type 1 diabetes case presentation

Type 1 Diabetes Mellitus Clinical Presentation

  • Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD  more...
  • Sections Type 1 Diabetes Mellitus
  • Practice Essentials
  • Pathophysiology
  • Epidemiology
  • Patient Education
  • Physical Examination
  • Complications
  • Laboratory Studies
  • Tests to Differentiate Type 1 from Type 2 Diabetes
  • Approach Considerations
  • Self-Monitoring of Glucose Levels
  • Continuous Glucose Monitoring
  • Insulin Therapy
  • Management of Hypoglycemia
  • Management of Hyperglycemia
  • Management of Complications
  • Glycemic Control During Serious Medical Illness and Surgery
  • Glycemic Control During Pregnancy
  • Consultations
  • Medication Summary
  • Antidiabetics, Insulins
  • Antidiabetics, Amylinomimetics
  • Hypoglycemia Antidotes
  • Monoclonal Antibodies
  • Allogeneic Islet Cells
  • Questions & Answers

The most common symptoms of type 1 diabetes mellitus (DM) are polyuria, polydipsia, and polyphagia, along with lassitude, nausea, and blurred vision, all of which result from the hyperglycemia itself.

Polyuria is caused by osmotic diuresis secondary to hyperglycemia. Severe nocturnal enuresis secondary to polyuria can be an indication of onset of diabetes in young children. Thirst is a response to the hyperosmolar state and dehydration.

Fatigue and weakness may be caused by muscle wasting from the catabolic state of insulin deficiency, hypovolemia, and hypokalemia. Muscle cramps are caused by electrolyte imbalance. Blurred vision results from the effect of the hyperosmolar state on the lens and vitreous humor. Glucose and its metabolites cause osmotic swelling of the lens, altering its normal focal length.

Symptoms at the time of the first clinical presentation can usually be traced back several days to several weeks. However, beta-cell destruction may have started months, or even years, before the onset of clinical symptoms.

The onset of symptomatic disease may be sudden. It is not unusual for patients with type 1 DM to present with diabetic ketoacidosis (DKA), which may occur de novo or secondary to the stress of illness or surgery. An explosive onset of symptoms in a young lean patient with ketoacidosis always has been considered diagnostic of type 1 DM.

Over time, patients with new-onset type 1 DM will lose weight, despite normal or increased appetite, because of depletion of water and a catabolic state with reduced glycogen, proteins, and triglycerides. Weight loss may not occur if treatment is initiated promptly after the onset of the disease.

Gastrointestinal (GI) symptoms of type 1 DM are as follows:

Nausea, abdominal discomfort or pain, and change in bowel movements may accompany acute DKA

Acute fatty liver may lead to distention of the hepatic capsule, causing right upper quadrant pain

Persistent abdominal pain may indicate another serious abdominal cause of DKA (eg, pancreatitis

Chronic GI symptoms in the later stage of DM are caused by visceral autonomic neuropathy

Neuropathy affects up to 50% of patients with type 1 DM, but symptomatic neuropathy is typically a late development, developing after many years of chronic prolonged hyperglycemia. Peripheral neuropathy presents as numbness and tingling in both hands and feet, in a glove-and-stocking pattern; it is bilateral, symmetric, and ascending.

History in patients with established diabetes

It is important to inquire about the type and duration of the patient’s diabetes and about the care the patient is receiving for diabetes. Determination of the type of diabetes is based on history, therapy, and clinical judgment. The chronic complications of diabetes are related to the length of time the patient has had the disease.

Ask about the type of insulin being used, delivery system (pump vs injections), dose, and frequency. Also ask about oral antidiabetic agents, if any. Of course, a full review of all medications and over-the-counter supplements being taken is crucial in the assessment of patients with type 1 DM.

Patients using a pump or a multiple-injection regimen have a basal insulin (taken through the pump or with the injection of a long-acting insulin analogue) and a premeal rapid-acting insulin, the dose of which may be determined as a function of the carbohydrate count plus the correction (to adjust for how high the premeal glucose level is). In these patients, ask about the following:

Basal rates (eg, units per hour by pump, generally 0.4-1.5 U/h, potentially varying on the basis of time of day); the total daily dose as basal insulin is a helpful value to know

Carbohydrate ratio (ie, units of insulin per grams of carbohydrate, generally 1 unit of rapid-acting insulin per 10-15 g carbohydrate)

Correction dose (ie, how far the blood glucose level is expected to decrease per unit of rapid-acting insulin, often 1 U of insulin per 50-mg/dL decrease, though individuals with insulin resistance may need 1 U per 25-mg/dL decrease)

Some patients may be taking premeal pramlintide (an amylin analogue)

A focused diabetes history should also include the following questions:

Is the patient’s diabetes generally well controlled, with near-normal blood glucose levels? (Patients with poorly controlled blood glucose levels heal more slowly and are at increased risk for infection and other complications)

Does the patient have severe hypoglycemic reactions? (If the patient has episodes of severe hypoglycemia and therefore is at risk for losing consciousness, this possibility must be addressed, especially if the patient drives)

Does the patient have diabetic nephropathy that might alter the use of medications or intravenous (IV) radiographic contrast material?

Does the patient have macrovascular disease, such as coronary artery disease (CAD), which should be considered in the emergency department (ED)?

Does the patient self-monitor his or her blood glucose levels? (Note the frequency and range of values at each time of day; an increasing number of patients monitor with continuous sensors)

When was the patient’s hemoglobin A 1c (HbA 1c ) value (an indicator of long-term glucose control) last measured? What was it?

In assessing glycemic exposure of a patient with established type 1 DM, review of self-monitored blood glucose levels is necessary. Ideally, this done by uploading time- and date-stamped levels from the patient’s meter to assure full understanding of the frequency of testing and the actual levels.

Questions regarding hypoglycemia and hyperglycemia

Hypoglycemia and hyperglycemia should be considered. Ask the following questions as needed:

Has the patient experienced recent polyuria, polydipsia, nocturia, or weight loss?

Has the patient had episodes of unexplained hypoglycemia? If so, when, how often, and how does the patient treat these episodes?

Does the patient have hypoglycemia unawareness (ie, does the patient lack the adrenergic warning signs of hypoglycemia)? (Hypoglycemia unawareness indicates an increased risk of subsequent episodes of hypoglycemia)

Questions regarding microvascular complications

Microvascular complications, such as retinopathy and nephropathy, should be considered as well. Ask the following questions as appropriate:

When was the patient’s last dilated eye examination? What were the results?

Does the patient have known kidney disease?

What were the dates and results of the last measurements of urine protein and serum creatinine levels?

Questions regarding macrovascular complications

Macrovascular complications should be explored. Questions should include the following:

Does the patient have hypertension? What medications are taken?

Does the patient have symptoms of claudication or a history of vascular bypass?

Has the patient had a stroke or transient ischemic attack?

What are the patient’s most recent lipid levels?

Is the patient taking lipid-lowering medication?

Questions regarding neuropathy

Potential neuropathy should be taken into account. Ask whether the patient has a history of neuropathy or symptoms of peripheral neuropathy or whether autonomic neuropathy is present (including erectile dysfunction if the patient is a man).

Other questions

The possibility of foot disease should be addressed. Inquire as to whether the patient has a history of foot ulcers or amputations or whether any foot ulcers are present. (See Diabetic Foot and Diabetic Foot Infections .)

The possibility of infection also should be considered. Be sure to inquire about whether frequent infections are a problem and, if so, at what sites.

In new cases of diabetes, physical examination findings are usually normal. Patients with DKA, however, will have Kussmaul respiration, signs of dehydration, hypotension, and, in some cases, altered mental status.

In established cases, patients should be examined every 3 months for macrovascular and microvascular complications. They should undergo funduscopic examination for retinopathy and monofilament testing for peripheral neuropathy.

Diabetes-focused examination

A diabetes-focused physical examination includes assessment of vital signs, funduscopic examination, limited vascular and neurologic examinations, and foot examination. Other organ systems should be assessed as indicated by the patient’s clinical situation. A comprehensive examination is not necessary at every visit.

Assessment of vital signs

Patients with established diabetes and autonomic neuropathy may have orthostatic hypotension. Orthostatic vital signs may be useful in assessing volume status and in suggesting the presence of an autonomic neuropathy. Measurement of the pulse is important, in that relative tachycardia is a typical finding in autonomic neuropathy, often preceding the development of orthostatic hypotension. If the respiratory rate and pattern suggest Kussmaul respiration, DKA must be considered immediately, and appropriate tests must be ordered.

Funduscopic examination

The funduscopic examination should include a careful view of the retina. Both the optic disc and the macula should be visualized. If hemorrhages or exudates are seen, the patient should be referred to an ophthalmologist as soon as possible. Examiners who are not ophthalmologists tend to underestimate the severity of retinopathy, which cannot be evaluated accurately unless the patients’ pupils are dilated.

Foot examination

The dorsalis pedis and posterior tibialis pulses should be palpated and their presence or absence noted. This is particularly important in patients who have foot infections: poor lower-extremity blood flow can delay healing and increase the risk of amputation.

Documenting lower-extremity sensory neuropathy is useful in patients who present with foot ulcers because decreased sensation limits the patient’s ability to protect the feet and ankles. If peripheral neuropathy is found, the patient should be made aware that foot care (including daily foot examination) is very important for the prevention of foot ulcers and lower-extremity amputation. (See Diabetic Foot and Diabetic Foot Infections .)

Infections cause considerable morbidity and mortality in patients with diabetes. Infection may precipitate metabolic derangements, and conversely, the metabolic derangements of diabetes may facilitate infection. (See Infections in Patients with Diabetes Mellitus .)

Patients with long-standing diabetes tend to have microvascular and macrovascular disease with resultant poor tissue perfusion and increased risk of infection. The ability of the skin to act as a barrier to infection may be compromised when the diminished sensation of diabetic neuropathy results in unnoticed injury.

Diabetes increases susceptibility to various types of infections. The most common sites are the skin and urinary tract. Dermatologic infections that occur with increased frequency in patients with diabetes include staphylococcal follicular skin infections, superficial fungal infections, cellulitis, erysipelas, and oral or genital candidal infections. Both lower urinary tract infections and acute pyelonephritis are seen with greater frequency.

A few infections, such as malignant otitis externa, rhinocerebral mucormycosis, and emphysematous pyelonephritis, occur almost exclusively in patients with diabetes, though they are fairly rare even in this population. Infections such as staphylococcal sepsis occur more frequently and are more often fatal in patients with diabetes than in others. Infections such as pneumococcal pneumonia affect patients with diabetes and other patients with the same frequency and severity. [ 84 ]

A study reported that out of 178 adult patients hospitalized with coronavirus disease 2019 (COVID-19), at least one underlying condition was found in 89.3%, the most common being hypertension (49.7%), obesity (48.3%), chronic lung disease (34.6%), diabetes mellitus (28.3%), and cardiovascular disease (27.8%). [ 85 ]

According to a report by Stokes et al, out of 287,320 US cases of COVID-19 in which the patient’s underlying health status was known, diabetes was the second most common underlying condition (30%), after cardiovascular disease (32%), which in this study included hypertension. [ 86 , 87 ]

The aforementioned study by Barrera et al found the overall prevalence of diabetes in patients with COVID-19 to be 12%, with the prevalence being 18% in severe COVID-19. [ 63 , 64 ]

In patients with type 1 DM who were diagnosed with COVID-19, a study by Ebekozien et al found that high blood glucose (48.5%), elevated temperature (45.5%), dry cough (39.4%), excess fatigue (33.3%), vomiting (33.3%), shortness of breath (30.3), nausea (30.2%), and body aches/headaches (21.2%) were the most prevalent presenting symptoms reported. Moreover, diabetic ketoacidosis was the most prevalent adverse outcome (45.5%) among these patients. [ 88 , 89 ]

The Centers for Disease Control and Prevention (CDC) includes type 2 DM in the list of conditions that increase the likelihood of severe illness in persons with COVID-19, and type 1 DM in the list of conditions that may increase this likelihood. [ 90 ]

Ophthalmologic complications

Diabetes can affect the lens, vitreous, and retina, causing visual symptoms that may prompt the patient to seek emergency care. Visual blurring may develop acutely as the lens changes shape with marked changes in blood glucose concentrations.

