Context Hyperglycemic emergencies such as diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) and new-onset diabetes mellitus (DM) have been reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. Hyperglycemia is a predictor of poor prognosis in COVID-19 disease. Objectives The objective of this work is to describe a case series of HHS and/or DKA likely triggered by the COVID-19 vaccine. The aim is to alert physicians of the potential hyperglycemic complications from the COVID-19 vaccination and to provide further insight into the underlying mechanism of the bidirectional relationship between SARS-CoV-2 and DM. Case description All 3 patients developed HHS and/or DKA within 2-10 days of the COVID-19 vaccination. PCR testing for SARS-CoV-2 was negative and other clinical precipitating factors were excluded. Two patients had a history of type 2 DM (T2DM) with pre-admission HbA1c levels of 7.0-7.5% while one patient was newly diagnosed with T2DM during the hospitalization. They were each treated with insulin infusion and were discharged on subcutaneous insulin therapy. Due to the rapid resolution of the hyperglycemia, insulin was discontinued in all patients within 8 weeks and they remain well-controlled on oral DM medications. Conclusion Severe hyperglycemia including HHS and DKA may be triggered by COVID-19 vaccination. Early evaluation and screening of patients with hyperglycemic symptoms after COVID-19 vaccination is recommended. The vaccine-induced hyperglycemia may provide further insight into the underlying pathogenesis caused by the SARS-CoV-2 infection itself. The underlying robust inflammatory response and “cytokine storm” may be the primary precipitant.
Transgender individuals are medically underserved in the United States. Based on the National Transgender Discrimination Survey, 19% transgender population were refused healthcare, 50% had providers with no knowledge of transgender care and 28% had to delay medical care because of discrimination based on the sexual orientation [1]. The Friedman Transgender Health and Wellness Program (FTHWP) was established in 2017 at Lenox Hill Hospital to provide clinical, legal and social services to transgender individuals. These services include pediatric and adult endocrinology services, primary care, mental health, gynecological services, HIV/AIDS testing and care, referrals for hair removal, vocal cord training and gender confirming surgery, legal services, specialty referrals and social work assistance. There were 10 participants at FTHWP in June 2017. The number of participants increased to 60 by September 2018. The patients’ ages range from 11 years to 80 years old. 32 are Caucasians (53%), 13 are African American (21%), 10 are Asian (16%) and 6 are Hispanic (10%). 29 patients are trans-male, 28 patients are trans-female, 4 patients are gender-fluid. 39 patients have received previous hormone therapy, while 22 patients initiated hormonal therapy in our program. From this limited initial experience we concluded that the demand for comprehensive transgender medical services exists and that the patients display diverse demographic and clinical characteristics. Endocrinologists are well positioned to establish transgender health centers because of their background in both internal medicine and hormone therapy. Reference: [1] Grant JM, Mottet LA, Tanis J, Harrison J, Herman JL, Keisling M. Injustice at Every Turn: A Report of the National Transgender Discrimination Survey . Washington, DC: National Center for Transgender Equality and National Gay and Lesbian Task Force; 2011.
