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Biomedical subjects

F Streiff

Publications and source records attributed to F Streiff.

At least 73 records · Page 4Linked to original sources

HLA typing in a new family with Fletcher factor deficiency.

In a nonrelated white family, the Fletcher factor level in the father was 0.41 U/ml and in the mother, 0.30 U/ml (controls, 0.75-1.25 U/ml). One sibling with recurrent epistaxis had a level of 0.012 U/ml, whereas the other without tendency to spontaneous bleeding had levels between 0.75 and 0.32 U/ml. This suggests autosomal recessive transmission with clinical symptoms when the defect is homozygous. HLA antigens were studied to determine whether characters of the histocompatibility system and this defect are linked: we determined that the gene(s) of the disease is (are) not shared on the HLA complex.

Adult↗

Treatment by plasma exchange of a patient with hyperlipidemia and diabetic ketoacidosis with lesional pulmonary edema and acute pancreatitis.

The authors report a case of severe hypertriglyceridemia (148.5 mmol/l) in a 27-year-old woman admitted for coma of unknown origin. Initial investigations revealed ketoacidosis, pancreatitis and noncardiogenic pulmonary edema. The diabetes was unknown. Ketoacidosis was rapidly controlled. The hypertriglyceridemia was corrected by one course of plasma exchange (4,400 ml) during which the patient returned to consciousness. The patient recovered without any sequelae. Only 2 similar cases, treated by plasma exchange, have been reported in the literature until now.

Acute Disease↗

A family demonstrating the independence between Lutheran and Auberger loci.

The family presented here demonstrates the absence of a close relationship between the Auberger loci on one hand and the Lutheran and secretor loci on the other. This absence of a close relationship between the Lutheran and Auberger loci is important in understanding the inhibition mechanism of the Au antigen when in the presence of the dominant In(Iu) allele.

Alleles↗

[Acquired coagulation inhibitors. 10 cases (author's transl)].

A circulating anticoagulant with antiprothrombinase activity was detected in 10 patients, 4 of whom had systemic lupus erythematosus. Clinically, haemorrhages occurred only in patients with associated thrombopenia; some developed thrombosis. Recalcification time and activated partial thromboplastin time were prolonged in the patients' plasma and in mixed patients' and control plasma. In 5 cases the anticoagulant was isolated by chromatography as IgG or IgM.

Adolescent↗

[HLA-DRw7 in psoriasis vulgaris].

40 unrelated patients with Psoriasis vulgaris were studied for their HLA-A, B and DRw antigen phenotypes. All underwent a skin biopsy to confirm diagnosis. Like most of the authors, we observed an increase in B13 and B17 antigens (17,50 and 25%) whereas in the healthy population the percentage was (5 and 6,02%) respectively. The strong increase in DRw7 suggests that psoriasis vulgaris was associated with DRw7 antigens, with an unbalanced linkage between the B13 and DRw7 antigens and between the B17 and DRw7 antigens.

Adult↗

[Anti-varicella-zona immunoglobulins. Discovery of antibodies and method of formation].

The screening of zoster's antibodies has been performed in blood donors population and persons convalescing from herpes zoster. The results show that 25% of blood donors and 83,5% of convalescents have respectively a titer of CF antibody of 8. Plasma units were pooled and the pool had a final titer of CF antibody of 16. Varicella zoster immunoglobulin prepared by alcohol fractionation had a fluorescent antibody titer of 1 024 and a CF antibody of 512. These results are discussed and compared with those of literature.

Adult↗

[HLA-DRw typing in 40 patients with psoriasis].

40 unrelated patients with psoriasis vulgaris were studied for their HLA-A, B and DRw antigens phenotypes. All underwent a skin biopsy to confirm diagnosis. Like most of the authors, we observed an increase in B 13 and B 17 antigens (17,50 % and 25 %) whereas in the healthy populations the percentage was (5 % and 6,02 %) respectively. The strongest increase in DRw7 suggest that the psoriasis vulgaris was associated with DRw7 antigens, with a linkage desequilibrium between the B 13 and DRw7 antigens and between the B 17 and DRw7 antigens.

Genetic Linkage↗

[Genetics of insulin-dependent juvenile diabetes].

Since the works of Singal and al. and Nerup and al., an increase in B 8, B 15 and B 18 antigens has been found in Insulin Dependent Diabetes. Thomson and al., Rubinstein and al. and the authors of this paper have shown an stronger association with DRw 3 and DRw 4 antigens. We investigated the genetic predisposition to juvenile diabetes in 22 families of 48 cases and 96 members. The study of one affected child in each family showed that DRw 3 was found in 63,63% and DRw 4 in 59,59% (healthy 16,22%)--RR = 9,0 and 7,49. The hypothesis of overdominance proposed by Nerup can be confirmed by our data, when I.D.D.M. share two different alleles (DRw 3 and DRw 4). 3 particular haplotypes with linkage imbalance are therefore observed in our series: B 8-Bf S-DRw 3, B 15-Bf F-DRw 4 and B 8-Bf F 1-DRw 3. Our date show a excessive transmission of the diabetic haplotype by parents who are either diabetics or carriers of the gene.

Antigens↗

[Bf groups in ankylosing spondylitis].

The phenotypes Bf were studied in 50 patients (42 men and 8 women) with definite ankylosing spondylitis and in certain of their relatives. The alleles BfF and BfS were most frequently encountered and the rare allele BfF1 in one case only. There may exist a preferential transmission of the haplotype HLA B27- Bf S. In 11 patients without B27 antigen, the distribution of the phenotypes was similar to that in a control group. It is probable that the locus Bf cannot be used as a preferential marker for ankylosing spondylitis.

Complement Factor B↗

[Ankylosing spondylitis in monozygous twins. Study of HLA complex (author's transl)].

A study of HLA complex (HLA A, B, C, DRw, Bf, chiddo) in monozygous twins suffering from ankylosing spondylitis with different clinical courses. All the markers studied were identified. The results would tend to suggest that hereditary factors are not alone responsible in the course of ankylosing spondylitis. Furthermore, they are not the sole causative factor of the disease since the literature contains reports of discordant pairs of twins.

Adolescent↗