Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum procollagen type I carboxyterminal propeptide (PICP) has been shown to be a useful marker of bone formation in patients undergoing haemodialysis. However, PICP levels has not been evaluated in depth in patients maintained on continuous ambulatory peritoneal dialysis (CAPD). Therefore serum and dialysate levels of PICP, its peritoneal clearance (Clp), mass transfer (MTp), and its possible relationship with osteocalcin, parathyroid hormone (PTH), and bone histomorphometry were studied in a group of CAPD patients. Serum PICP was just above the normal range with significant amounts detected in the dialysate but no correlations were found between levels of serum PICP, dialysate PICP, and Clp-PICP. One patient with systemic lupus and osteitis fibrosa had extraordinarily high serum and dialysate levels of PICP. The patient later developed sclerosing peritonitis. No associations were seen between serum PICP and Clp-PICP and any of the 18 bone histomorphometric parameters evaluated. Dialysate level of PICP correlated negatively with mineral appositional rate (r = -0.62, P < 0.01) and mineralization lag time (r = 0.64, P < 0.01). MTp-PICP correlated positively with mineral appositional rate (r = 0.65, P < 0.01). Serum osteocalcin and serum PTH levels did not correlate to serum, dialysate, Clp or MTp measurements of PICP. These results suggest that measurements of PICP in CAPD patients do not give substantial information as an non-invasive marker of bone histology.
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PMID:Type I procollagen propeptide in patients on CAPD: its relationships with bone histology, osteocalcin, and parathyroid hormone. 859 3

Although osteoporosis has traditionally been considered a disease of women, men also incur substantial bone loss with aging, and elderly men have age-specific hip fracture incidence rates and vertebral fracture prevalence rates that are at least half those in women. Early postmenopausal bone loss (which results in the syndrome of type I osteoporosis) is due to the direct skeletal consequences of estrogen deficiency, manifested by an increase in bone resorption without an adequate increase in bone formation. Recent evidence indicates that even late postmenopausal bone loss (type II or 'smile' osteoporosis) in women may be due to estrogen deficiency. In particular, the late consequences of estrogen deficiency in elderly women result in abnormalities in calcium homeostasis and increases in parathyroid hormone secretion, leading to increased bone resorption and bone loss. The etiology of bone loss in aging men has remained relatively unclear. Recent evidence from a male deficient in estrogen receptor-alpha and in two males with aromatase deficiency indicate that estrogen may play a significant role in bone metabolism in men. Moreover, several large epidemiologic studies have found that bone mineral density correlates better with serum estrogen than testosterone in aging men. Thus estrogen deficiency may lead to bone loss in men.
Lupus 1999
PMID:Osteoporosis: gender differences and similarities. 1045 20

We studied the effect of alphacalcidol (1-alpha-hydroxycholecalciferol) on bone metabolism in patients who were placed on glucocorticoid therapy. We selected 41 women (age: 32-52 yrs) who were recently diagnosed with systemic lupus erythematodes, multiple sclerosis, rheumatoid arthritis or asthma bronchiale. Patients did not have other disease or take drugs known to influence bone metabolism. Patients were randomly enrolled into two groups and were given 5-25 mg prednisone daily. After 4 weeks, group A (n = 21) received 0.5-1.0 microgram (mean = 0.54 +/- 0.03 microgram) alphacalcidol and group B (control; n = 20) was given 500 mg calcium daily for three years. There were no significant differences in age and steroid doses between groups. Serum calcium (Ca), osteocalcin (OC), collagen I C-terminal propeptide (PICP), parathyroid hormone (PTH), and urinary calcium and deoxypyridinoline crosslink excretion (DPD) were measured before corticosteroid administration, and before alphacalcidol or calcium treatment as well as 6 weeks, 6 months, and 1, 2, and 3 years later. Bone mineral density (BMD) was examined before treatment and 6 months, 1, 2, and 3 years later by DEXA and SPA. OC and PICP decreased significantly after 4 weeks on steroid in both groups and increased in group A but not in group B after 6 weeks of treatment with alphacalcidol and remained unchanged for 3 years. Serum PTH increased in both groups after 4 weeks of glucocorticoid treatment and was reduced in group A, but not in group B, after 6 weeks on alphacalcidol. Serum Ca, urinary Ca, and DPD did not change significantly in either group during the study period. Lumbar spine and femoral neck BMD were significantly reduced in group B after 6 months and 1 year, respectively, and continued to decrease during the study, while no significant change in group A was observed. BMD of the radius did not change in either group for 2 years but there was a significant reduction by the third year in group B. Based on these results, alphacalcidol treatment appears to be effective in preventing glucocorticoid-induced bone loss in these patients by reducing secondary hyperparathyroidism and stimulating bone formation.
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PMID:Prevention of corticosteroid-induced osteoporosis by alfacalcidol. 1076 37