Introduction: The role of plasmapheresis (TPE) in thyrotoxicosis management is not well established. Its use may be determined on an individualized basis (1). We report a case of a critically ill patient where TPE was utilized as first-line therapy for refractory thyrotoxicosis. Clinical Case: A 33-year-old woman with Graves’ disease complicated by medication non-adherence presented with rapidly ascending paralysis and bulbar weakness. Primary work up was consistent with acute inflammatory demyelinating polyneuropathy (AIDP) based on EMG findings of motor fiber polyneuropathy with demyelinating features. Laboratory evaluation revealed uncontrolled hyperthyroidism (TSH <0.05 uU/mL, N 0.3-4.2 uU/mL; fT4 3.9 ng/dL, N 0.6-1.5 ng/dL; tT3 318, N 60-160 ng/dL). Initially, there was low concern for thyrotoxicosis based on a Burch-Wartofsky score of 15 (2). Standard dose methimazole and aggressive beta-blockade were initiated. Hospital course was complicated by hypoxic respiratory failure due to progressive paralysis requiring intubation and septic shock from Klebsiella pneumonia requiring initiation of pressors and broad-spectrum antibiotics. Biochemical evaluation showed increasing fT4 (3.8 ng/dL) and tT3 (419 ng/dL) levels. Burch-Wartofsky score increased to 55, consistent with a thyrotoxic crisis. Due to the patient’s critical condition, TPE was rapidly initiated along with standard therapy for thyrotoxic crisis (high dose methimazole, esmolol drip, stress dose corticosteroids, cholestyramine, and potassium iodide) as a bridge to definitive management with thyroidectomy. Rapid clinical improvement with a decline in fT4 levels (3.8 to 2.1 ng/dL) was noted after initiation of TPE with normalization in fT4 (1.5 ng/dL) and tT3 (54 ng/dL) after three sessions. Thyroidectomy was pursued after clinical stabilization. Surgical pathology showed diffuse papillary hyperplasia consistent with Graves’ disease. Due to persistent respiratory failure, the patient underwent tracheostomy placement. Repeat EMG revealed severe myopathic dysfunction without demyelinating features favoring a diagnosis of acute thyrotoxic myopathy over AIDP. Patient was ultimately discharged to a long term acute care facility due to slow neurological recovery. Conclusion: TPE should be considered as first line management in conjunction with conventional medical therapy in critically ill patients with thyrotoxicosis as a bridge to thyroidectomy due to rapid time to effect and patient stabilization. References: (1) Padmanabhan A, et al. J Clin Apher. 2019 Jun;34(3):171-354. (2) Bahn Chair RS, et al. Thyroid. 2011 Jun;21(6):593-646.
Introduction Adrenal insufficiency (AI) has been reported due to the use of budesonide and itraconazole. We report an unusual presentation of adrenal insufficiency from the use of triamcinolone and itraconazole. Clinical Case 46-year-old man with a history of NASH and alcoholic cirrhosis requiring liver transplant presented to ER with two weeks of progressive lower extremity weakness. He reported difficulty climbing stairs and getting up from a chair. He denied anorexia, nausea, vomiting, abdominal pain, or lightheadedness. He was treated with itraconazole for diffuse histoplasmosis for over one year and received one dose of intra-articular triamcinolone 40mg for shoulder pain 2 weeks prior to the hospital admission. Physical exam was significant for proximal weakness, ecchymoses on upper and lower bilateral extremities, mild truncal obesity, but no violaceous striae, moon facies, dorsocervical fat pad or supraclavicular fullness. Laboratory evaluation was notable for sodium 129 mEq/L (n: 135-145), potassium 5.9 mEq/dl (n: 3.5-5), albumin 2.9 g/dl (n: 3.5-5) and glucose 345 mg/dl (n: 70-140), ACTH of 6 pg/ml (6-20) AM cortisol of <1 ug/dl (n: 4-20), aldosterone <1 ng/dl (n: 3-16), and plasma renin activity (PRA)20.54 ng/mL/h (n: 0.25-5.82). Serum cortisol increased to 3.4 ug/dl at 60 minutes of cosyntropin stimulation test, consistent with adrenal insufficiency. Synthetic glucocorticoid panel detected triamcinolone. Patient was discharged on hydrocortisone and fludrocortisone with marked clinical improvement. Abdominal MRI 3 months after admission did not show any adrenal involvement by histoplasmosis. Fludrocortisone was slowly titrated off and only hydrocortisone continued. Repeat evaluation 6 months after last triamcinolone injection demonstrated recovery of HPA axis with peak cosyntropin stimulation cortisol level 16.3 ug/dL (assay by Abbott Alinity) and recovery of renin/angiotensin/aldosterone axis (AM aldosterone 7 ng/dl, renin 2 ng/ml/h). Repeat synthetic glucocorticoid testing confirmed clearance of triamcinolone. Conclusion Itraconazole is CYP3A inhibitor that has been shown to decrease the metabolism and clearance of different corticosteroids. While our patient's lab results supported a diagnosis of AI, it was unclear if the etiology was primary (PAI) or central AI (CAI). The Na+, K+, aldosterone and PRA levels support a diagnosis of PAI; whereas the suppressed ACTH level supports CAI. We believe that our patient had an atypical presentation of both PAI due to histoplasmosis and CAI due to itraconazole/triamcinolone. This confounding picture can potentially be explained by an underlying PAI that may have been masked and exacerbated by the HPA axis suppression of the itraconazole/triamcinolone combination. Presentation: No date and time listed
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