IgA deficiency in Czech healthy individuals and selected patient groups.

BACKGROUND: Selective IgA deficiency (IgAD) is the most common immunoglobulin deficiency with a variety of clinical manifestations. The frequency of IgAD differs depending on the ethnic origin and clinical symptoms of investigated persons. METHODS: The prevalence of IgAD (serum IgA level <0.05 g/l) was determined in 5,310 Czech blood donors, 10,326 patients who had undergone immunological investigation, and 246 first-degree relatives of IgAD and common variable immunodeficiency (CVID) patients. RESULTS: IgAD was detected in 13 (1/408; 0.24%) of the blood donors. The prevalence of IgAD was increased both in children (48/3,113; 1.5%) and adults (33/3,824; 0.9%) referred for frequent respiratory tract infections (in both cases p<0.001) compared to the healthy population. The frequency of IgAD was 12/189 (6%) in first-degree relatives of IgAD patients and 9/57 (16%) in relatives of CVID patients, with the highest frequency observed in children of CVID patients. CONCLUSIONS: The prevalence of IgAD in the Czech healthy population is comparable to that in other Caucasians. The frequency is increased in children with recurrent respiratory tract infections and especially in relatives of patients with immunoglobulin deficiencies.

[IgG subclasses and autoantibodies in adult patients with selective IgA deficiency]. / Podtrídy IgG a autoprotilátky u dospelých pacientu se selektivním deficitem IgA.

Selective IgA deficiency is the most common primary immunodeficiency disease, but the etiopathogenesis is unknown. In a portion of patients disturbed IgA production is accompanied by various immunological abnormalities. Serological laboratory results of 30 female and 22 male adult patients with selective IgA deficiency were compared with sex- and age-matched healthy controls. Hypergammaglobulinemia IgG was observed in 31 patients and only in 2 control persons. Serum IgG1 was increased in 12 and/or IgG3 in 18 patients, the increase in IgG2 was less common (6 persons). The number of persons with increased IgE did not differ from the control group. The occurrence of autoantibodies (antinuclear antibodies, rheumatoid factor, antithyroglobulin and anti-thyroid microsomal antibodies, anti-gastric parietal cells, reticulin, smooth muscle, anticardiolipin, and anti-gliadin antibodies) did not differ significantly from the control group. IgG hypergammaglobulinemia, which, according to our results, is the most frequent accompanying serological abnormality in IgA deficiency, may be caused by compensatory increased production, but may also reflect more profound immunological dysregulation in the disease.

[Helicobacter pylori and nonspecific intestinal inflammation]. / Helicobacter pylori a nespecifické strevní zánety.

In 50 subjects with non-specific inflammations of the gut the total prevalence of Helicobacter pylori positive antibodies was 28%, while in the control group of blood donors its was 54% Patients with ulcerative colitis had lower antibodies--18%, in Crohn's disease the serum positivity was 33%. The lowest value of antibodies was found in patients taking Sulfasalazine--11%. The serum positivity was substantially higher in inactive ulcerative colitis and Crohn's disease--35% than in patients with signs of high activity--13%. In 28 patients with non-specific inflammations of the gut endoscopy was performed, in 60% with a pathological outcome. Histologically confirmed gastritis was in the majority Helicobacter pylori negative. It may be stated that in patients with non-specific inflammations of the gut there is a lower incidence of Helicobacter pylori than in the general population, in particular those subjects who were or are treated with Sulfasalazine. The explanation of this fact is however only speculative.

Mutation analysis of the receptor for colicins E1-E7. A pilot study.

Thirty eight mutant clones of the colicin indicator strain Escherichia coli K 12 ROW, selected by their insensitivity to any of the colicins E1-E7, were isolated. Comparison of their sensitivity-resistance patterns to colicins E1-E7 enabled us to draw a rough preliminary map of the receptor for E colicins. In this receptor, the highly specific binding site for colicin E1 partially overlaps with the domain shared by all colicins E2 through E7. A specific binding site of this domain appears to be common for colicins E3 and E6; a part of the E3 and E6 binding site is also common for colicins E4 and E5 and a small, least specific, part also for colicins E2 and E7. Using colicin assay experiments, the binding capacity of colicin E receptor mutants could be estimated. A decreased, but not completely lost ability of certain mutants to bind colicins E, correlated to their lowered sensitivity to them, was found. Thus the phenomenon of partial colicin resistance was established, showing that colicin sensitivity--resistance is not a qualitative but a quantitative marker.