Severe thyrotoxicosis can present with a myriad of cardiovascular complications. It may be mild features such as palpitations, tachycardia, and exertional dyspnea or may progress to life-threatening consequences such as atrial fibrillation, tachyarrhythmias, heart failure, myocardial infarction, and shock. In rare cases, they may present with myocardial ischemia secondary to coronary artery vasospasm. We report a case of a 59-year-old Malay gentleman who presented with fast atrial fibrillation and tachycardia-mediated heart failure that evolved to a silent myocardial infarction secondary to severe coronary artery vasospasm with undiagnosed severe thyrotoxicosis. He had complete resolution of heart failure and no further recurrence of coronary artery vasospasm once treatment for thyrotoxicosis was initiated and euthyroidism achieved. This life-threatening consequence has an excellent prognosis if recognised early and treated promptly.

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Summary Polycystic ovarian syndrome (PCOS) is associated with menstrual irregularities, ovulatory dysfunction, hirsutism, insulin resistance, obesity and metabolic syndrome but is rarely associated with severe hyperandrogenaemia and virilisation resulting in male pattern baldness and clitoromegaly. Total serum testosterone greater than twice the upper limit of the reference range or free androgen index of over five-fold elevated suggests a diagnosis other than PCOS. We reported a case of a 15 years old obese girl presented with secondary amenorrhoea, virilising signs: frontal baldness, clitoromegaly and prominent signs of insulin resistance and marked acanthosis nigricans. Her total testosterone level was markedly elevated at 9.4 nmol/L (0.5–1.7 nmol/L) and MRI pelvis revealed a right ovarian mass with fat and cystic component and a left polycystic ovary. The patient underwent laparoscopic right ovarian cystectomy and histologically confirmed mature cystic teratoma. Post-operatively, her testosterone level declined but did not normalise, menses resumed but remained irregular. Her fasting insulin was elevated 85.2 mIU/L (3–25 mIU/L) and HOMA-IR was high at 13.1 (>2) with persistent acanthosis nigricans suggesting co-existing HAIR-AN syndrome, an extreme phenotype of polycystic ovarian syndrome. Learning points Rapid onset of hyperandrogenic symptoms, especially if associated with signs of virilisation must raise the suspicion of an androgen-secreting tumour. Total serum testosterone greater than twofold the upper limit of the reference range or free androgen indices over fivefold suggest a diagnosis other than polycystic ovarian syndrome (PCOS). High levels of testosterone with normal levels of the DHEA-S suggest an ovarian source. Ovarian androgen-secreting tumour and HAIR-AN syndrome, an extreme spectrum of PCOS can co-exist.

Introduction: Antithyroid drugs (ATDs) are recommended effective treatment for uncontrolled Graves’ disease but achieves maximal antithyroid effects between 6 to 12 weeks. Cholestyramine sequesters thyroid hormones in the intestine and enhances its fecal excretion. Steroids inhibits the conversion of thyroxine to triiodothyronine peripherally and blocks thyroid hormone production. We hypothesize that adjunctive cholestyramine or prednisolone to ATDs may reduce circulating thyroid hormones and improve biochemical control. Methods: In this multicenter, open labelled, parallel-group trial, we randomly assigned in a 1:1:1 ratio, adult Graves’ disease patients with moderate to severe hyperthyroidism (FT4 levels > 40 pmol/L) to receive either adjunctive cholestyramine 4g twice daily or prednisolone 30 mg daily in tapering down doses in addition to standard treatment or standard treatment alone for 4 weeks. Standard treatment was carbimazole 30mg daily and propanolol 40mg BD for 4 weeks. The primary endpoint was change from baseline for FT4 and FT3 levels at the end of 2 and 4 weeks of intervention. Safety endpoints including gastrointestinal adverse events, hypokalemia, hypothyroid and hyperglycemia were recorded. Results: A total of 107 patients were screened and 97 patients randomised. Baseline demographics, clinical and biochemical characteristics were similar between the groups. The baseline median FT4 levels were 51.6 pmol/L (42.2-71.1) and FT3 levels 22.5 pmol/L (5.7-30.8). Both FT4 and FT3 declined at two and four weeks from baseline but were no different between the three groups. At week 2, median FT4 levels declined by 43.3% (25.8-53.3), 39.8% (19.1-55.1) and 33.4% (20.1-62.0) (p=0.988) and at 4 weeks, 50.9% (33.3-63.8), 57.8% (39-70.9), 55.8% (36.2-72.0) (p =0.362) in the cholestyramine, prednisolone and standard treatment group respectively. Median FT3 levels reduced by 51.2% (22.8- 58.9), 59.9% (38.9-69.3) and 50.9% (26.9-63.9) (p=0.084) at week 2 and 60% (39.2-67.9), 67.5% (38.4-78.4), 63.1% (45.7-69.3) (p=0.387) in the corresponding cholestyramine, prednisolone and standard treatment only group. A higher number of gastrointestinal adverse events: constipation, bloating, diarrhea, abdominal pain and vomiting were observed in the cholestyramine group in the first 2 weeks of treatment and no difference in the incidence of hypokalemia between groups. Conclusion: Adjunctive cholestyramine or prednisolone did not improve the biochemical control of uncontrolled moderate to severe Graves’ disease when added to ATDs. The additional use of cholestyramine resulted in a higher number of gastrointestinal adverse events but were mild and self-limiting.

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