Biomedical subjects
Publications and source records attributed to J Sennekamp.
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Esophageal function was investigated by quantitative intraluminal pressure measurements in three patients with Behçet's disease. All three had motility disorders partially resembling those described in diabetics and partially those from patients with scleroderma. These motility disturbances may be secondary to a neurological involvement in Behçet's disease.
The kinetoplast immunofluorescence test for the detection of antibodies against desoxynucleic acid (DNA) utilizes as a substrate the native double-stranded DNA containing kinetoplast of the hemoflagellate Crithidia luciliae, which is nonpathogenic in human beings. By studying the sera of 279 patients with dermatological and internal diseases, as well as the sera of 80 blood donors, this technique was assessed for its usefulness in routine diagnosis. DNA-antibodies were found most frequently in the sera of patients with systemic lupus erythematosus (34/53). Additionally DNA-antibodies were demonstrated in some patients with cicatrical pemphigoid (1/1), autoimmune hepatitis (4/25) and myasthenia gravis (1/3). According to the experience thus far the kinetoplast immunofluorescence test appears to be a specific and well reproducible method to demonstrate DNA-antibodies in a simple way.
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Sera from 41 children suffering with histologically proven coeliac disease and from 40 healthy control children were investigated for the presence of antireticulin antibodies and precipitating antibodies to a watery extract of wheat flour and to cow's milk. Antireticulin antibodies were demonstrated by means of indirect immunofluorescence using sections of fresh rat kidney as substrat. For the detection of precipitating antibodies a combination of electrophoresis and immunodiffusion was used. Serum antireticulin antibodies were found in 11/13 children (85%) with active coeliac disease, in 7/17 children (41%) with clinically and biochemically silent coeliac relapse and in 0/16 children with treated coeliac disease. Serum precipitating antibodies to wheat flour and cow's milk were found respectively in 3/13 children (23%) and 2/13 children (15%) with active coeliac disease and in 1/16 children (6%) with treated coeliac disease. Precipitating antibodies could not be detected in the sera of 17 patients with silent relapse of coeliac disease. In the sera of 40 controls neither antireticulin nor precipitating antibodies were detectable. The presence of antireticulin antibodies in serum did not correspond to the presence of serum precipitins to wheat flour and cow's milk. The significance of serum antireticulin antibodies for screening investigations and for follow-up studies is discussed.
The serum of 102 pigeon breeders was examined for circulating IgG antibodies against antigens localized in pigeon intestine by the indirect immunofluorescent technique. 15 symptomatic breeders with a positive response to inhalation challenge had antibodies against mucosa tissue. The majority of asymptomatic breeders demonstrated either a fluorescence of intestinal excrements combined with a weak fluorescence of mucosa tissue or had no detectable antibodies in their serum. By the indirect immunofluorescence, antibodies were found more frequently than by immunoprecipitin reactions in agar.
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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.
Fifteen women with pseudo-LE syndrome were studied. The dissease is characterized by recurrent attacks of fever, myalgia, arthralgia, visceral manifestations (pericarditis, myocarditis, pleurisy, pleural effusion and lung involvement). A prominent feature was an abnormal liver function with elevated GOT and GPT levels in serum, and impaired bromsuophalein elimination. The incidence of varicosities and thrombophlebitis was markedly increased. There was a correlation between complement-fixing antimitochondrial antibody (AMA) titres and the degree of activity of the disease. A reverse correlation was observed between antimitochondrial antibody titres and the absolute lymphocyte count in peripheral blood. In all instances the antimitochondrial antibodies were of polyclonal origin, belonging mainly to immunoglobulin class IgG and, in a few patients, IgM, IgA, or IgD. AMA titres, lymphocyte counts in peripheral blood, sedimentation rate, serum iron level and alpha1- and alpha2-globulins proved to be valuable in following the course of the disease. Other values (C-reactive protein, alpha1-acid glycoprotein, immunoglobulin and beta1c-globulin in serum) were not helpful.
Clinical, histological (including electron-microscopic), immunohistochemical and genetic studies were performed on two infants with alpha1-antitrypsin deficiency. The clinical picture was one of neonatal biliary stasis. Liver biopsies revealed multiple cytoplasmic acidophilic bodies within many cells of the liver parenchyma which were strongly periodic acid-Schiff-positive, diastase-resistant and stained selectively with fluorescein-labelled rabbit antihuman alpha1-antitrypsin. Ultrastructurally, the bodies were situated within enlarged cisterns of the endoplasmatic reticulum. Both infants were of the protease inhibitor (Pi) phenotype ZZ, having inherited on PiZ gene from each parent. Results of Pi typing of both families were consistent with an autosomal co-dominant inheritance. Both infants are clinically well except for slight hepatomegaly at one year of age. But transaminase and gamma-glutamyl transpeptidase activities have remained elevated.
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