scholarly journals Hyperosmolar Hyperglycaemic State and Diabetic Ketoacidosis in Nivolumab-Induced Insulin-Dependent Diabetes Mellitus

2021 ◽  
Author(s):  
Ahmed Osman Saleh ◽  
Ruba Taha ◽  
Shehab Fareed A. Mohamed ◽  
Mohammed Bashir
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Autoimmune Diabetes ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Glucose Levels ◽  
Testicular Lymphoma ◽  
Chemotherapy Protocol ◽  
Life Threatening ◽  
Insulin Dependent

Nivolumab is a monoclonal antibody directed against programmed cell death-1 receptor. It has an increasing application in the treatment of various advanced metastatic cancers. The incidence of autoimmune side effects associated with such agents is expected to increase. New-onset autoimmune diabetes mellitus associated with immune checkpoint inhibitor treatment is rare, occurring in less than 1% of patients. Nivolumab-induced diabetes often presents as diabetic ketoacidosis, which could be life-threatening if not recognized and treated promptly. We present the case of a patient who developed severe diabetic ketoacidosis concomitant with hyperosmolar hyperglycaemic state (HHS) after receiving nivolumab for metastatic testicular lymphoma. Pre-nivolumab blood glucose levels were normal, apart from transient hyperglycaemia related to steroids as part of the chemotherapy protocol. The diagnosis was confirmed with extremely low C-peptide in the clinic.

scholarly journals Myocardial dysfunction associated with diabetic ketoacidosis in a 5-year-old girl

2019 ◽  
Vol 7 ◽  
pp. 2050313X1984779 ◽  
Author(s):  
Amjad Halloum ◽  
Shaikha Al Neyadi
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Brain Edema ◽  
Myocardial Dysfunction ◽  
Insulin Dependent Diabetes Mellitus ◽  
Inotropic Support ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent ◽  
New Onset

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.

Diabetic ketoacidosis as a hallmark of autoimmune diabetes occurring after two cycles of cemiplimab

2021 ◽  
pp. 107815522110605
Author(s):  
Nasrin Saleh Jouneghani ◽  
John Phillip ◽  
Constantin A Dasanu
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Insulin Dependent Diabetes Mellitus ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

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.

scholarly journals Viruses as therapeutic agents. I. Treatment of nonobese insulin-dependent diabetes mice with virus prevents insulin-dependent diabetes mellitus while maintaining general immune competence.

1990 ◽  
Vol 171 (6) ◽  
pp. 2077-2089 ◽  
Author(s):  
M B Oldstone
Keyword(s):  
Diabetes Mellitus ◽  
Autoimmune Diabetes ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Lymphocytic Infiltration ◽  
Lymphocytic Choriomeningitis ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Beta Cell Destruction ◽  
Insulin Dependent

A situation in which virus can be used as a therapeutic agent to prevent a lethal autoimmune disease is explored. Nonobese insulin-dependent diabetes (NOD) mice spontaneously develop insulin-dependent diabetes mellitus (IDDM), characterized by lymphocytic infiltration into the islets of Langerhans and beta cell destruction, resulting in hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Infection of NOD mice with lymphocytic choriomeningitis virus (LCMV) aborts the autoimmune manifestations and resultant IDDM. The viruses' effect is on a subset of CD4+ lymphocytes. Ablating this autoimmune diabetes does not significantly alter immune responses to a variety of non-LCMV antigens that require CD4+ lymphocyte participation. The prevention of IDDM associated with viral therapy is maintained throughout the life spans of NOD mice.

Fluid Management of Children Who Have Diabetic Ketoacidosis

1995 ◽  
Vol 16 (8) ◽  
pp. 304-305
Keyword(s):  
Diabetic Ketoacidosis ◽  
Fluid Management ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Hydroxybutyric Acid ◽  
Acetoacetic Acid ◽  
Intracellular Space ◽  
Life Threatening ◽  
Insulin Dependent ◽  
Additional Water

Diabetic ketoacidosis (DKA) is a potentially life-threatening metabolic state that complicates insulin-dependent diabetes mellitus. In the absence of sufficient insulin, glucose is unable to enter cells, and the concentration in plasma increases. When the renal threshold is exceeded (generally at a concentration of about 180 mg/dL), an osmotic diuresis occurs, leading to dehydration. Additional water is lost through hyperventilation (an attempt to compensate for metabolic acidosis), vomiting, and in some cases, diarrhea. Water is drawn from the intracellular space to the plasma to equilibrate the tonicity of the two compartments, bolstering the circulation but producing further intracellular dehydration. Fat is metabolized for fuel because glucose without adequate insulin is not available to cells; beta-hydroxybutyric acid and acetoacetic acid are produced in the process and contribute to acidosis.

Sign in / Sign up

Export Citation Format

Share Document