Insulin-Dependent Diabetes Mellitus Presenting as Diabetic Ketoacidosis in Pregnancy

Author(s):  
Gary T. C. Ko ◽  
C. C. Chow ◽  
C. Y. Li ◽  
Vincent T. F. Yeung ◽  
Clive S. Cockram
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.


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.


1992 ◽  
Vol 7 (4) ◽  
pp. 199-211 ◽  
Author(s):  
Susan L. Bratton ◽  
Elliot J. Krane

Diabetic ketoacidosis (DKA) is a common and potentially life-threatening complication of diabetes mellitus, the second most common chronic childhood disease [1]. Prior to the introduction of insulin to clinical medicine by Banting and Best in 1922, DKA had a mortality rate greater than 60% [2]. As insulin was introduced into clinical practice, there was a gradual decrease in mortality associated with DKA over the subsequent 30 years. Recent epidemiological data reveal current mortality varies from 0 to 19% [3,4]. DKA continues to be the most common cause of death in patients younger than 24 years of age; it accounts for as many as 50% of deaths of young diabetic patients [5–7]. In elderly diabetics who have coexisting diseases, DKA carries a high mortality [8]. Despite many advances in the care of diabetic patients, the prevalence of DKA is not declining; it accounts for 14% of all diabetes-related hospital admissions [3, 4, 9]. The incidence of insulin-dependent diabetes mellitus continues to increase worldwide and has roughly doubled in each recent decade [10–13]. Because insulin-dependent diabetes mellitus is increasing, and preventative measures to avoid DKA in diabetic patients have not been successful, the incidence of DKA can also be expected to increase in coming years. Prevention of DKA is the ultimate goal (80% of hospital admissions for DKA occur in treated diabetics) [3,8]. It is necessary for clinicians to understand the pathophysiology and treatment of DKA to care for this increasing diabetic population. We discuss the pathophysiology of diabetic ketoacidosis, its management, and its complications.


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