Coronavirus disease-19 (COVID-19) can manifest as fever, cough, and shortness of breath and is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Occasionally, these patients may present with diabetic ketoacidosis (DKA). Patients with comorbidities such as diabetes mellitus and hypertension, as well as older age groups, are known to have a more severe disease progression and poor prognosis. In this review article, we attempt to better understand the disease process in diabetics and also discuss potential mechanisms by which diabetes may play a role in disease severity. This includes the effect of diabetes on the immune response and immune dysregulation. The role of diabetes mellitus in molecular processes including augmenting Angiotensin-Converting Enzyme 2 (ACE 2) levels is also discussed as potential mechanisms to explain the grave prognosis seen in these patients.
Introduction- Hypothyroidism is a common endocrine disorder, affecting about 4.6 percent of the U.S. population aged 12 and older. The most common treatment is synthetic thyroxine hormone supplementation-levothyroxine, starting at 1.6 mcg/kg.Hypersensitivity reactions to levothyroxine are rare. Two cases have been published of successful oral desensitization, for suspected IgE mediated reactions. There are no published protocols describing induction of drug tolerance to immunologic, non-IgE mediated reaction to levothyroxine. The objective of this case report is to describe a novel outpatient protocol, for oral desensitization to levothyroxine, in the setting of a delayed immunologic (non-IgE mediated) reaction. Case report- A 66 year old male with history of hypothyroidism, diagnosed in 2010 presented to outpatient endocrinology. Between 2010 and 2019, the patient was on multiple brands and formulations of levothyroxine. He noticed an itchy, raised rash on abdomen, chest and arms, within a few months after starting each of the above. No mucosal involvement or signs of end organ damage were noted. The rash was deemed a type IV delayed hypersensitivity reaction, based on history and histological findings on biopsy. The patient reported clearance of the rash when he was off any form of thyroid supplementation, and reappearance of the rash when he re-trialed it. The patient had normal thyroid stimulating hormone (TSH) levels while he was on supplementation despite the rash. The patient’s TSH after discontinuing treatment was 104 (uIU/mL) and free thyroxine (T4) was 0.13 ng/dl (0.9–1.7). All components of previous brands of levothyroxine were compared and no common ingredient was thought to be contributing to hypersensitivity reactions. Subsequently, an oral desensitization protocol was initiated at 0.075 mcg daily with weekly increase in doses over seven weeks to reach a target dose of 75 mcg. Discussion- The patient was tried on different brands of levothyroxine and dessicated thyroid hormone. He consistently developed a type IV hypersensitivity reaction within a few months after starting them. The patient had uncontrolled TSH levels after discontinuing the treatment and was at risk of complications of untreated hypothyroidism. This necessitated the need for desensitization. There have been previous case reports of oral or IV desensitization, in suspected IgE mediated reactions, but we describe the first case of induction of levothyroxine tolerance in an immunologic non-IgE mediated reaction. Subsequently, the patient tolerated a therapeutic dose of levothyroxine, with no appearance of rash or itching, for almost 6 months. This case report describes a novel approach to levothyroxine desensitization over a period of seven weeks in an outpatient setting in response to a delayed type hypersensitivity reaction.
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