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Caoimhe Casey University Hospital Kerry, Tralee, Co. Kerry, Ireland

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Tom Higgins University Hospital Kerry, Tralee, Co. Kerry, Ireland

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Summary

Subacute thyroiditis is an inflammatory disorder of the thyroid gland that has previously been described following viral illnesses and occasionally post vaccination such as influenza vaccine. 2021 was a revolutionary year for the development of SARS-CoV-2 vaccinations with multiple different vaccines now available. There are increasing numbers of case reports of thyroiditis following these vaccinations. We report a case of a 50-year-old female who developed subacute thyroiditis 6 days post ChAdOx1 nCoV-19 vaccine (AZD1222 produced by AstraZeneca Vaxzevria). The initial thyrotoxic phase was followed by overt hypothyroidism. This resolved spontaneously within 5 months without levothyroxine replacement. We hope that our case will add to the growing literature of cases of thyroiditis occurring after multiple different types of SARS-CoV-2 vaccination and create awareness of this rare but treatable adverse effect. We also review the literature on the proposed mechanisms behind this adverse effect.

Learning points

  • Subacute thyroiditis is an inflammatory disorder of the thyroid gland that can occur after a viral illness or vaccination against certain infections.

  • Subacute thyroiditis is a rare adverse effect that has been reported to occur after different types of SARS-CoV-2 vaccinations.

  • Subacute thyroiditis post vaccination is relatively straightforward to manage, with some patients requiring non-steroidal anti-inflammatory drugs and beta-blockers, while more severe cases may require corticosteroid therapy. This adverse effect should not dissuade vaccination use at a population level.

  • There are many postulated mechanisms for the development of subacute thyroiditis following vaccination including the presence of the ACE-2 receptor for SARS-CoV-2 on the thyroid gland, an inflammatory/immune response as is seen in COVID-19 infection itself and molecular mimicry between SARS-CoV-2 spike protein and healthy thyroid antigen.

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Adam I Kaplan Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Department of Endocrinology, Royal North Shore Hospital, Sydney, Australia

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Catherine Luxford Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Cancer Genetics Laboratory, Kolling Institute, Royal North Shore Hospital, Sydney, Australia

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Roderick J Clifton-Bligh Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Department of Endocrinology, Royal North Shore Hospital, Sydney, Australia
Cancer Genetics Laboratory, Kolling Institute, Royal North Shore Hospital, Sydney, Australia

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Summary

Biallelic pathological variants in the thyroid stimulating hormone (TSH) subunit β gene (TSHB) result in isolated TSH deficiency and secondary hypothyroidism, a rare form of central congenital hypothyroidism (CCH), with an estimated incidence of 1 in 65 000 births. It is characterised by low levels of free thyroxine and inappropriately low serum TSH and may therefore be missed on routine neonatal screening for hypothyroidism, which relies on elevated TSH. We describe a patient with CCH who developed recurrence of pituitary hyperplasia and symptomatic hypothyroidism due to poor compliance with thyroxine replacement. She was diagnosed with CCH as a neonate and had previously required trans-sphenoidal hypophysectomy surgery for pituitary hyperplasia associated with threatened chiasmal compression at 17 years of age due to variable adherence to thyroxine replacement. Genetic testing of TSHB identified compound heterozygosity with novel variant c.217A>C, p.(Thr73Pro), and a previously reported variant c.373delT, p.(Cys125Valfs*10). Continued variable adherence to treatment as an adult resulted in recurrence of significant pituitary hyperplasia, which subsequently resolved with improved compliance without the need for additional medications or repeat surgery. This case describes a novel TSHB variant associated with CCH and demonstrates the importance of consistent compliance with thyroxine replacement to treat hypothyroidism and prevent pituitary hyperplasia in central hypothyroidism.

Learning points

  • Pathogenic variants in the TSH subunit β gene (TSHB) are rare causes of central congenital hypothyroidism (CCH).

  • c.217A>C, p.(Thr73Pro), is a novel TSHB variant, presented in association with CCH in this case report.

  • Thyroxine replacement is critical to prevent clinical hypothyroidism and pituitary hyperplasia.

  • Pituitary hyperplasia can recur post-surgery if adherence to thyroxine replacement is not maintained.

  • Pituitary hyperplasia can dramatically reverse if compliance with thyroxine replacement is improved to maintain free thyroxine (FT4) levels in the middle-to-upper normal range, without the need for additional medications or surgeries.