This effect, which is caused by osmotic fluxes of water into and out of the lens, usually occurs as hyperglycemia increases, but it also may be seen when high glucose levels are lowered rapidly. In either case, recovery to baseline visual acuity can take up to a month, and some patients are almost completely unable to read small print or do close work during this period.

Patients with diabetes tend to develop senile cataracts at a younger age than persons without diabetes. Rarely, patients with type 1 DM that is very poorly controlled (eg, those with frequent episodes of DKA) can acutely develop a “snowflake” (or “metabolic”) cataract. Named for their snowflake or flocculent appearance, these cataracts can progress rapidly and create total opacification of the lens within a few days.

Whether diabetes increases the risk of glaucoma remains controversial; epidemiologic studies have yielded conflicting results. [ 91 ] Glaucoma in diabetes relates to the neovascularization of the iris (ie, rubeosis iridis diabetica).

Diabetic retinopathy is the principal ophthalmologic complication of DM. (See Diabetic Retinopathy .) Diabetic retinopathy is the leading cause of blindness in the United States in people younger than 60 years and affects the eyes in the following different ways:

Background retinopathy involves retinal small vessel abnormality leading to hard exudates, hemorrhages, and microaneurysms; it does not affect acuity

Proliferative retinopathy involves extensive proliferation of new retinal small blood vessels; a sudden loss of vision can occur because of vitreous hemorrhage from proliferating new vessels or retinal detachment

Maculopathy involves edema and hard exudate or retinal ischemia; it causes a marked reduction of acuity

Whether patients develop diabetic retinopathy depends on the duration of their diabetes and on the level of glycemic control. [ 92 , 93 , 94 ] The following are the 5 stages in the progression of diabetic retinopathy:

Dilation of the retinal venules and formation of retinal capillary microaneurysms

Increased vascular permeability

Vascular occlusion and retinal ischemia

Proliferation of new blood vessels on the surface of the retina

Hemorrhage and contraction of the fibrovascular proliferation and the vitreous

The first 2 stages of diabetic retinopathy are jointly referred to as background or nonproliferative retinopathy. Initially, the retinal venules dilate, then microaneurysms (tiny red dots on the retina that cause no visual impairment) appear. The microaneurysms or retinal capillaries become more permeable, and hard exudates appear, reflecting leakage of plasma.

Rupture of intraretinal capillaries results in hemorrhage. If a superficial capillary ruptures, a flame-shaped hemorrhage appears. Hard exudates are often found in partial or complete rings (circinate pattern), which usually include multiple microaneurysms. These rings usually mark an area of edematous retina.

The patient may not notice a change in visual acuity unless the center of the macula is involved. Macular edema can cause visual loss; therefore, all patients with suspected macular edema must be referred to an ophthalmologist for evaluation and possible laser therapy. Laser therapy is effective in decreasing macular edema and preserving vision but is less effective in restoring lost vision. (See Macular Edema in Diabetes .)

Preproliferative (stage 3) and proliferative diabetic retinopathy (stages 4 and 5) are the next phases in the progression of the disease. Cotton-wool spots can be seen in preproliferative retinopathy. These represent retinal microinfarcts from capillary occlusion and appear as off-white to gray patches with poorly defined margins.

Proliferative retinopathy is characterized by neovascularization, or the development of networks of fragile new vessels that often are seen on the optic disc or along the main vascular arcades. The vessels undergo cycles of proliferation and regression. During proliferation, fibrous adhesions develop between the vessels and the vitreous. Subsequent contraction of the adhesions can result in traction on the retina and retinal detachment. Contraction also tears the new vessels, which hemorrhage into the vitreous.

Diabetic nephropathy

About 20–30% of patients with type 1 DM develop evidence of nephropathy, [ 95 ] and all patients with diabetes should be considered to have the potential for renal impairment unless proven otherwise. Chronically elevated blood pressure contributes to the decline in renal function. The use of contrast media can precipitate acute renal failure in patients with underlying diabetic nephropathy. Although most recover from contrast medium–induced renal failure within 10 days, some have irreversible renal failure. (See Diabetic Nephropathy .)

Diabetic neuropathy

In the peripheral nerves, diabetes causes peripheral neuropathy. (See Diabetic Lumbosacral Plexopathy and Diabetic Neuropathy .) The 4 types of diabetic neuropathy are as follows:

Peripheral distal symmetrical polyneuropathy, predominantly sensory

Autonomic neuropathy

Proximal painful motor neuropathy

Cranial mononeuropathy (ie, cranial nerve III, IV, or VI)

Of these 4 types, distal symmetric sensorimotor polyneuropathy (in a glove-and-stocking distribution) is the most common. [ 96 ] Besides causing pain in its early stages, this type of neuropathy eventually results in the loss of peripheral sensation. The combination of decreased sensation and peripheral arterial insufficiency often leads to foot ulceration and eventual amputation.

Acute-onset mononeuropathies in diabetes include acute cranial mononeuropathies, mononeuropathy multiplex, focal lesions of the brachial or lumbosacral plexus, and radiculopathies. Of the cranial neuropathies, the third cranial nerve (oculomotor) is most commonly affected, followed by the sixth nerve (abducens) and the fourth nerve (trochlear).

Patients can present with diplopia and eye pain. In diabetic third-nerve palsy, the pupil is usually spared, whereas in third-nerve palsy due to intracranial aneurysm or tumor, the pupil is affected in 80-90% of cases.

It is important to consider nondiabetic causes of cranial nerve palsies, including intracranial tumors, aneurysms, and brainstem stroke. [ 97 ] Therefore, evaluation should include nonenhanced and contrast-enhanced compute4d tomography (CT) or, preferably, magnetic resonance imaging (MRI). Neurologic consultation is recommended. Acute cranial-nerve mononeuropathies usually resolve in 2-9 months. Acute thrombosis or ischemia of the blood vessels supplying the structure involved is thought to cause these neuropathies.

Macrovascular complications

People with diabetes experience accelerated atherosclerosis, affecting the small arteries of the heart, brain, lower extremity, and kidney. Coronary atherosclerosis often occurs at a younger age and is more severe and extensive than in those without diabetes, increasing the risk of ischemic heart disease. Atherosclerosis of the internal carotid and vertebrobasilar arteries and their branches predisposes to cerebral ischemia.

Severe atherosclerosis of the iliofemoral and smaller arteries of the lower legs predisposes to gangrene. Ischemia of a single toe or ischemic areas on the heel are characteristic of diabetic peripheral vascular disease; these result from the involvement of much smaller and more peripheral arteries.

Atherosclerosis of the main renal arteries and their intrarenal branches causes chronic nephron ischemia, which is a significant component of multiple renal lesions in diabetes. However, not all people with type 1 DM are at risk for nephropathy, because there are some polymorphisms in the various factors involved in its pathogenesis, which can modulate the course of this disease from one person to the other.

Risk factors for macrovascular disease

Macrovascular disease is the leading cause of death in patients with diabetes, causing 65-75% of deaths in this group, compared with approximately 35% of deaths in people without diabetes. Diabetes by itself increases the risk of myocardial infarction (MI) 2-fold in men and 4-fold in women, and many patients have other risk factors for MI as well.

The HbA1c value per se, rather than self-reported diabetes status or other established risk factors, robustly predicts MI odds. Each 1% increment in HbA1c independently predicts 19% higher odds for MI. [ 98 ] The risk of stroke in people with diabetes is double that of nondiabetic people, and the risk of peripheral vascular disease is 4 times that of people without diabetes.

Patients with diabetes may have an increased incidence of silent ischemia. [ 99 ] Diastolic dysfunction is common in patients with diabetes and should be considered in patients who have symptoms of congestive heart failure and a normal ejection fraction.

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Effects of insulin in relatives of patients with type 1 diabetes mellitus. N Engl J Med . 2002 May 30. 346(22):1685-91. [QxMD MEDLINE Link] .

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Herold KC, Bundy BN, Long SA, and the, Type 1 Diabetes TrialNet Study Group. An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes. N Engl J Med . 2019 Aug 15. 381 (7):603-13. [QxMD MEDLINE Link] . [Full Text] .

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Lei J, Coronel MM, Yolcu ES, et al. FasL microgels induce immune acceptance of islet allografts in nonhuman primates. Sci Adv . 2022 May 13. 8 (19):eabm9881. [QxMD MEDLINE Link] . [Full Text] .

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US Food and Drug Administration. FDA authorizes first interoperable, automated insulin dosing controller designed to allow more choices for patients looking to customize their individual diabetes management device system. Available at https://www.fda.gov/news-events/press-announcements/fda-authorizes-first-interoperable-automated-insulin-dosing-controller-designed-allow-more-choices?fbclid=IwAR3TSBssEd4n6b9hR5oe9Bzwmz3su1yQny8bcQeHVi0WFSsvURBh3nPjR-Y . December 13, 2019; Accessed: December 1, 2020.

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Hsiao-Chuan L, et al. Enterovirus infection is associated with an increased risk of childhood type 1 diabetes in Taiwan: A nationwide population-based cohort study. Diabetologia . 2014. [Full Text] .

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Contributor Information and Disclosures

Romesh Khardori, MD, PhD, FACP (Retired) Professor, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Eastern Virginia Medical School Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinology , American College of Physicians , American Diabetes Association , Endocrine Society Disclosure: Nothing to disclose.

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine George T Griffing, MD is a member of the following medical societies: American Association for Physician Leadership , American Association for the Advancement of Science , American College of Medical Practice Executives , American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Heart Association , Central Society for Clinical and Translational Research , Endocrine Society , International Society for Clinical Densitometry , Southern Society for Clinical Investigation Disclosure: Nothing to disclose.

