ABSTRACT
We report the case of a 76-year-old female who presented with a new onset of petechial rash in her lower extremities after the introduction of a new agent, semaglutide. She started taking this medication three months before her presentation at an initial dosage of 0.5 mg subcutaneously every week. She noticed a 15-pound weight loss and debilitating fatigue within that timeframe. She stopped taking the medication due to nontolerance and GI upset (nausea and vomiting) about a week before her hospitalization. She denied the use of any other agents. Initial lab work revealed elevated transaminases, alkaline phosphatase, total bilirubin, and inflammatory markers. A CT of the abdomen revealed mild cirrhosis and hepatosplenomegaly. Other causes for cirrhosis were effectively ruled out with negative viral hepatitis, ceruloplasmin levels, and the HFE gene. An autoimmune panel was conducted, yielding positive antinuclear antibody (ANA), anti-histone antibodies, elevated double-stranded DNA, as well as low complement levels supporting evidence of drug-induced lupus (DIL). Anti-mitochondrial M2 and anti-smooth antibodies were also detected, indicating a possible overlap syndrome with autoimmune hepatitis. Perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCA) and anti-neutrophil cytoplasmic autoantibodies (C-ANCA) were negative and ruled out the possibility of ANCA-associated vasculitis. The patient's condition improved with pulse-dose steroids, leading to an improvement in liver function tests. Consequently, the decision to perform skin and liver biopsies was deferred. She was discharged with a tapering dose of steroids and scheduled for outpatient follow-up to monitor her progress. This case report can offer insights to healthcare providers regarding the potential side effects of GLP-1 RAs in their patient population.
ABSTRACT
Bariatric surgery is a procedure performed to achieve weight loss and manage obesity. However, it can result in various complications including post-surgical hypoglycemia. Nesidioblastosis is a rare hypoglycemic syndrome marked by diffuse hyperplasia of pancreatic ß cells with distinct histologic features. Recent case reports have indicated an association of nesidioblastosis with certain bariatric procedures, often specifically linked to Roux-en-Y gastric bypass (RYGB) surgery. In this case report, we describe a 78-year-old male with a complex medical history who presented with altered mental status and severe hypoglycemia (13 mg/dL), despite having no history of diabetes or use of hypoglycemic medications. The patient's clinical condition improved after receiving a 50% intravenous dextrose injection and subsequently placed on a 10% dextrose infusion. Adrenal insufficiency was ruled out with normal cortisol level, and tests for ß-hydroxybutyrate, dehydroepiandrosterone (DHEA) sulfate, and hypoglycemia panels were all negative. However, further investigations were significant for elevated serum insulin, C-peptide, and proinsulin levels. The patient then underwent an abdominal computed tomography (CT) scan, which revealed a grossly normal liver, spleen, pancreas, and adrenal glands, along with evidence of prior gastric bypass surgery. Further evaluation confirmed a history of Roux-en-Y gastric bypass surgery, which was performed to address morbid obesity and obstructive sleep apnea. Following the procedure, the patient began experiencing hypoglycemic episodes. Subsequently, the patient was diagnosed with hyperinsulinemic hypoglycemia with possible nesidioblastosis. This diagnosis was made based on severe recurrent postprandial hypoglycemia, accompanied by elevated endogenous insulin production, and a pancreas that appeared grossly normal on imaging. The patient was treated with acarbose to prevent carbohydrate-driven blood sugar and insulin spikes, octreotide to inhibit insulin secretion, and dietary guidance to avoid high glycemic index foods. This case emphasizes the potential link between bariatric surgeries and metabolic disturbances, underscoring the importance of identifying uncommon hypoglycemic syndromes.
