Lymphocyte subpopulations in patients with multiple primary tumors.

BACKGROUND: Cancer patients with single tumors live longer today due to earlier detection and improved treatment methods. For this reason, the authors see more patients who develop a second primary tumor. The etiology of the second tumor can be the same as the first, whether treatment-induced or unknown. The prognoses of these patients usually depend on the behavior of the second tumor. METHODS: The authors investigated the lymphocyte subset in 88 of the more than 750 patients listed in the tumor registry at their treatment center who had at least one carcinoma of the breast or colon and a second primary of the same or another site. Mononuclear cells were obtained from heparinized blood by the standard fractionation Hypaque gradient centrifugation technique. Helper and suppressor cells were identified by using three murine monoclonal antibodies: CD3 for mature T lymphocytes, CD4 for helper inducer cells, and CD8 for suppressor cytotoxic cells. T-cell subset distribution was evaluated with flow cytometry. RESULTS: Most values of CD3, CD4, and CD4/CD8 were lower in patients than in healthy controls. The values of CD4 and CD4/CD8 were lower in patients who had a second tumor in the colon rather than in the breast. CONCLUSIONS: As tumors in patients with a second primary sometimes recur or the patient develops a third primary, the authors are prospectively following their patients to see whether those with immunosuppression have a greater tendency to develop recurrent disease or a third primary.

Nimesulide-induced acute hepatitis.

OBJECTIVE: To report the occurrence of nimesulide-induced acute hepatitis confirmed by biopsy and an in vitro lymphocyte toxicity assay. CASE SUMMARY: A 54-year-old Arabic woman treated with nimesulide for chronic low back pain was admitted to the hospital with acute hepatitis confirmed by biopsy. Her liver function test results returned to normal within one month after nimesulide discontinuation. An in vitro lymphocyte toxicity assay confirmed that the liver injury was due to nimesulide exposure. DISCUSSION: A case of acute hepatitis secondary to nimesulide, confirmed by biopsy and a laboratory in vitro assay, is described. Although the occurrence of clinically significant liver damage due to nonsteroidal antiinflammatory drugs (NSAIDs) is low, the enormous consumption of these drugs has made them an important cause of liver damage. Nimesulide, a relatively new NSAID commonly used in Europe, with a relative selectivity to cyclooxygenase type 2, can cause a wide range of liver injuries, from mild abnormal liver function to severe liver injuries. These effects are usually reversible on discontinuation of the drug, but occasionally can progress to fatal hepatic failure. CONCLUSIONS: Drug-induced acute hepatitis is a well-recognized adverse effect of many drugs, including nimesuilde. Identification of a drug as a cause for this life-threatening disease is important because the discontinuation of it may be life saving. This article confirms the occurrence of nimesulide-induced hepatitis. It also highlights the importance of monitoring liver function test results after initiating therapy with such a drug.

T-cell subpopulation in patients with metastatic renal cell carcinoma treated by recombinant interleukin-2, recombinant interferon-alpha, 5-fluorouracil, and vinblastine.

T-cell subpopulations were evaluated in 10 patients with metastatic renal cell carcinoma treated with recombinant interleukin-2, recombinant interferon-alpha, 5-fluorouracil, and vinblastine. T-cell subpopulation was tested by flow cytometry, and the results were compared with healthy control subjects. Mean T-cell values before treatment as compared with control were as follows: CD3, 68 vs. 73%; CD4, 34 vs. 53%; CD8, 38 vs. 31%; CD4/CD8, 1.1 vs. 1.8; CD4CD69, 20 vs. 47%, and CD8CD69, 24 vs. 19%. The difference in CD4, CD4/CD8, and CD4CD69 was statistically significant. After treatment (8 weeks), the values of CD4/CD8 ratio and CD4CD69 increased. Three patients achieved complete response, two partial response, and two had stabilization of the disease. After treatment, the CD4/CD8 ratio increased in complete responders, from 1.1 to 2.0, and CD4CD69 increased in complete and partial responders, from 11 to 37% and 23 to 31%, respectively. In nonresponders, no similar change was observed. In conclusion, increases in CD4/CD8 ratio and CD4CD69 levels in metastatic renal cell carcinoma patients may be associated with response to immunochemotherapy.