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H Schubothe

Publications and source records attributed to H Schubothe.

At least 19 recordsLinked to original sources
PubMed1983

[Clinical significance and pathogenesis of drug- or microbe-induced autoimmune hemolytic anemias].

Methyldopa and several other drugs, continuously taken over months or years, may induce autoimmunity in persons having a probably genetic predisposition. The autoimmunity is reversible after discontinuation of the drug. A number of infectious agents may lead to the same effect. The autoantibodies can react with different autologous targets, for instance red blood cells. This may occasionally cause an autoimmune haemolytic anaemia. The two pathogenetic cardinal points are discussed in the case of the methyldopa-induced autoimmune haemolytic anaemia: the induction of the process results very probably by inhibiting or blocking of the competent suppressor-T-lymphocytes, which normally prevent an autoantibody production, representing a form of chemical "contrasuppression". This has been demonstrated in cultures of peripheral human blood lymphocytes of patients on methyldopa therapy. The second pathogenetic cardinal point is the effect of the autoantibody after its binding to the drugs investigated up to now. Rarely it is pathogenic. This relation is exactly contrary to the idiopathic warm autoantibody anaemia and remains an unsolved problem. A reversible selective deficiency of suppressor-T-cells has also to be postulated for other autoimmune haemolytic anaemias and autoimmune diseases induced by drugs or infectious agents.

Adult↗
PubMed1982

[Methyldopa-induced autoimmune hemolytic anemia. Course and long-term observations on 11 patients].

Long-term studies on 11 patients suffering from methyldopa-induced autoimmune haemolytic anaemia suggest that this self limitable episode of disturbed immune tolerance is characterized by five main parameters: 1. The autoimmune pathogenic average daily drug dose: Unfortunately, it cannot be estimated exactly due to the individually rather variable absorption of methyldopa (7-62%). The lowest oral dose in our patients was 125 mg daily. 2. The period of autoimmune induction: between the start of the methyldopa administration and the beginning of autoantibody production. It has to be estimated somewhat shorter than the time up to the clinical manifestation of the haemolytic anaemia. This varied over a wide range from 2 to 52 months. 3. The period of the active autohemolysis: between the appearance of pathogenic autoantibodies and the withdrawal of methyldopa. It depends on the recognition of the cause of the disease. In our patients it varied between 2 and 32 weeks. 4. The period of the haematologic remission: between the withdrawal of methyldopa and the normalization of the red blood cell values. It ranged between 4 weeks and 4 months. Contrary to the other parameters, the clinical remission is almost uniform in all patients. It begins immediately when the drug is stopped. This fact suggests that the induction and maintenance of the disease needs a continuous application of methyldopa and its presence in blood and tissue. The normalization of the red blood cell turnover simultaneous with the cessation of therapy, although the direct antiglobulin test remains positive, reveals a change of the autoantibodies into those apathogenic variants known from the majority of methyldopa-induced autoimmunizations. 5. The period of immunologic remission: between the withdrawal of methyldopa and the definite extinction of autoantibody production. It varied between 4 and 12 months. Transition to or later development of an autonomous warm autoantibody anaemia were not observed. The disease remits spontaneously. Its prompt reversibility resembles the same phenomenon in autoantibody anaemias induced by infectious agents. An inhibition of methyldopa-sensitive suppressor-T-cells may initiate the disturbed tolerance disease.

Adult↗
PubMed1980

[Experimental models of human immune haemolytic anaemias (author's transl)].

In the last ninety years there were many attempts to induce immune haemolytic anaemia (IHA) in laboratory animals. The techniques employed were injections of modified autologous or incompatible erythrocytes as well as hyperimmunization with material of high antigen activity (e.g. egg albumin). Serious temporary IHA could be induced occasionally. The main pathogenetic mechanism in this immune reaction was related to the antigen. Another model used was the so called graft-host-reaction in which IHA is based on antibody formation of transplanted immunocompetent cells towards the host erythrocytes. So far, the best animal model is the spontaneous autoimmune haemolytic anaemia in NZB-mice. However this model has not been completely evaluated. In these animals AIHA is mediated by a genetically prescribed immunoregulatory defect which may be located at the level of T-lymphocytes.

