Recurrence of hyperparathyroidism (HPT) following total parathyroidectomy and autotransplantation (APTX) has been reported before. However, no data about the time interval between grafting and relapse and about morphology were given. Only 1 case of primary hyperparathyroidism with APTX has been extensively analyzed.
We have performed autotransplantation in 42 patients with HPT due to chronic renal failure. Implanted parathyroid tissue showed typical chief cell hyperplasia. Within 4–33 months, 6 patients developed recurrent HPT with serum iPTH levels being highest in venous blood of the grafted arm. Grafts had to be removed. Although only 20–40 mg of parathyroid tissue had been implanted, removed grafts weighed from 0.9 to 3.1 g. Explanted grafts were examined by light and electron microscopy. The size and DNA content of nuclei were determined. In all cases the explanted material showed a distinct invasive growth into the adjacent connective tissue and muscles and in 2 cases mitotic figures were demonstrated, a finding resembling malignant neoplasia of the parathyroid.
From our clinical and morphological observations we draw the following conclusions:
Surgical treatment of renal hyperparathyroidism by PTX + Auto‐TX unforeseeably may result in very accelerated growth of grafted tissue.
Because of invasive growth there exists the risk of uncontrolled spread of parathyroid tissue.
Graft removal may turn out to be difficult and possibly necessitate repeated and extensive surgery.
Before the observed phenomenon is totally understood, we no longer recommend PTX + Auto‐TX as an alternative to subtotal PTX in the surgical treatment of renal hyperparathyroidism.
In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.
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