[Surgical treatment of hyperparathyroidism due to parathyroid tumors].

OBJECTIVE: To study the clinical features of hyperparathyroidism due to parathyroid tumors, and evaluate the efficiency of surgical management. METHODS: Twenty-two patients with hyperparathyroidism resulted from parathyroid tumors were reviewed. The age ranged from 32 to 79 years, 9 males and 13 females. Recurrent laryngeal nerve was routinely exposed, and procedures were performed in normal tissue in initial surgery. Additional selective neck dissection of levels II, III, IV, and VI was taken in the cases with recurrent cancer. Local flaps were used to repair the esophageal defects after resecting tumors. The recurrent laryngeal nerves of 4 cases had to be sacrificed because they were embedded in the tumor tissues despite the nerves had normal function before operation. Prophylactic tracheostomy was performed in 5 cases. RESULTS: Eight cases were identified pathologically as parathyroid carcinoma, of them four with neck metastasis, and 14 cases as parathyroid adenoma after surgery. Their PTH dropped to normal level within two hours after surgery and hypercalcemia disappeared in two days postoperatively. The PTH and serum calcium were in normal range during the follow-up of 12 to 40 months. Recurrence occurred again in two cases in 6 and 8 months after the removal of the recurrent tumor tissues respectively. Esophageal fistula, chylous fistula and dehiscence of sternotomy developed in three cases separately. The tracheostomy was removed in four cases two weeks after operation and in one case six weeks after operation. One patient with parathyroid adenoma died of hypocalcemia about two weeks after operation and another one with recurrent parathyroid carcinoma also died of hypercalcemia 52 months after revised surgery. CONCLUSION: Extended resection of tumor and intraoperative PTH assay were strongly suggested for the managements of both benign and malignant parathyroid tumors.

Internal radiotherapy using 32P colloid or microsphere for refractory solid tumors.

OBJECTIVE: The aim of this work was to study the effectiveness of 32P colloids or microspheres, by arterial interventional administration or stromal injection in the treatment of refractory solid tumors. METHODS: By arterial intervention, under the guidance of computerized tomography, X-ray, ultrasonogram, or under direct vision of the surgical field, 32P microspheres (259-685 MBq) or radioactive colloid (281-666 MBq) was administered to 60 cases with refractory solid tumors. Tumor inhibition rate, side effects, survival period, and so on were observed. RESULTS: The tumor growth was obviously inhibited after the intratumoral injection of 32P colloid. The average survival time in the 60 cases was 35 months with a high tumor inhibition rate (93.4%). Thirty-one cases were completely relieved (51.7%), and 25 cases achieved partial remission (PR, 41.7%). One case with right lobe hepatocellular carcinoma has survived 90 months. The drug was ineffective only in four cases, including one patient who died of gastrointestinal hemorrhage and three of hepatic failure. No other obvious side effects were observed. Intratumoral necrosis, intense fibrosis in the tumor mass, and an integrated capsule encompassing the tumor were revealed by histological examination. CONCLUSIONS: Arterial interventional administration or stromal injection with 32P microspheres or colloid revealed a very fair clinical effectiveness in the treatment of refractory solid tumors. The range of safe effective dosage for 32P glass microspheres and 32P chromic phosphate in one treatment course is 555-740 MBq and 185-370 MBq, respectively.

Chromic-P32 phosphate treatment of implanted pancreatic carcinoma: mechanism involved.

AIM: To study the effects of chromic-P32 phosphate (32P colloids) interstitial administration in Pc-3 implanted pancreatic carcinoma, and investigate its anticancer mechanism. METHODS: Ninety-eight tumor bearing nude mice were killed at different time points after the injection of 32P colloids to the tumor core with observed radioactivity. The light microscopy, transmission electron microscopy (TEM) and immuno-histochemistry and flow cytometry were used to study the rates of tumor cell necrosis, proliferating cell nuclear antigen index, the micro vessel density (MVD). The changes of the biological response to the lymphatic transported 32P colloids in the inguinal lymph node (ILN) were dynamically observed, and the percentage of tumor cell apoptosis, and Apo2.7, caspase-3, Bcl-2, Bax-related gene expression were observed too. RESULTS: The half-life of effective medication is 13 d after injection of 32P colloids to the tumor stroma, in 1-6 groups, the tumor cell necrosis rates were 20%, 45%, 65%, 70%, 95% and 4%, respectively (F = 4.14-105.36, P<0.01). MVD were 38.5+/-4.0, 28.0+/-2.9, 17.0+/-2.9, 8.8+/-1.5, 5.7+/-2.3 and 65.0+/-5.2 (t = 11.9-26.1, P<0.01), respectively. Under TEM fairly differentiated Pc-3 cells were found. Thirty days after medication, tumors were shrunk and dried with scabs detached, and those in control group increased in size prominently with plenty of hypodermic blood vessels. In all animals the ILN were enlarged but in medicated animals they appeared later and smaller than those in control group. The extent of irradiative injury in ILN was positively correlated to the dosage of medication. Typical tumor cell apoptosis could be found under TEM in animals with intra-tumoral injection of low dosed 32P colloids. The peak of apoptosis occurred in 2.96 MBq group and 24 h after irradiation. In the course of irradiation-induced apoptosis, the value of Bcl-2/Bax was down regulated; Apo2.7 and caspase-3 protein expression were prominently increased dose dependently. CONCLUSION: 32P colloids intra-tumor injection having prominent anticancer effectiveness may reveal the ability of promoting cell differentiation. The low dose 32P colloids may induce human pancreatic carcinoma Pc-3 implanted tumor cell apoptosis; Apo2.7, caspase-3, Bcl-2 and Bax protein participated in regulating the process of irradiation induced cell apoptosis.