Clinical and metabolic aspects of adjuvant arthritis.
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Biomedical subjects
Publications and source records attributed to S Orloff.
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Two young siblings had a syndrome of growth retardation, severe rickets, anemia, renal insufficiency, and renal tubular dysfunction, the last including acidosis, aminoaciduria, and polyuria. There was moderate psychomotor developmental delay. Neither child had cystinosis. Renal biopsy in the older child revealed severe glomerular abnormalities, with capillary wall thickening reminiscent of the hemolytic-uremic syndrome. The proximal convoluted tubules were lined with short, cuboidal cells containing mildly abnormal mitochondria. There was also thinning of brush border microvilli and basolateral infoldings, perhaps as the result of regressive changes, and interstitial fibrous tissue was moderately increased. The etiology of the tubular and glomerular changes is uncertain. We believe these patients represent a previously unreported hereditary syndrome sharing certain clinical features with severe nephropathic cystinosis.
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A young female with osteomalacia complicating a blind loop syndrome associated with congenital megaduodenum is described. In this case, the correction of vitamin D malabsorption by administration of antibiotics highlights the role of massive intraluminal bacterial overgrowth from destruction of vitamin D, or decreased unicellar solubilization due to deconjugation of biliary acids. The importance of cutaneous vitamin D synthesis in patients with osteomalacia of gastrointestinal origin is emphasized. The detection of megaduodenum and megaesophagus in the patient's father may be the first report of a familial association of these gastrointestinal abnormalities.
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The effect of adjuvant-induced arthritis on the urinary excretion of hydroxyproline and hydroxylysyl glycosides (glc-gal-hyl and gal-hyl) was investigated in male Sprague-Dawley rats up to 70 days after the injection of Freund's complete adjuvant. In comparison with control animals the total urinary hydroxyproline is significantly increased in the arthritic rats at one day after injection, returns to normal level at one week and is further significantly increased between the 2nd to 7th week. The excretion of total glycosides in urine parallels the excretion of total hydroxyproline. However, the low ratio of glc-gal-hyl/gal-hyl provides circumstantial evidence in favour of the hypothesis of bone collagen degradation in the acute stage of adjuvant-induced arthritis in rats (between 2 and 3 weeks), while high absolute values but normal ratios of glc-gal-hyl/gal-hyl suggest degradation of both bone and skin collagen in equal amounts between the 4th and 7th week. No significant differences are found between control and arthritic groups in the later part of the experiment.
In a case of polyarthritis after salmonella gastroenteritis the levels of circulating immune complexes (CIC) (C1q-binding assay) correlated closely with disease activity. This observation suggests that systematically absorbed salmonella antigens may lead or contribute to the formation of CIC. CIC activate both the classical and alternate complement pathway and may be important in the pathogenesis of the arthritis associated with salmonella infection.
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