Posters

Presenting Author Academic/Professional Position

Shadi Jafari-Esfahani

Academic Level (Author 1)

Resident

Discipline/Specialty (Author 1)

Internal Medicine

Discipline Track

Patient Care

Abstract Type

Research/Clinical

Abstract

Background: Although there are not many studies regarding the effects of Covid-19 infection on Graves’ disease, few case reports demonstrate the association between the two. The SARS-CoV-2 uses the angiotensin II converting enzyme to gain entry into cells. This results in hyperactive immune response involving Th1 and Th17 lymphocytes which activates proinflammatory cytokines; IL-6 and TNF-alpha. Research shows elevation of IL-6 in patients with Graves’ disease.

Case report: A 22 years old man with no past medical history presented to the Emergency Room for the complaint of generalized weakness and dyspnea of one day. He had associated dry cough, palpitations, polydipsia, polyuria, and unintentional weight loss. He denied headache, or chest pain. Physical examination: afebrile, BP 173/68 mmHg, PR 129, RR 26, in respiratory distress, no signs of lid lag or exophthalmos. Thyroid gland normal in size and moved with swallowing. Cardiac, chest and abdominal examinations were normal. Laboratory is significant for metabolic ketoacidosis, hyperthyroidism and COVID-19 infection. Patient was admitted to the unit and started on IV fluid, regular insulin, oxygen, propranolol and methimazole. Thyroid peroxidase antibody and thyroid stimulating immunoglobulin were 2629 and 3.4 respectively, with diffuse enlargement of thyroid gland on ultrasound consistent with Graves’ Disease. Patient’s clinical status improved under the above medical therapy.

Conclusion: Covid-19 infection can trigger manifestation of thyroid disorder or worsening of the previously present symptoms. Therefore, it is imperative for physicians to have a high index of suspicion in diagnosing new onset thyroid disorders in patients who present with Covid-19 infection.

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Poster

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The impact of COVID 19 Infection on Graves' disease

Background: Although there are not many studies regarding the effects of Covid-19 infection on Graves’ disease, few case reports demonstrate the association between the two. The SARS-CoV-2 uses the angiotensin II converting enzyme to gain entry into cells. This results in hyperactive immune response involving Th1 and Th17 lymphocytes which activates proinflammatory cytokines; IL-6 and TNF-alpha. Research shows elevation of IL-6 in patients with Graves’ disease.

Case report: A 22 years old man with no past medical history presented to the Emergency Room for the complaint of generalized weakness and dyspnea of one day. He had associated dry cough, palpitations, polydipsia, polyuria, and unintentional weight loss. He denied headache, or chest pain. Physical examination: afebrile, BP 173/68 mmHg, PR 129, RR 26, in respiratory distress, no signs of lid lag or exophthalmos. Thyroid gland normal in size and moved with swallowing. Cardiac, chest and abdominal examinations were normal. Laboratory is significant for metabolic ketoacidosis, hyperthyroidism and COVID-19 infection. Patient was admitted to the unit and started on IV fluid, regular insulin, oxygen, propranolol and methimazole. Thyroid peroxidase antibody and thyroid stimulating immunoglobulin were 2629 and 3.4 respectively, with diffuse enlargement of thyroid gland on ultrasound consistent with Graves’ Disease. Patient’s clinical status improved under the above medical therapy.

Conclusion: Covid-19 infection can trigger manifestation of thyroid disorder or worsening of the previously present symptoms. Therefore, it is imperative for physicians to have a high index of suspicion in diagnosing new onset thyroid disorders in patients who present with Covid-19 infection.

 

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