Treatment of scleromyxedema with etretinate.
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Etretinate↗
Biomedical subjects
I Yust
Publications and source records attributed to I Yust.
Hepatic granuloma in polymyalgia rheumatica.
Hepatic granuloma occurs rarely in the polymyalgia rheumatica syndrome. A case was presented of a 62-year-old woman with polymyalgia rheumatica, elevated concentrations of hepatic enzymes, and granuloma of the liver. Low doses of corticosteroids produced a marked improvement in the patient's condition and a return of liver function tests to normal. This is apparently the first case of polymyalgia rheumatica associated with liver granuloma that has been reported in Israel.
Female↗
Acute embolic bilateral renal artery occlusions in an elderly patient--case report: importance of early diagnosis.
Acute bilateral renal artery occlusion by emboli is a rare event and diagnosis is very often delayed. There is a high mortality rate because of anuria and controversy exists concerning an appropriate therapeutic regimen. We present the case of an elderly patient with bilateral artery occlusion, treated conservatively with anticoagulants, fibrinolytic agents and dialysis, and a review of the pertinent literature.
Acute Disease↗
Lymphomatoid granulomatosis with impaired cellular immunity. Eight year survival without treatment.
Lymphomatoid granulomatosis (LYG), a non-neoplastic lymphoreticular disorder, was diagnosed in a 65-year-old woman. Chest radiographs demonstrated bilateral lower lobe nodular infiltrates. Percutaneous needle biopsy of the lung showed an infiltrate composed of plasma cells, lymphocytes and large histiocytic-like cells. Impairment of cellular immunity was found by in vivo as well as by in vitro tests. The clinical condition of the patient has remained stable for the last eight years without specific treatment.
Aged↗
Suppression of cortisol secretion by low-dose dexamethasone testing in Cushing's disease. Case report.
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Adenoma↗
Reiter's syndrome complicating dysentery epidemic in a small military unit: case reports.
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Adult↗
[Hemolytic anemia following methyldopa].
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Aged↗
Malabsorption syndrome, coccidiosis, combined immune deficiency, and fulminant lymphoproliferative disease.
Coccidia were found in a patient suffering from malabsorption syndrome. In addition, immunologic investigation showed combined humoral and cellular immunodeficiency. Treatment with metronidazole induced the disappearance of coccidia from the stool and clinical remission. Six months later, the patient was seen with acute lymphoproliferative disease and died thereafter. The possible relationship between malabsorption, immunodeficiency, coccidiosis, metronidazole, and malignancy is reviewed.
Adult↗
Simultaneous detection of two mechanisms of immune destruction of penicillin-treated human red blood cells.
Two separate processes of putative red-cell destruction in penicillin-induced immune hemolysis were measured simultaneously by a rapid (3 hour) assay utilizing 51Cr-labelled red blood cells (RBC). Antibody-dependent, cell-mediated cytotoxicity (ADCC) was estimated by release of 51Cr; and antibody-dependent phagocytosis (ADPh) by quantitation of 51Cr uptake into mononuclear phagocytes as well as by counts of engulfed RBC. Attacking cells were obtained by Ficoll-Hypaque separation of peripheral blood from normal donors. Phagocytosis as well as lysis were proportional to anti-penicillin antiserum concentration, to incubation time, and to the concentration of the attacking cells. Enrichment of mononuclear phagocytes in the attacking cell population by albumin gradient separation led to an increase in phagocytosis as well as in cytotoxicity. Depletion of mononuclear phagocytes resulted in a decline in both processes. Dilution of antiserum abolished ADCC but affected ADPh only slightly. Iodoacetate as well as colchicine inhibited both activities. These results indicate that both processes may be operative in the immune destruction of RBC in vivo.
Adult↗
Dermal vasculitis due to coumadin hypersensitivity.
A 65-year-old patient developed nonpruritic purpuric skin eruptions following 10 days of coumadin treatment. Skin biopsy revealed vasculitis and immunofluorescent studies demonstrated the presence of IgM and C3 deposits in the walls of the affected blood vessels. Rechallenge with coumadin was followed by reappearance of the skin eruptions. Indirect mast cell degranulation test and migration inhibiting factor test were positive in the presence of coumadin. These findings strongly suggest that the skin lesions were induced by an immunologic reaction to warfarin.
Aged↗
Mechanisms of immune haemolysis: cell-dependent destruction of autologous red blood cells in penicillin-induced haemolytic anaemia.
The mechanisms of red blood cell destruction in 2 patients with penicillin-induced immune haemolytic anaemia were investigated. Anti-penicillin antibodies of the IgG subclass were found in the patients' sera and in the eluates of their direct antiglobulin positive red blood cells. Using a rapid 51Cr in vitro assay it was shown that fresh peripheral blood mononuclear phagocytes and granulocytes but not lymphocytes from both patients lysed and phagocytosed autologous red blood cells previously treated in vivo or in vitro by penicillin and autologous anti-penicillin antibody. Antibody-dependent cell-mediated cytotoxicity (ADCC) as well as antibody-dependent phagocytosis (ADPh) were proportional to serum concentration and to the number of attacking cells. Anti-penicillin antibody from 1 patient activated the complement system in vitro but failed to induce lysis of penicillin-treated red blood cells in the presence of complement. These results suggest that ADCC as well as ADPh participate in the destruction of red blood cells in penicillin-induced haemolysis in vivo.
Adult↗
Antibody-dependent cell-mediated cytotoxicity (ADCC) of penicillin-treated human red blood cells.
