To the Editor: I read with interest the recent review of Paget’s disease by Walsh.1 I would recommend that calcium and phosphate levels should be included in the initial biochemical assessment, as both tests are cheap and readily available. As Paget’s disease predominantly afflicts the older population, coexisting vitamin D deficiency is likely. Low (but within the normal range) calcium and phosphate levels may support this diagnosis. Conversely, hypercalcaemia, a rare event in Paget’s disease except in prolonged immobilisation,2 may indicate primary hyperparathyroidism, which is significantly associated with Paget’s disease,3 or, less commonly, metastatic bone disease. Both these conditions have prognoses and management distinctly different from those of Paget’s disease.

Serum total alkaline phosphatase levels may not be elevated in 15% of active Paget’s disease.4 While bone-specific alkaline phosphatase level is more useful in these situations, this test is not readily available in some laboratories and, even among those in which it is available, some only provide qualitative results, making it less useful for monitoring Paget’s disease and the response to therapy. A suitable alternative test is urinary deoxypyridinoline/creatinine ratio, which can be done either on a random urine sample or a 24-hour urine collection.

In addition, the serum total alkaline phosphatase level can be spuriously low in malnourishment, and specifically in zinc deficiency,5 a frequent occurrence in elderly people. I describe here a case highlighting such a problem.

A 72-year-old socially isolated widower of 8 years presented with progressively worsening pain in his right hip in the preceding 3 months. He had poor appetite and had lost 6 kg in weight, but had no symptoms of malignancy. Clinical examination showed a thin man (body mass index, 20 kg/m2), who was otherwise normal with no features of zinc deficiency. A plain x-ray of the pelvis showed bilateral osteosclerosis. His total alkaline phosphatase level was 28 U/L (reference range, 35–110 U/L). Other investigations for metabolic bone disease gave normal results, including one for vitamin D level. Among other nutritional parameters, his zinc level was 5.2 mol/L (reference range, 10.0–18.0 mol/L).

A computed tomography scan of the thorax and abdomen showed no evidence of malignancy, and a bone scan was consistent with Paget’s disease. A zinc supplement was prescribed and his diet optimised.

At 6-week review, the serum zinc level had improved to 12.5 mol/L, but the serum total alkaline phosphatase level was 250 U/L. This confirmed that the patient’s acquired hypophosphatasia was secondary to zinc deficiency, with zinc being a critical cofactor for alkaline phosphatase activity.4

In light of the “correct” total alkaline phosphatase level, the patient was given intravenous pamidronate, with resulting marked resolution of his symptoms, including a 5-kg weight gain and normalisation of total alkaline phosphatase level.

Although this case is unusual, it nevertheless highlights the need to consider occult and coexisting nutritional morbidities in an elderly population.