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Biomedical subjects

W H Hitzig

Publications and source records attributed to W H Hitzig.

At least 37 records · Page 2Linked to original sources
PubMed1985

Transcobalamin II, a serum protein reflecting autoimmune disease activity, its plasma dynamics, and the relationship to established serum parameters in systemic lupus erythematosus.

Earlier investigations have shown that the activity of autoimmune diseases appears to correlate with increased levels of the vitamin B12 (cobalamin)-binding serum protein, transcobalamin II (M. Fráter-Schröder et al., Schweìz. Med. Wochensch 110, 1441, 1980; M. Fráter-Schröde et al., Lancet 2, 238, 1978). These preliminary findings were confirmed and extended with regard to SLE in the present prospective study. The correlation of serum levels with the degree of disease activity (determined by clinical scoring of 44 patients with systemic lupus erythematosus (SLE), fulfilling four or more of the American Rheumatoid Association criteria) was shown to be most reliable for transcobalamin II (P less than 0.001), when compared to other serological parameters. An answer to the question "what induces increased levels of transcobalamin II in active SLE?" was sought by injecting 15 SLE patients with cyanocobalamin which influences plasma dynamics of transcobalamin II. Results indicate that transcobalamin II-cobalamin "clearance" is probably unchanged in SLE, and that increased production or stimulation of transcobalamin II secretion may be the cause of elevated plasma levels in active SLE.

Antibodies, Antinuclear↗
PubMed1985

Uptake, intracellular activity, and influence of rifampin on normal function of polymorphonuclear leukocytes.

Quinone and hydroquinone forms of rifampin accumulated in normal polymorphonuclear leukocytes (PMN) (maximal cellular to extracellular concentration ratio [C/Emax] +/- standard error of the mean, 9.36 +/- 0.54 and 8.82 +/- 0.65, respectively, after 5 to 10 min) and chronic granulomatous disease PMN (C/Emax, 13.76 +/- 0.77 and 14.29, respectively). Uptake of rifampin was influenced by incubation temperature and extracellular pH but not by phorbol myristate acetate stimulation or metabolic inhibitors. At extracellular concentrations between 0.06 and 5.0 mg/liter, rifampin significantly reduced the number of staphylococci surviving inside chronic granulomatous disease PMN, thus compensating for the bactericidal defect inherent with this disease. Spontaneous migration and chemotaxis of normal PMN were unaffected by rifampin. However, phagocytosis of yeast particles and oxygen consumption of stimulated PMN were moderately depressed, and O2- production and chemiluminescence were significantly depressed in a dose-dependent manner. The bactericidal activity of normal PMN was not impaired. Inhibition of chemiluminescence and O2- release were also observed in a cell-free system. We conclude that rifampin possesses favorable characteristics for the effective elimination of intracellular microorganisms. Further studies are needed to evaluate the in vivo significance of ion scavenging by rifampin, which could be hazardous to immunocompromised patients.

Adult↗
PubMed1985

Chronic granulomatous disease: uptake and intracellular activity of fosfomycin in granulocytes.

In chronic granulomatous disease (CGD) polymorphonuclear leukocytes (PMN) are unable to kill phagocytized catalase-positive bacteria. Therefore, patients with CGD are prone to infections and dependent on antimicrobial agents able to penetrate PMN membranes and to act intracellularly. Owing to their good lipid solubility, trimethoprim/sulfamethoxazole and rifampicin passively diffuse the membrane. In contrast, fosfomycin is transported actively into the cell. In normal PMN, it reaches cellular-to-extracellular ratios of 1.83 after 15 min, in CGD-PMN 2.18 after 30 min. At concentrations between 16 and 200 mg/liter, fosfomycin was able to kill staphylococci surviving within CGD-PMN, thus compensating for the bactericidal deficiency in CGD. A combination of low concentrations of fosfomycin (8 mg/liter) plus rifampicin (0.06 mg/liter) was more effective at the intracellular level than either agent alone. Apart from a stimulation of PMN-chemiluminescence of yet unknown significance, the agent did not interfere with other neutrophil functions. Clinical investigations are indicated to study whether fosfomycin can be added to the small number of antibiotics useful in CGD.

Adolescent↗
PubMed1985

Congenital acatalasemia: a study of neutrophil functions after provocation with hydrogen peroxide.

Five Swiss subjects with hereditary acatalasemia (4 homo-, 1 heterozygous) were studied by a series of neutrophil function tests. H2O2 was added to a polymorphonuclear neutrophil leukocyte-suspension to produce a metabolic stress; neutrophil functions related to membrane deformation were subsequently found to be depressed, i.e., chemotaxis, membrane potential, and chemiluminescence. This mechanism might be one pathogenetic factor in the formation of mucosal ulcers in acatalasemic individuals.

Adult↗
PubMed1985

Surgery and granulocyte transfusions for life-threatening infections in chronic granulomatous disease.

We report two patients with chronic granulomatous disease (CGD) and life-threatening infections: a 10 10/12-year-old boy had Aspergillus fumigatus spondylitis with destruction of the 11th vertebral body and paravertebral abscess formation, and an 8 5/12-year-old boy had multiple Staphylococcus aureus hepatic abscesses with subphrenic abscess formation. Both patients failed to respond to intense antimicrobial therapy but showed a remarkable recovery following surgical drainage combined with granulocyte transfusions. These results suggest that antimicrobial therapy and surgical drainage followed by granulocyte transfusions may be the ideal mode of treatment for severe infections in patients with CGD.

Amphotericin B↗
PubMed1984

[Septic granulomatosis in adults].

