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1.
Ann Med Surg (Lond) ; 78: 103700, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1814095

ABSTRACT

Introduction: Coronavirus Disease 2019 (COVID-19) is predominantly manifested as respiratory distress. There are growing reports of extrapulmonary clinical manifestations of COVID-19 in addition to the respiratory symptoms. COVID-19 has been associated with the thyroid function through Angiotensin-converting enzyme 2 (ACE2), the central mechanism through Thyroid Stimulating Hormone (TSH), and direct replication of the virus. Case presentation: A 26-year-old woman presented with complaints of palpitation and abdominal pain for three days. Because the symptoms were worsening, she was brought to the emergency room. Her temperature was 37.9 °C without any symptoms of cough, coryza, sneezing, nor headache. Physical examination revealed tremor, tachycardia with 162 beats per minute (bpm), excessive sweating, hyperreflexia of patellar reflex, and no prominent lump in the neck. Electrocardiography (ECG) showed supraventricular tachycardic rhythm (SVT) and 150 J cardioversions were performed. The ECG converted to sinus rhythm, regular, with 120 bpm. Thyroid function tests showed an elevated fT4 level (>7.77 ng/dL) and low TSH level (<0.005 µIU/mL). Chest X-ray showed slight cardiomegaly without prominent abnormality in the lungs that was confirmed with thoracic computerized tomography. The result of the rapid antigen test for COVID-19 was positive and confirmed with polymerase chain reaction testing. She was then treated in the intensive isolation room with remdesivir, anti-hyperthyroid, and supportive therapy. As her condition improved, she was shifted to a non-intensive isolation room and was discharged from the hospital at day 7. Discussion: COVID-19 could present as a thyroid crisis as the initial clinical manifestation. Clinicians should be aware that presentation of thyroid dysfunction in a patient without previous endocrine disease could be due to COVID-19 infection. Early recognition, anti-hyperthyroid therapy, and following isolation procedures for COVID-19 are required in the emergency condition.

2.
AACE Clin Case Rep ; 7(1): 14-16, 2021.
Article in English | MEDLINE | ID: covidwho-1002210

ABSTRACT

OBJECTIVE: Graves' disease is an autoimmune thyroid disease that is thought to develop following environmental exposure in patients with genetic predisposition. Our objective is to present the first report of Graves' disease onset immediately following recovery from mild coronavirus disease 2019 (COVID-19), a close temporal occurrence that should be studied further. METHODS: We describe the clinical course and laboratory features, including thyroid function studies, antibody testing, and polymerase chain reaction testing for severe acute respiratory syndrome coronavirus 2. RESULTS: A 21-year-old woman with prediabetes, obesity, asthma, and gastroesophageal reflux disease presented to the emergency department reporting 3 days of tachycardia, palpitations, anxiety, and shortness of breath. Laboratory investigation revealed a thyroid-stimulating hormone level of 0.01 (0.30-5.00) mcIU/mL with a free thyroxine level of 3.8 (0.6-1.6) ng/dL, prompting endocrinology consultation. On physical examination, she had mild diffuse thyromegaly without tenderness and a history, which included hypothyroidism in her mother. Antibody testing results demonstrated thyroid-stimulating immunoglobulin and thyrotropin receptor antibody levels of 2.6 (<1.3) thyroid-stimulating immunoglobulin index and 17 (0.00-1.75) IU/L, respectively. Sixteen days before presenting to the ED, she was diagnosed with COVID-19 by polymerase chain reaction test after reporting typical symptoms, including fever. Infectious symptoms resolved within 10 days. She achieved clinical and laboratory improvements with a combination of methimazole and beta blocker therapy. CONCLUSION: This case documents the occurrence of Graves' thyrotoxicosis following mild symptomatic COVID-19. Whether the preceding infection is coincidental or contributed to GD development requires definitive studies. This presentation may align with the theory of a viral link in the development of autoimmune thyroid disease in those with genetic predisposition.

3.
AACE Clin Case Rep ; 7(1): 2-5, 2021.
Article in English | MEDLINE | ID: covidwho-1002207

ABSTRACT

OBJECTIVE: The objective of this report is to highlight the possible but little-known association between coronavirus disease 2019 (COVID-19) and delayed onset of central hypocortisolism, which may be of significant clinical importance. METHODS: We describe a patient who developed new-onset central hypocortisolism in the convalescent phase of mild COVID-19, which has not been previously reported. RESULTS: A 47-year-old man with recent COVID-19 upper respiratory tract infection developed new-onset persistent dyspepsia and eosinophilia for which multiple investigations were normal. He was eventually diagnosed with central hypocortisolism, as evidenced by 8 AM cortisol level of 19 nmol/L (normal, 133-537 nmol/L) and adrenocorticotropic hormone of 7.1 ng/mL (normal, 10.0-60.0 ng/mL). He was started on hydrocortisone, which led to resolution of both dyspepsia and eosinophilia. At the same time, an interesting thyroid function trend was observed-an initial increase in both free thyroxine and thyroid stimulating hormone was followed by temporary central hypothyroidism before subsequent spontaneous recovery. On follow-up 3 weeks later, the patient remained hypocortisolemic. CONCLUSION: COVID-19 may be associated with the delayed onset of central hypocortisolism in its convalescent phase. Although various mechanisms are possible, hypothalamic-pituitary activation during systemic illness, followed by a rebound decrease in activity after recovery, is consistent with the clinical course and thyroid function trend in this patient. It is essential that physicians consider endocrinopathies in the differential diagnosis of such cases, given the risk of life-threatening adrenal crises and their possible contribution to persistent symptoms following recovery from COVID-19.

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