Since kidney transplant recipients are at enhanced risk for developing severe upper gastrointestinal disease and Helicobacter pylori (Hp) is an important pathogen in active gastritis and peptic ulcer, we performed gastroduodenoscopic examination, coupled with assessment of Hp colonization in 29 renal allograft recipients complaining of recurrent dyspepsia. Results were compared with those of 25 chronically hemodialyzed patients and 16 subjects free from renal disease, also suffering from upper gastrointestinal symptoms of similar severity. We found that while transplant recipients have had a high prevalence of Hp infection (62 vs. 34.6% in dialysis and 43.6% in control dyspeptic patients), active gastritis was clearly less frequently seen in these patients than in control subjects (transplant group: 6.9%, dialysis 3.8%, control 31.3%) and peptic ulceration was totally absent. Prevalence of Hp colonization was even higher in renal graft recipients on triple posttransplant immunosuppression (82%). In dyspeptic transplant and dialysis patients, colonization with Hp did not account for development of active inflammatory lesions, an association frequently seen in subjects free from renal disease and immunosuppressive therapy.

On the basis of our study, we conclude that HMGI(Y) gene expression analysis could be helpful in differentiation between follicular carcinoma and adenoma.

Background: Some studies indicate that malignant melanoma occurs more frequently in renal transplant recipients than in the normal population. The development of excess benign melanocytic naevi is regarded as an indicator of the risk for malignant melanoma. Objective: This study was undertaken to evaluate the prevalence of benign melanocytic naevi in adult renal transplant patients. Method: All benign melanocytic naevi irrespective of size were counted in 76 patients with renal transplants and were compared to naevus counts in 55 sex- and age-matched healthy controls. Results: The mean total number of benign melanocytic naevi was significantly higher (p < 0.001) in renal transplant patients than in the control group: 93.6 ± 52.2 and 36.1 ± 29.9, respectively. The most evident increase occurred on the palms/soles and back/buttocks. A positive, although not significant, correlation between naevus counts and duration of immunosuppression was found. Conclusion: Renal transplant recipients have an increased number of benign melanocytic naevi and should be considered as a risk group for malignant melanoma.

Forty-nine follicular adenomas and 11 follicular carcinomas of the thyroid were investigated by immunohistochemistry for the expression of p53 protein and proliferating cell nuclear antigen (PCNA). The DNA ploidy and the S-phase fraction (SPF) of the neoplasms were analysed by flow cytometry. Twelve adenomas (24 per cent) and six carcinomas (55 per cent) were DNA non-diploid (P = 0.07). The carcinomas had a higher proliferation rate than the adenomas when assessed either by SPF size (median 9.9 per cent vs. 2.9 per cent, P = 0.0003) or by PCNA staining intensity (P < 0.0001). Some scattered nuclei in two (4 per cent) adenomas and in three (27 per cent) carcinomas stained positively for p53 (P = 0.04). The two adenomas with positive staining for p53 were subserially sectioned, but no signs of invasion were found; both patients are alive and well 6 and 7 years after surgery. One of the two adenomas showing positive p53 nuclear staining was DNA aneuploid, and both were positive in PCNA staining, but their SPFs were low (2.1 and 3.3 per cent). We conclude that p53 protein expression is not confined to follicular carcinomas; scattered p53-positive cells may also be present in histologically and clinically benign follicular adenomas. Because both follicular adenomas and carcinomas may be DNA aneuploid and their SPF and PCNA staining distributions overlap, the distinction between follicular adenoma and carcinoma should still be based on histological criteria.

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