Coronavirus disease 2019 (COVID-19) is a new pandemic the entire world is facing since December of 2019. Several risk factors are identified in developing severe disease and one of which is preexisting type 2 diabetes mellitus. Metformin is known to have host-directed anti-viral and anti-inflammatory properties. However, whether these effects offer lower mortality remains unclear. In this retrospective study, we aim to address whether metformin use prior to admission decreases mortality in patients with COVID-19 and pre-existing type 2 diabetes mellitus. A total of 1356 hospitalized patients with COVID-19 and pre-existing type 2 diabetes mellitus was analyzed by multivariable regression. Covariates that potentially confound the association were further adjusted using propensity score matching or inverse probability of treatment weighting. We found that metformin therapy prior to admission in patients with COVID-19 and type 2 diabetes mellitus was significantly associated with less primary outcome events including in-hospital mortality and hospice care enrollment with an odds ratio (OR) of 0.25 (95% CI 0.06–0.74) and less in-hospital length of stay, compared to the non-metformin group. Our results provide supporting evidence that metformin may confer increased survival in patients with COVID-19 and type 2 diabetes mellitus treated with metformin prior to hospitalization.
Introduction Glucagonoma is an uncommon neoplasm of the pancreatic neuroendocrine islet α-cells. At least 50% of cases will have metastatic disease when diagnosed. Glucagonomas can be associated with other tumors in Multiple Endocrine Neoplasia syndrome 1 (MEN 1), but this association is rare and comprises no more than 3% of glucagonomas. Glucagonoma syndrome is a rare paraneoplastic phenomenon characterized by necrolytic migratory erythema (NME), hyperglucagonemia, diabetes mellitus, anemia, weight loss, glossitis, cheilitis, steatorrhea, diarrhea, and venous thrombosis. Case presentation A 55-year-old Caucasian woman was admitted for acute onset of shortness of breath and she was seen by endocrinology team for persistent hyperglycemia. Her medical history revealed a long-standing uncontrolled type 2 diabetes mellitus and an episode of left lower extremity deep-vein thrombosis. Her physical exam revealed tachycardia, otherwise unremarkable, with no skin lesions. Laboratory results showed hyperglycemia (387 mg/dl), Hemoglobin A1C, 9%, and hypoalbuminemia (3.4 g/dl). Her Hemoglobin (13 g/dl), white cell count (6100/μL), and platelet level (19.3 × 104/μL) were within normal limits. The patient underwent CT pulmonary angiogram, which showed a large saddle pulmonary embolism as well as a distal pancreatic mass measuring 4.5×3.4 cm, which contains numerous coarse calcifications. Pancreatic mass was confirmed in a CT abdomen and pelvis with contrast. CA 19-9 was elevated to 51 U/ml (normal range, 0- 35U/ml). The GI team performed an Endoscopic Ultrasound, and samples were sent for FNA and flow cytometry which revealed a 4 cm irregular heterogeneous mass with calcifications at the distal pancreatic body, positive for Pankeratin (CK), Cam 5.2, Synaptophysin, Chromogranin A, and CD56, consistent with Pancreatic neuroendocrine Tumor. Her serum glucagon level was elevated to 447 pg/mL (normal range, 50 -150 pg/mL), while her levels of other hormones, such as somatostatin or gastrin, were within normal limits. Glucagonoma of the pancreas was diagnosed, and a spleen-preserving distal pancreatectomy was performed. Histopathological examination revealed a 5.9 cm alpha-cell pancreatic tumor without lymphovascular or perineural tumor invasion. (AJCC 8th edition staging II, pT3, pN0, MX, G1). Immunohistochemical staining was strongly positive for glucagon. A gallium-68 positron emission tomography (68Ga-PET, Netspot) did not show metastasis. Post resection surveillance showed normalization in Glucagon level and no evidence of recurrence in CT abdomen. Conclusion The diagnosis of glucagonoma is often delayed due to unusual initial manifestations of glucagonoma. Early diagnosis provides a good chance of complete surgical removal as the only curative treatment. Presentation: No date and time listed
