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Biomedical subjects

C Friman

Publications and source records attributed to C Friman.

69 records · Page 4Linked to original sources
PubMed1975

A case of disseminated hemangiomatosis with cutaneous, hepatic and skeletal manifestations and increased urinary excretion of glycosaminoglycans.

A case of disseminated hemangiomatosis with cutaneous hepatic and extensive skeletal manifestations is reported. The diagnosis was established by means of bone X-ray, hepatic angiography, and skin and bone biopsies. A moderately increased urinary excretion of glycosaminoglycans (GAG) was found. The main GAG fraction excreted was tentatively identified as a heparan sulphate.

Angiomatosis↗
PubMed1972

[Sanfilippo's syndrome].

Explore the source record for details and available documents.

Carbohydrate Metabolism, Inborn Errors↗
PubMedDate not supplied

Urinary excretion of glycosaminoglycans in malignant diseases of the haemopoietic and lymphatic tissues.

A study has been made of the urinary excretion of glycosaminoglycans (GAG) in 50 patients with malignancies, including 6 patients with acute myeloid leukaemia (AML), 11 with chronic myeloid leukaemia (CML), 10 with chronic lymphatic leukaemia (CLL), 10 with multiple myeloma (MM), 7 with Hodgkin's disease and 6 with mycosis fungoides (MF). The total urinary GAG were isolated by precipitation with cetyltrimethyl-ammoniumbromide (CTAB), and assayed in terms of their hexuronic acid content. A statistically highly significant increase in the excretion of total GAG was observed in all the disorders studied, except Hodgkin's disease, the highest value being seen in myeloid leukaemia (ML). Constant amounts of non-dialysable urinary GAG were electrophoresed in 0.5 M lithium acetate on cellulose acetate strips, and stained with alcian blue. The densitometric tracing derived from the electrophoresis strips were analysed with a Du Pont Curve Resolver. The electrophoretic data suggested the existence of a qualitative deviation in GAG excretion in CLL and in MF, in that patients with these diseases excreted on an average larger than normal amounts of slowly migrating GAG fractions. Pooled crude urinary GAG material from patients with CLL, MF, AML and CML and from control subjects was further purified and subjected to analytical studies. These indicated that a similar qualitative urinary GAG distribution exists in ML and in controls, whereas the urinary GAG in CLL and MF patients contained relatively more dermatan sulphate (DS, in terms of iduronate) than those of the controls.

Carbazoles↗
PubMedDate not supplied

Plasma glycosaminoglycans in experimental osteoarthritis caused by immobilization.

The right knees of adult rabbits were immobilized under conditions known to produce either "developing" osteoarthritic lesions or advanced, "chronic" lesions typical of osteoarthritis. The concentration of plasma glycosaminoglycans was assayed and found to be unchanged in "developing" osteoarthritis but significantly increased in animals with "chronic" lesions of the immobilized knee. Assays of plasma glycosaminoglycans may be useful in the assessment of osteoarthritis.

Animals↗
PubMedDate not supplied

Fetal outcome in women with primary Sjögren's syndrome. A retrospective case-control study.

OBJECTIVE: To study fetal outcome in women with primary Sjögren's syndrome (SS) compared to that in women with systemic lupus erythematosus (SLE) and healthy women, and to study the possible association of fetal loss with anticardiolipin antibodies (aCL) and antibodies to SS-A/Ro and SS-B/La in women with primary SS. METHODS: A retrospective analysis of the fetal outcome in 55 pregnancies in 21 patients with primary SS compared to that in 100 pregnancies in 42 patients with SLE and 94 pregnancies in 42 healthy women matched for age, parity and the onset of the autoimmune disease with respect to pregnancy. IgG-, IgM- and IgA-aCL were determined by a cofactor-dependent ELISA and antibodies to SS-A/Ro and SS-B/La by ELISA using human recombinant antigens and affinity-purified antigens. RESULTS: Of all the 55 pregnancies in patients with primary SS, 8 (15%) occurred after the onset of primary SS symptoms. Eleven (20%) of the 55 pregnancies ended in fetal loss. The relative risk (RR) for fetal loss in patients with primary SS was 2.7 (95% CI 1.1-6.5; p = 0.023), and after the exclusion of the patient with four spontaneous abortions it was 2.0 (0.7-5.3; p = 0.18). In SLE the level of risk was 2.2 (0.9-5.0; p = 0.065). Fetal loss in patients with primary SS was not associated with elevated levels of anticardiolipin antibodies (aCL) or autoantibodies to SS-A/Ro or SS-B/La. Newborns of mothers with primary SS were not more premature or growth retarded than newborns of healthy women, but the absolute and the relative birth weights of the newborns of mothers with SLE was significantly lower than in healthy controls (P < 0.001 and P < 0.0001, respectively). CONCLUSION: We conclude that the majority of pregnancies in women with primary SS occur before the onset of the disease and that these women have an increased risk of fetal loss, which is not associated with elevated levels of ACL or antibodies to SS-A/Ro or SS-B/La. The risk of fetal loss in primary SS is similar to that in women with SLE, but fetal growth retardation appears to be more common in SLE than in primary SS.

Adult↗