Anemia, Hemolytic, Autoimmune↗
PubMed1979

[Hemolytic crisis and acute kidney failure from rifampicin].

Two cases are reported of hemolytic crisis and acute anuria after intermittent rifampicin medication. Immunologic tests demonstrate that the hemolysis was of the drug-induced heteroimmune type whereas the pathogenesis of the anuria was uncertain. For both complications the prognosis is good.

Acute Kidney Injury↗
PubMed1979

[Progressive systemic sclerosis - long-term treatment with azathioprin (author's transl)].

The study presents the results of an Azathioprin long-term therapy in 19 of 60 patients with progressive systemic sclerosis (PSS). Average treatment was 47 months (6 to 114 months). The patients received 2-2,5 Azathioprin/kg bodyweight daily. In 16 cases no further progression of PSS was noted. One patient showed minor deterioration. In particular no further deterioration in the lung and kidney manifestations were found. Two patients died. A female patient showed signs of osteomyelofibrosis after being treated for 70 months. She died 3,5 years after Azathioprin had been discontinued. The second patient died of right heart failure after recurrent pulmonary emboli. On the whole treatment with Azathioprin over a long period of time seems in most cases to hold the progression of the disease. The unfavourable prognosis can therefore be much improved.

Adolescent↗
PubMed1976

[Complex formation between monoclonal IgM and albumin in a patient with macroglobulinaemia (author's transl)].

A remarkable interaction between a monoclonal IgM(x) protein and autologous albumin was found in the serum of a 76 year old male patient (Ke.E) without morphological characteristics of Waldenströms disease. The components were bound noncovalently. Immunoelectrophoretic analysis of 50 additional monoclonal IgM and 10 IgA sera showed a complex formation with albumin in 62% (IgM) and in 90% (IgA). The degree of interaction was, however, less pronounced in comparison with that observed in the serum of Ke.E.

Aged↗
PubMed1975

[On the question of drug-induced pseudo-LE syndrome: preliminary results in 58 cases (author's transl)].

Drug intake had been checked in 58 patients with pseudo-LE-syndrome. In view of the findings of the Zürich group a connection between the intake of Venopyronum¿ coated tablets and a pseudo-LE syndrome was strongly suspected in 45. In a further seven patients who also had taken the drug no definite connection could be shown because there was no temporal relationship between drug and disease. Three patients had taken Venopyronum-triplex capsules. Only three patients categorically denied ever having taken the drug in any form.

Acute Disease↗
PubMed1975

[Serum iron in hemolytic anemia (author's transl)].

Serum iron, hemoglobin, and reticulocytes were determined in 134 patients with hemolytic anemia (hereditary spherocytosis, pyruvate kinase- or glucose-phosphate isomerase deficiency, hemolytic anemia due to warm auto antibodies, cold agglutinin disease, paroxysmal nocturnal hemoglubinuria, hemolytic uremic syndrome). No correlation was found between iron concentration and degree of hemolysis. Only a few patients show a marked increase of serum iron.

Agglutinins↗
PubMed1975

[Mitochondrial antibodies induced by drug administration in patients with and without pseudo LE syndrome (author's transl)].

The pseudo LE syndrome was first described in 1972. It is a severe, sometimes fatal condition, in which high titres of mitochondrial antibodies are a constant feature. In the vast majority of cases detected, Venopyronum in dragée form (containing phenopyrazone, horse-chestnut extract, and cardiac glycosides from various plants), had been taken prior to onset of the clinical symptoms. It is probably commoner, that following intake of the drug mitochondrial antibodies appear without clinical manifestations. In both situations, disposition, dose and duration of treatment are important factors. There is reasonable ground to believe that not just a single component, but rather the combination of various substances in the preparation is responsible for the induction of an autoimmune process. At the present time it appears that an idiopathic form, without drug contact, also exists.

Adult↗