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Biomedical subjects

R I Rynes

Publications and source records attributed to R I Rynes.

At least 37 records · Page 2Linked to original sources
PubMed1983

Family study of the major histocompatibility complex in patients with systemic lupus erythematosus: importance of null alleles of C4A and C4B in determining disease susceptibility.

The families of 29 patients with systemic lupus erythematosus and 42 normal subjects were studied to determine the inheritance of the HLA-A, B, C, and DR antigens and also the complement polymorphisms for C2, C4A, C4B, and Bf, which are encoded in the same region of the sixth chromosome. Null (silent) alleles for C4A, C4B, or C2 were found in 24 of the 29 (83%) patients compared with 18 of the 42 (43%) normal controls. HLA-DR3 was present in 20 (69%) of the patients and seven out of 39 (18%) of the normal controls. There was strong linkage disequilibrium between DR3 and the null alleles for C4A and C4B. The data did not permit the relative contributions of DR3 and null factors of C4A and C4B as genetic risk factors to be distinguished. The known association of systemic lupus erythematosus with uncommon inherited and acquired deficiencies of complement components suggests, however, that the presence of null alleles for C4A and C4B, as well as C2, found in most of the patients, is relevant to their genetic susceptibility to this disease.

Adolescent↗
PubMed1983

Enhancement of granulocyte oxidative metabolism in sera from patients with C2 deficiency and systemic lupus erythematosus.

Serum or plasma from 3 patients with C2 deficiency (C2D) and systemic lupus erythematosus (SLE) significantly enhanced chemiluminescence and superoxide anion production by polymorphonuclear leukocytes (PMN) after stimulation with phorbol myristate acetate or latex beads. PMN from patients and normal individuals were supranormally activated when resuspended in plasma from these patients. No such effect was seen with plasma from a patient with C2D but with no evidence of SLE, from patients with SLE but not C2D, from patients with C1q or C8 deficiency, from C4-deficient guinea pigs, or NZB-NZW mice. Because oxygen-derived free radicals may cause joint or tissue damage, C2D patients who have or develop this activity in their plasma may be more prone to SLE or other collagen-vascular diseases.

Adolescent↗
PubMed1982

Lupus foot.

Explore the source record for details and available documents.

Adult↗
PubMed1982

Hydroxychloroquine. Seven-year experience.

Ninety-nine patients were treated with hydroxychloroquine sulfate for connective tissue diseases during a seven year period. All patients received the medication for at least one year and most were treated with a daily dosage of 400 mg. Four patients experienced toxic effects, but no patient sustained permanent loss of visual acuity. Toxicity did not seem to represent a cumulative dosage effect. Funduscopic and visual field examinations at six-month intervals are sufficient to detect the occasional adverse reactions and prevent serious retinal toxic effects when a maximum daily dosage of 400 mg is maintained.

Adult↗
PubMed1982

Deficiency of the second complement component association with the HLA haplotype A10, B18 in a normal population.

Serum C2 activity was measured in 135 individuals drawn from a panel of 418 tissue-typed blood donors. The study group included all donors with HLA antigens A10 and B18. Heterozygote C2 deficiency (C2Dhet) was defined by reference to the range of C2 activity in previously studied obligate heterozygotes. Five donors were C2Dhet. Family studies confirmed that C2Dhet was associated in all instance with an A10, B18 haplotype. The minimum frequency for C2Dhet was 1.2% in the panel of 418 donors and 62.5% in those donors with an A10, B18 haplotype.

Complement C2↗
PubMed1982

Phagocytosis, chemoluminescence, and intracellular killing of fungi by phagocytes from subjects with deficiency of the second component of complement.

The capacity of phagocytes from animals or humans with complement component deficiency to ingest and kill Candida albicans has been much disputed. We show that peripheral blood polymorphonuclear leukocytes and mononuclear phagocytes from subjects with hereditary C2 deficiency (C2D) ingested C. albicans or Saccharomyces cerevisiae at an abnormally slow rate. After preincubating C. albicans in C2D plasma, the slow rate of phagocytosis was corrected and subsequent intracellular killing of C. Albicans was normal. A normal number of C2D phagocytes reduced nitroblue tetrazolium after stimulation with either phorbol myristate acetate or ingestion of C. albicans. The rate at which chemoluminescence was generated in response to C. albicans was abnormally slow, but peak chemoluminescence produced by C2D phagocytes in response to C. albicans was normal.

Adult↗
PubMed1979

Ophthalmologic safety of long-term hydroxychloroquine treatment.

Ocular toxicity of long-term hydroxychloroquine treatment was assessed by regular ophthalmologic examinations in 99 patients. No patient developed significant loss of vision or visual field constriction to a white test object. Three patients had evidence of toxicity, but the medication had to be permanently discontinued in only one who subsequently had regression of all abnormalities except visual field constriction to a red test object. Neither duration of treatment nor the diagnosis of systemic lupus erythematosus predisposed patients to toxicity.

Accommodation, Ocular↗
PubMed1978

Heterogeneity of the clinical syndrome in patients with systemic lupus erythematosus and genetic deficiency of the second complement component.

Two patients with systemic lupus erythematosus associated with homozygous deficiency of the second complement component (SLE-C2D) illustrate the different clinical disease patterns found in patients with this illness. Despite the differences in extent and severity of clinical manifestations and serological findings, the renal disease was similar and kidney function was well preserved in both patients. Renal microscopic changes were focal and segmental, deposits of immuno-globulins and complement components were present by immunofluorescent staining, and dense deposits were seen by electron microscopy. Tubulo-reticular inclusion bodies were found in glomerular endothelial cells and lymphocytes of both patients, but not in the lymphocytes of a clinically healthy C2D sibling. The findings in these two patients stress the importance of careful evaluation to determine the presence of systemic disease in patients with SLE-C2D and suggest that an intact classic complement pathway is important in the development of severe lupus, nephritis, but is not needed in the pathogenesis of lupus skin lesions.

Adult↗
PubMed1978

Calcium pyrophosphate crystal deposition disease and hyperparathyroidism: a controlled, prospective study.

A prospective, controlled study of patients with primary hyperparathyroidism has been carried out to establish the relation of this endocrinopathy to calcium pyrophosphate dihydrate crystal deposition disease. Eight of 26 patients with documented hyperparathyroidism were found to have chondrocalcinosis compared to four of 104 individuals in the control group (p less than 0.01). Two of these eight patients had confirmed pseudogout attacks shortly after parathyroidectomy. Four other patients, including two without chondrocalcinosis, gave a history of typical pseudogout. Patients with hyperparathyroidism and chondrocalcinosis were significantly older than those without the articular lesion (p = 0.006). We could not delineate specific metabolic abnormalities of hyperparathyroidism which contributed to the development of chondrocalcinosis.

Adult↗
PubMed1977

Development of giant cell (temporal) arteritis in a patient 'adequately' treated for polymyalgia rheumatica.

A 70-year-old woman presenting with typical polymyalgia rheumatica (PMR) and a normal temporal artery biopsy appeared to respond completely to low-dose prednisone therapy. A subsequent biopsy showing temporal arteritis with a normal sedimentation rate and no recurrence of myalgic symptoms emphasizes the unpredictable course of treated PMR and the need for continued clinical as well as laboratory follow-up.

Aged↗