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha , American Academy of Emergency Medicine , American College of Chest Physicians , American College of Emergency Physicians , American College of Physicians , American Heart Association , American Thoracic Society , Arkansas Medical Society , New York Academy of Medicine , New York Academy ofSciences ,and Society for Academic Emergency Medicine

Aneela Naureen Hussain, MD, FAAFM Assistant Professor, Department of Family Medicine, State University of New York Downstate Medical Center; Consulting Staff, Department of Family Medicine, University Hospital of Brooklyn

Aneela Naureen Hussain, MD, FAAFM is a member of the following medical societies: American Academy of Family Physicians , American Medical Association , American Medical Women's Association , Medical Society of the State of New York , and Society of Teachers of Family Medicine

Anne L Peters, MD, CDE Director of Clinical Diabetes Programs, Professor, Department of Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, Los Angeles County/University of Southern California Medical Center

Anne L Peters, MD, CDE is a member of the following medical societies: American College of Physicians and American Diabetes Association

Disclosure: Amylin Honoraria Speaking and teaching; AstraZeneca Consulting fee Consulting; Lilly Consulting fee Consulting; Takeda Consulting fee Consulting; Bristol Myers Squibb Honoraria Speaking and teaching; NovoNordisk Consulting fee Consulting; Medtronic Minimed Consulting fee Consulting; Dexcom Honoraria Speaking and teaching; Roche Honoraria Speaking and teaching

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association , American Federation for Medical Research , Central Society for Clinical Research , and Endocrine Society

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Miriam T Vincent, MD, PhD Professor and Chair, Department of Family Practice, State University of New York Downstate Medical Center

Miriam T Vincent, MD, PhD is a member of the following medical societies: Alpha Omega Alpha , American Academy of Family Physicians , American Association for the Advancement of Science , Medical Society of the State of New York , North American Primary Care Research Group , Sigma Xi , and Society of Teachers of Family Medicine

Disclosure: Joslin Diabetes Group, Harvard Honoraria Speaking and teaching

Scott R Votey, MD Director of Emergency Medicine Residency, Ronald Reagan UCLA Medical Center; Professor of Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine

Scott R Votey, MD is a member of the following medical societies: Society for Academic Emergency Medicine

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists , American College of Endocrinology , American College of Physicians , American College of Physicians-American Society of Internal Medicine , American Diabetes Association , American Federation for Medical Research , American Medical Association , American Society for Bone and Mineral Research , California Medical Association , Endocrine Society , andInternational Society for Clinical Densitometry

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type 1 diabetes case presentation

Faculty and Disclosures

Zachary t bloomgarden, md.

Associate Clinical Professor of Medicine, Mount Sinai Medical School, New York, NY

Disclosure: Zachary T. Bloomgarden, MD, has disclosed that he receives research grant support from Hoechst Marion Roussel, Novartis, and TCPI Inc. He has consulting agreements with Hoechst Marion Roussel, Novartis, Parke-Davis, Bristol-Myers Squibb Company, Novo Nordisk, Pfizer Inc., Eli Lilly and Company, Takeda, and GlaxoSmithKline.

type 1 diabetes case presentation

Case Study 1: Patient with Newly Diagnosed Type 1 Diabetes

  • Authors: Author: Zachary T. Bloomgarden, MD
  • THIS ACTIVITY HAS EXPIRED FOR CREDIT

Target Audience and Goal Statement

This activity is intended for physicians and pharmacists.

This article reviews the physiologic consequences of diabetes mellitus and presents evidence that supports the benefits of aggressive intervention to achieve glycemic control. Real-life clinical scenarios will be presented to illustrate the practical clinical applications of insulin preparations in patients with diabetes.

  • Describe the physiologic consequences of diabetes mellitus.
  • Outline the importance of maintaining glycemic control in reducing the risk of diabetic complications.
  • Detail specific clinical applications of insulin therapy to achieve both basal and meal-related glycemic control.
  • Manage a patient's glycemic status by continuously refining the therapeutic approach.

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Case 1 History

Results of hospital laboratory studies (Table 1-1) revealed that the patient's initial blood glucose level was 1192 mg/dL and clinical presentation and laboratory findings were consistent with a diagnosis of diabetic ketoacidosis (DKA). The patient reported no family history of diabetes. His father died at age 35 of renal failure.

The patient was treated successfully for DKA and discharged from the hospital 3 days later on an insulin regimen consisting of 30 units of NPH/regular human insulin 70/30 mixture (70/30 mix) before breakfast, 15 units of regular human insulin before dinner, and 20 units of NPH insulin at bedtime.

On discharge, he was instructed to perform blood glucose measurements 4 times a day. The patient was seen as an outpatient 4 days after he is discharged from hospital.

Table 1-1. Hospital Laboratory Studies

2 AM 4 AM 5 AM 9 AM 11 AM 1 PM Plasma Glucose mg/dL 1192 958 718 358 288 222 Sodium mEq/L 154 -- 158 167 -- 161 Potassium mEq/L -- -- 3.3 4.0 -- 3.5 Creatinine (mg/dL) 1.7 1.6 -- -- 0.9 -- pH 7.34 -- -- -- -- -- Urine Acetone -- -- -- 2+ -- --

This patient presented to the emergency department with acute-onset diabetes with classic symptoms of insulin deficiency compatible with a diagnosis of type 1 diabetes. Approximately 25% of patients that present with DKA have new onset of type 1 diabetes. Antibody testing was not performed, presumably because of the typical type 1 presentation. During his hospital stay, the patient received instructions regarding diet, medication schedule, and home glucose monitoring.

The patient was discharged on an insulin regimen designed for ease of administration, consisting of a premixed 70/30 mix before breakfast. The evening insulin regimen included regular insulin before dinner and NPH at bedtime. Because the peak action of NPH is expected approximately 8-10 hours following administration, giving the evening dose of NPH at bedtime rather than before dinner avoids the nocturnal (2-3 AM) hypoglycemia that is often associated with dinnertime NPH administration.

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Nursing Case Study for Type 1 Diabetes

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Michael is a 14-year-old male brought into a small ER by his mother. They were driving a long distance after he competed in a wrestling tournament. He had not felt well on the bus ride with the team so his mother decided he should ride with her. His mother denies a history of chronic illness but did say he had “like a cold but with a stomachache” about 3 months ago.

She also says that he has been very thirsty, and they had to stop several times for him to urinate. She is also worried because he almost missed his wrestling “weight class” parameters because he was significantly lighter this past weekend than he has been in the past. And that is even with him eating more than usual.

What symptoms are most worrisome to the triage nurse?

  • He has 2 of the 3 “p’s” – polydipsia (thirst), polyuria (frequent urination), polyphagia (hunger) which are trademarks of diabetes mellitus (DM) and/or diabetic ketoacidosis (DKA). They happen in response to the body lacking insulin and its response is to try to achieve homeostasis with these mechanisms. His weight loss could be indicative of DM as well. 
  • They describe a recent viral-like illness which may precipitate a diagnosis of DM (it is thought the body has an inappropriate immune response to the illness leading to DM)

In triage, the nurse obtains a point-of-care blood glucose (BG) level and the machine gives no value. Instead, an error message indicating “hi” displays on the machine.

Why did the nurse do this test? What should they do next?

  • Clues point to possible DM or DKA. Getting a BG immediately can help guide care. Always follow the facility protocol/procedure on “hi” or “lo” (often spelled this way on glucometers) readings. The protocol might dictate (standing order) stat venous draw and send it to the lab. It may be advised to try again on a different machine with a new sample. Whatever the guidance, a BG level is imperative for this patient.

Michael is AAO x 4. He complains of a “stomachache” and reports he has nausea and experienced vomiting shortly before arrival. His skin is warm and dry, but his face is flushed. When asked about pain, he says he has a headache, and his vision is blurry. The nurse notices a fruity odor on his breath when obtaining vital signs. 

BP 90/54 mmHg SpO 2 98% on Room Air

HR 122 bpm and regular

RR 26 bpm at rest

The patient and his mother are placed into an exam room immediately and the triage nurse verbally reports this to the accepting nurse.

How does the nurse interpret these symptoms?

  • Michael’s symptoms are consistent with hyperglycemia (link here to cheatsheet?) DKA

What orders does the accepting nurse anticipate?

  • Labs, ABGs, urinalysis, IV access (bilateral upper extremities, largest possible in case patient deteriorates). One lab, in particular, can give the provider an idea of the last 2-3 month BG average, the hemoglobin A1C.

The provider orders stat labs, urinalysis and ABGs then examines the patient. 

Why stat orders?

  • This patient’s condition could deteriorate rapidly, and treatment should begin ASAP. Labs are needed to guide the plan of care. The nurse should watch for changes in the level of consciousness, respiratory changes, his response to potential fluid & electrolyte imbalances. Place on continuous cardiac monitoring as well.

Lab results are as follows:

WBC 15000 cells/mcL

Glucose 420 mg/dl

BUN 21 mg/dl

Creatinine 0.77 mg/dl

Anion gap 12

Glucose positive

Ketones positive

What do these results mean?

  • CBC WBC 15000 cells/mcL – an immune response, possibly to viral illness or another issue HgbA1C 9% – indicates the average BG over the past 2-3 months has been about 212mg/dLBMP Glucose 420 mg/dl – hyperglycemia K 5.8 – electrolyte imbalance, can cause cardiac changes and need to monitor closely if IV insulin is started (will need frequent checks of this and BG) BUN 21 mg/dL – fluid imbalance Creatinine 0.77 mg/dL – normal but necessary to check for kidney function Anion gap 12 – indicative of DKAABG – metabolic acidosis Ph 7.25 HCO3 15 PaCo2 35 PaO2 88Urine – indicative of DKA Glucose positive Ketones positive

What medication orders should the nurse anticipate?

  • IV fluids, insulin (either IV or SQ). NOTE: only REGULAR INSULIN can be given IV, and if it is, then IV dextrose and potassium chloride should be included in the insulin IV titration protocol/order). SQ insulin may be ordered using a sliding scale. O2 via NC possibly due to potential respiratory concerns (Kussmaul respirations)

The provider tells Michael and his mother that he suspects diabetic ketoacidosis which is not uncommon for new type I diabetics. He plans to transfer Michael to a nearby city via helicopter for a higher level of care.  The patient’s mother asks why he has to be transferred.

How does the nurse explain the transfer to the mother and patient?

  • DKA requires monitoring in a critical care unit. Because of his age and new-onset DM, a higher level of care is recommended in order to have access to the best resources

The flight team arrives and assesses the patient. The ER completes a report using SBAR format at the bedside. The patient and his mother are given the chance to ask questions.

What are the transport team’s priorities as they move this patient?

  • Airway, breathing, and circulation (ABC) status; Mental status; Volume status.

Upon arrival to the higher level of care, Michael is admitted to the ICU overnight. By the morning he is transferred to a pediatric floor for further observation. His mother remains at his bedside. They plan to return to their home after discharge. 

How should the pediatric medical unit prepare this family for discharge? What specific teaching should be provided?

  • Condition-specific education is vital including DM management with medications, exercise, nutrition, psychosocial concerns, preventative care (i.e. vaccinations), parental/family involvement. A specialized diabetic educator and/or dietician would be ideal. Assessing their education preferences and literacy level is important as well. How to give insulin injections and check BG (glucometer use) are key takeaways (have patient and parent return-demonstrate). Case management may need to get involved for prescription/supplies. An endocrinologist may be consulted so education about his specialist is also important.

References:

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Nursing case studies.

Jon Haws

This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

Cardiac nursing case studies.

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Mental health nursing case studies.

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A case report: First presentation of diabetes mellitus type 1 with severe hyperosmolar hyperglycemic state in a 35-month-old girl

Affiliations.

  • 1 Division of Pediatric Intensive Care Department of Pediatrics Shiraz University of Medical Sciences Shiraz Iran.
  • 2 Division of Pediatric Metabolism and Endocrinology Department of Pediatrics Shiraz University of Medical Sciences Shiraz Iran.
  • PMID: 34765201
  • PMCID: PMC8572339
  • DOI: 10.1002/ccr3.4984

Hyperglycemic hyperosmolar syndrome (HHS) is a rare complication of diabetes mellitus among pediatric patients. Since its treatment differs from diabetic ketoacidosis (DKA), hence, pediatricians should be aware of its diagnosis and management.

Keywords: case report; diabetes mellitus; hyperglycemic hyperosmolar syndrome (HHS); pediatric patients; rhabdomyolysis; thrombosis.

© 2021 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.

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Conflict of interest statement

The authors declare that they have no competing interests.

