ABSTRACT
We report a 59-year-old woman diagnosed with metastasic colorectal cancer who developed immune hemolytic anemia during FOLFOX chemotherapy (oxaliplatin/leucovorin/5-fluorouracil). Immunohematologic studies demonstrated that immune hemolysis was oxaliplatin-mediated. On the basis of this case and in a review of the literature in which 13 cases of previously reported oxaliplatin-induced immune cytopenia have been identified, we suggest some clinical clues regarding the use of oxaliplatin in cancer patients.
Subject(s)
Anemia, Hemolytic, Autoimmune/chemically induced , Antineoplastic Agents/adverse effects , Organoplatinum Compounds/adverse effects , Adenocarcinoma/complications , Adenocarcinoma/drug therapy , Adenocarcinoma/pathology , Antidotes/administration & dosage , Antimetabolites, Antineoplastic/administration & dosage , Antineoplastic Agents/administration & dosage , Antineoplastic Combined Chemotherapy Protocols/adverse effects , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Autoantibodies/analysis , Colorectal Neoplasms/complications , Colorectal Neoplasms/drug therapy , Colorectal Neoplasms/pathology , Erythrocytes/immunology , Female , Fluorouracil/administration & dosage , Hemoglobins/metabolism , Humans , Leucovorin/administration & dosage , Liver Neoplasms/pathology , Liver Neoplasms/secondary , Lymphatic Diseases/pathology , Middle Aged , Organoplatinum Compounds/administration & dosage , Oxaliplatin , Platelet CountABSTRACT
OBJECTIVE: To compare the serum levels of beta2-microglobulin (beta2M), neopterin (NP), TNF-alpha and soluble receptors of TNF-alpha (sTNF-R55 and sTNF-R75) and interleukin-2 (sIL-2R) in a population of intravenous drug abusers according to whether or not they had HIV-1 infection and to the stage of the HIV-1 infection. METHODS: A cross-sectional study was performed at four drug detoxification centers in Barcelona, and the HIV outpatient clinic at Hospital Clínic in Barcelona. Three cohorts of intravenous drug abusers (IVDAs)-105 HIV-1-uninfected patients (cohort A), 174 with asymptomatic HIV-1 infection (cohort B) and 39 with AIDS (cohort C)-were enrolled. On the first visit, the following laboratory tests were performed: hemogram and platelet count, hepatitis B surface antigen (HBsAg), anti-hepatitis C antibodies, B2M, NP, sIL-2R, TNF-alpha, and TNF receptors (sTNF-R55 and sTNF-R75). RESULTS: The three cohorts were homogeneous according to sex, type of drug, average number of intravenous doses of drug in 1 day, and hepatitis B infection. Patients with AIDS were older than those of cohort A and B (p<0.0001). HIV-negative IVDAs were co-infected with hepatitis C virus less frequently than were HIV-positive IVDAs (80% versus 91%, p<0.03). Among HIV-1-negative IVDAs (cohort A), almost all (from 86% to 95%, depending on the marker) individual values were within the normal boundaries of our laboratory. With a single exception (level of sTNF-R55 in cohort B compared with cohort A, p=0.15), levels of all markers were significantly higher in asymptomatic HIV-1-infected (cohort B) when compared with uninfected patients (cohort A), and in AIDS patients (cohort C) when compared with both cohorts A and B. There was a significant positive correlation between levels of ss2M and NP (r=0.56; p<0.01), ss2M and TNF (r=0.65, p<0.01) and NP and TNF (r=0.76, p<0.01). There was no correlation between levels of sIL-2R and levels of ss2M, NP or TNF and its receptors. CONCLUSIONS: Intravenous drug abuse does not modify serum levels of ss2M, NP, sIL-2R, TNF-alpha, and TNF receptors (sTNF-R55 and sTNF-R75). Levels of these markers increase significantly when an HIV-1 infection occurs and when there is progression to AIDS.
