ABSTRACT
Monckeberg medial calcific sclerosis (MCS) is an infrequent finding in the temporal artery and can clinically present almost indistinguishably from giant cell arteritis (GCA). To our knowledge, there have been only two case reports of suspected GCA found to be MCS only after a temporal artery biopsy (TAB). Herein, we present two cases. The first case is a 69-year-old female with hypertension, type-2 diabetes mellitus, and chronic headaches who presented with left temporal headaches and scalp tenderness. She had a prominently dilated, tortuous, and tender left temporal artery. Initial labs showed a leukocyte count of 11.1x103/L, erythrocyte sedimentation rate (ESR) of 29 mm/hr, and C-reactive protein (CRP) of 5.8 mg/L. The patient was started on prednisone 60 mg for presumptive GCA. Left TAB was negative for inflammatory changes, with findings consistent with MCS. Steroids were discontinued, and symptoms resolved. The second case is a 67-year-old male with hypertension, asthma, hyperlipidemia, status-post left eye cataract phacoemulsification, with intraocular lens insertion one-month prior, who presented with left eye blurriness in the inferior visual field and intermittent headache for 15 days. Left ophthalmoscopy showed retinal pallor and edema. Initial labs revealed ESR of 25 mm/hr, CRP of 11.2 mg/L, leukocyte count of 13.01x103/L. The patient was given solumedrol 120 mg once and prednisone 70 mg daily for presumptive GCA. Left TAB was negative for GCA but reported damaged elastic fibers by calcification consistent with MCS. Partial visual blurriness remained, and steroids were discontinued. This report accentuates the importance of MCS as a temporal GCA simulator. Physicians should be aware that TAB potentially changes management and may help surface underlying conditions.
ABSTRACT
Sodium-glucose cotransporter 2 (SGLT2) inhibitors are increasingly used as add-on therapy in patients with poorly controlled type 2 diabetes mellitus (T2DM). Although pancreatitis is not a known side effect of SGLT-2 inhibitors, there have been case reports of SGLT-2 inhibitor use being associated with pancreatitis. Case Presentation. A 51-year-old male with a history of type 2 diabetes, dyslipidemia, and status-post cholecystectomy presented to the emergency room with a four-day history of periumbilical pain radiating to the back. He denied any history of recent alcohol intake or prior episodes of pancreatitis. On physical examination, his abdomen was diffusely tender to palpation without guarding or rebound. Initial labs were notable for a leukocyte count of 9.3 × 109/L, creatinine level of 0.72 mg/dL, calcium level of 9.5 mg/dL, lipase level of 262 U/L, and triglyceride level of 203 mg/dL. His last HbA1c was 8.5%. CT scan of his abdomen and pelvis showed findings consistent with acute pancreatitis with no biliary ductal dilatation. Careful review of his medications revealed the patient was recently started on dapagliflozin five days prior to admission in addition to his longstanding regimen of insulin detemir, sitagliptin, metformin, and rosuvastatin. His symptoms resolved after discontinuation of sitagliptin and dapagliflozin. A year later, due to increasing HbA1c levels, a decision was made to rechallenge the patient with dapagliflozin, after which he developed another episode of acute pancreatitis. His symptoms resolved upon cessation of dapagliflozin. Conclusion. This case highlights the possible association of SGLT-2 inhibitors and pancreatitis. Patients should be informed about the symptoms of acute pancreatitis and advised to discontinue SGLT-2 inhibitors in case such symptoms occur.