Introduction Pituitary hypophysitis is an inflammatory disorder classified as primary or secondary. The five histologic subtypes of primary hypophysitis are lymphocytic, granulomatous, xanthomatous, IgG4-related, and necrotizing. Idiopathic granulomatous hypophysitis (IGH) has an incidence of 1 in 10 million and accounts for < 1% of cases involving panhypopituitarism, headache, and visual disturbances. We present the case of IGH in a patient initially suspected to have pituitary adenoma. Case Presentation A 54-year-old female with a history of hypertension presented to the emergency department with nausea, vomiting, and acute worsening of a chronic headache of 1-week duration. Her past medical history was significant for a suspected pituitary macroadenoma of 1.7 cm, which was incidentally detected 7 months before the current presentation. She reported a history of 9 lb weight gain in one month, hot flashes, and diplopia, but denied hirsutism, polyuria, polydipsia, and galactorrhea. Prior evaluation revealed normal prolactin, TSH, and visual field testing. Her medication and familial history were unremarkable. Physical exam during the current presentation revealed stable vital signs, left eye exophthalmos, left anisocoria, decreased sensation in the left V1 and V2 trigeminal nerve distribution, and right abducens nerve palsy. Her initial laboratory workup was consistent with panhypopituitarism. Brain Magnetic Resonance Imaging (MRI) revealed an extensive, locally invasive, exuberantly enhancing infiltrative process measuring at least 5.6 cm in maximal transverse diameter involving the pituitary gland with bilateral cavernous sinus and Meckel's caves invasion and extension into bilateral superior orbital fissures. The patient underwent supraorbital craniotomy with subtotal resection of the tumor. Tuberculosis, sarcoidosis, and neoplasm were ruled out by appropriate tests, and the patient was diagnosed to have IGH on histology. Her symptoms improved postoperatively and the patient was discharged on levothyroxine and hydrocortisone. Conclusion Clinically and radiologically, IGH is a rare pathology that can closely mimic a pituitary adenoma. Through this case, we highlight the importance of performing a comprehensive evaluation with a full hormonal workup and imaging, with the exclusion of secondary causes while assessing patients with a sellar mass. Presentation: No date and time listed
Introduction Metformin is the first-line drug for treatment of Type 2 diabetes. A meta-analysis of 70,490 patient-years of metformin use reported no lactic acidosis. We present a case of a patient who developed lactic acidosis while on Metformin; with other contributing factors. Case Description A 72-year old male with dementia, diabetes, hypertension, hypothyroidism and “muscular dystrophy” was admitted with encephalopathy. Medications included levothyroxine, donepezil, insulin glargine and metformin. A Brain CT scan revealed frontal lobe atrophy and lacunar infarcts. Admission blood work revealed lactic acidosis of 5.6. Sepsis workup was negative. Metformin was discontinued, and the patient improved with intravenous hydration. Upon discharge, Metformin was restarted. Follow-up lactic acid was normal. After a subsequent hospitalization with similar presentation and peak lactic acid of 4.7, metformin was stopped altogether. The patient was referred to a neuromuscular specialist and a diagnosis of Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) was made. The “muscular dystrophy” was likely mitochondrial disease. A third hospitalization (while not on Metformin) saw a peak lactic acid of 2.8. We concluded that the lactic acidosis was secondary to MELAS, but Metformin had caused the significant spikes seen during the first two hospitalizations. Discussion Mitochondrial disorders must be in the differential diagnosis for patients diagnosed with muscular dystrophy. The hallmark of MELAS syndrome is stroke-like episodes that result in hemiparesis, hemianopia, or cortical blindness. Other features include seizures, recurrent headaches, vomiting, short stature, and muscle weakness. Patients with mitochondrial diseases also have a high incidence of diabetes. Lactic acidosis occurs during stress. DNA testing is the gold standard for diagnosis. Conclusion Metformin is contraindicated in patients with mitochondrial disease and diabetes due to the predisposition for lactic acidosis. This is not part of the current package inserts for prescribers and patients- and we strongly recommend inclusion of this language.
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