Penicillin-treated human red blood cells (RBC) were lysed by the cooperation of autologous nonsensitized peripheral blood mononuclear cells and human anti-penicillin serum. Using a rapid (3 h) assay of antibody-dependent cell-mediated cytotoxicity (ADCC), lysis was proportional to serum (anti-penicillin antibody) concentration, to incubation time and to the concentration of attacking cells, which were obtained from normal human peripheral blood by Ficoll-Hypaque separation. Incubation of these lymphoid effector cells on a nylon column prior to the tests depleted the number of phagocytic (latex positive) cells in the effluent; there was a concomitant drop in cytotoxic activity. Enrichment of mononuclear phagocytes in the attacking cell population by albumin gradient separation led to an increase in cytotoxicity. Granulocytes separated by Ficoll-Hypaque were not active in this system. Using specific antisera the antibody was found to be of the IgG1 sub-class. Anti-penicillin antibody activated the complement system in vitro, but failed to induce lysis of penicillin-treated RBC in the presence of complement without attacking cells. These results suggest that ADCC may participate in the destruction of RBC in penicillin-induced haemolysis in vivo.
Adult↗
Chlorpropamide-induced Syndrome of Inappropriate Antidiuretic Hormone Secretion.
The Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is a rare but serious complication of chlorpropamide therapy. In 2 elderly women who had diabetes mellitus, the SIADH developed two months after the chlorpropamide dosage had been increased to 500 mg daily. The syndrome disappeared after withdrawal of the drug. In one of these patients, re-administration of chlorpropamide resulted in recurrence of the SIADH. A review of the current literature disclosed certain common denominators, i.e., most of the patients are elderly women whose dosage of chlorpropamide was increased shortly before the development of the SIADH.
Aged↗
Lethal occult pulmonary hemorrhage in drug-induced thrombocytopenia.
A patient with drug-induced thrombocytopenia who died because of massive pulmonary hemorrhage is described. The patient had a clinical picture of acute respiratory distress resembling pulmonary edema, but there was no hemoptysis. Chest x-ray films showed granular density in the pulmonary fields, and the electrocardiograms revealed a pattern of acute biatrial enlargement. The diagnosis was confirmed at autopsy.
Acute Disease↗
Antibody-dependent, cell-mediated cytotoxicity against human red blood cells: correlation of effector cell type with enzymatic alteration of the target cell surface.
Target cell factors, which contribute to the determination of the effector cell type in an antibody-dependent, cell-mediated cytotoxicity system were studied. Human red blood cells (RBC) were treated with papain and investigated by transmission and scanning electron microscopy (TEM and SEM). Both untreated (native) and treated 0 Rh+ RBC were labeled with 51Cr, sensitized with anti-D immunoglobulin and incubated with unfractionated autologous peripheral blood mononuclear cells. With native RBC, immune lysis was proportional to the number of phagocytes: enrichment of effectors in phagocytes increased lysis, while depletion of phagocytes from effectors decreased lysis. Following papain treatment of target RBC, lysis by unfractionated mononuclear effectors was markedly augmented; since this effect was not diminished by decrease of phagocytes to less than 2%, the augmented lysis was not due to the number of phagocytic effectors. TEM and SEM of enzyme-treated RBC showed spherocytosis with varying degrees of crenation and blurring and irregularities of the cellular membranes. The results suggest that papain-induced alterations in the target RBC rendered them susceptible to lysis by interaction between anti-D antibody and peripheral blood lymphocytes.
Antibody-Dependent Cell Cytotoxicity↗
Cholestatic jaundice: an immune response to prajmalium bitartrate.
Cholestatic jaundice associated with chills, pruritus and blood eosinophilia developed in a patient who received prajmalium bitartrate therapy for ventricular arrhythmia following acute myocardial infarction. Discontinuation of the drug resulted in a spontaneous improvement in the clinical and biochemical findings. Challenge by prajmalium bitartrate caused rapid reappearance of the clinical and biochemical features. In immunological studies, deposits of IgG and IgA were detected at the bile canaliculi by fluorescent staining, and the patient's lymphocytes produced macrophage migration inhibition after in vitro incubation with prajmalium bitartrate. Thus, laboratory results support the assumption of an allergic mechanism.
Ajmaline↗
Hemolysis due to human antibody-dependent cell-mediated cytotoxicity. Lysis of erythrocytes treated with anti-D serum.
Antibody-dependent cell-mediated cytotoxicity against Rh+ red blood cells was detected in human anti-D sera. We used a rapid 4-h 51Cr-release assay to show that cytotoxic activity was proportional to serum concentration, incubation time and the attacking cell concentration. Attacking cells were obtained from normal human peripheral blood by Ficoll-Hypaque separation. Incubation of these lymphoid cells on a nylon column prior to the test depleted the number of phagocytic (latex-positive) cells in the effluent concomitantly with a drop in cytotoxic activity. Enrichment of the attacking cell population in mononuclear phagocytes by albumin gradient separation led to an increase in cytotoxicity. Granulocytes separated by Ficoll-Hypaque were not active in this system. Antibody activity was found in the 7S region following Sephadex G-200 fractionation of anti-D serum. Antibody activity was also studied after its elution from antiserum-coated red blood cells by diethyl ether. The eluate contained IgG and mediated cell-dependent lysis. Cell-free antiserum did not mediate lysis of coated red blood cells in the presence of complement.
Antibody-Dependent Cell Cytotoxicity↗
Subendocardial infarction and thrombocytopenia.
Two female patients who suffered from drug-induced thrombocytopenic purpura and subendocardial myocardial infarction are presented. One of them died from cerebral haemorrhage and diffuse subendocardial punctate haemorrhages were found at post-mortem. The abnormal haemostasis which is associated with thrombocytopenia might induce diffuse damage of the myocardium and might impair heart performance. This finding may be more frequent than hitherto appreciated and calls for serial electrographic tracings in thrombocytopenic patients.
Anti-Inflammatory Agents↗