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Mone Murashita Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Norio Wada Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Shuhei Baba Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Hajime Sugawara Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Arina Miyoshi Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Shinji Obara Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Summary

We report a 26-year-old Japanese man who visited our outpatient clinic presenting fever immediately after i.m. injection of the second dose of a coronavirus disease 2019 (COVID-19) vaccine (Moderna®). At the first visit, the patient had a fever of 37.7°C and a swollen thyroid gland with mild tenderness. He was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free tri-iodothyronine, 32.3 pg/mL; free thyroxine, >7.77 ng/dL; and thyroid-stimulating hormone (TSH) < 0.01 μIU/mL), high C-reactive protein level (7.40 mg/dL), negative TSH receptor antibody, and characteristic ultrasound findings. His HLA types were A*02:01/24:02, B*15:11/35:01, Cw*03:03, DRB1*09:01/12:01, DQB1*03:03, and DPB1*05: 01/41:01. He was initially administered prednisolone 15 mg/day, following which the fever subsided. After 10 days, he developed limb weakness and could not walk. The serum potassium level decreased to 1.8 mEq/L, which confirmed the diagnosis of thyrotoxic periodic paralysis (TPP). Potassium supplementation was initiated. The muscle weakness gradually decreased. Prednisolone therapy was terminated 6 weeks after the first visit. His thyroid function returned to normal 5 months after the first visit, through a hypothyroid state. To our knowledge, this is the first reported case of TPP-associated SAT following COVID-19 vaccination. Persistent fever following vaccination should be suspected of SAT. Additionally, TPP may be associated with SAT in Asian male patients.

Learning points

  • Following coronavirus disease 2019 (COVID-19) vaccination, subacute thyroiditis may develop regardless of the vaccine type.

  • If persistent fever, anterior neck pain, swelling and tenderness of thyroid gland, and symptoms of thyrotoxicosis are observed immediately after the COVID-19 vaccination, examination in consideration of the onset of subacute thyroiditis is recommended.

  • HLA-B35 may be associated with the onset of subacute thyroiditis after the COVID-19 vaccination.

  • Although rare, subacute thyroiditis can be associated with thyrotoxic periodic paralysis, especially in Asian men.

  • Glucocorticoid therapy for subacute thyroiditis may induce thyrotoxic periodic paralysis through hypokalemia.

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Farooq Khan Department of Endocrinology, Tipperary University Hospital, Clonmel, Co. Tipperary, Ireland

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Mary Jane Brassill Department of Endocrinology, Tipperary University Hospital, Clonmel, Co. Tipperary, Ireland

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Summary

There is emerging evidence of an association between COVID-19 vaccination and subacute thyroiditis. We present the case of a 42-year-old female healthcare worker who was diagnosed with subacute thyroiditis 4 days after receiving her second dose of Pfizer-BioNTech vaccine. Her clinical course followed the classical pattern for thyroiditis with spontaneous return to euthyroidism at 6 months post-presentation. The autoimmune/inflammatory syndrome induced by adjuvants has been implicated as a cause of autoimmune conditions post-vaccination and is a potential mechanism for subacute thyroiditis in our case.

Learning points

  • Subacute thyroiditis should be considered in all patients who receive any kind of vaccine for COVID-19 and subsequently develop symptoms or signs of hyperthyroidism or neck pain.

  • Subacute thyroiditis is a self-limiting condition, and recognising it is important as no specific thyroid treatment (antithyroid drugs or thyroid hormone replacement) is necessary for most patients.

  • The autoimmune/inflammatory syndrome induced by adjuvants may be an under-recognised cause of endocrinopathies and should particularly be considered post-vaccination.

Open access
S Ludgate Department of Diabetes and Endocrinology, Dublin, Ireland

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S P Connolly Department of Infectious Diseases, Dublin, Ireland

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D Fennell Department of Diabetes and Endocrinology, Dublin, Ireland

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M F Muhamad Department of Diabetes and Endocrinology, Dublin, Ireland

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I Welaratne Department of Radiology, Mater Misericordiae University Hospital, Dublin, Ireland

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A Cotter Department of Infectious Diseases, Dublin, Ireland
School of Medicine, University College Dublin, Dublin, Ireland

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S E McQuaid Department of Diabetes and Endocrinology, Dublin, Ireland
School of Medicine, University College Dublin, Dublin, Ireland