Low vitamin D levels have been found in patients with autoimmune diseases, including type I diabetes, rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus. The main source of vitamin D is exposure to sunlight, but the same solar radiation is known to exacerbate lupus erythematosus. We investigated the prevalence of vitamin D insufficiency in patients with cutaneous lupus erythematosus (CLE). We designed a cross-sectional study including 55 patients with CLE to measure their serum 25-hydroxyvitamin D (25(OH)D) by chemiluminescence immunoassay and compare it with a control group consisting of 37 healthy sex and age-matched subjects recruited from the patients' relatives as well as healthcare workers. Correlations with clinical and demographic variables were determined. Approximately 95% of patients with CLE had less than 30 ng/ml of serum 25(OH)D, which is accepted as the lower limit for vitamin D adequacy. Mean serum vitamin D values were significantly lower than controls (p = 0.038) and were associated with higher levels of parathyroid hormone (p = 0.050). A history of CLE was a strong predictor of insufficiency of vitamin D (odds ratio 4.2; 95% confidence interval 1.0-17.4). The results suggest a role of CLE in the metabolism of the vitamin and provide guidance for future studies looking at a potential role for vitamin D in the prevention and treatment of CLE. Lupus (2010) 19, 810-814.
Lupus 2010 Jun
PMID:Serum 25-hydroxyvitamin D levels in patients with cutaneous lupus erythematosus in a Mediterranean region. 2030 48

Calciphylaxis is a frequent entity in patients with chronic renal failure of diverse etiology. The main pathogenic mechanism of calciphylaxis is impairment of either calcium and phosphate metabolism or plasma levels of parathyroid hormone. There are communications of patients with normal renal function, and in some cases with chronic inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE) and antiphospholipid syndrome. We report a patient with SLE and no renal failure or hyperparathyroidism who developed severe calciphylaxis.
Lupus 2012 Mar
PMID:Calciphylaxis in a patient with systemic lupus erythematosus without renal insufficiency or hyperparathyroidism. 2199 68

There is a high prevalence of hyperuricemia (HUA) in the chronic kidney disease (CKD) population. However, there's a dearth of research on HUA's prevalence, subtypes, early detection, and treatment strategies of HUA in lupus nephritis (LN) patients. The aim of this study is to address these knowledge gaps. LN patients presenting to the Department of Nephrology at Shanghai Rui Jin Hospital from January 2011 to January 2016 were recruited. The effective sample size was derived using the power analysis. The demographic, clinical and laboratory characteristics of the LN patients with HUA were compared with those of patients without HUA. Two statistical models for analyzing HUA were built and compared using the receiver operating characteristic (ROC) curve analysis. The total prevalence of HUA in the cohort was 40.11%. The subtypes of HUA included urate underexcretion-type, overproduction-type and combined-type, which proportion being 67.7%, 9.7% and 22.6% respectively. The CKD stage was closely associated with the prevalence of HUA in patients with LN. The other significant associated factors were hypertension, triglycerides, serum creatinine, serum albumin, hemoglobin, parathyroid hormone, phosphorus, calcium, etc. The statistical algorithm successfully identified LN patients at risk of HUA. In conclusion, there was a high prevalence of HUA in LN patients at CKD stages 1-3, and renal underexcretion hyperuricemia was the most prevalent subtype. The occurrence of HUA in LN may be related to renal insufficiency, metabolic disorder and lupus itself. Early care coordination programs can employ risk models to improve HUA prevention and target interventions in LN patients.
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PMID:The prevalence, subtypes and associated factors of hyperuricemia in lupus nephritis patients at chronic kidney disease stages 1-3. 2891 57