There are not many publications describing long-term follow-up of persistent hyperparathyroidism requiring surgical treatment after kidney transplantation (PHSKT). In some patients adenomas, rather than multiglandular disease, have been incriminated as the cause of PHSKT. We reviewed the charts of 45 patients followed for 12 to 146 months (median 45 months) after parathyroidectomy for PHSKT. We compared them with (1) those of 951 patients receiving a kidney graft during the same period but not submitted to parathyroidectomy or (2) 90 matched controls selected from this cohort to determine the characteristics of PHSKT patients. The duration of pretransplant dialysis was significantly longer in PHSKT patients than in controls (5.78 +/- 0.41 vs. 3.41 +/- 0.24 years; p < 0.0001). A total of 166 glands were removed or biopsied. Except for one questionable case, no true adenoma was observed even when only one gland was enlarged. The outcome of surgery was not influenced by the technique (subtotal parathyroidectomy versus total parathyroidectomy and autografting) but depended on the amount of resected parathyroid tissue: no failures and 4 cases of hypoparathyroidism in 34 cases with no missing gland at cervical exploration; 3 failures and no permanent hypoparathyroidism in 11 cases with one or two missing glands. Excision of the enlarged glands only was sufficient to cure the patient. No recurrence was observed. Our results suggest that single gland enlargement in PHSKT results in most cases from different rates of involution of the parathyroids after successful kidney transplantation. When fewer than four glands are discovered, resection of all visible glands with or without grafting corrects hypercalcemia in more than 70% of the cases.

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Intact parathormone (inPTH) has a short half-life. Its blood level on the first day after total parathyroidectomy and subcutaneous parathyroid implantation (PTX + G) should therefore allow an early diagnosis of missed residual parathyroid tissue. We tested this hypothesis in 72 uremic patients who were followed for 6 to 110 months after operation. Nine were reoperated for recurrence of the disease. Graft removal was successful in four patients who had post-PTX inPTH levels of 16 pg/ml or lower. In five patients, an overlooked parathyroid gland had to be resected. All of them had elevated post-PTX inPTH blood levels ranging from 72 to 791 pg/ml (upper normal limit 55 pg/ml). Three of these patients had presented with hypocalcemia after PTX. We conclude that the inPTH blood concentration on the first day after PTX allows more precise evaluation of the efficacy of the surgical procedure than the postoperative evolution of blood calcium levels. It is also useful for localizing the source of excessive PTH secretion (graft or overlooked gland) when the disease recurs.

The effect of surgery on inflammation was studied in male Wistar R/A rats using the carrageenin-induced edema model. Swelling of the paw was measured in standardized arbitrary units 2, 4, and 6 hr after a subcutaneous injection of carrageenin iota in the subplantar region of the right hind limb. It was significantly depressed in rats submitted to laparotomy (5.0 +/- 0.4, 8.0 +/- 1.0, 13.7 +/- 1.9) when compared with controls simply anesthetized with ether (6.2 +/- 0.5, 15.5 +/- 1.2, 23.7 +/- 0.6) (p less than 0.001 at 4 and 6 hr). This inhibition lasted for at least 24 hr and was also observed after amputation, although in these experiments, the difference between operated animals and controls was not significant. Alterations of the inflammatory cellular infiltrate were studied using polyurethane sponges soaked with carrageenin lambda implanted subcutaneously in control animals and rats undergoing laparotomy or amputation. The total number of cells recovered from these sponges 5 hr after implantation was smaller in operated rats (2.9 +/- 0.4 x 10(6) cells after laparotomy, 3.1 +/- 1.0 x 10(6) cells after amputation) when compared with controls (11.1 +/- 1.9 x 10(6) cells and 10.3 +/- 1.3 x 10(6) cells) (p less than 0.001 for laparotomy and p less than 0.005 for amputation). The inhibitory effect of operative trauma was not abolished by bilateral adrenalectomy performed 12 days before laparotomy. In rats, surgical trauma induces a depression of remote inflammatory reactions. This phenomenon is not related to increased corticosterone levels.