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Introduction: The gene coding for the angiotensin I-converting enzyme is known for its polymorphism revealed by the presence or absence of a 287-base pair fragment. The question arises whether ACE gene polymorphism in the recipient and donor has any effect on renal graft function., Material and Methods: This prospective study enrolled 94 renal graft recipients. 27 ACE donor genotypes were ascertained. Creatinine clearance after cimetidine, laboratory tests, and episodes of acute and chronic rejection were analyzed. None of the recipient genotype subgroups differed significantly as to creatinine clearance. Only in the group of patients not on ACE inhibitors were there significantly higher creatinine concentrations in recipients with II genotype as compared with ID and DD genotypes pooled together. No differences were found between the genotype subgroups as to the frequency of rejection episodes. Ultimately, donor ACE genotype had no effect on graft function., Results: In conclusion, the I/D genotype is not an independent prognostic factor for renal graft survival during the first four years after transplantation. The use of ACE inhibitors may modify the effect of the genotype on some parameters of renal function.

Objectives: The purpose of our study was to analyze the rate of hypersensitivity reactions (HSRs) to paclitaxel in patients with advanced ovarian carcinoma. We also analyzed the possibility of re-administration paclitaxel with adequate treatment after hypersensitivity reactions., Materials and Methods: The incidence of HSRs was analyzed retrospectively in 112 patients who received 24-hr infusions of paclitaxel (135 mg/m2) for advanced ovarian cancer at the Department of Gynecology Medical University of Gdańsk between the January 2000 and the February 2002. Before each course of the paclitaxel administration patients received orally dexamethasone (20 mg p.o., 12 and 6 hours prior to the chemotherapy) and thirty minutes prior to the infusion of paclitaxel all patients received, diphenhydramine (50 mg), and cimetidine (300 mg) intravenously (i.v.). When HSR was observed administration of paclitaxel was temporally stopped and before the re-challenge additional intravenous dosage of hydrocortisone (200-500 mg) and diphenhydramine (25 mg) was given., Results: Severe hypersensitivity reactions occurred in 9 patients (8%) and the administration of paclitaxel was withdrawn. Mild hypersensitivity reactions were observed in 8 patients (7%) and all of these patients were successfully retreated with paclitaxel without HSRs., Conclusion: We conclude that this premedication and treatment strategy provides lower hypersensitivity reactions rate and allows for continuing administration of paclitaxel in patients with advanced ovarian carcinoma.

An effect of cimetidine on parathyroid glands functioning in healthy subjects was evaluated. Serum calcium, phosphate, and magnesium concentrations together with renal excretion++ of these ions in healthy subjects as well as cAMP excretion++ in selected individuals were determined before and following intravenous administration of cimetidine (Altratmet Lek Ljublijana) in total dose of 500 mg (50 mg injected rapidly as a bolus following with 450 mg in an intravenous infusion during 60 minutes). No significant changes in serum calcium, phosphates, and magnesium concentrations were noted. Renal clearance of calcium and magnesium remained unchanged whereas renal phosphate excretion++ increased from 10.69 +/- 4.9 mL/min to 15.1 +/- 5.41 mL/min (p less than 0.02). Excretion++ of 3.5 cAMP increased from 2.65 +/- 2.19 nM/min to 5.16 +/- 2.0 nM/min (p less than 05). The obtained results do not exclude stimulating effect of intravenous cimetidine on parathyroid glands. Cimetidine given intravenously in the bleeding gastric or duodenal ulcers in the course of the primary hyperparathyroidism+ may decrease serum phosphate levels due to increased exretion of this ion with the urine.

Increased inhibition of gastric acid release through simultaneous blockade of H2-receptors and muscarine-receptors or administration of gastroprotective agent is theoretically justified in patients with peptic ulcer unresponsive to cimetidine. The study involved 70 patients with peptic ulcer previously treated with cimetidine in daily dose 1000 mg for 6 weeks without an effect. Patients were divided into two groups: group 1 treated with cimetidine plus pirenzepine, and group 2 given sucralfate in daily dose 4.0 g. Pirenzepine to patients of group 1 was given in a single dose of 50 mg before bedtime. Both groups were comparable in age, sex, disease onset, smoking, gastric acid secretion, and ulcer size. Healing was evaluated with endoscopic technique following 2 and weeks of therapy. Ulceration healed up within 2 weeks in 40% of patients treated with cimetidine combined with pirenzepine and in 31.4% patients treated with sucralfate. After 4 weeks, healing of ulceration was 71.4% and 68.6%, respectively. Large ulcers (over 1 cm in diameter) and previous partial gastrectomy did not affect healing rate. The obtained results suggest that administered therapies enable recovery in over 2/3 of patients with peptic ulcer unresponsive to a 6-week therapy with cimetidine alone.