Predominance of T cells in pleural fluid of a patient with systemic lupus erythematosus.
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Biomedical subjects
Publications and source records attributed to A Many.
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Peripheral blood lymphocytes from 20 patients with systemic lupus erythematosus (SLE), 3 patients with drug-induced lupus and 20 normal controls were studied. The absolute number of E-rosette-forming cells (ERFC) and surface immunoglobulin-bearing cells were determined during active and inactive stages of the disease. An attempt was made to establish the relationship between the number of ERFC and the clinical stages of the disease on one hand and treatment on the other. A decrease in ERFC was observed in all SLE patients, but it was most prominent in patients with active disease. No correlation was found between treatment and the decreased numbers of ERFC.
The distribution of thymus-dependent (T cells) and bone marrow-derived lymphocytes (B cells) was studied in 74 patients with Hodgkin's disease and 33 normal controls. A T cell deficit was found in untreated patients as well as in long-term survivors in remission. Therapy slightly enhanced the T cell depletion in Hodgkin's disease patients. Concomitant with this finding was slight increase of B cells.
The findings of Factor XI (plasma thromboplastin antecedent) deficiency in a patient with Gaucher's disease was investigated. A family study, which included measurements of leukocyte glucocerebrosidase activity and Factor XI levels, revealed that the two genetic disorders segregated independently. One of 12 additional unrelated patients with Gaucher's disease showed a diminished Factor XI level and two of seven unrelated Factor XI-deficient patients showed decreased glucocerebrosidase activity. It is possible that the common occurrence of both genetic disorders results from a high gene frequency of both defects in Ashkenazic Jews.
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Xanthine dehydrogenase/oxidase (XDH, EC 1.1.1.204, XO, EC 1.2.3.2) produces uric acid, and in the oxidase form also generates the free radical superoxide. Previous reports failed to demonstrate XDH/XO activity in human placenta. Our objective was to determine evidence of XDH/XO in human placenta. We developed a cDNA probe for human XDH/XO and used it to detect mRNA by Northern hybridization. Immunohistochemical localization of the enzyme in placental tissue was performed using a specific antibody for XDH/XO and ABC-peroxidase. Enzyme activity assay was determined by the conversion of [14C] xanthine to [14C] uric acid. mRNA was detected in all placental samples (n = 4). Villous and non-villous trophoblast cells expressed immunohistochemical staining for XOD (n = 4). Enzyme activity was detected in all placentae (n = 6). Despite previous reports, we found mRNA, XDH/XO protein and enzyme activity in human placenta localized to trophoblast cells. Enzyme activity was much lower than in liver. Several conditions in the maternal-fetal unit could potentially increase XDH/XO activity and conversion of the enzyme to its oxidase form.
Serum immunoglobulin levels were periodically determined in 70 CLL patients and the changes were correlated with several clinical and laboratory parameters. It was found that the IgG and IgA levels decreased significantly as the disease progressed. A low IgG concentration was found at the time of diagnosis in 18.7% and after six years in about 50% of the patients. The IgM concentration, although initially low, increased during the follow-up in 43% of the patients and in four of them a monoclonal fraction appeared in the serum. The changes in the immunoglobulins did not correlate with age, sex or initial leukocyte count. Stage O patients as well as untreated patients also had a decrease in their immunoglobulin levels but advanced disease stage and especially continuous chemotherapy seemed to augment the drop in the immunoglobulin levels. Neither the initial immunoglobulin levels nor the subsequent changes, absolute or relative, had a significant prognostic value.
The effect of cyclophosphamide pulse therapy given in relatively small doses (10 mg/kg per pulse) in 17 females with lupus nephritis has been studied. Four females developed menopause; in one transient amenorrhea occurred. No changes in menstrual cycle were noted in the other 11 females, four of whom subsequently delivered five normal babies. These data suggest the relative safety of small doses of cyclophosphamide pulse therapy on gonadal function in females under age 40 years.
Most authors agree upon the causal association between antiphospholipid antibodies [lupus anticoagulant (LAC) and/or anticardiolipin antibodies] and adverse pregnancy outcome. Placental insufficiency, caused by thrombosis, infarction and maldevelopment, is thought to be the main cause of fetal loss in patients with LAC. Therapy given thus far to prevent fetal loss can be divided into (1) immunosuppression by corticosteroids, azathioprine, or intravenous gamma globulin (IVGG), (2) anti-aggregants to overcome imbalance of thromboxane/prostacycline production in patients with LAC, and (3) anticoagulants to neutralize the possible impairment of clotting inhibitor systems. Different therapeutic success rates have been reported by various authors who used the same combination of therapy. We report the results of different therapy regimens in 154 pregnancies in 31 women with LAC. These patients suffered from SLE with LAC or from APLA syndrome and experienced either recurrent miscarriages or thromboembolic phenomena in the past. With no therapy there were seven (6.8%) live births and 95 (93.2%) failures. Various combinations of corticosteroids, anti-aggregants and anticoagulants were used for treatment. Of 52 treated pregnancies, 27 (51.9%) were successful. Sixteen (69.1%) of 23 pregnancies treated by all three modalities ended in live births. Four of these successful pregnancies occurred after failure of treatment by prednisone and anti-aggregants only. In order to minimize osteoporosis caused by the combination of steroids and heparin, we have used warfarin in the second trimester and have lately substituted low molecular weight heparin for heparin. In the absence of a therapeutic schedule predicated on a large prospective study, therapy during pregnancy in patients having LAC should be individualized according to their obstetric and medical history.(ABSTRACT TRUNCATED AT 250 WORDS)