Chronic granulomatous disease is a usually X-linked disorder of granulocyte bacterial killing. At least 8 variants can be distinguished biochemically. Two male patients aged 20 and 24 years with a relatively benign clinical course are presented. A partial defect of the membrane-bound cytochrome b-245 with a residual bactericidal capacity was detected in both. Due to continuous antibacterial prophylaxis (trimethoprim/sulfamethoxazol) and treatment of infections with intracellularly accumulating agents (e.g. rifampicin, fosfomycin, clindamycin), even patients with complete defects of bacterial killing can reach adulthood today. Physicians and surgeons should be aware of this disorder, which is no longer a "fatal granulomatous disease of childhood".

Adult↗
PubMed1984

Oral chloramphenicol therapy for multiple liver abscesses in hyperimmunoglobulinemia E syndrome.

In a patient with Hyper-IgE-syndrome multiple liver abscesses developed in spite of prophylactic treatment with trimethoprim and sulfamethoxazol. Ultrasound confirmed the clinical diagnosis and percutaneous needle aspiration under ultrasonographic guidance and culture of the aspirated pus allowed specific antibiotic treatment by oral chloramphenicol alone without surgical drainage. The isolated Staph.aureus strain was resistant to trimethoprim and sulfamethoxazol.

Candidiasis↗
PubMed1984

Human IgG antibodies to carbohydrate and protein antigens in mouse protection tests with group B streptococci.

The protective effect of four commercial human gammaglobulin batches (I-IV) in mice was studied using six different strains of group B streptococci (GBS): types Ia; Ib; II, R-protein negative (R-); II, R+; III, R-; and III, R+. Each mouse received 1.0 ml gammaglobulin and 0.5 ml bacteria, 10(6)-10(8) colony forming units (CFU). There was a close correlation between antibody levels measured by the use of radiolabeled protein A and the mouse-protective effect of the gamma-globulins. The mouse-protection tests demonstrated that batch I protected against GBS types Ia and III, R- at low concentration (65 mg/kg mouse weight), against type Ib at medium (260 mg/kg) and against type III, R+ at high concentration. Batch IV protected against types Ia and Ib, although the doses were four times higher than those in batch I, but did not protect against type III, R+. There was no mouse protection by any of the batches against type II. Antibody levels against Ibc and R, protein antigens, were substantially lower in batch IV. Because the results of these mouse-protection studies indicate the importance of such antibodies against protein antigens, batches I-III might be more useful for therapy of neonatal GBS-septicemia.

Animals↗
PubMed1983

[Humoral immunodeficiencies and their substitution treatment].

Missing antibodies can be effectively and rapidly replaced by injections of immunoglobulins. For practical reasons this method is restricted to prophylaxis, repeated replacements and acute treatment. Provided they are administered at an early stage, small amounts of immunoglobulins are sufficient for prophylaxis or passive immunization. Acute treatment is based on the same principle, but much higher doses are required since it is given late to patients with clinical symptoms. Replacement therapy proper is used in patients who are clearly unable to produce antibodies in sufficient amounts. Regularly repeated administration makes replacement therapy very expensive. Comparisons between different preparations of immunoglobulins indicate that the best are those which are well tolerated by the intravenous route. In our experience, Sandoglobulin fulfills all the clinicians' requirements.

Antibody Formation↗
PubMed1983

Chronic granulomatous disease, a heterogeneous syndrome.

Chronic granulomatous disease (CGD) is a clinical syndrome, the unifying characteristics of which are a severe predisposition to bacterial and fungal infections, an impaired ability of phagocytic leukocytes to kill certain microorganisms and the failure of these cells to produce microbicidal oxygen metabolites. In CGD the causal biochemical defect and the mechanism of genetic transmission vary from family to family. At least six different molecular defects have been found to underly the X-linked and at least three other the autosomal recessive form of CGD. Diagnosis of carriers is possible in most instances, and prenatal diagnosis by fetoscopic placental vessel puncture has become feasible.

Bone Diseases↗
PubMed1983

Granulocyte function in untreated pernicious anaemia.

Neutrophil granulocyte functions were evaluated in nine patients with pernicious anaemia (PA). Membrane potential, oxygen consumption, nitroblue tetrozolium reduction, and phagocytosis and killing of staphylococci were determined prior to the institution of vitamin B12 therapy. There were no significant alterations in these granulocyte functions as compared with normal controls, although in several patients low values were seen. We conclude that in PA the oxidative metabolism and microbicidal functions of granulocytes in general are normal, even in severely anaemic patients.

Aged↗
PubMed1983

Protean appearances of immunodeficiencies: syndromes and inborn errors involving other systems which express associated primary immunodeficiency.

Developmental defects interrupting the normal evolution of immunocytes can explain many of the congenital immunodeficiency syndromes. Observations accumulated during the last decade have, however, shown that this is not the only cause, and that many diseases have signs of immunodeficiency as an accompanying feature. Severe combined immunodeficiency (SCID) is a good example of the multiple etiology of similar clinical features--they are phenocopies of a well-delineated hereditary disease. A number of recently described syndromes are reviewed, albeit an incomplete list. Metabolic disorders due to inactivity of enzymes may present characteristic ID. Some of them are explained by lack or increased need of co-enzymes (like biotin or zinc). In other syndromes, better understanding of the pathogenesis might pin down the primary failure to one single point, as shown in the hyper IgE syndrome. Other fundamental disturbances are located in the chromosome itself, eg decreased repair capacity, deletion, translocation. An attempt is made to propose a general classification accommodating all etiologic factors known to date which lead to immunodeficiency. It is obvious that within this framework the same clinical syndrome may be repeated.

Adenosine Deaminase↗