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Summary

Both human immunodeficiency virus (HIV) and antiretroviral therapy (ART) are associated with endocrine dysfunction (1). The term 'immune reconstitution inflammatory syndrome' (IRIS) describes an array of inflammatory conditions that occur during the return of cell-mediated immunity following ART. Graves’ disease (GD) occurs rarely as an IRIS following ART. In this study, we describe the case of a 40-year-old Brazilian female who was diagnosed with HIV following admission with cryptococcal meningitis and salmonellosis. At this time, she was also diagnosed with adrenal insufficiency. Her CD4 count at diagnosis was 17 cells/µL which rose to 256 cells/µL over the first 3 months of ART. Her HIV viral load, however, consistently remained detectable. When viral suppression was finally achieved 21 months post diagnosis, an incremental CD4 count of 407 cells/µL over the following 6 months ensued. Subsequently, she was diagnosed with a late IRIS to cryptococcus 32 months following initial ART treatment, which manifested as non-resolving lymphadenitis and resolved with high-dose steroids. Following the initiation of ART for 45 months, she developed symptomatic Graves’ hyperthyroidism. At this time, her CD4 count had risen to 941 cells/µL. She has been rendered euthyroid on carbimazole. This case serves to remind us that GD can occur as an IRIS post ART and typically has a delayed presentation.

Learning points

  • Endocrinologists should be aware of the endocrine manifestations of HIV disease, in particular, thyroid pathology.

  • Endocrinologists should be aware that IRIS can occur following the initiation of ART.

  • Thyroid dysfunction can occur post ART of which Graves' disease (GD) is the most common thyroid manifestation.

  • GD as a manifestation of ART-induced IRIS can have a delayed presentation.

  • Infectious disease physicians should be aware of endocrine manifestations associated with HIV and ART.

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Clare E Bonnar Centre for Diabetes, Endocrinology & Metabolism

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John F Brazil Centre for Diabetes, Endocrinology & Metabolism

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Julie O Okiro Department of Nephrology, Endocrinology & Metabolism

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Louise Giblin Department of Nephrology, Endocrinology & Metabolism

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Yvonne Smyth Department of Cardiology, Galway, Ireland

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Paula M O’Shea Department of Clinical Biochemistry, Galway University Hospitals, Saolta University Healthcare Group, Galway, Ireland

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Francis M Finucane Centre for Diabetes, Endocrinology & Metabolism

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Summary

A 32-year-old Caucasian male presented to the emergency department with a one-day history of acute severe bilateral lower limb weakness, three days after competing in a bodybuilding competition. He consumed large quantities of carbohydrate-rich foods following the competition. His past medical history was significant for anxiety, and family history was non-contributory. Examination was normal except for reduced power and hyporeflexia in both legs, despite his muscular physique. He was noted to have severe hypokalaemia (K+= 1.9 mmol/L). His thyroid function tests were consistent with thyrotoxicosis. He reported taking thyroxine and several other agents to facilitate muscle mass generation before the bodybuilding competition. His presentation was reminiscent of thyrotoxic periodic paralysis, albeit uncommon with Caucasian ethnicity. He also had transient hyperglycaemia at presentation with concomitant hyperinsulinaemia, which could be attributed to the carbohydrate load and may have exacerbated his hypokalaemia through a transcellular shift. Urine toxicology screen subsequently ruled out the use of diuretics but confirmed the presence of a long-acting beta agonist (clenbuterol) which, along with other substances, may have aggravated the hypokalaemia further. After 12 h of i.v. replacement, the potassium level normalised and leg weakness resolved. The patient agreed to stop taking thyroxine and beta agonists and was well during the clinic visit at one month follow-up. This case highlights the potential for thyrotoxicosis factitia to exacerbate hypokalaemia and muscle weakness from other causes in bodybuilders presenting with acute severe weakness, irrespective of ethnicity.

Learning points

  • In patients presenting with muscle weakness and hypokalaemia, early consideration of thyrotoxicosis is essential, even in the absence of a past history of thyroid disease or specific symptoms of thyrotoxicosis, in order to allow prompt initiation of appropriate treatment and to prevent recurrence.

  • Bodybuilders may constitute a uniquely ‘at-risk’ group for thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia, especially where there is concomitant use of beta-adrenergic agonists, even in the absence of diuretic use.

  • Although rare and usually described in patients of Asian or Polynesian ethnicity, this case highlights that thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia can also occur in patients with Caucasian ethnicity.

  • We speculate that consuming large quantities of carbohydrates may induce hyperinsulinaemia, which could theoretically contribute to worse hypokalaemia, though mechanistic studies would be needed to explore this further.

