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Biomedical subjects

S Havelka

Publications and source records attributed to S Havelka.

At least 19 recordsLinked to original sources

A model for the role of HLA-DQ molecules in the pathogenesis of juvenile chronic arthritis.

Restriction fragment length polymorphism (RFLP) typing of MHC-class II loci DRB, DQA1, DQB1, DQA2 and DPB1 was performed in 94 patients with seronegative juvenile chronic arthritis (JCA) and 184 random controls. Analysis of allele frequencies and MHC-class II 4-loci haplotypes indicate: (1) Susceptibility to JCA is more strongly associated with the HLA-DQ subregion than with the HLA-DR subregion, especially in early onset pauciarticular JCA (EOPA-JCA). (2) Haplotype and sequence analysis show two independent MHC-class II associations for susceptibility to EOPA-JCA, one located in DQA1, the other in DPB1. (3) Two RFLP defined patterns of the DQA1 locus, DQA1.5 (DQA1*0501) and DQA1.8 (DQA1*0401, *0601) are strongly associated with the disease. (4) Analysis of amino-acid (AA) sequences coded in exon 2 of DQA1 reveals an AA sequence of six AAs common to all three associated DQA1 alleles. This suggests a model that includes a functional role for HLA-DQ molecules in the pathogenesis of JCA.

Alleles

Sulphasalazine and Delagil--a comparative study in patients with juvenile chronic arthritis.

Thirty nine consecutive patients with pauciarticular and polyarticular juvenile chronic arthritis were randomised to treatment with either sulphasalazine or Delagil (chlorochinum diphosphoricum) in a parallel 6 month clinical trial. We compared clinical and laboratory signs of activity before and after the treatment. Of 21 patients with Sulphasalazine 10 were improved, 7 unchanged and in 4 patients had the therapy to be withdrawn. Of 18 patients with Delagil 5 were improved, 12 without effect and withdrawal was necessary in 1.

Anti-Inflammatory Agents, Non-Steroidal

Syndrome of secondary polymyositis with leukemia.

A boy with neurofibromatosis suffered mumps at the age of 5. A full-blown juvenile polymyositis developed shortly afterwards. First hematological consultation was done for monocytosis in peripheral blood at the age of 7. He suffered varicella at the age of 8. Diagnosis of acute nonlymphocytic leukemia with monosomy 7 was done before the age of 9. The boy died at the age of 10.

Child, Preschool

[Sulfasalazine in the treatment of chronic juvenile arthritis].

In 38 children with juvenile chronic arthritis the authors tested Sulphasalazine in an open clinical trial. The drug was administered for 26 weeks, 20-30 mg/kg/day. The action of the drug was followed up with regard to clinical (number of criteria of juvenile chronic arthritis, functional state, period of morning stiffness, number of affected joints painfulness of joints) and laboratory (red cell sedimentation rate, circulating immunocomplexes) indicators. A favourable effect (improvement of at least five of the above indicators) was recorded in 42.1% of the children. Undesirable effects were found in 11 children (30%) incl. six where they were the cause of discontinuation of treatment. All undesirable effects were reversible. The majority of them (exanthema, headache, leukopenia, microscopic haematuria) developed during the first 3-4 weeks of treatment.

Adolescent

[The incidence of antibodies against collagen in patients with juvenile chronic arthritis].

Using the ELISA method, the authors assessed titres of antibodies to collagen type I, II and III in serum of patients with juvenile chronic arthritis (JCA). The results were compared with antibody titres in patients with rheumatoid arthritis (RA). Elevated antibody titres to all collagen types were found, as compared with age-matched controls. The mean titres in patients with RA were higher than in the group with JCA. Investigation of a correlation between the collagen antibody titres and values of the sedimentation rate after one hour revealed a statistical relationship only in collagen type II in patients with RA.

Adolescent

Anticollagen antibodies in patients with juvenile chronic arthritis.

Using ELISA antibodies, titres to collagen type I, II and III in sera of patients with juvenile chronic arthritis (JCA) were assayed. Results were compared with titres of patients with rheumatoid arthritis (RA). Increased antibodies titres to all three collagen types were found in comparison with healthy individuals of the same age. Average titres in patients with RA were higher than those of the JCA group. When antibodies titres were correlated with erythrocyte sedimentation rate in 1 hour (ESR/1h) statistical significance was found only in RA group for collagen type II.

Adolescent