The incidence of gout has more than doubled over the recent 20 years. This increase together with the more frequent occurrence of comorbid conditions and cardiovascular risk factors represents a significant public health challenge.

Hospitalization increased the risk of gout flares 10-fold. In-hospital gout flares were associated with longer hospitalization.

Fahr’s disease, also known as familial idiopathic basal ganglia calcification, is a neurodegenerative disorder affecting cerebral microvessels, mainly the basal ganglia, and presenting with diverse neuropsychiatric manifestations. It is considered to be mainly hereditary, with autosomal dominant inheritance. In light of its various presentations and incomplete penetrance, Fahr’s disease is known to be underestimated and underdiagnosed. Here, an early-onset case of Fahr’s disease is presented mainly with pure psychiatric symptoms. Given the diversity of the presenting symptoms, and variations in the age of onset, further investigation of organic etiologies in patients presenting with neuropsychiatric symptoms, family members of patients with Fahr’s disease, and patients with unexplained cerebral calcification is recommended.

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.

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