Palpitations and Fatigue Post COVID: A Harbinger of Silent Thyroiditis!

Background: Subacute thyroiditis is a self-limiting condition brought about by an inflammatory reaction often linked to a recent viral infection. SARS-COV2 (COVID-19), an RNA coronavirus that started a global pandemic in December 2019 has been linked mostly to severe acute respiratory distress syndrome. However, there have been increasing reports of its effect on other organ systems. We present a case of a 32-year-old female recovering from COVID-19, only to develop silent thyroiditis afterwards. Clinical Case: A 32-year-old female with anxiety disorder but otherwise in excellent health was diagnosed with COVID-19 via nasal swab RT-PCR after experiencing low grade fever and cough. She quarantined at home and was on her way to recovery when, a few weeks later, she began to experience increasing bouts of chest pain with no relation to activity, intermittent headaches and lower extremity edema. This prompted her to visit the emergency department. Work-up done at that time was unremarkable and her symptoms were attributed mostly to anxiety. She was advised to follow-up as an outpatient with a cardiologist. One month later, due to the persistence of her fatigue, low exercise tolerance and tremors, she decided to seek consult with a cardiologist. An electrocardiogram done during that visit showed normal sinus rhythm with poor-R wave progression and early repolarization changes. Both the echocardiogram and 24-hour Holter monitoring, which were subsequently done, were unremarkable. Blood work-up, however, revealed a significantly low thyroid stimulating hormone (TSH) level of 0.17 mU/L, for which she was referred to an endocrinologist. A month later, she sought consult with an endocrinologist. Thyroid gland was non-tender on palpation. Repeat blood work-up showed an elevated TSH level (23.50 mU/L) with a low Free T4 (0.42 ng/dL) and an elevated thyroid peroxidase antibody (TPO-Ab) level (900 mU/mL), indicative of subacute thyroiditis, but without associated neck pain. Thyroid sonography done showed diffusely heterogeneous thyroid lobes with no evidence of a dominant mass or nodule. A decision was made to start her on low dose levothyroxine. Two months into treatment, she underwent repeat thyroid hormone levels. Normal TSH and normal free T4 were observed. However, TPO-Ab was still elevated. It was decided to continue her therapy for one more month before gradually tapering her levothyroxine dose. She was told to follow-up in a month for further monitoring. Conclusion: Subacute thyroiditis associated with COVID-19 infection has become a more common occurrence as more cases of COVID-19 are noted worldwide. Our patient followed the usual course of subacute thyroiditis, initially presenting with a thyrotoxicosis phase which typically lasts 4-10 weeks, then subsequently developing hypothyroidism, inadvertently needing thyroid hormone replacement. What made this case more intriguing was that she did not have severe anterior neck pain, the classic clinical presentation of subacute thyroiditis. While there is a very strong association between COVID-19 and respiratory failure, there is paucity of evidence linking COVID-19 to dysfunction of other body systems. This case of thyroiditis presenting post COVID-19 illness, buttresses the versatility of COVID-19. Physicians should keep this in mind when evaluating a COVID-19 survivor who continue to present with persistent tachycardia or palpitations with or without anterior neck pain even after a month or two from infection. Routine follow-up TSH assay on COVID-19 survivors may be a valuable consideration.

