Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

Rupture of the extensor mechanism of the knee is not an unusual occurrence. Bilateral simultaneous rupture, however, is rare. Most cases of bilateral simultaneous rupture occur in association with systemic disease, i.e., systemic lupus erythematosus, arteriosclerosis, diabetes, or secondary hyperparathyroidism. Only three cases without predisposing conditions have been reported. A case report of a 48-year-old black male without apparent risk factors who sustained spontaneous simultaneous rupture of the patella tendons is presented. Histologic evidence supports Davidsson's theory of multiple recurrent microtears within the tendon substance as a cause of rupture.
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PMID:Bilateral simultaneous infrapatellar tendon rupture: support for Davidsson's theory. 305 Aug 16

We describe a patient with systemic lupus erythematosus, chronic renal failure and secondary hyperparathyroidism who developed laxity and elongation of the patellar tendon, followed by its rupture one year later. Hydroxyapatite and urate crystals were identified from the chalky material surrounding the patellar tendon observed at surgery. These findings suggest that tendon laxity and elongation could possibly be detected before its rupture and that secondary hyperparathyroidism could be considered as another causative factor of tendon damage in patients with systemic lupus erythematosus.
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PMID:Laxity and rupture of the patellar tendon in systemic lupus erythematosus. Association with secondary hyperparathyroidism. 317 17

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

The deposition of calcium and phosphorous salts in the soft tissues can be classified into three categories: metastatic calcification, dystrophic calcification, and calcinosis. Metastatic calcification occurs when the calcium-phosphorous levels are elevated. The calcifications involve normal tissues. Associated disease include hyperparathyroidism, neoplasms, milk-alkali syndrome, hypervitaminosis D, and tumoral calcinosis. Dystrophic calcification occurs in the presence of normal metabolism in damaged or devitalized tissues. Disorders included in this classification are: Ehlers-Danlos syndrome, pseudoxanthoma elasticum, arteriosclerosis obliterans, venous calcifications, crystal deposition disorders, and calcification resulting from neurologic disorders. Calcinosis is also found in persons with normal metabolism. It occurs most often in subcutaneous tissues, skin, and related connective tissues. Associated disorders include: calcinosis universalis, calcinosis circumscripta, scleroderma, dermatomyositis, and systemic lupus erythematosus.
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PMID:A review of soft tissue calcifications. 404 12

Two patients with patellar tendon rupture and underlying systemic disease are described. One had systemic lupus erythematosus and the other had chronic renal failure and secondary hyperparathyroidism. There have been 13 other cases of patellar tendon rupture in patients with systemic disease reported in the literature and they are reviewed. Patellar tendon rupture has occurred spontaneously in more than one-half of the cases and has been associated with rupture of the contralateral extensor tendon mechanism in 87%. Although patellar tendon rupture almost always occurs at the tendinous insertion, on a rare occasion (as in one case described in this report), the tear may involve the main substance of the tendon, which is the part of the tendon with the greatest tensile strength. The relation between systemic disease and patellar tendon rupture is discussed and the clinical and radiographic findings are described.
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PMID:Patellar tendon rupture with underlying systemic disease. 677 17

A 31-year-old woman with systemic lupus erythematosus (SLE), diabetes mellitus, and chronic renal failure developed digital ischemia, myocardial dysfunction, abnormal ECG, and elevated CPK levels. Radiographic studies revealed calcification of the peripheral vasculature although coronary angiography was unremarkable. An endomyocardial biopsy demonstrated intra and extracellular myocardial calcification without evidence of vasculitis or primary myocarditis. A diagnosis of calciphylaxis, as a result of secondary hyperparathyroidism, was made. This case demonstrates that calciphylaxis can mimic the cardiovascular manifestations of SLE. Early differentiation of these disparate diseases is important because treatment strategies employed in SLE may exacerbate calciphylaxis.
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PMID:Systemic lupus erythematosus: calciphylaxis induced cardiomyopathy. 769 81

A case is reported of bilateral patellar tendon rupture in a fit man after a fall. He had a history of repeated local steroid injections into both tendons and histology confirmed steroid-induced changes. The history of repeated local steroid administration has to be implicated as the cause of this extremely rare injury in this patient, which can also be associated with hyperparathyroidism, systemic lupus erythematosus, diabetes and rheumatoid arthritis. All doctors performing repeated local steroid injections into the patellar tendon should be aware of the possible dangers of inducing tendon rupture and should ensure that the steroids are not delivered into its substance.
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PMID:Bilateral patellar tendon rupture secondary to repeated local steroid injections. 877 66

Brown tumors (osteoclastomas) are histologically benign lesions that are caused by primary or secondary hyperparathyroidism. Secondary hyperparathyroidism is a frequent complication of chronic renal failure. Skeletal brown tumors are relatively uncommon, and brown tumors that involve the spine are considered very rare. The authors present the case of a 37-year-old woman with systemic lupus erythematosus and hemodialysis-dependent anuric renal failure, in whom spinal cord compression developed due to a brown tumor and pathological fracture at T-9. The patient underwent transthoracic decompressive surgery and spinal reconstruction in which cadaveric femoral allograft and instrumentation were used. Brown tumors of the vertebral column require surgical treatment if medical therapy and parathyroidectomy fail to halt their progression or if acute neurological deterioration occurs. In patients with renal failure bone healing is delayed and there is an increased risk that healing will fail because the metabolic derangements can result in severe osteoporosis. Surgical reconstruction of the spine may require the use of augmentation with instrumentation and aggressive treatment of hyperparathyroidism to achieve successful outcomes.
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PMID:Chronic renal failure causing brown tumors and myelopathy. Case report and review of pathophysiology and treatment. 1019 56

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


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