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)

Hypercalcaemia is a common electrolyte abnormality. The vast majority of patients will be shown to have either hyperparathyroidism or malignancy. In less than 10% of patients other, less common causes of hypercalcaemia will be present. Systemic lupus erythematosus is a very rare cause of hypercalcaemia. It may be associated with lymphadenopathy and pleuritis to constitute a distinct clinical entity described as 'hypercalcaemia-lymphoedema syndrome'. In these cases the pathophysiology of the hypercalcaemia is not completely understood. In some cases it is associated with elevated levels of parathyroid-related peptide (PTHrP). In others the level of PTHrP is normal, and it has been suggested that autoantibodies may cause hypercalcaemia by activating the PTH receptor. We describe a case of a woman who presented with severe hypercalcaemia, developed the hypercalcaemia-lymphodema syndrome and fulfilled the diagnostic criteria of systemic lupus erythematosus.
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PMID:Hypercalcaemia in systemic lupus erythematosus. 1134 30

A patient with end stage renal disease secondary to systemic lupus erythematosus (SLE) ultimately required amputation of the four extremities and developed mesenteric ischemia. The patient presented with widespread medial calcification involving various small to medium sized arteries, although no noticeable secondary hyperparathyroidism was observed. We speculated that SLE associated with systemic vasculitis and uremic milieu over a number of years may represent the perfect preexisting condition for calcific arteriolopathy to occur following which several factors including chronic administration of corticosteroids, photosensitivity in lupus, and significant weight loss may have contributed to acral gangrene and mesenteric ischemia.
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PMID:Calciphylaxis in a patient with end-stage renal disease secondary to systemic lupus erythematosus associated with acral gangrene and mesenteric ischemia. 1181 38

1alpha,25-Dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)], the active metabolite of vitamin D(3), is known for the maintenance of mineral homeostasis and normal skeletal architecture. However, apart from these traditional calcium-related actions, 1,25-(OH)(2)D(3) and its synthetic analogs are being increasingly recognized for their potent antiproliferative, prodifferentiative, and immunomodulatory activities. These actions of 1,25-(OH)(2)D(3) are mediated through vitamin D receptor (VDR), which belongs to the superfamily of steroid/thyroid hormone nuclear receptors. Physiological and pharmacological actions of 1,25-(OH)(2)D(3) in various systems, along with the detection of VDR in target cells, have indicated potential therapeutic applications of VDR ligands in inflammation (rheumatoid arthritis, psoriatic arthritis), dermatological indications (psoriasis, actinic keratosis, seborrheic dermatitis, photoaging), osteoporosis (postmenopausal and steroid-induced osteoporosis), cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), secondary hyperparathyroidism, and autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis, and organ transplantation). As a result, VDR ligands have been developed for the treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism. Furthermore, encouraging results have been obtained with VDR ligands in clinical trials of prostate cancer and hepatocellular carcinoma. This review deals with the molecular aspects of noncalcemic actions of vitamin D analogs that account for the efficacy of VDR ligands in the above-mentioned indications.
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PMID:Noncalcemic actions of vitamin D receptor ligands. 1579 98

Treatment of giant cell lesions of the jaws is currently a subject of acute interest in the maxillofacial community. Based on their presumptive histological and biological similarities to both the "brown tumors" of hyperparathyroidism as well as proliferative vascular lesions, both calcitonin and interferon alpha administration have been attempted in patients suffering from these lesions. We present a case report of one young female in which both of these treatment modalities were instituted. We also discuss a rarely reported complication consisting of drug-induced lupus erythematosis and pancreatitis secondary to interferon alpha use.
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PMID:Complications of alpha-interferon therapy for aggressive central giant cell lesion of the maxilla. 1612 54

