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Clinical Protocols↗
Biomedical subjects
R Bettigole
Publications and source records attributed to R Bettigole.
Human T-lymphotropic virus type I-associated benign transient immature T-cell lymphocytosis.
We describe a case of human T-lymphotropic virus type I (HTLV-I)-associated transient benign immature T-cell lymphocytosis in a black female patient, which over the course of several months underwent spontaneous complete remission. The patient presented with a white blood cell count of 20,000/microliter and a T4/T8 ratio of 1.7:1. The majority of cells appeared to be lymphoid in origin, and cell marker analyses established that the circulating lymphocytes were predominantly immature T-cells. HTLV-I was detected at this time by a p19 indirect immunofluorescent slide assay. Over a 1-month period of time the patient's clinical status evolved into a mature T-lymphocytosis with a T4/T8 ratio of 4.5:1. HTLV-I was detected by anti-p19 immunofluorescence by cell sorter analyses and by dot-bloc nucleic acid hybridization. Serological testing demonstrated that the patient had anti-HTLV-I antibodies and antimembrane antibodies specific for an HTLV-I producing cell line. In a competitive HTLV-I ELISA assay only HTLV-I proteins could effectively compete out the seroreactivity. The patient also had a high serum level of soluble interleukin-2 (IL-2) receptors, which is associated with HTLV-I infection. This is the first reported case of immature T-lymphocytosis in a patient infected with HTLV-I. The patient's HTLV-I markers disappeared with time, and her lymphocytosis subsequently spontaneously resolved. She remains disease free and virus negative after 2 years of follow-up study.
Antibodies, Viral↗
Studies on vasoocclusive crisis of sickle cell disease. I. Effect of pentoxifylline.
A method was developed to induce and continuously monitor vasoocclusive crisis of sickle cell disease in non-human primates. Pentoxifylline, a phosphodiesterase inhibitory agent, showed significant preventive effect. This may be based on its ability to increase intracellular cAMP levels and consequently to decrease platelet aggregation and to increase red cell deformability.
Anemia, Sickle Cell↗