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  • Pediatric Diabetic Ketoacidosis With Hyperosmolarity: Clinical Characteristics and Outcomes. Agrawal S, Baird GL, Quintos JB, Reinert SE, Gopalakrishnan G, Boney CM, Topor LS. Agrawal S, et al. Endocr Pract. 2018 Aug;24(8):726-732. doi: 10.4158/EP-2018-0120. Epub 2018 Aug 7. Endocr Pract. 2018. PMID: 30084686
  • A Rare Presentation of New-Onset Type 1 Diabetes Mellitus in a Developmentally Delayed Child With an Overlap of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. Parra Villasmil MG, Patel S, Tansey M, Badheka A, Chegondi M. Parra Villasmil MG, et al. Cureus. 2022 Sep 9;14(9):e28983. doi: 10.7759/cureus.28983. eCollection 2022 Sep. Cureus. 2022. PMID: 36237743 Free PMC article.
  • Combined diabetic ketoacidosis and hyperosmolar hyperglycemic state in type 1 diabetes mellitus induced by immune checkpoint inhibitors: Underrecognized and underreported emergency in ICIs-DM. Zhang W, Chen J, Bi J, Ding N, Chen X, Wang Z, Jiao Y. Zhang W, et al. Front Endocrinol (Lausanne). 2023 Jan 4;13:1084441. doi: 10.3389/fendo.2022.1084441. eCollection 2022. Front Endocrinol (Lausanne). 2023. PMID: 36686495 Free PMC article. Review.
  • Severe hypernatremia in soft drink ketoacidosis and hyperglycemic hyperosmolar state at the onset of type 2 diabetes mellitus: a case series of three adolescents. Choo SJ, Lee HG, Kim CJ, Yang EM. Choo SJ, et al. Clin Pediatr Endocrinol. 2022;31(2):81-86. doi: 10.1297/cpe.2021-0075. Epub 2022 Feb 16. Clin Pediatr Endocrinol. 2022. PMID: 35431447 Free PMC article.
  • Treatment of Diabetic Ketoacidosis (DKA)/Hyperglycemic Hyperosmolar State (HHS): Novel Advances in the Management of Hyperglycemic Crises (UK Versus USA). Dhatariya KK, Vellanki P. Dhatariya KK, et al. Curr Diab Rep. 2017 May;17(5):33. doi: 10.1007/s11892-017-0857-4. Curr Diab Rep. 2017. PMID: 28364357 Free PMC article. Review.
  • Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. 2018;19(Suppl 27):155‐177. 10.1111/pedi.12701 - DOI - PubMed
  • Zeitler P, Haqq A, Rosenbloom A, Glaser N, Drugs and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society . Hyperglycemic hyperosmolar syndrome in children: pathophysiological considerations and suggested guidelines for treatment. J Pediatr. 2011;158(1):9‐14.e142. 10.1016/j.jpeds.2010.09.048 - DOI - PubMed
  • Klingensmith GJ, Connor CG, Ruedy KJ, et al. Presentation of youth with type 2 diabetes in the Pediatric Diabetes Consortium. Pediatr Diabetes. 2016;17(4):266‐273. 10.1111/pedi.122814 - DOI - PubMed
  • Agrawal S, Baird GL, Quintos JB, et al. Pediatric diabetic ketoacidosis with hyperosmolarity: clinical characteristics and outcomes. Endocr Pract. 2018;24(8):726‐732. 10.4158/EP-2018-0120 - DOI - PubMed
  • Rosenbloom AL. Hyperglycemic hyperosmolar state: an emerging pediatric problem. J Pediatr. 2010;156(2):180‐184. 10.1016/j.jpeds.2009.11.057 - DOI - PubMed

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An atypical presentation of type 1 diabetes

Brandon w. knopp.

1 Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA

Parvathi Perumareddi

2 Department of Integrated Medical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA

Type 1 and type 2 diabetes have been described historically as occurring in distinct patient populations; however, atypical demographics are becoming more frequent as the prevalence of diabetes increases, crossing boundaries of ages. Some of these cases can be challenging to diagnose clinically as the patient symptomatology and progression can differ from the standard features of type 1 and 2 diabetes. Our case is an example of a patient whose type 1 diabetes presented atypically with characteristics often associated with type 2 diabetes. Patient presentations such as this are uncommon, with our patient having presented with the “textbook” characteristics of type 2 diabetes. When first diagnosed with diabetes mellitus type 2, the patient was 60 years old, had a BMI around 30 and experienced a gradual onset of symptoms over the course of several months. At the age of 64, the patient tested positive for GAD65 autoantibodies following a year of declining glycemic control and was re-evaluated and classified as a type 1 diabetes patient. Subsequent insulin injections resolved his diabetes-related complications which included polyuria, weakness and weight loss and improved his glycemic control. This case provides an example of an unusual clinical presentation of type 1 diabetes and serves to raise awareness for atypical presentations of diabetes to improve accurate classifications at earlier stages.

Introduction

Diabetes mellitus is a metabolic disease characterized by insulin deficiency and/or insulin resistance. Type 1 diabetes results from the autoimmune destruction of pancreatic β cells and is typically found in younger patients while type 2 diabetes occurs due to insulin resistance and is most often found in middle aged to older adults. Each type has been associated with a distinct patient population, however, there are reports of cases with atypical demographics characterized by a crossover in age, weight and other factors [ 1 , 2 ].

These rare cases are difficult to identify clinically and may require antibody testing to confirm the diagnosis. The incidence of atypical presentations of diabetes mellitus is unknown, however, with the rise in diabetes cases over the past several decades and an expected increase of 54% between 2015 and 2030 [ 3 ], a concomitant increase in atypical cases can be reasonably expected.

Case report

This case describes a 64-year-old Caucasian male who was referred for evaluation and treatment of diabetes mellitus which was first diagnosed at the age of 60. At the age of 60 he presented with minimal clinical signs of diabetes mellitus, including mild fatigue, and was diagnosed with type 2 diabetes due to hyperglycemia and elevated HbA1c. He was treated as a type 2 diabetes patient for four years before being placed on insulin at the age of 64 following a significant deterioration in glycemic control. He had no known risk factors for diabetes mellitus and was screened with self-monitoring of blood glucose (SMBG). His past medical history was significant for elevated thyroid stimulating hormone (TSH), but otherwise no significant abnormalities.

Clinical Progression

On 10/28/2020, the patient presented with a multi-day history of polyuria and weakness with deterioration since his previous visit on 7/3/20. Following a weight loss of 5.4 kg during the previous several days, the patient weighed 84.4 kg with a BMI of 29.1. He rarely checked his blood glucose but measured a value of almost 500 mg/dL at home during this time and a value of close to 400 mg/dL in office. On a physical exam, the patient did not appear weak or ill and reported no changes in vision or neurologic symptoms. He reported consistency in taking metformin and glimepiride, with sertraline being added a few months prior. Because of the significant hyperglycemia and concerns of potential diabetic ketoacidosis, he was injected with 20 units of insulin degludec, given 5 units of insulin lispro with instructions for later use and asked to drink 5 cups of water while in office. ( Note : treatments vary among providers)

At his follow up on 11/5/2020, he improved with no significant incidences of hyperglycemia, though he experienced blood sugar spikes after breakfast. Along with dietary interventions to mitigate post-breakfast spikes, Insulin degludec increased to 23 units daily and 5 units of insulin lispro with meals. Metformin and Glimepiride were discontinued.

During his visit on 3/29/2021, the patient stated his diabetes was not well-controlled and had variable glucose ranges with hypoglycemia typically occurring before dinnertime. He had a temperature of 36.4 o C, weight of 90.7 kg, height of 171.5 cm and BMI of 30.86. The physical exam findings were normal with no foot ulcers or other visible abnormalities. He also had an intact sensory exam. The patient had a recent c-peptide of 0.5 ng/mL on 12/24/2020 and an HbA1c of 7.4% (normal 4.2–5.7%).

During his visit on 5/17/2021, the patient stated his diabetes was well-controlled. He used an insulin pump and continuous glucose monitoring (CGM) sensor between 5/4/2021 and 5/17/2021. Between those dates, his blood glucose was 88% in range with no significant hypoglycemia since beginning insulin pump use. He gained 3.6 kg since 3/29/2021 with no new development of diabetes-related symptoms. Table 1 presents the most important laboratory parameters.

Select laboratory results

Insulin Growth Factor 1255 ng/mL (high)Normal: 46-219 ng/mL
Fibrinogen530 mg/dL (high)Normal: 276-471 mg/dL
Urea nitrogen25 mg/dL (high)Normal: 6-23 mg/dL
Creatinine1.1 mg/dlNormal: 0.7–1.3 mg/dl

Diagnosis and outcome

The patient tested positive for a concentration of 16 IU/mL of GAD 65 autoantibodies on 3/29/2021, indicating a diagnosis of type 1 diabetes. Likewise, he tested positive for Thyroid Peroxidase antibodies (TPO) at 499 IU/mL, confirming his diagnosis of autoimmune thyroid disease, Hashimoto thyroiditis in this case.

As indicated on Table 2 , the patient’s HbA1c levels rose from 9.1% to 13.5% in about 9 months before being treated with insulin in November 2020. While taking insulin in the form of insulin lispro and insulin degludec, his HbA1c levels dropped from 13.5% to 7.4% in under 4 months. Based on the continuous glucose monitoring (CGM) values between 5/4/21 and 5/17/21, the Glucose Management Indicator (GMI) predicted an HbA1c of 6.4% just 7 months after the first insulin injection. Likewise, his glycemic control improved with a blood glucose 88% in range with no significant lows as of 5/17/21.

HbA1c level evolution

DateHbA1c
1/13/209.1%
7/3/2010.4%
10/29/2013.5%
12/24/208.8%
2/18/217.4%
5/4/21-5/17/21 Expected HbA1c (GMI) = 6.4%

Discussions

Type 1 and 2 diabetes have clinically distinct pathophysiologic etiologies. These discrete pathologies lead to unique presentations for each type and are useful in informing clinical diagnostic practices as well as treatment regimens. The clinical determination of type 1 vs. 2 diabetes is made with consideration of factors including the patient’s age, body composition, symptom progression and clinical presentation. Type 1 diabetes typically manifests in young patients, often before the age of 14, who frequently appear thin and have a sudden onset of symptoms, with diabetic ketoacidosis presenting as the first sign of disease in many cases. Type 2 diabetes, on the other hand, often develops around the age of 45 or later and is associated with obesity and metabolic syndrome and usually has a gradual onset.

As both types of diabetes generally have distinct etiologies, diagnosis can often be made based on patient demographics. However, atypical cases can exist in contravention of diagnostic norms. The case detailed above discusses one such patient whose clinical characteristics and progression matched closely with the criteria for type 2 diabetes, even though his pathophysiology pointed to type 1 diabetes. While his initial diagnosis of type 2 diabetes was made based on his clinical characteristics, antibody tests significant for glutamic acid decarboxylase 65 autoantibody (GAD 65 ) confirmed his diagnosis with type 1 diabetes [ 3 ]. While rare, similar atypical cases of diabetes have been reported [ 1 , 2 ]. With the increasing number of diabetes cases expected in the coming years [ 4 ], unusual cases such as the case presented above may become more common. To ensure timely and accurate diagnosis and management of patients with atypical cases of diabetes, we seek to raise awareness of cases which do not adhere to presentational or diagnostic norms.

Key Messages

  • It is known that atypical cases of diabetes exist and can complicate the diagnosis of diabetes mellitus.
  • This manuscript provides evidence that atypical cases can present with symptoms typically associated with another type of diabetes.
  • The case described is an example of a type 1 diabetes patient presenting with several classic features of type 2 diabetes.

Conflicts of interest

There are no personal, financial, or other conflicts of interest to disclose.

