Introduction Antiretroviral therapy, especially protease inhibitors are a cause of hyperglycemia in 5% of patients with HIV. However most people develop hyperglycemia of mild degree. We present a rare case in which an Integrase Strand Inhibitor (Dolutegravir) led to the development of profound hyperglycemia over a short period of time. Case: Patient is a 48 year old transgender patient (male to female) with a past medical history of HIV/AIDS, Hepatitis B and strokes. Patient was being treated with Emtricitabine-tenofovir and efaverinz until 2013 after which she did not follow up and stopped her medication. In June 2018, infectious disease clinic restarted her on Emtricitabine-tenofivir and added Doletugravir. Her Hba1c was 5.9% at that time. In July 2018, she was found to have a blood glucose of 467 mg/dl on random lab testing. Patient was started on Metformin 500 mg BID. In August 2018, she presented to the hospital with altered mental status and shock. Laboratory work up was consistent with hyperosmotic hyperglycemic state with a glucose of 1700 mg/dl, serum osmolality of 391 mOsm/kg , Hba1c 12.9%, anion gap of 28 mmol/l, bicarbonate of 17 mmol/l, lactate of 3.1 mmol/l and trace ketones in the urine. An insulin drip was initiated and patient was subsequently transitioned to basal bolus regimen. A thorough review of medical records failed to elicit any other medication that could have caused hyperglycemia including steroids. Other etiologies such as infections were ruled out. C peptide was 1.6 with a fasting glucose of 141 mg/dl. Insulin Ab, islet cell Ab and Glutamic acid decarboxylase were all negative. There was no history of autoimmunity in the family. Due to the absence of other potentially causative factors, we think Doletugravir could be the cause of her diabetes mellitus. Conclusion: To our knowledge, this is the second case report identifying Doletugravir causing diabetes mellitus and especially hyperosmolar syndrome. The mechanism of action hypothesized has been the medications ability to chelate magnesium which in turn affects the glucose transport via GLUT 4 receptor and gluconeogenesis causing insulin resistance.

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Context We describe a patient with metastatic malignant pheochromocytoma who was found to have germline SDHB and TP53 mutations occurring together. Case Description A 39-year-old male presented with neck pain. Magnetic resonance imaging of the neck revealed a C3 vertebral body collapse and an underlying C3 lesion. Computed tomography (CT) of the thorax, abdomen, and pelvis showed multiple skeletal lesions, a sternal mass, bilateral pulmonary nodules, bilateral adrenal masses, and an aortocaval lymph node conglomerate. He underwent biopsy of the sternal mass, which revealed metastatic pheochromocytoma and subsequent blood work showed serum epinephrine levels of 200 pg/mL (normal 10–200 pg/mL), norepinephrine 28 241 pg/mL (normal 80–520 pg/mL), and dopamine 250 pg/mL (normal 0–20 pg/mL). Genetic testing revealed both SDHB and TP53 germline mutations. He was started on α- and β-blockers and calcium channel blockers to control hypertension and tachycardia. Two months after the diagnosis, a CT of the abdomen and pelvis showed progression of disease, with enlargement of the right adrenal mass as well as the aortocaval conglomeration. His plasma metanephrines were significantly elevated. He was started on systemic chemotherapy with cyclophosphamide, dacarbazine, and vincristine. He required several antihypertensive agents, including metyrosine, to control his blood pressure in preparation for chemotherapy. Conclusion This is the first reported case of simultaneous SDHB and TP53 germline mutations occurring in an individual with a highly aggressive clinical course of pheochromocytoma. We speculate that the simultaneous occurrence of these 2 oncogenic mutations may have led to an aggressive tumor progression.

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