Hyperglycemic nonketotic coma in insulin-dependent diabetes mellitus. Report of a patient with previous history of diabetic ketoacidosis and pituitary stalk section

JAMA ◽  
1968 ◽  
Vol 203 (7) ◽  
pp. 461-463 ◽  
Author(s):  
H. D. Kolodny
2019 ◽  
Vol 7 ◽  
pp. 2050313X1984779 ◽  
Author(s):  
Amjad Halloum ◽  
Shaikha Al Neyadi

In this study, we report a case of a 5-year-old girl with new onset of insulin-dependent diabetes mellitus, who presented with severe diabetic ketoacidosis associated with brain edema and severe myocardial dysfunction, needing intubation and inotropic support. To our knowledge, this is the youngest reported case with severe diabetic ketoacidosis complicated with myocardial dysfunction.


1994 ◽  
Vol 39 (8) ◽  
pp. 1704-1707 ◽  
Author(s):  
Giuseppe Del Favero ◽  
Alessandro Caroli ◽  
Tamara Meggiato ◽  
Antonio Volpi ◽  
Paola Scalon ◽  
...  

2021 ◽  
pp. 107815522110605
Author(s):  
Nasrin Saleh Jouneghani ◽  
John Phillip ◽  
Constantin A Dasanu

Introduction Clinical indications of immune checkpoint inhibitors have expanded to a variety of malignancies. Nearly 50% of patients with advanced cutaneous squamous cell carcinoma, respond to the programmed-death 1 inhibitor cemiplimab. To date, insulin-dependent diabetes mellitus has been documented with the use of several immune checkpoint inhibitors but not cemiplimab. Case report We report herein the first case of a patient with cutaneous squamous cell carcinoma who developed diabetic ketoacidosis and insulin-dependent diabetes mellitus following only two cycles of cemiplimab. A score of 6 on the Naranjo nomogram makes the causality relationship between cemiplimab use and the insulin-dependent diabetes mellitus probable. Management and outcome The patient's developed diabetic ketoacidosis was managed with intravenous fluids and intravenous insulin, with a prompt resolution. Cemiplimab was discontinued, and the patient was discharged on long-acting and short-acting insulin therapy, with a follow-up with endocrinology. Discussion/conclusions The mechanism by which cemiplimab caused insulin-dependent diabetes mellitus is most likely due to lack of endogenous insulin production in the setting of immune-mediated loss of pancreatic beta-cells. Patients may benefit from fasting blood glucose monitoring and early immune checkpoint inhibitor discontinuation where elevated serum glucose is detected.


2007 ◽  
Vol 43 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Elizabeth R. Bryson ◽  
Elisabeth C.R. Snead ◽  
Chantal McMillan ◽  
Lori MacDougall ◽  
Andrew L. Allen

A 10-year-old golden retriever with a 3-year history of insulin-dependent diabetes mellitus was presented with recurring episodes of hypoglycemia and seizures. A presumptive diagnosis of an insulinoma was made based on hypoglycemia with concurrent endogenous hyperinsulinemia and unremarkable radiographic and ultrasonographic images of the chest and abdomen. A beta cell carcinoma of the pancreas with metastasis to the liver and a mesenteric lymph node was confirmed by surgery and histopathology.


1997 ◽  
Vol 136 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Birgit Nyholm ◽  
Sanne Fisker ◽  
Sten Lund ◽  
Niels Møller ◽  
Ole Schmitz

Abstract Objective: To explore a possible association between serum concentration of leptin, insulin sensitivity and non-insulin-dependent diabetes mellitus (NIDDM). Design: Forty first-degree relatives of NIDDM patients and 35 control subjects matched for age, gender and body mass index underwent a hyperinsulinaemic (insulin infusion rate 0·6 mU/kg per min) euglycaemic clamp combined with indirect calorimetry. Serum leptin was measured in fasting blood samples obtained before the clamp. Results: All subjects had a normal oral glucose tolerance test. Insulin-stimulated glucose uptake (M) was decreased in the relatives compared with the control subjects (4·58 ± 0·27 versus 606 ± 0·25 mg/kg per min, P < 0·001). Conversely, serum leptin was increased in the relatives (9·6·/÷ 1·1 versus 6·1·/÷ 1·2 ng/ml (geometric mean·/÷ antilog s.e.m.). P < 0·05). A positive correlation was observed between circulating levels of leptin and percentage body fat (P < 0·001) and inverse correlations were found between leptin, M (P < 0·01), maximal aerobic capacity (VO2 max) (P < 0·01), and energy expenditure (P ≤ 0·01) in both groups. In multiple linear regression analysis, percentage body fat, gender and M significantly determined the level of leptin (r2 = 0·71, P < 0·001) whereas family history of NIDDM and VO2 max did not. Conclusion: Serum leptin is increased in insulin-resistant offspring of NIDDM patients. The association between leptin, anthropometric measures and insulin sensitivity is, however, comparable with that of a control group. The increased concentrations of serum leptin in the relatives appear to be associated with the insulin resistance, but not with a family history of NIDDM. European Journal of Endocrinology 136 173–179


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