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

Bilateral simultaneous and spontaneous patellar tendon ruptures are exceedingly rare. The diagnosis is established by clinical examination. Early diagnosis and surgical repair is essential to provide a satisfactory functional result. A case of patella tendon rupture on the right side and a fracture of the tuberositas tibiae on the other one after minor trauma in an 31-year-old woman with osteomalacia is presented. In case of spontaneous and bilateral tendon ruptures other diseases, especially generalized bone diseases, systemic lupus erythematodes, metabolic diseases and rheumatoid arthritis should be excluded.
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PMID:[Spontaneous and simultaneous rupture of the right patellar ligament and avulsion fracture of the left tibial tuberosity in osteomalacia]. 280 10

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17

Lobulated fibers have been observed in biopsies of 13 patients with various neuromuscular disorders including limb-girdle muscular dystrophy (3), distal myopathy (2), scapuloperoneal muscular dystrophy (2), congenital myopathy, Kugelberg-Welander syndrome, hypothyroidism, steroid myopathy, osteomalacia and systemic lupus erythematosus (on steroids). In all cases there were fibers characterised by small subsarcolemmal triangular aggregates or more diffuse collections extending into the interior of the muscle fiber. These were strongly reactive with oxidative enzymes, acid phosphatase, periodic acid-Schiff (PAS), Verhoeff-van Gieson (VVG) and also stained red with the Gomori trichrome technique. In 5 cases core-like fibers were also seen. Morphometric analysis of the NADH-tetrazolium reductase (NADH-TR) preparations in 11 cases showed atrophy of the lobulated fibers. Ultrastructural studies of lobulated fibers disclosed large peripheral mitochondrial aggregates and focal areas with Z-line streaming and disrupted myofibrils. We consider this structural change of the muscle fiber as a reflection of muscle cell disruption and suggest that they may progress from lobulated fibers to more atrophic core-like fibers.
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PMID:Lobulated fibers in neuromuscular diseases. 316 2

The first treatment of pregnant women with antiphospholipid antibody syndrome (APLS) employed high doses of corticosteroids, plus low dose aspirin, with the goal of suppressing production of the autoantibody. Corticosteroids (usually prednisone), even when much lower doses are used, and even when tapered after midpregnancy, have been associated with significant maternal and obstetric risks and side effects: the most important are osteomalacia and preterm delivery (often precipitated by premature rupture of the membranes). Since the publication of a randomized trial demonstrating equivalent live birth rates of about 75% whether heparin or prednisone was used for treatment (plus low dose aspirin), the use of adjusted doses of heparin, together with low dose aspirin, has replaced prednisone for treatment of pregnant women; although prednisone may still be needed to treat manifestations of associated autoimmune disorders. A recent randomized trial has shown that the addition of heparin to aspirin is probably superior to treatment with aspirin alone. To achieve prophylactic levels of plasma heparin equivalent to those measured in patients who are not pregnant and are treated with the usual dose of standard heparin of 5000 IU every 12 h, the heparin dose required for treatment of pregnant women is usually higher. For that reason, heparin doses should be adjusted using the nadir APTT, or better plasma heparin measured by a factor Xa inhibition assay at the 2 h post-injection peak. Although low molecular weight heparin has been shown to be useful in prevention of fetal resorption in a mouse model, and appears to be equally safe for treatment of pregnant women, we still have no published data to show therapeutic equivalency, with respect to treatment of APLS-complicated pregnancy, to standard heparin preparations, and none that demonstrate any lower risk for the complication of most concern when heparin is given to pregnant women-osteopenia. Similarly, intravenous infusion of gamma globulins (IVG) appears on the basis of case reports to be effective additional treatment in cases where standard therapy has failed. Gamma globulin preparations contain anti-idiotypic antibodies that have been shown to bind to patient antiphospholipid antibodies. The place for the addition of IVG to standard therapy has not been defined, but clinically significant and corticosteroid-resistant thrombocytopenia complicating antiphospholipid antibody syndrome might be one indication for primary treatment with IVG +/- low dose aspirin. Overall, live birth rates in most treatment studies are in the range of 70-80%. The reported birth rate information, however, cannot be compared between studies. None of the studies reported have used tools such as logistic regression analysis to allow for such significant predictors of live birth as the number of prior miscarriages, maternal age, medical history, or a history of fetal death (loss of a viable and chromosomally normal fetus after the 10th gestational week).
Lupus 1996 Oct
PMID:Prevention of fetal death in the antiphospholipid antibody syndrome. 890 84

