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Hashimoto’s Thyroiditis Presenting With Hoffman’s Syndrome in a Patient With the Coronavirus Disease 2019 (COVID 19): Hormone Replacement in the Time of the Pandemic

Introduction: Hoffmann’s syndrome is a very rare and reversible manifestation of hypothyroidism presenting as classic features of hypothyroidism with muscle stiffness, weakness, and pseudohypertrophy. Clinical Case: A 62-year-old man was admitted to our institution due to dyspnea. He also had progre...

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Detalles Bibliográficos
Autores principales: Larrazabal, Ramon Bagaporo, Chiu, Harold Henrison Chang, Magnaye, Franz Michael Millar, Acampado, Laura T
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089815/
http://dx.doi.org/10.1210/jendso/bvab048.1906
Descripción
Sumario:Introduction: Hoffmann’s syndrome is a very rare and reversible manifestation of hypothyroidism presenting as classic features of hypothyroidism with muscle stiffness, weakness, and pseudohypertrophy. Clinical Case: A 62-year-old man was admitted to our institution due to dyspnea. He also had progressive muscular weakness and recurrent cramps four months prior. On admission, he was seen in respiratory distress and was eventually intubated and hooked to mechanical ventilation for acute respiratory failure brought about by COVID-19 pneumonia (confirmed by a reverse transcriptase-polymerase chain reaction of a nasopharyngeal swab on admission). He had an unremarkable head and neck examination; both of his calf muscles were hypertrophied. On neurological examination, he had mild proximal lower limb muscle weakness (power 4/5) and deep tendon reflexes were sluggish (+1). The patient was subsequently admitted into the intensive care unit. Laboratory data showed inflammatory markers associated with COVID-19 were elevated: Lactate Dehydrogenase (857 u/L; NV: 120-246 u/L) and Interleukin-6 (137 pg/mL; NV: 0-50 pg/mL). He was given tocilizumab, convalescent plasma therapy, and underwent hemoperfusion. His serum chemistry was unremarkable. Thyroid function tests were consistent with primary hypothyroidism from Hashimoto’s thyroiditis: TSH (22.6712 UIU/mL; NV: 0.35-4.94 UIU/mL), fT3 (<2.30 PMOL/L; NV: 2.89-4.88 PMOL/L), fT4 (<5.15 PMOL/L; NV: 9.01-19.05 PMOL/L), anti-Tg Ab (1810.3 IU/mL; NV: <50 IU/mL) and Anti-TPO Ab (2610.4 IU/mL; NV: <100 IU/mL). There was a consideration of Hoffman’s syndrome; muscle enzymes were noted to be elevated also: CK-Total (2589 U/L; NV: 55-170 U/L) and CK-MB (85.7 U/L; NV: 0-16 U/L). This is consistent with Hoffman’s syndrome. He was supposed to start hormone replacement therapy. However, he developed ileus (attributed to sepsis and hypothyroidism) which precluded the use of oral levothyroxine. To circumvent this roadblock, levothyroxine was given as an enema via the rectal route at 300 mcg once daily (approximately twice the oral dose). Upon initiation of hormone replacement, his sensorium, hemodynamic parameters, and bowel movement improved. Thus, we were able to shift to oral levothyroxine eventually. Unfortunately, he went into sudden cardiac arrest and expired after the 11th hospital day. Conclusion: COVID 19 infection could lead to exacerbations of pre-existing conditions such as Hashimoto’s Thyroiditis (in this case, manifesting with Hoffman’s syndrome). Hormone replacement is still the treatment of choice. Concomitant COVID 19 infection and treatment is not a contraindication to delay hormone replacement. Reference: (1) Senanayake, Hemal Ms et al. “Hoffmann syndrome: a case report.” International archives of medicine vol. 7,1 2. 6 Jan. 2014, doi:10.1186/1755-7682-7-2.