Consent for publication

Written informed consent from the patient has been taken and is available for review by Editor in chief of the journal.

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Our rationale for choosing this condition:

Throughout our clinical experiences, previous careers, and personal lives, diabetes has been prevalent. As practitioners, we will continue to see this condition often and have to recognize/treat it in our patients. In light of this, we wanted to have a good understanding of Type 1 diabetes, its presentation, and its treatment.


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CASE PRESENTATION ON DIABETES MELLITUS

This document presents a case study of a 75-year-old patient with diabetes mellitus, chronic asthma, and heart failure. The patient's current medications were interacting and not well-controlled. The presenting doctor assessed the patient and created a new treatment plan including Dapagliflozin, insulin glargine, pantoprazole, salbutamol, beclomethasone, prednisolone, and ibuprofen. The doctor also provided counseling to the patient on lifestyle modifications, medication adherence, and monitoring of blood sugar, heart rate, and response to the new treatment plan. Read less

type 1 diabetes case presentation

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  • 1. CASE PRESENTATION ON DIABETES MELLITUS BY MS. VARSHA R WADNERE (PD539)
  • 2. INTRODUCTION A disease in which the body’s ability to produce or respond to the hormone insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood. Sign and symptoms- Excessive Thirst, Frequent Urination, Ongoing Fatigue, Delayed Healing, Vision Problems, Mood Swings, Numbness and Tingling in Extremities, Food Cravings. Types- • Type I Diabetes Mellitus • Type II Diabetes Mellitus Risk Factors- • Obesity • Poor diet stress • Family history of DM • High BP
  • 3. SUBJECTIVE DATA Name- xyzzy, age- 75 years C/O- Feeling unwell and lethargic, breathlessness at night and kept awake, pain in knee OBJECTIVE DATA • Glycosuria • Last two glycosylated hemoglobin- 11.3% and 12.0% ( less than 5.7 and more than 6.5 indicates diabetes mellitus) Personal data- Lives alone and has poor eyesight
  • 4. TREATMENT CHART Current medication for chronic asthma , heart failure, and knee pain is- 1. BENDROFLUMETHIAZIDE 10MG EACH MORNING 2. PREDNISOLONE 20MG DAILY 3. SALBUTAMOL INHALER 2 PUFFS- 6 HOURLY 4. BECLOMETHASONE INHALER 2 PUFFS- 6 HOURLY 5. MAGNESIUM TRISILICATE 10 ML S.O.S 6. GLIPIZIDE 15MG Q8H 7. METFORMIN 850MG 3 TIMES DAILY 8. NAPROXEN 750MG QH • Patient was on non insulin dependent DM treatment(since 15 years) now doctor has advised insulin therapy.
  • 5. ASSESSMENT • Diagnosis- diabetes mellitus, chronic asthma, heart failure
  • 6. INTERVENTION • PREDNISOLONE INTERACT WITH MAGNESIUM TRISILICATE • BENDROFLUMETHIAZIDE INTERACT WITH PREDNISOLINE, SALBUTAMOL, GLIPIZIDE • GLIPIZIDE INTERACT WITH METFORMIN INDICATION- THIS THERAPY NEEDED TO BE MONITORED
  • 7. MY PLAN 1. DAPAGLIFLOZIN- 5MG- 1-0-0 2. INSULIN GLARGINE- 0.2MG/KG- 0-0-1 3. PANTOPRAZOLE -40 MG 1-0-0 4. SALBUTAMOL- INHALER- 2 PUFFS- 6 HOURLY 5. BECLOMETHASONE- INHALER- 2 PUFFS- 6 HOURLY 6. PREDNISOLONE- 20MG- DAILY- 1-0-0 7. IBUPROFEN- 400MG- 0-1-0
  • 8. MONITORING PARAMETERS • BLOOD SUGAR LEVEL • HEART RATE • PATIENT RESPONSE TO THERAPY (ACCORDING TO MY PLAN) • MONITOR RESPONSE OF CURRENT THERAPY
  • 9. PATIENT COUNSELLING On drugs- • Do not repeat the dose if missed • Take medication on time On disease- • Drink jamun and karela juice • Drink sabza soaked in water
  • 10. PATIENT COUNSELLING Lifestyle modification- • Drink jamun and karela juice. • Drink sabza soaked in water. • Consume healthy fats- almond, tuna, salmon, walnuts, flax seeds. • Have a balanced diet. • consume 8 glasses of water. • Consume seasonal and local fruits and vegetables. • Take a walk after dinner.
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  • Diabetes & Primary Care

Interactive case study: MODY – a strong family history of diabetes

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type 1 diabetes case presentation

Diabetes & Primary Care ’s series of interactive case studies is aimed at all healthcare professionals in primary and community care who would like to broaden their understanding of diabetes.

These two scenarios review the most common subtypes of maturity-onset diabetes of the young (MODY), signs and symptoms, differential diagnosis and management.

The format uses typical clinical scenarios as tools for learning. Information is provided in short sections, with most ending in a question to answer before moving on to the next section.

Working through the case studies will improve our knowledge and problem-solving skills in diabetes care by encouraging us to make evidence-based decisions in the context of individual cases.

Readers are invited to respond to the questions by typing in their answers. In this way, we are actively involved in the learning process, which is hopefully a much more effective way to learn.

By actively engaging with these case histories, readers will feel more confident and empowered to manage such presentations effectively in the future.

George , a 31-year-old chef, comes to the surgery asking to be tested for diabetes. He reports symptoms of thirst and explains that there is a strong family history of diabetes. His BMI is 25.2 kg/m 2 and a capillary blood glucose reading is 13.4 mmol/L. How would you proceed from here?

Nadia , 27 years old, has, amongst a set of otherwise normal routine blood investigations, a mildly elevated fasting blood glucose level, confirmed on repeat testing, and is diagnosed with diabetes. Her BMI is 23.2 kg/m 2 and her HbA 1c is 49 mmol/mol (6.6%). She has no relevant past medical history and her only medication is the combined contraceptive pill. Her father was diagnosed with type 2 diabetes at the age of 43, and this is controlled by diet. What type of diabetes might you suspect?

By working through this interactive case study, we will consider the signs, symptoms, differential diagnosis and management of maturity-onset diabetes of the young (MODY).

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Clinical pearls, case study: type 1 diabetes with subacute presentation during pregnancy.

Michelle L. Griffith, MD, is a fellow, and Shubhada M. Jagasia, MD, is an attending physician in the Division of Diabetes, Endocrinology, and Metabolism at Vanderbilt University Medical Center, in Nashville, Tenn.

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Michelle L. Griffith , Shubhada M. Jagasia; Case Study: Type 1 Diabetes With Subacute Presentation During Pregnancy. Clin Diabetes 1 April 2009; 27 (2): 86–87. https://doi.org/10.2337/diaclin.27.2.86

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T.S. presented at age 17 with apparent gestational diabetes mellitus (GDM) in her first pregnancy. Her past medical history included allergic rhinitis and acne vulgaris; she had no history of polycystic ovarian syndrome, impaired glucose tolerance, or impaired fasting glucose. She also had no complaints of hirsutism, prior menstrual irregularity, or weight gain. Her family history was notable for diabetes in both parents. Her prepregnancy BMI was 26.2 kg/m 2 .

At diagnosis of pregnancy at ~ 5 weeks gestational age, a fingerstick glucose was 224 mg/dl; home testing at ~ 10 weeks revealed continued elevated glucose levels in the 200 mg/dl range, and the patient also had polyuria and polydipsia. She subsequently had a 50-g oral glucose tolerance test with a result of 262 mg/dl. She was diagnosed with GDM and started on nutritional therapy and glyburide once daily.

At the time of initial consultation with endocrinology, she was at 23 weeks gestational age. She had continued polyuria and polydipsia. Exam revealed a gravid young woman with stable vital signs. She had normal thyroid and cardiac exams and no acanthosis nigricans.

Because of her young age, relatively low BMI, and lack of stigmata of insulin resistance, labs were sent to look for evidence of autoimmune diabetes. Laboratory data included an A1C of 6.5%, C-peptide of 2.3 ng/ml (reference range 0.9-7.1 ng/ml), and GAD antibody of < 1.00 (reference range < 1.46).

Review of her glucose meter download showed poor control with persistent hyperglycemia and average blood glucose of 155 mg/dl. Because her diabetes was not adequately controlled with glyburide, it was discontinued at the first endocrinology visit, and she was started on an insulin regimen of glargine and aspart with carbohydrate counting for her mealtime doses.

The rest of the pregnancy was complicated by poor adherence, difficulty with carbohydrate counting, and continued hyperglycemia, with occasional hypoglycemia. Her regimen was adjusted several times. At the time of delivery at 39 and 3/7 weeks of pregnancy, however, she had not returned for follow-up in the prior 8 weeks, nor had she sent blood glucose data to the clinic. She delivered a healthy 10 lb, 3 oz infant. She had also developed pregnancy-induced hypertension.

At ~ 6 weeks postpartum, she presented to an internist to establish care. She had stopped insulin therapy but continued to have nocturia. At that visit, labs included a random glucose of 492 mg/dl, A1C of 11.7%, and C-peptide of 0.7 ng/ml. Insulin antibodies were not checked. She was diagnosed with type 1 diabetes and started back on intensive insulin therapy.

The patient returned for follow-up with endocrinology ~ 4 weeks later. On repeat labs, C-peptide was 0.4 ng/ml, islet cell IgG antibody was < 1:4, and GAD antibody was positive at 1.75. Insulin doses were increased to improve her glycemic control; however, adherence remained a problem. Although 2-week follow-up was scheduled, the patient did not keep this appointment and presented to the hospital with altered mentation in diabetic ketoacidosis within a month.

What proportion of patients presenting with diabetes during gestation will subsequently be diagnosed with type 1 or type 2 diabetes?

What clinical features are suggestive of type 1 diabetes or latent autoimmune diabetes in adults (LADA)?

What antibodies should be tested when autoimmune diabetes is suspected?

GDM, defined as carbohydrate intolerance that begins or is first recognized during pregnancy, affects ~ 7% of pregnancies annually, with a higher incidence in some ethnic groups. 1   Even normal pregnancy is a state of increased insulin resistance induced by weight gain and placental hormone secretion, including human placental lactogen and growth hormone variant. By the third trimester, insulin sensitivity is about 50% less. 2   In a normal pregnancy, insulin secretion increases by ~ 30% to compensate for this defect. Thus, GDM results from a combination of increased resistance and lack of sufficient compensatory insulin increase, leading to relative insulin deficiency.

Some patients with GDM may still have relatively normal insulin resistance in the nonpregnant state. Other patients who are diagnosed with GDM may also have underlying impaired glucose tolerance that is exacerbated by pregnancy. More rarely, type 1 diabetes may be first detected in pregnancy, when the prodromal phase of the disease is present in the pregestastional time period. 3   The physiological stressor of pregnancy may then unmask the disease.

Fewer than 1 in 10,000 women may become pregnant during the prodromal phase of type 1 diabetes. 1   More frequently, type 2 diabetes may be first detected in pregnancy when the pregnancy exacerbates hyperglycemia or as a result of patients receiving routine medical care while pregnant. Among patients with GDM in the United States, it has been estimated that 50% will develop overt diabetes within 10 years after delivery. 2   In Finland, where the 6-year risk for diabetes after GDM is estimated at 10%, 4.6% of patients developed type 1 diabetes after GDM, and 5.3% eventually developed type 2 diabetes. 4  

Among patients with a new diagnosis of diabetes, be it during gestation or not, several clinical features may suggest an underlying diagnosis of type 1 diabetes or LADA. LADA is considered by some to be a distinct disease state and by others to be on the continuum of type 1 diabetes, but a characteristic feature is antibody positivity; disease onset is often insidious. Features that may raise suspicion include age < 50 years; presentation with acute symptoms such as weight loss, polyuria, or polydipsia; personal history of autoimmune disease; family history of autoimmune disease; and BMI < 25 kg/m 2 .