Patients whose symptoms include widespread, diffuse musculoskeletal pain are commonly referred for rheumatological evaluation, even when the underlying cause may lie out with the remit of rheumatology. A diagnosis of fibromyalgia may seem highly probable even from the referral letter, or after a few leading questions during the consultation. However, the lack of specificity of the many symptoms associated with widespread pain means that other diagnoses have to be considered. The history and examination must bear in mind alternative and concomitant musculoskeletal disorders, such as mild systemic lupus erythematosus, polyarticular osteoarthritis, rheumatoid arthritis, polymyalgia rheumatica, hypermobility syndromes and even osteomalacia. Non-rheumatological diseases may also have symptomatic similarities to fibromyalgia, including neoplastic and neurological diseases, hypothyroidism and other endocrine disorders, chronic infections, as well as a variety of psychiatric conditions. A rational approach to investigation will usually allow other diagnostic possibilities to be excluded without reinforcing the abnormal illness behaviour so common in chronic pain states.
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PMID:The differential diagnosis of generalized pain. 1056 69

The purpose of this article is to review the causes, the clinical manifestations and the management of the more frequent drug-induced rheumatic disorders. These include: (i) articular and periarticular manifestations induced by fluoroquinolones, nonsteroidal anti-inflammatory drugs, injections of corticosteroids, and retinoids; (ii) multisystemic manifestations such as drug-induced lupus and arthritis induced by vaccination, Bacillus Calmette-Guerin therapy and cytokines; (iii) drug-induced disorders of bone metabolism (corticosteroid-induced osteoporosis, drug-induced osteomalacia and osteonecrosis); and (iv) iatrogenic complex regional pain syndromes. Disorders caused by nonpharmacological and rarely used treatments have been deliberately excluded. Knowledge of these drug-induced clinical symptoms or syndromes allows an earlier diagnosis and treatment, and earlier drug withdrawal if necessary. With the introduction of new medications such as the recombinant cytokines and antiretroviral treatments, the number of drug-induced rheumatic disorders is likely to increase.
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PMID:Drug-induced rheumatic disorders: incidence, prevention and management. 1105 Dec 16

Many drugs can induce adverse effects such as rheumatoid disorders, which we need to be aware of in order to best detect and manage them. New drugs are constantly entering the marketplace and can cause an increasing number of disorders. Through this article, we review the prevention and pharmacological management of drug-induced rheumatic disorders. These include articular and peri-articular manifestations induced by fluoroquinolones, retinoids, cyclosporin, drug-induced disorders of bone metabolism such as corticosteroid-induced osteoporosis and drug-induced osteomalacia, and multisystemic manifestations including drug-induced lupus and arthritis induced by vaccinations and cytokines.
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PMID:The pharmacological management of drug-induced rheumatic disorders. 1182 5

Fibromyalgia is a chronic pain syndrome of unknown etiology characterized by diffuse pain and tender points, which have been present for more than 3 months. Many patients with systemic illnesses can have diffuse pain similar to that found in fibromyalgia, including rheumatic diseases such as polymyalgia rheumatica, rheumatoid arthritis, idiopathic inflammatory myopathy, systemic lupus erythematosus, and joint hypermobility. Osteomalacia and thyroid disease are also in the differential diagnosis of diffuse pain and are imminently treatable. In addition, there has been interest throughout the past 10 years in infectious diseases including hepatitis C, Lyme disease, coxsackie B, HIV, and parvovirus infection, which may cause or trigger fibromyalgia. This paper provides a framework to use when identifying these diseases as part of the evaluation of a patient with chronic widespread musculoskeletal pain.
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PMID:Rheumatic mimics and selected triggers of fibromyalgia. 1209 63

Secondary osteoporosis is common among patients being evaluated for osteoporosis. All men and premenopausal women with unexplained bone loss or a history of a fragility fracture should undergo a work-up for secondary osteoporosis. Also, postmenopausal women with risk factors for secondary osteoporosis should be carefully evaluated. The evaluation should include a thorough history, physical examination, bone mineral density testing, and laboratory testing. While there is no consensus for a cost-effective laboratory evaluation, some recommendations include: 25-hydroxyvitamin D, parathyroid hormone (PTH), serum and urine calcium, phosphate, creatinine, liver function tests, a complete blood count, testosterone in men, and thyroid-stimulating hormone. After a thorough review of the evaluation for secondary osteoporosis, this chapter reviews the pathophysiology and treatment of secondary osteoporotic disorders, including vitamin D insufficiency, osteomalacia, the osteoporosis of erosive inflammatory arthritis, ankylosing spondylitis, systemic lupus erythematosus, and osteoporosis related to anti-androgenic therapy for prostate cancer and aromatase inhibitor therapy for breast cancer. Physicians have a significant responsibility to evaluate and treat the underlying medical problem that is the cause of secondary osteoporosis and to optimize bone health in the individual patient.
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PMID:The management of secondary osteoporosis. 1630 Nov 95


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