Nephrotoxicity from non-steroidal anti-in ammatory drugs (NSAID) is well recognized. We report a case of severe hypokalaemia and weakness due to renal tubular acidosis in a young woman who was taking 40-60 tablets per day of Nurofen Plus 1 (ibuprofen 200 mg and codeine phosphate 12 ¢ 8 mg). Proprietary brands of ibuprofen are freely available to the public and those containing codeine may be potentially subject to abuse. This case highlights the need to be aware of this potential and of the life-threatening electrolyte and acid-base disturbances that might be encountered with the widespread availability of these types of NSAID. Case reportA 28-year-old woman presented to the emergency department with a 2-day history of severe generalized weakness. She was unable to stand up or hold her neck straight. She said that she had one episode of vomiting on the day before admission and that, 2 weeks earlier, she had bronchitis for which her general practitioner prescribed amoxycillin. She was taking pantoprazole for a duodenal ulcer, diagnosed 7 months earlier. She was also taking over-the-counter analgesics for relapsing knee pains. She had a history of depression and alcohol dependence for which she had previously received psychiatric counselling.On examination, she was afebrile (36¢78C), her pulse rate was 90 per min, regular, and blood pressure 110/60 mmHg. She had severe generalized muscle weakness but no neurological de¢cit. Body mass index was 20¢4 kg/m 2 . The ECG showed prolonged QT intervals and inverted T waves.Blood tests on admission, showed serum potassium 1Í4 mmol/L (3Í6-5Í3), sodium 141 mmol/L (138-146), urea 6Í4 mmol/ L (2Í5-7Í5), creatinine 64 mmol/L (50-130), calcium 2Í54 mmol/ L (2Í2-2Í6) and phosphate 0Í43 mmol/ L (0Í8-1Í4). Further investigations revealed serum bicarbonate 14Í7 mmol/ L (21-28), chloride 112 mmol/ L (96-104) and an anion gap of 15Í7 mmol/L (12-16). Urinary potassium was inappropriately high at 26Í6 mmol/ L and the renal tubular maximum reabsorption of phosphate (TmP/GFR) was low at 0 Í31mmol/ L GFR (0 Í8-1Í4).In view of the hypokalaemia, hyperchloraemia, low serum bicarbonate and normal anion gap, the diagnosis of renal tubular acidosis was made. She was treated with intravenous potassium therapy over the following 4 days (a total of 340 mmol) and her serum potassium rose gradually to 3Í7 mmol/ L and bicarbonate to 23Í9 mmol/ L by day 4; 2 days later, and without any further treatment, her serum potassium was 4Í9 mmol/ L and bicarbonate 26Í5 mmol/ L. The TmP/GFR was normal (1Í4 mmol/ L GFR) and the fractional excretion of bicarbonate was 1%. An ammonium chloride acidi¢cation test was undertaken but was inconclusive because she vomited shortly after ingesting the ammonium chloride.A review of her notes revealed that, 8 months earlier, she was admitted to hospital with an episode of abdominal pain and diarrhoea. Her serum potassium at the time was 2Í4 mmol/ L and had normalized with intravenous and oral potassium. Her hypokalaemia was thought to be due to the diarrhoea and she...

Cryptogenic fibrosing alveolitis (CFA) is an interstitial lung disease, which by definition is of unknown aetiology. Recent evidence has suggested that smoking and occupational exposure to dusts may be environmental risk factors for the disease, but there has been little research into potential host risk factors. One previous study has suggested that the prevalence of abnormal alpha1-antitrypsin phenotypes may be increased in patients with CFA. Since alpha1-antitrypsin is important in regulating inflammation within the lung in response to environmental exposures, such abnormalities may be of aetiological importance in this disease. We have compared the alpha1-antitrypsin phenotypes of 189 patients with CFA with 189 age-, sex-, and community-matched controls. This sample size was sufficient to provide more than 95% power to detect an odds ratio (OR) of 2.5. Alpha1-antitrypsin phenotype was established by isoelectric focusing, and the prevalence of abnormal phenotypes in cases and controls was compared by conditional logistic regression. Personal smoking histories were obtained by postal questionnaire. The prevalence of abnormal alpha1-antitrypsin phenotypes was similar in cases and controls (12.7 versus 15.3%; OR 0.88; 95% confidence interval 0.49-1.57; p=0.66). No interaction was found between the presence of abnormal alpha1-antitrypsin phenotypes and a history of smoking. We conclude that cryptogenic fibrosing alveolitis is not associated with abnormal alpha1-antitrypsin phenotypes.

did not drink any alcohol. Physical examination on admission revealed bilateral swellings across the medial aspects of both thighs, with overlying bruising and purpura (Fig 1a ). He was haemodynamically stable and respiratory, abdominal and neurological examinations were unremarkable. There was no palpable lymphadenopathy. His dentition was poor, with the majority of teeth absent.Blood tests showed a normocytic anaemia (haemoglobin [Hb] A 73-year-old man presented with bilateral leg pain and swelling, and no history of trauma or bleeding disorders. Clinical examination, biochemistry and magnetic resonance imaging of the thighs were suggestive of muscle haematomas. These progressed signifi cantly during the admission, requiring blood transfusion. Normal vascular anatomy on computed tomography, renal and liver function, and absence of infection made a bleeding diathesis more likely. This may be caused by coagulation defects, platelet disorders and vascular fragility. An undetectable serum ascorbic acid level confi rmed the clinical suspicion of scurvy, and administration of vitamin C resulted in rapid improvement. Our case provides a structured approach to the diagnosis of bleeding disorders and scurvy, a treatable and potentially fatal disease which is often forgotten. KEYWORDS : Muscle haematomas , scurvy , bleeding disorders Case historyA 73-year-old man of Asian origin with a background of ischaemic heart disease, hypertension and type 2 diabetes presented to our London hospital complaining of severe bilateral thigh and leg pain. He described a dull ache throughout the lower limbs, which was of gradual onset and deteriorated over a period of 5 months. This was exacerbated by movement rendering him unable to walk. There were no constitutional symptoms, history of trauma or alterations to his medications in the past year. He took no non-steroidal anti-inflammatory drugs (NSAIDs), anticoagulant or antiplatelet agents, and there was no family history of any bleeding disorders. The patient lived alone, was previously fully independent, a non-smoker and

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