One study using these criteria found that, among patients with two or more of these features, 75% had LADA, whereas 24% had type 2 diabetes. 5   For patients meeting only one criterion, 98% did not have antibodies indicative of LADA. Despite a lower BMI being suggestive of an autoimmune process, most patients with LADA are overweight or obese. Similarly, a family history of type 2 diabetes did not predict against LADA. 5   However, testing for antibodies and clinical suspicion for an autoimmune process should be considered in patients with two or more of these clinical features.

Diabetes-associated antibodies include antibodies to GAD, islet cell antibodies, antibodies to the protein tyrosine-phosphatase-related protein 2 (IA2), and insulin antibodies. 4 , 6   These autoantibodies have been studied in relatives of patients with type 1 diabetes, and their presence, in the absence of apparent metabolic abnormalities, has a high predictive value for diabetes in those relatives. Patients can develop diabetes in the setting of one or more antibodies being positive, although some studies have correlated increased numbers of antibodies as well as higher titers of antibodies with increased risk for frank diabetes. 5   The insulin antibodies and IA2 are more likely to be positive in children with type 1 diabetes, whereas GAD antibodies are more frequently detected in adult patients. Among patients with diabetes who are not insulin-requiring at diagnosis, antibody positivity predicts requirement for insulin in 80% of cases. 7   Other autoimmune diseases are also increased in frequency in these patients. Although at this point there is no definite way to prevent diabetes in patients with positive antibodies, animal and human studies are ongoing.

GDM affects ~ 7% of pregnancies. When it is diagnosed, clinicians should keep in mind the possibility of a new diagnosis of type 1 or type 2 diabetes.

Clinical features can be used to assess risk of autoimmune diabetes in patients with a new diagnosis and to guide appropriate antibody testing.

Although a lower BMI may suggest LADA or type 1 diabetes, the majority of patients with LADA are overweight, so an elevated BMI should not exclude consideration of this diagnosis.

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GLP-1 receptor agonists may enhance the effects of desmopressin in individuals with AVP deficiency: a case series and proposed mechanism

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type 1 diabetes case presentation

  • Afif Nakhleh   ORCID: orcid.org/0000-0003-1206-1516 1 , 2 , 3 , 4 ,
  • Naim Shehadeh 1 , 2 , 3 &
  • Bshara Mansour 1  

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have diverse effects on sodium and water homeostasis. They decrease thirst perception, potentially inhibit arginine vasopressin (AVP) production, and induce natriuresis. We present three cases of AVP deficiency (AVP-D) where GLP-1 RA initiation led to desmopressin dose reduction.

Three patients with AVP-D on stable desmopressin therapy started GLP-1 RAs for type 2 diabetes mellitus or obesity. Following weight loss and decreased thirst, all patients reduced their desmopressin dose while maintaining normal thirst and urine output.

GLP-1 RAs influence sodium and water homeostasis through various mechanisms. In individuals with intact AVP systems, GLP-1 RAs may directly suppress AVP production and induce natriuresis in the kidney leading to increased water excretion. In AVP-D, with exogenous desmopressin replacing endogenous AVP, the osmotic permeability of collecting ducts is primarily influenced by desmopressin dose. Thus, increased distal fluid delivery may allow for lower desmopressin doses to maintain water balance.

Our findings indicate a potential interaction between GLP-1 RAs and desmopressin in AVP-D. Clinicians should reassess desmopressin dosage upon initiating GLP-1 RA therapy.

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Introduction

Glucagon-like peptide-1 (GLP-1) plays a multifaceted role in maintaining sodium and water homeostasis in humans. In the brain, GLP-1 plays a direct role in modulating thirst perception and leads to decreased water intake [ 1 ]. It is also thought to directly inhibit arginine vasopressin (AVP) production [ 2 ]. In the gut, GLP-1 reduces sodium absorption [ 1 ]. In the kidney, GLP-1 has a natriuretic effect and can potentially enhance renal hemodynamics [ 3 ].

The viability of GLP-1 receptor agonists (GLP-1 RAs) as a potential treatment for primary polydipsia has come to attention recently. Winzeler et al. presented evidence that suggests the potential of GLP-1 RAs as a viable therapeutic option for primary polydipsia. Patients with primary polydipsia who were administered dulaglutide, a GLP-1 RA, showed a significant reduction in fluid intake and thirst perception as compared to those who were given a placebo [ 4 ].

AVP deficiency (AVP-D), also known as central diabetes insipidus, is another cause for polyuria-polydipsia syndrome. This condition is characterized by hypotonic polyuria (50 ml/kg body weight per 24 h) and polydipsia (> 3 L per day). Desmopressin is the primary treatment for AVP-D. It targets AVP receptor 2 and improves excessive urination and thirst [ 5 ].

In this report, we present three patients diagnosed with AVP-D who required a reduction in their desmopressin dosage following initiation of GLP-1 RA. We propose a hypothesis to explain why desmopressin's antidiuretic effect may be increased when combined with GLP-1 RA.

Cases presentation

A 70-year-old man with a history of AVP-D following resection of a third ventricle colloid cyst 24 years ago. He was maintained on a stable daily dose of desmopressin (400 mcg) for the past 5 years, with a weekly intentional omission of 200 mcg. His condition was well-controlled without symptoms of polydipsia or polyuria (Table  1 ). The anterior pituitary function was normal. The patient presented to our clinic for the management of a recently diagnosed type 2 diabetes mellitus (T2DM). Comorbid conditions included obesity (BMI = 30.3 kg/m 2 ), hypertension managed with enalapril (20 mg/day) and lercanidipine (10 mg/day), hyperlipidemia on atorvastatin (40 mg/day) and depression treated with escitalopram (10 mg/day). He was started on semaglutide, and the dose was gradually increased to 1 mg weekly. Following 4 months of semaglutide treatment, he reported a 6 kg weight loss (98 to 92 kg) and a noticeable reduction in thirst and desire to drink water, but no significant change in urinary frequency. Laboratory evaluation showed mild hyponatremia (Table  1 ). His desmopressin dose was gradually tapered to 200 mcg daily (decreased by 200 mcg/day). Three months later, the patient reported a return to normal thirst levels, and his 24-h urine volume was 2400 ml. Further laboratory results are provided in Table  1 .

A 49-year-old woman with a history of AVP-D following resection of a non-secreting pituitary macroadenoma 4 years ago, currently controlled with desmopressin 250 mcg/day. The patient followed a once weekly desmopressin omitting strategy. Her medical history includes secondary hypothyroidism well-controlled with levothyroxine (100 mcg/day), depression treated with venlafaxine (37.5 mg/day), psoriatic arthritis on methotrexate (10mg weekly) and obesity (BMI = 34.3 kg/m 2 ). She underwent single anastomosis gastric bypass 5 years ago.

Liraglutide was initiated for weight management, with a gradual increase in dose over 4 weeks to 3mg/day. After four months of liraglutide therapy, she experienced a weight reduction from 99 to 92 kg. The patient reported a modest decrease in thirst and desire to drink water, with no alterations in urinary frequency. Laboratory assessments were performed (Table  1 ), and the desmopressin dose was titrated down to 150 mcg/day (decreased by 100 mcg/day). Three months later, she reported returning to her previous thirst and drinking habits, and her 24-h urine volume was 2300 ml. Additional laboratory findings are presented in Table  1 .

A 67-year-old woman, with a 14-year history of AVP-D following surgical removal of a pituitary stalk granular cell tumor, was maintained on desmopressin (200 mcg/day) with a weekly omission strategy. She has secondary hypoadrenalism, treated with prednisolone (5 mg/day), secondary hypothyroidism well-controlled on levothyroxine (100 mcg/day), hypertension controlled with valsartan (160 mg/day) and amlodipine (5 mg/day), hyperlipidemia managed with atorvastatin (20 mg/day) and a newly diagnosed T2DM. For the management of her diabetes, the patient was started on semaglutide, with the dose gradually increased to 1 mg weekly over two months. After three months of semaglutide treatment, the patient reported weight loss (from 87 to 82 kg) and a slight decrease in thirst and water intake, but no change in urinary frequency (Table  1 ). Consequently, her desmopressin dose was reduced to 100 mcg/day (decreased by 100 mcg/day). Three months later, the patient reported a return to normal thirst, and her 24-h urine volume was 2100 ml. Detailed laboratory results are in Table  1 .

We present three patients with a history of AVP-D and stable desmopressin treatment who initiated GLP-1 RA therapy for type 2 diabetes mellitus or obesity. Following weight loss and a self-reported decrease in thirst, all three patients were able to reduce their desmopressin dosage while maintaining normal thirst and urine output. None of the patients were taking diuretics, lithium, or following a low-sodium diet. Although all patients experienced weight loss after starting GLP-1 RAs, this 6–7% reduction in weight is insufficient to explain the 40–50% decrease in desmopressin dosage. These cases suggest a potential impact of GLP-1 RAs on desmopressin requirements in AVP-D. Herein, we discuss the possible interactions between these medications and propose a hypothesis to explain the enhanced antidiuretic effect of desmopressin when combined with GLP-1 RA.

GLP-1 plays a complex role in regulating sodium and water homeostasis. It acts on the brain to decrease thirst and potentially suppress AVP production. GLP-1 has been shown to significantly reduce water intake by 36% in healthy subjects after a salty meal, without affecting their blood sodium levels [ 1 ]. This effect is thought to be mediated by a direct influence on drinking behavior, as supported by evidence in rats demonstrating reduced fluid intake with GLP-1 RAs independent of food intake [ 6 ]. Interestingly, a recent study utilizing Brattleboro rats, a model of hereditary hypothalamic diabetes insipidus, revealed an augmented response to centrally administered GLP-1 RAs, leading to a greater reduction in fluid intake compared to wildtype rats [ 7 ]. However, both wildtype and Brattleboro rats exhibited similar reductions in food intake following GLP-1 RA treatment. This suggests that Brattleboro rats may have a specific dysfunction in the GLP-1 pathway that regulates water intake [ 7 ].

In rats, GLP-1 receptor signaling in hypothalamic neurons can directly inhibit the production of AVP [ 2 ]. Furthermore, GLP-1 could decrease water consumption by reducing sodium absorption in the gut via inhibition of the intestinal sodium-hydrogen exchanger-3 (NHE3) [ 1 ].

The GLP-1 receptor is expressed in various renal locations, including preglomerular vascular smooth muscle cells and juxtaglomerular cells [ 8 ]. Multiple studies on experimental models, healthy volunteers, overweight individuals, and diabetic patients have shown that GLP-1 RAs stimulate natriuresis and diuresis [ 9 , 10 , 11 , 12 ]. This effect is likely mediated by NHE3 inhibition in the proximal renal tubule. When GLP-1 binds to its receptor, it activates protein kinase A (PKA). This activation leads to the phosphorylation of NHE3, which ultimately results in the inhibition of sodium reabsorption in the proximal tubule leading to less fluid reabsorption at this site and increased distal delivery [ 12 , 13 ].

In the kidney, AVP binds to vasopressin V2 receptors, regulating urine concentration by increasing sodium reabsorption in the thick ascending limb of the loop of Henle and enhancing aquaporin 2 (AQP-2) expression in the apical membrane of collecting duct principal cells, thereby increasing their osmotic permeability [ 14 ].

