Brugada syndrome is a genetic disease with a characteristic electrocardiogram (ECG) findings of ST elevation in leads V1-V3 with a right bundle branch block (RBBB) appearance called Brugada ECG pattern and a tendency to develop malignant polymorphic ventricular arrhythmias that may lead to syncope or cardiac arrest. Common triggers for Brugada ECG pattern include fever, tricyclic antidepressants, lithium, cocaine and alcohol. This ECG pattern together with clinical findings mentioned above is termed Brugada Syndrome. We report a case of a 51-year-old male with a past medical history of hypertension presented to emergency department with 2-day complaint of fever, chills, sore throat, nasal congestion, malaise, productive cough, was positive for Influenza B and on ECG found to have type-I (coved) Brugada ECG pattern. Influenza fever associated with Brugada ECG pattern is a rare manifestation; in fact, to the best of our knowledge, only three case reports have been published in the literature to date.
There is a well-established association between hyperglycemia and severe coronavirus disease 2019 (COVID-19) infection, regardless of the diagnosis of diabetes prior to the infection. However, it is unusual for patients with a mild infection to present with severe hyperglycemia and insulin resistance requiring intravenous insulin therapy. Uncontrolled hyperglycemia is associated with worse outcomes in COVID-19, making it crucial to achieve optimal glycemic control, which occasionally requires IV insulin therapy. We report a patient with type 1 diabetes mellitus (T1DM), on hemodialysis, who presented with diabetic ketoacidosis (DKA) due to non-adherence to insulin. He was found to be incidentally positive for COVID-19 on admission. Although he was asymptomatic and did not require steroids for the treatment of COVID-19, he was noted to have persistent severe hyperglycemia requiring unusually high levels of intravenous insulin. This proposes that even a mild infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can trigger a systemic response that can lead to downstream manifestations including insulin resistance and severe hyperglycemia. Interestingly, our patient had three admissions within the past six months as well as another admission two weeks after the current presentation with DKA secondary to insulin non-compliance, all of which required IV insulin for <24 hours following which he was transitioned to a basal-bolus insulin regimen with well-controlled glucose levels.
Introduction Covid-19 infection (CI) is known to cause hyperglycemia and insulin resistance in patients with and without diabetes. Prior reports have correlated the degree of hyperglycemia to the severity of the CI. However, not much data is available regarding severe insulin resistance in patients with mild CI who are otherwise asymptomatic and not on steroids. Case We report a 48-year old male with type-1 diabetes, asymptomatic CI and renal failure, on dialysis who was admitted with diabetic ketoacidosis (DKA). Patient had refused insulin and hemodialysis treatments for one week and was noted to be confused by staff in his long-term facility. Upon presentation, he was initiated on intravenous (IVIT) insulin infusion therapy and transitioned to subcutaneous (SQ) insulin the following morning. That evening, hyperglycemia worsened (>500 mg/dl), necessitating reinstatement of the IVIT. Hyperglycemia persisted (no excess carbohydrate intake reported by nursing) and IVIT was continued as attempts to change to SQ therapy were unsuccessful. He was dialyzed for two consecutive days after admission and then changed to alternate day schedule. On day 4, hyperglycemia worsened to >500 mg/dl persistently, IVIT rate was increased to 24 units/hr but blood sugars persisted in the >500 range. Work up for evaluating Covid-related inflammation and insulin resistance was sent. After 6 hours of IVIT at 24 U/hr, he was given a relatively higher dose of SQ-insulin (insulin glargine 20 units and insulin lispro 30 units SQ). IVIT rate was gradually tapered based on blood sugars and stopped 6 hours after SQ-insulin was given. Approximately eight hours after receiving SQ-insulin, he was noted to be hypoglycemic, and he received two amps of D-50. His blood sugar stabilized, and he continued to do well subsequently and was maintained on basal-bolus therapy. The on-call nurse confirmed good IV access for the IVIT access line. The IV insulin infusion fluid from bag was sent for analysis which showed that insulin was present in the infusion bag. Inflammatory markers showed high levels of cortisol, ferritin, growth hormone, C-reactive protein and sedimentation rate. Insulin antibodies were also present. D-dimer was normal, and fibrinogen was only mildly elevated. Conclusion This is a rare case of severe insulin resistance in a patient with mild Covid-19 infection and underlying type 1 diabetes, who developed severe insulin resistance with poor response to high doses IV insulin. He ultimately responded a combination of high dose subcutaneous insulin and high doses IV insulin infusion therapy with resolution of ketoacidosis and hyperglycemia. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
ACTH-secreting pituitary adenomas account for about two-thirds of cases of endogenous Cushing's syndrome and are considered the most common cause of endogenous hypercortisolemia. Silent corticotroph adenomas (SCAs) are pituitary tumors that stain positive for adrenocorticotropic hormone (ACTH) but do not produce biochemical levels of excess ACTH or cortisol. These tumors account for approximately 20% of all corticotroph adenomas and 5.5% of nonfunctioning pituitary adenomas. New immunohistochemical (IHC) techniques continue to be the gold standard in diagnosis, while having prognostic implications. Presentation: No date and time listed
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