Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2) was declared a pandemic by WHO in March 2020. The causative organism has since undergone a series of mutations. COVID-19 primarily being a respiratory illness causes pre-existing pulmonary diseases to show worse clinical outcomes.
About one-third of the world’s population is thought to be infected with latent
Mycobacterium tuberculosis
(MTB). Both previous and newly developed tuberculosis (TB) infection are risk factors for COVID-19 and are associated with poor outcomes. T lymphocytes play a pivotal role in defense against MTB and with evidence suggesting depletion of T lymphocytes in COVID-19, it can be postulated that COVID-19 can increase the risk of reactivation of latent TB.
Given that a large population around the globe is infected with latent tuberculosis, it is interesting to study and note cases where the virus leads to the reactivation of latent tuberculosis infection. Herein, we present a 76-year-old Brazilian male recently treated for COVID-19 pneumonia, presenting with new-onset cough and weakness diagnosed with latent MTB reactivation.
Inherited thrombophilia is an important cause of venous thrombosis. The Factor V Leiden (FVL) is the most commonly encountered mutation, followed by the prothrombin G20210A gene mutation (PTM). The typical venous thrombotic events (VTEs) associated with PTM mutations are deep vein thrombosis (DVT) and pulmonary embolisms (PE). The PTM is inherited in an autosomal dominant pattern with variable penetrance. While heterozygous PTM mutations are more frequent and well documented in the literature, rare cases of homozygous PTM mutations are also reported. In this report, we discuss a 56-year-old male with a past medical history of homozygous prothrombin gene mutation (G20210A) who presented with an unprovoked DVT of the right lower extremity involving both the proximal and distal veins associated with multiple bilateral PEs. This case is unique in terms of the homozygous PTM inheritance, the age at which the patient presented (usually presentation is earlier in life), and the fact that he had a recurrence of both DVT and PE simultaneously.
Myxedema coma is a life-threatening manifestation of hypothyroidism associated with altered mental status, hypothermia, and symptoms related to the slowing of other organ systems. It can occur as a culmination of severe, longstanding hypothyroidism or be precipitated by acute stressors such as infection, myocardial infarction, cold exposure, and surgery in patients with poorly controlled hypothyroidism. Given the high mortality rate and acuity with which the disease presents, treatment with thyroid hormone replacement should be initiated upon suspicion of the disease even prior to obtaining laboratory confirmation. Stress doses of hydrocortisone should also be given until coexisting adrenal insufficiency is excluded. We present a case of a 58-year-old male who presented to the emergency department after being found on the floor of his house. Physical examinations and laboratory results were significant for myxedema coma and the patient was given levothyroxine with improvement of symptoms and mild change in thyroid hormone levels during hospitalization.
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