In individuals with intact AVP system, GLP-1 RA treatment is thought to reduce AVP secretion and induce natriuresis, increasing fluid delivery to the distal nephron and collecting ducts. The GLP-1 RA-induced decrease in AVP should reduce the osmotic permeability of collecting duct, allowing excretion of sodium-free water and restoring osmotic homeostasis (Fig.  1 A).

figure 1

Proposed mechanism of GLP-1 RA impact on sodium and water homeostasis in the kidney. A In individuals with normal AVP production, administration of GLP-1 RAs decreases AVP secretion and induces natriuresis. Reduced endogenous AVP levels result in decreased V2 receptor-mediated sodium reabsorption in the distal nephron. Additionally, reduced endogenous AVP levels decrease the osmotic permeability of collecting ducts, leading to increased water excretion. B GLP-1 RAs promote natriuresis and increased fluid delivery to the distal nephron. In patients with AVP-D receiving desmopressin replacement, V2 receptor-mediated sodium reabsorption and collecting duct water permeability are primarily regulated by exogenous desmopressin dosage, not endogenous AVP levels. This may account for the observed amplification of desmopressin effects

We propose that GLP-1 RAs will also induce natriuresis and increased distal fluid delivery in patients with AVP-D. However, as these individuals receive exogenous desmopressin to replace AVP, the osmotic permeability of the collecting ducts is primarily influenced by desmopressin dosage, not endogenous AVP levels. This may account for the observed amplification of desmopressin effects and subsequent reduction in desmopressin dosages in our cases (Fig.  1 B). In other words, the increased distal fluid delivery caused by GLP-1 RAs may allow for lower desmopressin doses to maintain water balance.

This hypothesis is supported by observations of increased hyponatremia risk when desmopressin is combined with other medications that increase distal fluid delivery in the nephron, such as thiazides [ 15 ].

GLP-1 RAs may interact directly with the renin–angiotensin–aldosterone system (RAAS) by inhibiting angiotensin II formation, although their effect on renin release remains unclear. Two potential mechanisms have been proposed: indirect inhibition of renin release through tubuloglomerular feedback activation secondary to natriuresis (induced by NHE3 in the proximal tubule), and direct inhibition of angiotensin II production in tissues [ 16 ]. Nevertheless, this interaction does not appear to undermine our hypothesis.

In the case of patient 3, who is treated with valsartan, an angiotensin II type 1 receptor (AT1R) antagonist, an additional interaction may exist. AT1R antagonists inhibit sodium reabsorption in the proximal tubule leading to natriuresis via activation of unblocked angiotensin II type 2 receptors by angiotensin III [ 17 ]. This could theoretically attenuate the natriuretic effect of GLP-1 RAs. Despite this, patient 3 was able to decrease her desmopressin dosage by 50% after initiating GLP-1 RA.

In the kidneys, the angiotensin-converting enzyme (ACE) maintains a balance between the vasodilatory and natriuretic actions of bradykinin and the vasoconstrictive and salt-retentive effects of angiotensin II. By disrupting this balance, ACE inhibitors promote natriuresis [ 18 ]. This could theoretically weaken the natriuretic effect of GLP-1 RAs in patients taking ACE inhibitors. However, patient 1, who was on enalapril, still achieved a 50% reduction in desmopressin dose after starting GLP-1 RA treatment.

While desmopressin can increase hyponatremia risk in older adults [ 19 ], this does not explain the 50% dosage decrease in patients 1 and 3, who had stable doses and normal serum sodium levels before GLP-1 RA initiation.

Another factor to consider in patients 2 and 3 is their secondary hypothyroidism. If chronically uncontrolled, it may be associated with a decreased capacity for free water excretion and hyponatremia. This is due to elevated AVP levels, mainly attributed to the hypothyroidism-induced decrease in cardiac output [ 20 ]. This interaction seems less relevant in patients 2 and 3, who have AVP-D and were well-controlled with levothyroxine.

An additional factor to consider in patient 3 is secondary hypoadrenalism. Glucocorticoid deficiency can lead to impaired renal free water clearance, causing water retention and dilutional hyponatremia [ 21 ]. Additionally, cortisol deficiency stimulates the hypothalamus to increase production of corticotropin-releasing hormone (CRH), which in turn promotes the secretion of AVP [ 21 ]. However, our patient has AVP-D and her hypoadrenalism was controlled with prednisolone. Therefore, these interactions are unlikely to be relevant in this case.

This report is limited by its small sample size, observational design, reliance on self-reported data, and lack of specific measurements such as urinary sodium, which precluded assessment of fractional excretion of sodium.

Nonetheless, existing evidence supports our hypothesis and provides a plausible explanation for the observed decrease in desmopressin requirements in patients with AVP-D treated with GLP-1 RAs. However, further research is needed to confirm this hypothesis and elucidate the underlying mechanisms.

Data availability

The raw data supporting the conclusions of this article will be made available by the authors without undue reservation.

Abbreviations

Aquaporin 2

Arginine vasopressin

  • Desmopressin

Glucagon-like peptide-1 receptor agonist

Sodium ions

Vasopressin V2 receptors

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Acknowledgements

The authors gratefully acknowledge the patients whose cases are presented in this publication for their gracious consent.

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Afif Nakhleh, Naim Shehadeh & Bshara Mansour

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Conceptualization: Afif Nakhleh, Bshara Mansour. Data curation: Afif Nakhleh, Bshara Mansour. Formal analysis: Afif Nakhleh, Bshara Mansour. Investigation: Afif Nakhleh, Naim Shehadeh, Bshara Mansour. Methodology: Afif Nakhleh, Bshara Mansour. Project administration: Afif Nakhleh. Resources: Afif Nakhleh. Supervision: Afif Nakhleh, Naim Shehadeh. Visualization: Afif Nakhleh. Writing—original draft: Afif Nakhleh. Writing—review & editing: Afif Nakhleh, Naim Shehadeh, Bshara Mansour.

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Nakhleh, A., Shehadeh, N. & Mansour, B. GLP-1 receptor agonists may enhance the effects of desmopressin in individuals with AVP deficiency: a case series and proposed mechanism. Pituitary (2024). https://doi.org/10.1007/s11102-024-01451-7

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Preserving insulin function in diabetes: a case report

  • Masaru Oota 1  

Journal of Medical Case Reports volume  18 , Article number:  416 ( 2024 ) Cite this article

Metrics details

This case report explores the long-term dynamics of insulin secretion and glycemic control in two patients with diabetes mellitus type 2 over 20 years. The observations underscore the impact of lifestyle interventions, including weight loss and calorie restriction, on insulin secretion patterns and glucose levels during 75 g oral glucose tolerance tests. Additionally, the role of hemoglobin A1c fluctuations, influenced by various factors such as body weight, exercise, and pharmacological interventions, is investigated.

Case presentation

Case 1 involves a Japanese woman now in her late 70s who successfully maintained her hemoglobin A1c below 7% for over two decades through sustained weight loss and lifestyle changes. Despite a gradual decline in the homeostasis model assessment of β cell function, the patient exhibited remarkable preservation of insulin secretion patterns over the 20-year follow-up. In case 2, a Japanese woman, now in her early 70s, experienced an improvement in hemoglobin A1c to 6.3% after a period of calorie limitation due to a wrist fracture in 2018. This incident seemed to trigger a temporary rescue of pancreatic β cell function, emphasizing the dynamic nature of insulin secretion. Both cases highlight the potential for pancreatic β cell rescue and underscore the persistence of insulin secretion over the 20-year follow-up. Additionally, we have briefly discussed three additional cases with follow-ups ranging from 10 to 17 years, demonstrating similar trends in glucose and insulin ratios.

Conclusions

Long-term lifestyle interventions, such as weight loss and calorie restriction, can preserve pancreatic β cell function and maintain glycemic control in type 2 diabetes patients over 20 years. Two patients showed stable or improved insulin secretion and favorable hemoglobin A1c levels, challenging the traditional view of irreversible β cell decline. The findings highlight the importance of personalized, nonpharmacological approaches, suggesting that sustained lifestyle changes can significantly impact diabetes management and potentially rescue β cell function.

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Type 2 diabetes mellitus (DM) presents a global health challenge characterized by insulin resistance and impaired insulin secretion [ 1 ]. Previous research, particularly using homeostatic model assessment (HOMA), has indicated that β cell function is already destroyed by approximately 50% by the time patients are diagnosed with DM. Subsequently, β cell function declines by around 4% each year. The traditional understanding suggests that β cell function experiences irreversible loss, necessitating insulin treatment once specific thresholds (15%) are reached [ 1 , 2 , 3 ]. This relationship is expressed by the following equation: HOMA-β = [immunoreactive Insulin (IRI) μU/mL × 360/fasting plasma glucose (FPG) mg/dL − 63]. However, emerging studies, such as the one conducted by Gregg et al . in 2012, propose that intensive lifestyle interventions (ILI) may contribute to partial remission of type 2 diabetes, challenging the prevailing belief in irreversible decline [ 4 ]. Furthermore, investigations have demonstrated the reversal of diabetes through a very low-calorie diet (VLCD). During VLCD therapy, volunteers adhered to the following regimen: (1) consuming 600–700 kilocalories a day for 8 weeks, (2) gradually returning to eating food over the next 2 weeks, and (3) undergoing follow-up once a month and supported with a maintenance program over the next 6 months. On average, volunteers lost 14 kg in body weight. A total of 40% (12/30) of patients diagnosed with diabetes less than 10 years prior reversed their condition, and 6 months later, they remained diabetes-free [ 5 , 6 , 7 ].

This backdrop establishes the foundation for our case series, spanning over 20 years, aiming to explore the long-term dynamics of insulin secretion and glycemic control in patients with DM. The objective is to investigate the role of lifestyle modifications, including weight loss and dietary changes, in influencing the disease course and challenging established paradigms regarding β cell function decline.

The existing literature emphasizes the significance of personalized approaches to diabetes management, considering factors beyond pharmacological interventions [ 1 ]. Our case series contributes to this evolving narrative by presenting two cases with sustained insulin secretion patterns over two decades, offering insights into the potential impact of lifestyle interventions on pancreatic β cell function.

Case 1: housewife currently in her late 70s

A Japanese woman, currently in her late 70s, presented to the clinic for a medical check-up over 21 years ago. She had been treated for essential hypertension for 20 years at another clinic without a DM diagnosis. The patient had not previously experienced symptoms of thirst, polyuria, or polydipsia but had a sibling with diabetes. Upon physical examination, her blood pressure was 170/100 mmHg. Her height was 151.5 cm and her weight was 94 kg, yielding a body mass index (BMI) of 40.9 kg/m 2 . Urinalysis was negative for glucose, protein, ketones, and urobilinogen normal positive, with a pH of 6. The patient’s FPG was 128 mg/dL, and her hemoglobin A1c (HbA1c) was 6.6%. After 1 week, 75 g OGTT was performed to explore treatment options.

The patient received metformin (250 mg) three tablets/day for diabetes and manidipine hydrochloride (10 mg) two tablets/day for hypertension. In 2003, amlodipine (5 mg) one tablet and LOSARRHYD.LD (losartan potassium, hydrochlorothiazide) one tablet were both prescribed. In 2006, her BP was 120–130/70–80 mmHg. In early 2002, total cholesterol (TC) was 346 mg/dL, high-density lipoproteins—cholesterol (HDL-C) was 49 mg, triglyceride (TG) was 205 mg, and low-density lipoproteins—cholesterol (LDL-C) was 256 mg/dL. Atorvastatin (10 mg, one tablet) was started. In early 2003, TC was 228 mg/dL, HDL-C was 57 mg/dL, TG was 148 mg/dL, and LDL-C was 141 mg/dL.