Open access
P A D M Kumarathunga Diabetes and Endocrinology Unit, National Hospital Kandy, Kandy, Sri Lanka

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N S Kalupahana Department of Physiology, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka

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C N Antonypillai Diabetes and Endocrinology Unit, National Hospital Kandy, Kandy, Sri Lanka

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Summary

Whey protein is a popular dietary supplement that is claimed to provide multiple health benefits. It has been shown to delay gastric emptying and impair ileal nutrient absorption. Additionally, some of the other additives like papain enzyme, soy lecithin in these protein supplements could interfere with L-thyroxine absorption. There is no evidence in the literature for the effects of protein supplements on L-thyroxine absorption. Herein, we describe a case of a 34-year-old lady who was on endocrinology follow up for primary hypothyroidism with stable thyroid-stimulating hormone (TSH) levels within the normal range while on L-thyroxine with a dose of 125 µg daily for the last 3 years, presenting with mild hypothyroid symptoms and elevated TSH level following a recent introduction of a protein supplement by her physical care adviser. Her treatment adherence and ingestion technique were good throughout, she was not on other medications or herbal remedies, there were no other changes in her food pattern or features suggestive of malabsorption, she was not pregnant, was taking the same L-thyroxine brand and TSH test was done from the routine lab. Since the only factor which could have contributed to the deranged TSH levels was the recent introduction of the whey protein supplement, we advised her to stop the protein supplement while continuing the same dose of L-thyroxine. Her TSH level was repeated in 6 weeks and was found to be normal (1.7 mIU/L). Our case report demonstrates that over-the-counter protein supplements could interfere with L-thyroxine absorption. Therefore, patients on L-thyroxine should be cautious when taking them.

Learning points

  • Over-the-counter protein supplements could interfere with oral L-thyroxine absorption.

  • The underlying mechanism could be the effect of whey protein by delaying gastric emptying and reduced responsiveness of organic anion transporters in the ileum, and there may be a contribution from other additives like papain and soy lecithin present in these supplements.

  • When there is an elevation of previously stable thyroid-stimulating hormone (TSH) value in a hypothyroid patient on oral L-thyroxine, the patient's assessment should include inquiring for a recent introduction of protein supplement, in the absence of other well-known risk factors.

  • Discontinuation of protein supplement results in normalization of thyroid function tests.

  • Patients on oral L-thyroxine should be cautious when taking over-the-counter protein supplementation.

Open access
Ayesha Ghayur Department of Medicine, McMaster University, Hamilton, Ontario, Canada

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Qurrat Elahi Department of Family Medicine, Pikeville Medicine Center, Pikeville, Kentucky, USA

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Chinmay Patel Department of Nephrology, Southern Kidney Associates, Shreveport, LA, USA

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Rishi Raj Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Pikeville Medical Center, Pikeville, Kentucky, USA

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Summary

Hypothyroidism is a common medical condition and is often easily managed with excellent outcomes, when treated adequately. Compliance with levothyroxine (LT4) therapy is often compromised because of the need for a daily and lasting schedule. Overt rhabdomyolysis due to under-treatment or non-compliance is a rare occurrence. We report a case of rhabdomyolysis leading to acute kidney injury (AKI) on chronic kidney disease (CKD) requiring hemodialysis (HD) in a 68-year-old Caucasian male due to non-compliance with levothyroxine (LT4) therapy. Our patient 'ran out of levothyroxine' for approximately 4 weeks and developed gradually progressive muscle pain. The diagnosis of severe AKI due to rhabdomyolysis was made based on oliguria, elevated creatinine kinase (CK), and renal failure. Resuming the home dose of LT4 failed to correct CK levels, and there was a progressive decline in renal function. Although increasing doses of LT4 and three cycles of HD improved CK levels, they remained above baseline at the time of discharge. The patient recovered gradually and required HD for 4 weeks. CK levels normalized at 6 weeks. Through this case report, we highlight that non-compliance with LT4 therapy can lead to life-threatening complications such as renal failure and hence the need to educate patients on the significance of compliance with LT4 therapy should be addressed.

Learning points

  • Non-compliance to levothyroxine therapy is common and can lead to serious complications, including rhabdomyolysis.

  • Rhabdomyolysis is an uncommon presentation of hypothyroidism and severe rhabdomyolysis can result in renal failure requiring hemodialysis.

  • Rhabdomyolysis associated with hypothyroidism can be further exacerbated by concomitant use of statins.

