Marked hypercalcaemia in sepsis-induced multiple organ failure

Sir, A 58-year-old man was referred to our intensive care unit, because of retropharyngeal abscess and Staphylococcus aureus bacteraemia. On admission, he showed tachyponea, wheezing and oliguria. Laboratory examination revealed hypoxia, cardiac failure, lung congestion, renal dysfunction and marked inflammatory signs ( Table 1 ). He was diagnosed as having multiple organ failure due to sepsis, was intubated on a ventilator, and started on treatment with inotropes and antibiotics. This intensive treatment improved his clinical condition and laboratory abnormalities; however, on day 10, he showed marked hypertension (200/100 mmHg) and a new rise of serum creatinine level. An intravenous infusion of a calcium antagonist was thus initiated. On day 16, renal function was improved, but marked hypercalcaemia was noticed ( Table 1 ). The patient was treated with a single dose of intravenous pamidronate at 45 mg. Laboratory findings included normocalciuria, a low level of intact-parathyroid hormone (iPTH) and 1,25-dihydroxyvitamin D, an undetected iPTH-related protein level and normal thyroid and adrenal gland function. Six days after the dose of pamidronate, the plasma ionized calcium levels were reduced to normal ranges (1.27 mmol/l), and hypertension was improved. On day 27, his clinical condition was markedly improved, and he was transferred to the general ward; after rehabilitation, the patient was discharged on day 60. Changes in the laboratory data in the present case a Reference range, 8.6–10.32 mg/dl; b reference range, 1.13–1.28 mmol/l; c reference range, 2–4%; d reference range, 2.5–4.5 mg/dl; e reference range, 10–65 pg/ml; f reference range, 10–55 ng/ml; ND, not determined. Changes in the laboratory data in the present case a Reference range, 8.6–10.32 mg/dl; b reference range, 1.13–1.28 mmol/l; c reference range, 2–4%; d reference range, 2.5–4.5 mg/dl; e reference range, 10–65 pg/ml; f reference range, 10–55 ng/ml; ND, not determined. We have described here, a patient with sepsis-induced multiple organ failure who developed marked hypercalcaemia. The patient showed depressed PTH and vitamin D levels, and his hypercalcaemia was effectively treated with pamidronate. Critically ill patients have been reported to have a high prevalence of bone hyper-resorption [ 1 , 2 ], progressing to marked hypercalcaemia in some patients [ 2 ]. Urinary bone resorption markers (amino terminal cross-linked telopeptide of type I collagen and deoxypyridinoline) were increased in our case. These bone abnormalities are thought to be caused by immobilization bone hyper-resorption in a PTH-independent manner [ 1 ] and biochemically responding to treatment with pamidronate [ 1 , 2 ]. In the present case, extremely high serum C-reactive protein levels were observed on admission, indicating that levels of circulatory pro-inflammatory cytokines were probably markedly increased. Since these cytokines, particularly interleukin-6, are known to enhance bone resorption via increasing osteoclast activity and inhibiting osteoblast activity, it is hypothesized that these inflammatory reactions may have caused the alteration of calcium metabolism in this patient. Moreover, PTH levels were not completely suppressed in spite of marked hypercalcaemia, and maximal tubular reabsorption of phosphorous per glomerular filtration rate (TmP/GFR) was decreased, suggesting that our patient might have been in a mild hyperparathyroid state. During acute oliguric renal failure, low ionized calcium levels, 1.09 mmol/l, could, in our case, stimulate PTH secretion; this parathyroid hyperactivity might persist even after recovery of renal function. Jeffries et al . [ 3 ] have described this type of hyperparathyroid state after recovery from multiple organ failure as a life-threatening tertiary hyperparathyroidism. We speculate that several factors, i.e. immobilization, the sepsis-induced marked inflammatory reactions and the parathyroid hyperactivity, might have contributed to the development of hypercalcaemia in our case. Unrecognized hypercalcaemia in critically ill patients is thought to be very dangerous, as it can cause cardiovascular dysfunction [ 3 ]. Indeed, also in our case, renal dysfunction and marked hypertension occurred during developing hypercalcaemia. Our study suggests that nephrologists should be alert for this type of hypercalcaemia during the course of multiple organ failure with sepsis. Conflct of interest statement . None declared.