January 22, 2019 : DCMS #433

DISASTERS AVERTED — Near Miss Case Studies

Warn, Teach, and Revisit Metformin

EXCLUSIVE INTERVIEW — Candid Video Interviews with Top Practitioners

Tracey Brown on Her Vision for the ADA

HOMERUN SLIDES — Great Clinical Presentation Highlights

Endocrinology Jeopardy: Adrenal for $300!

CLINICAL GEMS — The Best from Diabetes Texts

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #161: Immunopathogenesis of Type 1 Diabetes in Western Society Part 4

MOST POPULAR ARTICLES OF THE MONTH

#1 Interview: New Drug Cocktail That Increases Human Beta Cell Proliferation at Rapid Rates
#2 Confusing Insulins Still A Common Mistake
#3 What Can Happen When Patients Take Diabetes Holidays

Most medical professionals agree that type 1 diabetes is an autoimmune disease, and more often than ever before we see patients in their 40’s to their late 60’s who are newly diagnosed with insulin requiring diabetes. These patients are classified as having type 2 diabetes because of characteristics such as age, BMI, insulin use and the like.

The question is: do they really have type 2 diabetes, or do they actually have type 1 diabetes–people who had an extremely late bout of an autoimmune disease?

This week in part 4 four of our Clinical Text on the Immunopathogenesis of Type 1 Diabetes in Western Society, we look how genetics and viruses may be a major factor in the increase in late onset of type 1 diabetes.

Dave Joffe

Editor-in-chief

If this happens in my practice, I’m sure it likely happens with your patients too.

So many of our patients take metformin. They may be new to using metformin or have been taking it for many years. Either way it’s not unusual to have untoward GI side effects from taking it. They may have done fine taking it for years, so they don’t even think about it being their metformin.

Tracey D. Brown, MBA, BChE is Chief Executive Officer of the American Diabetes Association (ADA), the nation’s largest voluntary health organization and a global authority on diabetes.

Tracey joined the ADA in June 2018 after her tenure as senior vice president of operations and chief experience officer at Sam’s Club, a division of Walmart, Inc., where she was responsible for creating meaningful member experiences, directing member strategy, marketing and branding, go-to-market execution, data and analytics and membership operations.

In this week’s Homerun Slides, another question from the Adrenal category in Dr. Claude Lardinois’ Endocrinology Jeopardy! This week’s clue: 44-year-old male with hypertension, headache, tachycardia, and hyperhidrosis.

Genes and environment: a moving target?

Studies from multiple populations have shown shifts of the typical HLA class II gene associations during the last few decades. Indeed, fewer patients carry the high risk heterozygous HLA-DR/DQ genotype, except among younger children [59–63], in whom the disease is becoming more common [4]. In contrast, more patients now carry moderate risk HLA types and genotypes. Such shifts in HLA associations may be explained by stronger environmental pressures that enhance HLA-mediated genetic predisposition and/or broaden the spectrum of diabetogenic gene–environment interactions. Viruses, and especially enteroviruses, rank at the top of the list of environmental factors that have been linked to T1DM.

Diabetes in Control is pleased to bring you an exclusive interview with Dr. Andrew Stewart. Dr. Stewart and his fellow researchers at the Icahn School of Medicine at Mount Sinai have discovered a novel combination of two classes of drugs that induces the highest rate of proliferation ever observed in adult human beta cells—the cells in the pancreas that produce insulin. The result is an important step toward a diabetes treatment that restores the body’s ability to produce insulin. 

I have a patient who has type 2 diabetes. He was started on long-acting insulin 8 months ago. Before adding the insulin, he was taking a daily GLP-1. He had experienced diabetic ketoacidosis (DKA) while on a SGLT-2, and did not tolerate metformin due to GI side effects. Therefore, these two were no longer options. …

Man, 36 years of age, type 2 diabetes, obesity class II, fatty liver, was taking metformin 1,000mg twice daily, and lower dose of SGLT-2. A1C was elevated 9% due to steroids; had been in the 6-7% range. Came in for 3-month follow up — A1C 9.9%, glucose 359, urine positive for glucose and for ketones, gained 19 pounds since last office visit, B/P 126/78-HR 78 and regular.

The patient reports he took a “holiday” from everything during the holidays. He ate and drank anything and everything he wanted, including alcohol, and stopped his medications. He complained of  increased hunger and thirst. Very thirsty.