Table 1 presents the 75 g OGTT results. These data indicated a diabetic glucose profile in 2002. However, the glucose curve showed an almost normal pattern in 2017 as compared with 2002. The ratio of glucose area under the curve (AUC) in 2017/2002 was 0.89 (155.5 mg.h/dL and 173.2 mg.h/dL). The ratio of insulin AUC in 2017/2002 was 9.53 (34.3 μU.h/mL and 3.6 μU/mL). These ratios show that insulin secretion increased, resulting in a normal glucose curve.

After 5 years, 75 g OGTT was performed again (Table  1 ). The ratio of glucose AUC 2022/2002 was 0.95 (165.5 mg.h/dL and 173.2 mg.h/dL). The ratio of insulin AUC 2022/2002 was 10.2 (36.7 μU.h/mL and 3.6 μU.h/mL). The AUC of both glucose and insulin were almost the same in 2017 and 2022. In particular, insulin secretion remained stable for more than 20 years. In terms of HOMA-β, β cell function gradually declined (50.0% in 2002, 31.3% in 2017, and 22.9% in 2022). Figure  1 illustrates the correlation between weight and HbA1c over 20 years. To avoid any potential bias or intention, these data points were systematically extracted from the same month every year, spanning almost every month’s laboratory data of patients diagnosed with diabetes.

figure 1

Weight versus hemoglobin A1c over 20 years in case 1. The patient lost approximately 30 kg in body weight over 10 years. BMI was 27.7 kg/m 2 and was maintained

Case 2: housewife now in her early 70s

A Japanese woman, now in her early 70s, presented to the clinic for further examination almost 21 years ago, as her blood glucose level was found to be high at a group medical checkup. She had a history of thirst since 2000, and polyuria, polydipsia, and easy fatigue were recognized since mid 2002. A family history of DM was found in her two brothers. On physical examination, her height was 155 cm and her weight was 56 kg, yielding a BMI of 23.3 kg/m 2 . Urinalysis revealed glucose positive 3 (around 300 mg/dL) without protein or ketones and a pH of 5. The 2 hour postprandial plasma glucose level (PG) was 419 mg/dL, and HbA1c was 10.4%.

Nutrition counseling was directed to a dietary and behavioral program. Metformin (250 mg, three tablets/day) was prescribed. When first diagnosed with DM, the patient had high motivation to improve her condition. Her HbA1c has improved to below 8% within 3 months. She lost 4 kg in body weight over 8 years and maintained good control for around 10 years (Fig.  2 , similar to case 1, the data points presented in case 2 were collected systematically following a time-controlled approach). However, her HbA1c rose to around 8% even when her weight was maintained between 52 and 53 kg. Therefore, a DPP-4 inhibitor (one tablet) and glimepiride (1 mg, two tablets) were prescribed in 2013.

figure 2

Weight versus hemoglobin A1c over 20 years in case 2. The patient lost 4 kg over 8 years. Despite this, her hemoglobin A1c increased to 8%. However, a significant short-term calorie reduction after a right wrist fracture in early 2018 may have contributed to the improvement of her hemoglobin A1c level to nearly normal

On 20 January 2018, a 75 g OGTT was performed to assess the glucose and insulin profiles. C-peptide index (CPI), calculated using the formula CPI = blood C-peptide (fasting)/FPG (fasting plasma glucose) × 100 (1.4/147 × 100) was 0.93.

Eventually, the patient was persuaded to use insulin and was taught how to prepare and inject. However, in early 2018, she accidentally sustained a fracture of the right wrist before initiating insulin treatment. The patient was unable to cook and did not consume sufficient calories for 3 months. Our dietitian estimated she was taking more than 1800 kcal before the surgery, which has reduced to less than 1200 kcal for the first month postsurgery. On 16 May her blood glucose was 90 mg/dL, and her HbA1c was 6.3%. Only INISYNC (alogliptin: DPP-4 inhibition and metformin) was prescribed.

In contrast to the accident in 2018, she broke her left wrist in early 2009. At that time, she could cook and eat sufficiently using her right hand. As she could not work outside and had to stay home, her HbA1c increased to 7.9%.

In mid 2018, a 75 g OGTT was performed again to assess any profile changes in glucose and insulin (Table  2 ). The ratio of glucose AUC in May/January was 0.46 (37.3 mg.h/dL and 193 mg.h/dL). The ratio of insulin AUC in May/January was 3.74 (24.55 μU.h/mL and 6.55 μU.h/mL). This experience indicates that the shock of sudden calorie limitation may reactivate β cell function.

The 75 g OGTT results from late 2022 were compared with that in early 2018. The ratio of glucose AUC in 2022/2018 was 0.36 (70.2 mg.h/dL and 193 mg.h/dL), and the ratio of insulin AUC in 2022/2018 was 3.3 (21.6 μU.h/mL and 6.55 μU.h/mL). These data indicate a similar tendency to the above data. Insulin secretion was maintained in 2022, after she was diagnosed with type 2 diabetes more than 20 years ago. HOMA-β cell function was 11.65% in the beginning of 2018, 14.41% in mid 2018, and 11.56% in 2022. Neither hypertension nor hyperlipidemia were found over 20 years during the follow-up.

Overall, the patient’s HOMA-β cell function declined below 15%, except in mid 2018. The AUC of insulin and glucose in the 75 g OGTT indicated that insulin therapy was not yet required.

Outcome and follow-up

Similar to the aforementioned cases, we have also monitored three additional individuals (A.T., J.T., and M.K.) albeit for 17 years, 15 years, and 10 years, respectively. They also showed a decrease in the ratio of glucose and an increase in the ratio of insulin AUC. Case A.T. was a Japanese woman in her early 80s who had a ratio of glucose AUC 2022/2005 of 0.46, a ratio of insulin AUC of 4, and HOMA-β of 9.4% in 2005 and 27.4% in 2022. Case J.T. was a man in his late 70s who had a ratio of glucose AUC in 2022/2008 of 0.99, a ratio of insulin AUC of 4, and HOMA-β of 9.4% in 2008 and 8.8% in 2023. Case M.K. was a Japanese woman in her early 70s who had a glucose AUC 2019/2012 of 0.9, a ratio of insulin AUC of 3.7, and HOMA-β of 15.2% in 2012 and 41.3% in 2019.

Discussion and conclusions

The traditional view of β cell function decline posits that this decline involves a progressive and irreversible loss in patients with type 2 diabetes [ 1 , 2 , 3 ]. In 2012, Greg et al . suggested that ILI is associated with a greater likelihood of partial remission of T2DM, compared with diabetes support and education [ 4 ]. Besides, multiple authors have shown that diabetes could be reversed by a VLCD [ 5 , 6 , 7 ].

In our case 1, the pancreatic function was retained following weight loss, improving the insulin secretion pattern in the 75 g OGTT compared with 20 years prior. In case 2, HbA1c was maintained at around 8% from 2013 to 2017, even though the patient maintained her weight at around 52 kg and was prescribed additional medication. We intended to initiate insulin therapy at the beginning of 2018. However, in early 2018, before starting insulin treatment, the patient broke her right wrist. She was forced to maintain a low-calorie diet in the month following this accident. Insulin secretion on 28 May was improved compared with that in early 2018. This substantial calorie limitation over a short period may be responsible for rescuing pancreatic cells.

In 2017, Perry suggested three major mechanisms to explain the blood glucose concentration lowering effect of VLCD in diabetic rodents in the liver: (1) decreasing the concentration of lactate and amino acids into glucose, (2) decreasing the rate of liver glycogen conversion to glucose, and (3) decreasing fat content, which improves the response of the liver to insulin [ 8 ].

In 2018, using cross-sectional magnetic resonance imaging (MRI), Taylor et al . showed that high-fat liver at baseline (30.4%) decreased to 1.3% after weight loss intervention, with similar findings in terms of pancreas fat (8.9 to 7.5%). The twin cycle hypothesis suggests that type 2 diabetes develops due to an accumulation of excess liver fat, leading to an increased supply of fat to the pancreas. Consequently, dysfunction occurs in both organs [ 9 ].

The UKPDS cohort of patients with T2DM (enrolled between 1977 and 1991) had a median BMI of only 28 kg/m 2 . One in three of those studied had a BMI of less than 25 kg/m 2 . Each individual could have a personal fat threshold (PFT), and surpassing this threshold would likely lead to the development of T2DM. Maintenance of a BMI below their level of susceptibility resulted in the return of normal glucose control. The authors hypothesized that PFT is independent of BMI [ 10 ]. According to the PFT theory, our two cases seemed to remain within their respective PFTs.

In case 1, the patient’s height was 152 cm, and her weight was 94 kg (BMI 40.7) in 2002, but she lost weight, falling to 64 kg (BMI 27.7) in 2017 (Fig.  1 ), which she has been able to maintain. During this time, her HOMA-IR improved from 3.3 to 0.85. Table 1 presents that the ratio of insulin AUC was 9.53 (2017/2002), and the ratio of glucose AUC was 0.89 (2017/2002). With regards to the intake of metformin, based on the findings from the TODAY study [ 11 ], it is evident that metformin, when used in combination with other treatments, can significantly improve insulin sensitivity and β-cell function initially; however, the long-term effectiveness in maintaining glycemic control does not differ significantly among various treatment groups. The patients’ weight loss may have also played a role in effectively lowering blood pressure, reducing cholesterol and triglyceride levels, and facilitating the remission of T2DM [ 12 ].

In case 2, the patient’s height was 155 cm, weight was 57 kg (BMI 23.7) at the beginning of 2018, and by 2 May, her weight had reduced to 46 kg (BMI 19.1) (Fig.  2 ). During this time, her HOMA-IR improved from 0.85 to 0.56. Table 2 presents that the ratio of insulin AUC was 3.74 (mid 2018/beginning of 2018), while the ratio of glucose AUC was 0.46 (mid 2018/beginning of 2018). As presented in Table  2 , the AUC of glucose and insulin was almost the same in mid 2018 and 2022, meaning pancreas function remained stable for 4 years. Neither hypertension nor dyslipidemia were found over the 20 years.

This case report emphasizes the importance of maintaining insulin secretion patterns using the 75 g OGTT over long periods, as well as maintaining a healthy lifestyle including body weight by calorie intake exercise and pharmacological intervention. All these factors are important to keep a better HbA1c. Both HOMA-β and the AUC of insulin are considered indicators of pancreatic β cell function, but neither indicator was consistent in our data [ 13 , 14 ].

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Abbreviations

Area under the curve

Body mass index

C-peptide index

Diabetes mellitus

Dipeptidyl peptidase-4

Fasting plasma glucose

High-density lipoproteins-cholesterol

Homeostatic model assessment

Homeostatic model assessment of insulin resistance

Insulin (immunoreactive insulin)

Low-density lipoproteins-cholesterol

Magnetic resonance imaging

Oral glucose tolerance test

Personal fat threshold

Triglycerides

United Kingdom prospective diabetes study

  • Very low-calorie diet

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Acknowledgements

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MO conducted the analysis and interpretation of the data for both case reports on Diabetes Mellitus. MO also performed the clinical examination, and interpretation of the labra and was the sole contributor to manuscript writing. The final manuscript has been reviewed and approved by MO.

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Oota, M. Preserving insulin function in diabetes: a case report. J Med Case Reports 18 , 416 (2024). https://doi.org/10.1186/s13256-024-04714-w

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