423(85 %) of patients require insulin therapy. Incretin-based therapies should be
avoided in these individuals. Pancreatic enzyme supplements are recommended
in patients with steatorrhea, and fat soluble vitamins should be adequately
replenished. For pain abdomen, analgesics (non-opioid/opioid) may be used. If
pain is unbearable or nonresponsive to medical management, surgical interven-
tion should be considered.- What is ketosis-prone diabetes?
Ketosis-prone diabetes refers to a heterogeneous group of disorders with pro-
pensity to develop diabetic ketosis/ketoacidosis either at onset or during the
course of disease. The classification of ketosis-prone diabetes (KPD) based on
the presence or absence of autoimmunity (A + or A-) and β-cell function (β+ or
β-) is summarized in the table given below.Types of KPD Autoimmunity β-cell function
Type 1A (A +β−) + −
Type 1B (A −β−) − −
Type 2A (A +β+) + +
Type 2B (A − +) − +This classification was based on the characteristics of adult patients admitted
with DKA and followed up thereafter. However, this classification adds confu-
sion to the existing nomenclature of diabetes and has limited utility in clinical
practice.- What is Flatbush diabetes?
Flatbush diabetes was described in African–American young adults residing in
an area named Flatbush in New York City, USA. These individuals presented
with DKA, required insulin for a short time, and subsequently were able to
discontinue insulin therapy, while maintaining euglycemia (with or without
OHA) for several months to years. The majority of patients were overweight/
obese (67 %) and had strong family history of diabetes (88 %). Evidence of islet
autoimmunity was conspicuously absent, and β-cell function was relatively
preserved in these patients.- Why do patients with Flatbush diabetes present with DKA despite preserved
β-cell function?
The key determinant of DKA despite preserved β-cell function in patients
with Flatbush diabetes remains elusive. The mechanisms proposed include
severe oxidative stress, and glucotoxicity-mediated β-cell dysfunction and
insulin resistance. The high prevalence of G6PD deficiency in these patients12 Diabetes in the Young