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CASE PRESENTATION ON DIABETES MELLITUSThis 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 More Related Content
Interactive case study: MODY – a strong family history of diabetesShare this article + Add to reading list – Remove from reading list ↓ Download pdf 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). Editorial: The importance of getting the correct diabetes diagnosisPcds committee elections (2024): call for candidates, prescribing pearls: a guide to pioglitazone, diabetes distilled: diabetes remission in the real world, hypertension case finding and treatment to target as part of the nhs diabetes eye screening programme, q&a: lipid management – part 3: triglycerides and use of non-statin drugs. Jane Diggle tackles the challenges of getting the diabetes diagnosis right. How to stand for election to the PCDS Committee. Understanding pioglitazone: The essential information in one place. Early data from the NHS Type 2 Diabetes Path to Remission programme show it is effective in achieving remission at scale outside of clinical trials. Sign up to all DiabetesontheNet journals
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PRESENTATIONClinical 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.
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 Download citation file:
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. Email alerts
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This Feature Is Available To Subscribers OnlySign In or Create an Account Advertisement 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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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. Similar content being viewed by othersArginine vasopressin deficiency: diagnosis, management and the relevance of oxytocin deficiencyTolvaptan in hyponatraemia secondary to syndrome of inappropriate secretion of antidiuretic hormone: a guide to its use in the eu. Glucagon-Like Peptide-1 Infusion Suppresses Aldosterone Levels in Healthy Normal-Weight Individuals: Double-Blind, Placebo-Controlled Crossover StudyAvoid common mistakes on your manuscript. IntroductionGlucagon-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 presentationA 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). 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 availabilityThe raw data supporting the conclusions of this article will be made available by the authors without undue reservation. AbbreviationsAquaporin 2 Arginine vasopressin
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Disord Fluid Electrolyte Metabol 52:80–92 Article CAS Google Scholar Download references AcknowledgementsThe authors gratefully acknowledge the patients whose cases are presented in this publication for their gracious consent. Open access funding provided by Bar-Ilan University. The authors have not disclosed any funding. Author informationAuthors and affiliations. Maccabi Healthcare Services, Haifa, Israel Afif Nakhleh, Naim Shehadeh & Bshara Mansour Institute of Endocrinology, Diabetes and Metabolism, Rambam Health Care Campus, Haifa, Israel Afif Nakhleh & Naim Shehadeh Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel Diabetes and Endocrinology Clinic, Maccabi Healthcare Services, 54 Simcha Golan St., Haifa, Israel Afif Nakhleh You can also search for this author in PubMed Google Scholar ContributionsConceptualization: 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. Corresponding authorCorrespondence to Afif Nakhleh . Ethics declarationsConflict of interest. The authors state that they do not have any conflicts of interest to disclose. Additional informationPublisher's note. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Rights and permissionsOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . Reprints and permissions About this articleNakhleh, 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 Download citation Accepted : 23 August 2024 Published : 06 September 2024 DOI : https://doi.org/10.1007/s11102-024-01451-7 Share this articleAnyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative
Preserving insulin function in diabetes: a case report
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 presentationCase 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. ConclusionsLong-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. Peer Review reports 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 70sA 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. 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 70sA 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. 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-upSimilar 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 conclusionsThe 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 ]. Availability of data and materialsNot applicable. AbbreviationsArea 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
Park SY, Gautier JF, Chon S. Assessment of insulin secretion and insulin resistance in human. Diabetes Metab J. 2021;45(5):641. https://doi.org/10.4093/dmj.2021.0220 . Article PubMed PubMed Central Google Scholar Wysham C, Shubrook J. Beta-cell failure in type 2 diabetes: mechanisms, markers, and clinical implications. Postgrad Med. 2020;132(8):676–86. https://doi.org/10.1080/00325481.2020.1771047 . Article CAS PubMed Google Scholar Wang Z, York NW, Nichols CG, Remedi MS. Pancreatic β cell dedifferentiation in diabetes and redifferentiation following insulin therapy. Cell Metab. 2014;19(5):872–82. https://doi.org/10.1016/j.cmet.2014.03.010 . Article CAS PubMed PubMed Central Google Scholar Gregg EW, Chen H, Wagenknecht LE, et al . Association of an intensive lifestyle intervention with remission of type 2 diabetes. JAMA. 2012;308(23):2489–96. https://doi.org/10.1001/jama.2012.67929 . Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. 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Obesity. 2008;16(6):1349–54. https://doi.org/10.1038/oby.2008.226 . Kim SH, Silvers A, Viren J, Reaven GM. Relationship between insulin sensitivity and insulin secretion rate: not necessarily hyperbolic. Diabet Med. 2016;33(7):961–7. https://doi.org/10.1111/dme.13055 . Download references AcknowledgementsEditorial support, in the form of medical writing, assembling tables, and creating high-resolution images based on authors’ detailed directions, collating author comments, copyediting, fact checking, and referencing, was provided by Editage, Cactus Communications. The study did not receive any external funding. Author informationAuthors and affiliations. Oota Internal Medicine and Dental Clinic, 13-3, Hassamu, Nishi Ku, Sapporo, 063-0833, Japan Masaru Oota You can also search for this author in PubMed Google Scholar ContributionsMO 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. Corresponding authorCorrespondence to Masaru Oota . Ethics declarationsEthics approval and consent to participate, consent for publication. Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Competing interestsThe author declares that there are no competing interests. Additional informationPublisher’s note. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. 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To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ . Reprints and permissions About this articleCite this article. 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 Download citation Received : 15 April 2024 Accepted : 20 July 2024 Published : 07 September 2024 DOI : https://doi.org/10.1186/s13256-024-04714-w Share this articleAnyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative
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Registered dietitians (RDs) who have earned the Board Certified-Advanced Diabetes Manager (BC-ADM) credential hold a master's or doctorate degree in a clinically relevant area and have at least 500 hours of recent experience helping with the clinical management of people with diabetes.1 They work in both inpatient and outpatient settings, including diabetes or endocrine-based specialty ...