A case of thyrotoxicosis-induced anemia in a patient with painless thyroiditis

Background There have been several reports of secondary anemia associated with Graves’ disease. There are no reports of secondary anemia resulting from thyrotoxicosis due to painless thyroiditis (silent thyroiditis). We report the case of a patient with pancreatic diabetes who developed anemia caused by thyrotoxicosis due to painless thyroiditis. Case presentation The patient was a 37-year-old man who visited the hospital complaining of fatigue, palpitations, and dyspnea. His hemoglobin was 110 g/l (reference range, 135–176), and mean corpuscular volume was 81.5 fl (81.7–101.6). His free thyroxine (FT4) was high, at 100.4 pmol/l (11.6–21.9); the free triiodothyronine (FT3) was high, at 27.49 pmol/l (3.53–6.14); TSH was low, at < 0.01 mIU/l (0.50–5.00); and TSH receptor antibody was negative. Soluble IL-2 receptor (sIL-2R) was high, at 1340 U/ml (122–496); C-reactive protein (CRP) was high, at 6900 μg/l (< 3000); and reticulocytes was high, at 108 109 /l (30–100). Serum iron (Fe) was 9.5 (9.1–35.5), ferritin was 389 μg/l (13–401), haptoglobin was 0.66 g/l (0.19–1.70. Propranolol was prescribed and followed up. Anemia completely disappeared by 12 weeks after disease onset. Thyroid hormones and sIL-2R had normalized by 16 weeks after onset. He developed mild hypothyroidism and was treated with L-thyroxine at 24 weeks. Conclusions This is the first case report of transient secondary anemia associated with thyrotoxicosis due to painless thyroiditis. The change in sIL-2R was also observed during the clinical course of thyrotoxicosis and anemia, suggesting the immune processes in thyroid gland and bone marrow.

Clinical Course

The various clinical presentations of Hashimoto's thyroiditis (HT) include euthyroidism and goiter, subclinical hypothyroidism and goiter, primary thyroid failure, hypothyroidism, adolescent goiter, painless thyroiditis or silent thyroiditis, post-partum painless thyrotoxicosis, and alternating hypo- and hyper-thyroidism. Generally, the progress from euthyroidism to hypothyroidism is considered “irreversible” due to thyroid cell damage and loss of thyroidal iodine stores. Myxedema psychosis is a relatively uncommon consequence of hypothyroidism. Myxedema coma, a rare, life-threatening condition, occurs late in the progression of hypothyroidism when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection, medication, environmental exposure, or other metabolic-related stresses. Several unusual syndromes that are believed to be associated with HT include amyloidosis, interstitial pneumonitis, Vitiligo, hives, and alopecia. Hashimoto's encephalopathy and Hashimoto's ophthalmopathy are rare complications of HT. This chapter explores the clinical course of Hashimoto's disease.

Simultaneous onset of type 1 diabetes mellitus and silent thyroiditis under durvalumab treatment

Summary Durvalumab, a human immunoglobulin G1 kappa monoclonal antibody that blocks the interaction of programmed cell death ligand 1 (PD-L1) with the PD-1 and CD80 (B7.1) molecules, is increasingly used in advanced neoplasias. Durvalumab use is associated with increased immune-related adverse events. We report a case of a 55-year-old man who presented to our emergency room with hyperglycaemia after receiving durvalumab for urothelial high-grade non-muscle-invasive bladder cancer. On presentation, he had polyuria, polyphagia, nausea and vomiting, and laboratory test revealed diabetic ketoacidosis (DKA). Other than durvalumab, no precipitating factors were identified. Pre-durvalumab blood glucose was normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. Simultaneously, he presented a thyroid hormone pattern that evolved in 10 weeks from subclinical hyperthyroidism (initially attributed to iodinated contrast used in a previous computerised tomography) to overt hyperthyroidism and then to severe primary hypothyroidism (TSH: 34.40 µU/mL, free thyroxine (FT4): <0.23 ng/dL and free tri-iodothyronine (FT3): 0.57 pg/mL). Replacement therapy with levothyroxine was initiated. Finally, he was tested positive for anti-glutamic acid decarboxylase (GAD65), anti-thyroglobulin (Tg) and antithyroid peroxidase (TPO) antibodies (Abs) and diagnosed with type 1 diabetes mellitus (DM) and silent thyroiditis caused by durvalumab. When durvalumab was stopped, he maintained the treatment of multiple daily insulin doses and levothyroxine. Clinicians need to be alerted about the development of endocrinopathies, such as DM, DKA and primary hypothyroidism in the patients receiving durvalumab. Learning points: Patients treated with anti-PD-L1 should be screened for the most common immune-related adverse events (irAEs). Glucose levels and thyroid function should be monitored before and during the treatment. Durvalumab is mainly associated with thyroid and endocrine pancreas dysfunction. In the patients with significant autoimmune background, risk–benefit balance of antineoplastic immunotherapy should be accurately assessed.