SUMMARY Methods : Fifty patients with relapsing or complicated Helicobacter pylori positive duodenal ( n = 41) or gastric ulcer disease ( n = 9) and failure of a combined treatment with omeprazole plus amoxycillin to eradicate H. pylori infection were re‐treated with either oral triple therapy (bismuth subsalicylate, metronidazole, tetracycline) plus ranitidine [group I: n = 22] or high‐dose omeprazole (40 mg b.d. to t.d.s.) plus amoxycillin (1 g t.d.s.) [group II: n = 28]. Results : Patients of group I and II had similar demographic and clinical characteristics. The overall proportion of eradication of H. pylori infection was 81.8% in group I and 78.6% in group II ( P = N.S.) as judged from negative bacterial findings by means of an urease test, specific culture and histology after modified Giemsa stain. Ulcer healing was observed in all patients after a maximum duration of 10 weeks. Ten patients on triple therapy and only one patient on omeprazole plus amoxycillin (45.5% vs . 3.6%; P < 0.001) complained of side effects without necessity of discontinuation of the study medication in either group. Twenty patients (group I: n = 10: group II: n = 10) with relapsing duodenal ulcer disease and successful cure were prospectively followed for one year without any evidence of ulcer relapse or H. pylori re‐infection. Conclusion : Oral triple therapy plus ranitidine or highdose omeprazole plus amoxycillin remain highly effective in eradicating H. pylori infection in patients with peptic ulcer disease and treatment failure of omeprazole/amoxycillin, but the omeprazole enhanced antibiotic monotherapy seems to be superior with regard to side effects. Thus, high‐dose omeprazole/amoxycillin is recommended as the treatment of first choice in these selected patients. Triple therapy should be reserved for patients intolerant of amoxycillin
Abstract. Since its discovery, human plasminogen (PLG) polymorphism has received widespread acceptance in population genetics and forensic haematology. Due to the large number of variant alleles described, a PLG reference typing and Plasminogen Symposium was held, at which a nomenclature proposal was inaugurated. The technology of comparing PLG variants was based on isoelectric focusing and subsequent detection by caseinolytic overlay and ‘Western’ blotting. Typing results permitted comparison of so far described variant designations and resulted in a new nomenclature proposal for PLG polymorphism. It is recommended that the two most common alleles found in all investigated races be called: PLG*A (previously also PLG*1 ) and PLG*B (previously also PLG*2 ), the known variants with acidic pI: PLG*A1 to *A3 , intermediate variants: PLG*M1 to *M5, PLG*M5 being functionally inactive, and basic variants: PLG*B1 to *B3. For future classification of newly discovered variants, samples should be compared at any of the laboratories participating in the reference typing.
The two genes for the C4A and C4B isotypes of the fourth component of human complement are located in the MHC class III region. Previous studies have demonstrated the unusual expression of C4 genes in the form of aberrant or duplicated haplotypes. Null alleles of C4A or C4B (AQ0 or BQ0) have been defined by the absence of gene products and occur at frequencies of 0.1-0.3. However, only some C4 null alleles are due to gene deletions, the remainder were thought to be nonexpressed genes. We have analyzed the C4 gene structure of 26 individuals lacking either C4A or C4B protein. The DNA of individuals with apparently nonexpressed C4 genes was tested for the presence of C4A- and C4B-specific sequences using restriction fragment analysis and isotype-specific oligonucleotide hybridization of DNA amplified by polymerase chain reaction. All nondeleted AQ0 allels had C4A-specific sequences and may thus be described as pseudogenes, whereas the nondeleted BQ0 alleles had C4A-instead of C4B-specific sequences. Gene conversion is the probable mechanism by which a C4A gene is found at the second C4 locus normally occupied by C4B genes.
Forty-four cases of insulin-dependent diabetes mellitus with cutaneous allergic reactions to insulin were typed for HLA-A and -B antigens. HLA-B7, which commonly is negatively associated with insulin-dependent diabetes mellitus, showed a positive association with insulin allergy. A second antigen, HLA-Bw21 may also be positively associated with local insulin allergy. These data were discussed in relation to heterogeneity of insulin-dependent diabetes mellitus and to the existence of B7-associated immune response genes for allergic-immunoreactivity to insulin.