CASE PRESENTATION. A previously healthy 35‐month‐old girl was brought to the emergency room of the Namazi hospital, Shiraz, Iran, due to reduced level of consciousness. ... First presentation of diabetes mellitus type 1 with severe hyperosmolar hyperglycemic state in a 35‐month‐old girl. Clin Case Rep. 2021; 9:e04984. 10.1002/ccr3.4984 ...
Presentation of Case. Dr. Max C. Petersen (Medicine): A 34-year-old woman was evaluated in the diabetes clinic of this hospital for hyperglycemia. Eleven years before this presentation, the blood ...
A 59-year-old woman with type 1 diabetes and a 2-year history of cognitive decline presented with obtundation. There was diffuse, symmetric hypointensity in the brain on T2-weighted images and abno...
Case 6-2020: A 34-Year-Old Woman with Hyperglycemia
Type 1 Diabetes Mellitus Clinical Presentation
Adult-Onset Type 1 Diabetes: Current Understanding and ...
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.
from uptodate: Epidemiology, presentation, and diagnosis of type 1 diabetes mellitus in children and adolescents-Authors:Lynne L Levitsky, MDMadhusmita Misra, MD, MPH, updated Oct, 2021; Overview of the management of type 1 diabetes mellitus in children and adolescents ... This wraps up the case study on type one diabetes. Please take a look at ...
Presentation of Case. ... Janež A, Guja C, Mitrakou A, et al. Insulin therapy in adults with type 1 diabetes mellitus: a narrative review. Diabetes Ther 2020;11:387-409. Crossref.
In this new paradigm, a preclinical stage 1 case of type 1 diabetes is defined as the presence of two or more autoantibodies, ... is slightly more common in men and boys than in women and girls. 23 Two HLA class 2 haplotypes involved in anti gen presentation, HLA DRB1*0301-DQA1*0501-DQ*B10201 (DR3) ...
Case 1. An obese 40 year-old woman is admitted for asthma. She received a dose of methylprednisolone in the ED at 7pm and will now be receiving 40 mg of oral prednisone daily in the AM. She had not been on any steroids for many years. Random finger-stick blood glucose when she gets to the floor at 10pm is 275 mg/dL. Her last meal was at 5pm.
Pathophysiology and Clinical Presentation. Pathophysiology: Type 1 Diabetes Mellitus is a syndrome characterized by hyperglycemia and insulin deficiency resulting from the loss of beta cells in pancreatic islets (Mapes & Faulds, 2014). Nonimmune (type 1B diabetes), occurs secondary to other diseases and is much less common than autoimmune (type ...
A case report: First presentation of diabetes mellitus type 1 with severe hyperosmolar hyperglycemic state in a 35-month-old girl Clin Case Rep. 2021 Nov 6;9(11):e04984. doi: 10.1002/ccr3.4984. ... Clinical Case Reports published by John Wiley & Sons Ltd. Publication types
The most recent National Health and Nutrition Examination Survey noted that 30% of adolescents are now overweight, 2 and there has been a commensurate rise in the number of cases of type 2 diabetes found in adolescents. 3 Recently, in a cohort of obese adolescents, 20% were noted to have impaired glucose tolerance, and 4% had undiagnosed type 2 ...
Case study on Diabetes Mellitus | PPT
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 ...
11. Introduction Type1 diabetes Insulin Dependent diabetes mellitus, or Juvenile onset DM. Average onset is in childhood or early adulthood (usually before 30 years of age) Due to pancreatic islet destruction predominantly by an autoimmune process. Cell mediated response: - Type 1 diabetes is caused by a T cell mediated autoimmune destruction ...
In light of this, we wanted to have a good understanding of Type 1 diabetes, its presentation, and its treatment. If you have a disability and experience difficulty accessing this content, please email [email protected] or call 614-292-5000 for assistance. The content of this site is published by the site owner (s) and is not a statement of advice ...
Last Update: Updated Chapter 4, Chapter 11 slideset. For comments, corrections or to contribute teaching slides please contact Dr. George Eisenbarth at: [email protected]. Updated Chapter 4 slideset. Banting Slideset (2009) Type 1 Diabetes: Cellular, Molecular & Clinical Immunology Edited by George Eisenbarth. TABLE OF CONTENTS.
Open the PDF Link PDF for Case 3: An Unusual Clinical Presentation of Diabetes Eventually Diagnosed as a Monogenic Form in another window. Case 4: A Case of Monogenic Diabetes. By ... Open the PDF Link PDF for Case 41: New-Onset Type 1 Diabetes, Addison's Disease, and Hypothyroidism: A Case of Autoimmune Polyendocrine Syndrome Type 2 in ...
varshawadnere. 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 ...
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.
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 ...
Background 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. Cases Three patients with AVP-D on stable ...
Background 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 ...