As this journal thuds onto the work-place desk, in deepest mid-winter, the thoughts of most will be far from outdoor sporting activities – least of all those involving personal participation. In an earlier Piscatorial annotation, the problems confronting the World Anti-Doping Agency, in relation to steroid and hormone abuse in sport, were discussed. The challenge of keeping elite sports free of drugs is ongoing as increasingly more sophisticated strategies are developed to circumvent detection. In this respect, I was unaware of the use of osteocalcin as a marker of growth hormone abuse. To establish the normal variation in osteocalcin in response to exercise, a study was undertaken of 15 male recreational athletes participating in a half-marathon of 21 km (Clin Chem 2008;545:1093–5). One would think that stress of competition was enough without being subjected to venepuncture on completion of the event – pointless to measure cortisol at any rate. Both osteocalcin and parathyroid hormone (PTH) were measured prerace and at timed intervals of up to 24 h after the race. There were exercise-induced increases in both PTH and osteocalcin observed immediately after the race but these returned to basal concentrations within 3 h. The authors state that it is important that the acute and transitory increase in osteocalcin should be recognized to avoid false allegations of growth hormone abuse. For the record, a previous study (Int J Sports Med 2007;28:576–9) documented the changes in PTH (and cortisol) after an ultramarathon of 245 km – can't have been many volunteers for that.

Continuing the theme of bone metabolism, a recent review examines what the authors regard as a ‘common’ clinical problem – hypoparathyroidism (N Engl J Med 2008;359:391–403). This is published under the Clinical Practice banner and will be a good source of CPD points from self-directed learning. As is typical of the journal, there are impressive coloured illustrations to facilitate ease of understanding of the more complicated hormonal interactions together with a detailed listing of the various categories of hypoparathyroidism. In this regard, I did not know that deposition of heavy metals such as iron (in thalassaemia and haemochromatosis) and rarely copper (as in Wilson's disease) can damage the gland. Similarly, the more recently identified genetic causes of hypoparathyroidism are presented – while the relatively familiar Di George syndrome, for example, has an incidence of 1:4000 to 1:5000 live-births, activating mutations in the extracellular calcium-sensing receptor are much less common. There is also discussion of the conditions owing to hormone resistance. Guidelines for clinical treatment of the hypocalcaemia are presented as are recommendations for the biochemical monitoring of response to vitamin D treatment. The authors acknowledge that there is limited data on replacement therapy with injectable human PTH, which may be the only viable treatment for defects in the calcium-sensing receptor.

The British Medical Journal has also dedicated a clinical review to the topic of hypocalcaemia (BMJ 2008;336:1298–302). Interestingly, the authors refer an incidence of hypocalcaemia of 85% among patients in intensive care. This is a less sophisticated examination of the topic but probably more of use to hard-pressed physicians, which distinguishes the commonplace from the rare. In the investigation of hypocalcaemia, the authors recommend measurement of PTH as a front-line test with it being placed high up the diagnostic algorithm. Brief mention is made of the diagnostic usefulness of alkaline phosphatase and the measurement of phosphate has ‘limited value’. So now we know.

A study of the long-term follow-up of patients with hyperparathyroidism, who were treated conservatively, has been published (JCEM 2008;93:3462–70). Due mention was made of the history of opportunistic identification of cases of hyperparathyroidism when blood samples were first submitted to unselective, multi-channel analysis in the 1970s.

The unexpected finding of hypercalcaemia duly lead to the demonstration of raised PTH. The clinical profile of the disease at presentation changed from one in which there was significant skeletal and renal disease to one where patients were essentially asymptomatic. This paper supplements the information published after an initial decade of follow-up and extends the period of observation to 15 years. The cohort was 116 patients of whom 91 were female – 85% of the cohort was asymptomatic at recruitment. Approximately half the cohort underwent parathyroidectomy – the patients had higher serum calcium and PTH than those conservatively managed. Of the latter, nearly half did meet the consensus clinical criteria for surgery at recruitment but refused intervention initially. During the 15-year follow-up, the majority of the non-intervention group remained asymptomatic but nonetheless, half of them did ultimately proceed to successful surgery. The authors found evidence of decline in cortical bone density in the conservatively managed group, which they felt was indicative of disease progression. They felt that non-interventional management should be limited to the first decade of follow-up. They also stress the need for continued long-term surveillance of biochemical indices in all patients with mild disease who do not undergo surgery – for the purposes of the study this involved thrice yearly routine serum ‘bone profile’ with measurement of urinary calcium excretion, PTH and vitamin D.

Small wonder that the laboratory workload is increasing exponentially.