To the Editor: Senna is widely used in laxatives, but the results of its misuse are not inconsequential. We describe a 36-year-old woman admitted with hypercalcaemia and renal failure. She had a 6-year history of anorexia nervosa and ingestion of 50–100 senna tablets daily for weight loss. Examination revealed clubbing of the fingers and toes, a body mass index (BMI) of 17.7 kg/m2 and postural hypotension. Laboratory findings on admission are shown in Box 1. Results of autoimmune studies and protein electrophoresis, and the serum angiotensin-converting enzyme level were normal. Parathyroid hormone-related peptide was absent. She had a bland urinary sediment, trace proteinuria (150 mg/24 h; reference range, < 150 mg/24 h) and a urine pH of 5.0 (physiological range, 4.5–8.0).

Computed tomography scans did not detect malignancy or infection, but showed bilateral medullary renal calcifications. Renal biopsy confirmed extensive nephrocalcinosis and the absence of primary glomerular disease. A skeletal survey showed prominent periosteal reaction and new bone formation at the ends of long bones (Box 2, A). A bone scan revealed increased tracer uptake in a pattern consistent with hypertrophic osteoarthropathy (HOA; Box 2, B). Interestingly, bone mineral density (BMD) scans showed increased lumbar and femoral T scores (1.2 and 1.3, respectively). Four years later, the renal failure, clubbing and HOA persisted despite a reduction in senna intake.

Low urine volume is a prerequisite for urolithiasis, but hypercalcaemia is the key requirement for nephrocalcinosis.3 The suppressed parathyroid hormone level and elevated serum calcium level excludes primary hyperparathyroidism and made familial hypocalciuric hypercalcaemia unlikely. The serum and urine biochemistry was inconsistent with thiazide diuretic use or renal tubular acidosis. Hence, exogenous calcium is the likely cause of hypercalcaemia. Each of the senna (calcium sennosides) tablets the patient ingested contained 12.5 mg of calcium. Chronic ingestion, in addition to dehydration (with low calcium excretion) and a low BMI may contribute to a vicious circle of calcium phosphate retention, renal failure and nephrocalcinosis. Indeed, hydration increased her calcium excretion to 6.23 mmol/day and normalised her serum calcium and phosphate levels after a week.

The association between finger clubbing and senna misuse, and the reversibility of finger clubbing, were reported in 1975.4 Several reports have followed, but only one noted concurrent HOA on plain x-rays.5 We believe that our report is the first to show the extent and distribution of HOA related to this disorder. It remains unknown whether HOA is reversible with abstinence from senna. Patients with anorexia are also more likely to have a low BMD, and the increased BMD scores seen in our patient might be the result of metastatic calcification or periosteal new bone formation. Neither could be conclusively proven.

The development of nephrocalcinosis in anorexic patients is more common than is generally appreciated. Clubbing and HOA are useful clues to senna misuse, and BMD measurements should be interpreted with caution in this setting.

2 Ankle x-ray and full bone scan