Objectives. To describe 2 cases of thyrotoxic periodic paralysis. Methods. We report of 2 cases of thyrotoxic periodic paralysis in 2 individuals from 2 different backgrounds with emphasis on their presentation and treatment. We also conducted a literature search to put together an update review of thyrotoxic periodic paralysis. Results. A 47-year-old Chinese and 28-year-old Caucasian male presented with profound yet reversible weakness associated with hypokalemia on admission bloods and thyrotoxicosis. Both were given definitive therapy to prevent recurrence of attacks with any future relapse of thyrotoxicosis. Conclusion. Thyrotoxic periodic paralysis (TPP) is a rare but potentially serious complication of thyrotoxicosis resulting in temporary but severe muscle weakness. Recent discovery of a novel mutation in the KCNJ18 gene which codes for an inwardly rectifying potassium channel and is controlled by thyroid hormones may provide greater insight into the pathogenesis of TPP.

A 31-year-old lady presented to hospital with a two-week history of shortness of breath, pleuritic chest pain and productive cough. She had been unable to keep solids down for the previous month and was only able to tolerate small sips of fluid before vomiting for the week prior to admission. She had a gastric band fitted one year previously and had lost 50 kg since, but had no history of diabetes mellitus. She had no previous psychiatric history and denied taking excess alcohol, anti-freeze or tricyclic antidepressants.On examination, blood pressure was 128/93 mmHg, pulse 108/minute, respiratory rate 18/minute and oxygen saturation 96% on room air. She looked pale, chest and abdominal examination were unremarkable. Initial arterial blood analysis demonstrated a normal pH (7.372), PCO 2 of 3.52kPa (4.7-6.0kPa), PO 2 12.95kPa (9.3-13.3kPa) and HCO 3 15.0 mmol/l (22-26 mmol/l), base excess of -8.5 (-2 to 2 mmol/l). Her anion gap was raised at 18.1 mmol/l (8-16 mmol/l) and lactate was normal at 0.6 mmol/l (Ͻ2 mmol/l). Electrocardiogram (ECG) demonstrated sinus tachycardia with non-specific ST changes in V3-V6. Chest X-ray demonstrated normal heart size and a small area of shadowing in the left middle zone. She was admitted with a provisional diagnosis of viral respiratory infection with pleurisy. She was treated initially with intravenous (iv) fluids.Urinalysis was strongly positive for ketones (ϩϩϩ). Her full blood count, urea and electrolytes and C-reactive protein were normal. Salicylate levels were negative. A computed tomography pulmonary angiogram (CTPA) showed patchy consolidation of midzones and right upper lobe, and fluid distension within the oesophagus and a pouch of this was isolated by the band, herniating into the hiatus hernia. There was no free fluid or gas in the abdomen and no evidence of pulmonary embolism (Fig 1). Differential diagnosisShe had a high anion gap, metabolic acidosis with normal lactate levels. The differential diagnosis of metabolic acidosis is highlighted in Fig 3. Careful consideration of her history (especially not eating and drinking, vomiting), and exclusion of other causes of a high anion gap acidosis (normal lactate, glucose, salicylate levels and no features to suggest other poisoning) led to the suspicion that she had starvation ketoacidosis and aspiration pneumonia. Initial managementInvestigations were carried out to exclude the different causes of her high anion gap metabolic acidosis including lactate, salicylate levels, blood glucose levels, urine (ideally blood ketone metre readings), calcium oxalate crystals on urine microscopy and/or a high osmolar gap (obtained by comparing the patient's measured serum osmolality against predicted osmolality) may suggest ethylene glycol poisoning especially if clinically A Lulsegged, 1 consultant physician, endocrinology and diabetes; E Saeed, 2 foundation year 1, general medicine; E Langford, 2 consultant physician, cardiology; C Duffield, 3 foundation year 1, general surgery; S El-Hasani, 3 general surgeon; N Pareek, 2 specialis...

Aim. Despite an incidence of parathyroid “incidentalomas” of 0.2%–4.5%, only approximately 135 cases have been reported in the literature. We present eight patients in whom an incidental abnormal parathyroid gland was found during routine thyroid surgery. We have reviewed the literature and postulate whether these glands could represent further evidence of a preclinical stage of primary hyperparathyroidism. Methods. A retrospective analysis of all 236 thyroid operations performed by a single surgeon was performed to identify patients in whom abnormal parathyroid tissue was removed at surgery. Results. 8/236 patients (3.39%) had a single macroscopically abnormal parathyroid gland removed and sent for analysis. Seven patients were found to have histological evidence of a parathyroid adenoma or hyperplasia. None of the patients had abnormal serum calcium detected preoperatively. Postoperatively, four patients had normal calcium, three had temporary hypocalcaemia and one refused followup. No patients had recurrent laryngeal nerve impairment. Conclusions. Despite the risk of removing a histologically normal gland, we believe that when parathyroid “incidentalomas” are found during surgery they should be excised and sent for histological analysis. We have found this to be a safe procedure with minimal morbidity to the patient. As the natural history of primary hyperparathyroidism is better understood, these glands found in normocalcaemic patients may in fact represent the early or preclinical phase of the disease. By removing them at the original operation, the patient is saved redo neck surgery with its high complication rate as or when clinically apparent primary hyperparthryoidism develops in the future.

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