We herein describe a patient with non-occlusive mesenteric ischemia (NOMI) potentially associated with the administration of a sodium glucose co-transporter 2 (SGLT2) inhibitor. A 60-year-old man with type 1 diabetes was transferred to our hospital due to vomiting and respiratory distress. He was treated with insulin, metformin and a SGLT2 inhibitor, which had recently been added. He was diagnosed with intestinal ischemia complicated by diabetic ketoacidosis and lactic acidosis. Urgent exploratory surgery was performed, and the gangrenous bowel was resected. Histological findings confirmed the diagnosis of NOMI. The administration of SGLT2 inhibitors therefore requires certain exceptions for type 1 diabetes and cautious monitoring for the occurrence of these possible adverse effects.

E3V4M6 on the Glasgow Coma Scale) and slight neck rigidity were present. Neurological and general findings showed no other abnormality. Laboratory data on admission were erythrocyte sedimentation rate 109 mm/1h; white blood cells (WBC) 11,170/mm 3 ; and C-reactive protein (CRP) 6.3 mg/dl. Other laboratory tests, including HbA1c and urine analysis, were normal. HIV antibody was negative. Computerized brain tomography (CT) showed slight brain edema. The open pressure was raised to 300 mmH 2 O on lumbar puncture on admission. Her cerebrospinal fluid (CSF) was cloudy with 1833/mm 3 WBC (78.5 % polymorphonuclear cells), 44 mg/dl glucose (simultaneous blood sugar 130 mg/dl), and 344 mg/dl protein.A chest radiograph and cardioechograph were normal. Her CT of the abdominal, chest, and cervical regions revealed no focus of infection or malignancy. No CSF leakage or sinusitis was found in otolaryngological medical examinations. We immediately started the antibiotics ceftriaxone and vancomycin with dexamethazone, the standard therapy for acute bacterial meningitis. Gram staining of her CSF showed gram negative rods. Because on hospital day two a culture grew the pseudomonas genus, she was placed on ceftazidime and gentamycin. Later, the P. putida found in both her CSF and blood cultures was susceptible to ceftazidime, gentamycin, meropenem and imipenem. Her consciousness slowly improved, becoming clear on hospital day four. Her laboratory data for hospital day two showed a WBC count of 12090/ mm 3 and a CRP of 17.6 mg/dl. In the CSF study performed on the same day, her WBC count was 7753/mm 3 . Subsequent blood and CSF tests showed improvement, and no bacteria were detected in her CSF. Because drug-induced

Traumatic brain injury is frequently involved in cases of hypopituitarism. We report a case of panhypopituitarism due to transection of the pituitary stalk that we diagnosed 9 years after the traumatic brain injury. If a patient develops unexplained or non-specific symptoms, the physician should consider the possibility of hypopituitarism.

Gonadotropin-releasing hormone (GnRH) agonists have been used for the treatment of various diseases. Although autoimmune thyroid disease has been reported as a rare complication of these agents, the symptoms are almost always transient and non-life-threatening. We herein report a rare case of an 83-year-old man receiving GnRH agonist treatment for prostate cancer who developed myxedema coma complicated by acute pancreatitis. This is the first report of myxedema coma potentially associated with a GnRH agonist. The follow-up of the thyroid function is necessary for patients undergoing treatment with GnRH agonists, especially those known to have or to be susceptible to autoimmune thyroid disease.

No abstract