Open access
Edmond Puca Service of Infection Diseases, University Hospital Center, Tirane, Albania

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Entela Puca Service of Endocrinology, Amerikan Hospital, Tirane, Albania

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Pellumb Pipero Service of Infection Diseases, University Hospital Center, Tirane, Albania

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Holta Kraja Service of Anaesthesia and Reanimation, University Hospital Center, Tirane, Albania

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Najada Como Service of Infection Diseases, University Hospital Center, Tirane, Albania

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Summary

Comorbidities are a risk factor for patients with COVID-19 and the mechanisms of disease remain unclear. The aim of this paper is to present a case report of an COVID-19 patient with severe hypocalcaemia. This is a report of an 81-year-old female, suffered from myalgia and fatigue for more than 3–4 weeks. Fever and cough appear 2 days before she presented to the emergency room. On physical examination, she was febrile with a temperature of 38.8°C, accompanied by cough, sore throat, headache, fatigue, and muscle ache. Her past medical history was remarkable with no chronic disease. She had lymphopenia. Laboratory test revealed moderate liver dysfunction, hypoalbuminemia, and severe hypocalcaemia (serum corrected calcium level: 5.7  mg/dL). Parathyroid hormone (PTH) was 107.9 pg/mL (range: 15–65) and 25(OH)2D levels was 4.5 ng/mL (range: 25–80). Chest CT scan detected peripheral ground-glass opacity. Throat swab for coronavirus by RT-PCR assay tested positive for the virus. She was treated with lopinavir/ritonavir, third generation cephalosporin, anticoagulant, daily high-dose calcium acetate, vitamin D3, fresh frozen plasma and oxygen therapy. She was discharged after two negative throat swab tests for coronavirus by conventional RT-PCR.

Learning points:

  • Comorbidities are a risk factor for patients with COVID-19.

  • Laboratory findings are unspecific in COVID-19 patients; laboratory abnormalities include lymphopenia, elevated of LDH, CPK and the inflammatory markers, such as C reactive protein, ferritinemia and the erythrocyte sedimentation rate.

  • In addition to inflammatory markers, in COVID-19 patients it is crucial to check the level of vitamin D and calcium.

  • There may be a correlation between vitamin D deficiency and the severity of COVID-19 disease.

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Colin L Knight Department of Endocrinology and Diabetes, University Hospital Geelong, Geelong, Victoria, Australia

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Shamil D Cooray Department of Endocrinology and Diabetes, University Hospital Geelong, Geelong, Victoria, Australia

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Jaideep Kulkarni Department of Endocrinology and Diabetes, University Hospital Geelong, Geelong, Victoria, Australia

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Michael Borschmann Ear, Nose and Throat, Head and Neck Surgery, St. John of God Hospital, Geelong, Victoria, Australia
Director of Otolaryngology, University Hospital Geelong, Geelong, Victoria, Australia

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Mark Kotowicz Department of Endocrinology and Diabetes, University Hospital Geelong, Geelong, Victoria, Australia
Deakin University School of Medicine, Geelong, Victoria, Australia
Melbourne Clinical School-Western Campus, Department of Medicine, The University of Melbourne, St. Albans, Victoria, Australia

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A 51 year old man presented with sepsis in the setting of thioamide-induced agranulocytosis. Empiric broad-spectrum antibiotics was followed by directed narrow-spectrum antibiotics, and his neutrophil count recovered with support from granulocyte-colony stimulating factor (G-CSF) analogue transfusions. After a brief period of multi-modal therapy for nine days including potassium iodide (Lugol’s iodine), cholestyramine, propanolol and lithium to temper his persisting hyperthyroidism, a total thyroidectomy was performed while thyroid hormone levels remained at thyrotoxic levels. Postoperative recovery was uncomplicated and he was discharged home on thyroxine. There is limited available evidence to guide treatment in this unique cohort of patients who require prompt management to avert impending clinical deterioration. This case report summarises the successful emergent control of thyrotoxicosis in the setting of thioamide-induced agranulocytosis complicated by sepsis, and demonstrates the safe use of multi-modal pharmacological therapies in preparation for total thyroidectomy.

Learning points:

  • Thioamide-induced agranulocytosis is an uncommon but potentially life-threatening complication of which all prescribers and patients need to be aware.

  • A multi-modal preoperative pharmacological approach can be successful, even when thioamides are contraindicated, when needing to prepare a thyrotoxic patient for semi-urgent total thyroidectomy.

  • There is not enough evidence to confidently predict the safe timing when considering total thyroidectomy in this patient cohort, and therefore it should be undertaken when attempts have first been made to safely reduce thyroid hormone levels.

  • Thyroid storm is frequently cited as a potentially severe complication of thyroid surgery undertaken in thyrotoxic patients, although the evidence does not demonstrate this as a common occurrence.

Open access