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Measurement of serum ionized calcium was performed daily for 7 days after admission in 8 consecutive patients with acute pancreatitis. The results support the findings of our previous study that the most common cause of the low serum calcium often found in patients with this disease is a low serum albumin; when correction of serum calcium is made for hypo-albuminaemia, most patients are found to be normocalcaemic. The occasional hypocalcaemia as shown by the ‘corrected’ serum calcium or by serum ionized calcium measurement is usually mild and transient, indicating that the normal homoeostatic mechanisms of the body can efficiently maintain the physiologically active fraction of the serum calcium within, or close to, the normal range. These findings explain the rarity of overt and subclinical tetany in acute pancreatitis. This study has shown that correction of serum calcium for albumin provides similar information to the direct measurement of serum ionized calcium. The value of ‘apparent’ hypocalcaemia in assessing severity of acute pancreatitis requires reappraisal, while greater attention should be directed towards the investigation and management of hypoalbuminaemia in this disease.

Sequential daily measurements of plasma parathyroid hormone (PTII) have been performed in 89 patients with acute pancreatitis. A total of 439 PTH assays was obtained during 98 episodes of the disease. Three main patterns of PTH response were found. These responses were correlated with severity of disease graded by objective criteria and also to corrected serum calcium levels. The first type of PTH response was characterized by significantly elevated PTH levels soon after hospitalization with a subsequent decrease in levels to within the normal range by the third or fourth day of illness. This type of response was specifically associated with transient severe hypocalcaemia (corrected calcium <2·0 mmol/1). It was also associated with the most severe forms of disease and 6 of the 7 deaths. The second type of PTH response revealed initial PTH values in the upper level of the normal range (400–600 ng/l) while persistently low PTH levels were characteristic of the third type of response. Persistently low PTH levels were associated with normocalcaemia, and no patient in this group died. None of a group of 14 control patients exhibited the type 1 PTH response. An effective PTH response to an unidentified hypocalcaemic stimulus results in satisfactory calcium homeostasis in most patients with acute pancreatitis.

Twenty adult epileptic out-patients who had received anticonvulsant therapy for a mean duration of 15 years were assessed for clinical, biochemical, radioisotopic and bone biopsy evidence of osteomalacia. Occasional biochemical abnormalities were demonstrated but no individual subject was found to have osteomalacia. There is increasing evidence to cast doubt on the existence of a strong relationship between anticonvulsant drugs and osteomalacia. This evidence is reviewed and it is concluded that in the presence of adequate sunlight exposure anticonvulsant therapy alone is most unlikely to lead to osteomalacia in adults.

1. Foetal rat hemi-calvaria were incubated in organ culture with sera from patients with active rheumatoid arthritis. 2. Increased 45Ca resorption was produced by sera from patients who were hypercalcaemic. 3. This bone-resorbing effect could be inhibited by calcitonin.