Ageing lung cancer patients may be at increased risk of Cisplatin (Cp) nephrotoxicity, because of comorbidities leading to accelerated ageing of the kidneys. Therefore, the Cp-induced impairement of renal function was compared between no comorbidity (NC) and hypertension plus ischaemic heart disease (CD) patients or others having diabetes mellitus plus ischaemic heart disease (DMIH).In a preliminary study, glomerular filtration rate (GFR) was measured by clearance of technetium 99m-labelled diethylene-thiamine penta-acetate in 38 lung cancer patients with normal serum creatinine concentration ([creat]). Then, the incidence of nephrotoxicity was analysed retrospectively over 1st-4th cycles of Cp treatment among 242 lung cancer patients with initially normal [creat]. GFR was repeatedly estimated using calculated creatinine clearance.Pre-treatment GFR was 57¡3 mL?min -1 ?m -2 in those with normal (n515) and 42¡2 mL?min (n552) subgroups. Within the overall dropout rate from further Cp chemotherapy, nephrotoxicity was responsible in 14% of NC, 38% in CD and 75% in DMIH patients. A major portion of our ageing lung cancer patients suffered from comorbidities leading to reduced renal resistance to Cp nephrotoxicity.
PTH level determination from tissue aspirates is a highly reliable, quick, and simple method to differentiate parathyroid and nonparathyroid tissues during parathyroidectomy. This method can obviate frozen sections in patients undergoing surgery for hyperparathyroidism.
According to earlier reports, a decrease below 50% of baseline of intraoperative PTH levels measured 5 min after resection of the parathyroid adenoma predicts a cure of hyperparathyroidism. To reveal previously unrecognized pitfalls of intraoperative PTH measurements, we reviewed surgical failures in our series of parathyroidectomies combined with intraoperative PTH sampling. PTH measurements were performed in 251 patients with primary hyperparathyroidism (PHPT) between November 1999 and December 2002. PHPT due to parathyroid hyperplasia were found in 8 cases, double parathyroid adenomas in 6 cases, parathyroid carcinoma in 1 case and single parathyroid adenomas in 236 cases, all confirmed by histological examination. Of the 236 cases of single adenomas, initial surgery failed to cure PHPT in 4 patients. In 3 patients a false-positive decrease of intraoperative PTH (from 269 to 40 pg/ml, from 211 to 27 pg/ml, and from 140 to 59 pg/ml) was observed, whereas in the fourth patient a true-negative decrease of intraoperative PTH (from 758 to 401 pg/ml) was mistakenly interpreted as indication for a cure of PHPT. In each of the 4 patients in whom initial surgery failed the intervention included thyroid surgery and reoperative parathyroid surgery resulted in a permanent cure of PHPT. These observations support the possibility that thyroid surgery may compromise the blood supply of parathyroid adenomas resulting in a misleading drop of intraoperative PTH levels. Therefore, a careful evaluation of intraoperative PTH levels and, perhaps, other intraoperative aids such as histological evaluation of frozen sections are recommended when parathyroid surgery is combined with simultaneous thyroid intervention.
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