Dermatologists are in the unique position to be able to diagnose serious systemic diseases through skin findings; in addition, cutaneous manifestations can be associated with internal symptoms and clarify the pathogenesis and treatment of challenging new syndromes. Calciphylaxix, now renamed Calcific Uremic Arteriolopathy, primarily affects patients with end-stage renal disease with concomitant hyperphosphatemia, increased calcium-phosphate product and hyperparathyroidism, skin biopsy and wound care are crucial parts of the diagnosis and treatment. Hyperhomocysteinemia may play a very important role in many cutaneous and systemic diseases including, chronic cutaneous wounds, systemic lupus erythematosus, Behcet's disease and psoriasis. Through a skin biopsy and biochemical analysis of the proteoglycans accumulation it may be possible to diagnose a new systemic mucinosis and prevent sudden death in patients with severe mitral valve prolapse. Nephrogenic Fibrosing Dermopathy is a newly described fibrosing disorder occurring in patients with end stage renal disease, the etiology and pathogenesis are still unknown, and the ultimate course of this disease has not been defined.
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PMID:New clinical syndromes in dermatology. 1690 97

The pathogenesis of calciphylaxis, which has a rising incidence in the chronic dialysis population and a high mortality rate, is poorly understood. Abnormalities in the calcium-phosphorus-parathyroid axis are clinically related to calciphylaxis, but alone, they cannot explain this condition. Here, we present two patients who had chronic inflammatory conditions and hyperparathyroidism and who developed calciphylaxis. A 41-year-old white woman on hemodialysis following scleroderma, hepatitis C, liver transplant, and failed kidney transplant, developed progressive ulcerative lower extremity calciphylaxis lasting more than 3 years. She had evidence of severe hyperparathyroidism and elevated serum C-reactive protein (CRP). A 39-year-old white woman on continuous ambulatory peritoneal dialysis for 6 years for renal failure secondary to lupus nephritis, with sustained lupus activity during the dialysis period, developed rapidly progressing ulcerative calciphylaxis of the lower and upper extremities not responding to adequate treatment of hyperphosphatemia and hyperparathyroidism. Her condition culminated in death within 2 months of the appearance of the skin lesions. Her serum CRP was elevated on a sustained basis before the development of the calciphylaxis and rose to a very high level after appearance of the skin lesions. Inflammation may assist in the development of calciphylaxis through depression of serum levels of fetuin-A, an endogenous inhibitor of calcification that is also a negative acute-phase reactant. The interactions between inflammation-mediated changes in the levels of endogenous inhibitors of calcification and abnormalities in calcium-phosphorus metabolism merit intensive study in the future as potential mechanisms of calciphylaxis.
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PMID:Association between calciphylaxis and inflammation in two patients on chronic dialysis. 1698 64

Simultaneous bilateral patellar tendon ruptures are a rare complication of rheumatoid arthritis (RA). Systemic inflammatory diseases (RA, systemic lupus erythematosus (SLE), chronic renal failure, primary and secondary hyperparathyroidism, diabetes mellitus, obesity, sports activity, older age (>50) and drugs (prolonged use of high doses of steroids, local steroid injections and quinolones) are considered as potent predisposing factors for tendon rupture. We report a case of an alcoholic patient with RA and bilateral spontaneous tendon ruptures of the knees. Circumstantial evidence suggest that in this patient, chronic alcohol consumption, a very frequent cause of toxicity to striated and cardiac muscle, contributed to the injury.
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PMID:Chronic alcohol consumption as a predisposing factor for multiple tendon ruptures in unusual sites in a patient with rheumatoid arthritis. 1763 46

The active metabolite of vitamin D3 - 1,25-(OH)2D3 - exerts most of its physiological and pharmacological actions through its nuclear receptor (VDR), regulating the transcriptional machinery of a variety of cell types. Basic research motivated by the detection of VDR in numerous target cells, has indicated potential therapeutic applications of VDR ligands in osteoporosis, cancer, secondary hyperparathyroidism and autoimmune diseases such as psoriasis, systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes and multiple sclerosis. In recent years vitamin D analogs, particularly calcipotriol and tacalcitol, have been used as topical therapeutic agents in vitiligo, an autoimmune pigmentary disorder characterized by aberrant loss of functional melanocytes from involved epidermis. The presence of cytotoxic T cells targeting melanocyte antigens and imbalance of the cytokine network were described as characteristics of the disease, eventually leading to melanocyte damage and death. Vitamin D ligands are designed to target the local immune response in vitiligo, acting on specific T cell activation, mainly by inhibiting the transition of T cells from early to late G1 phase and by inhibiting the expression of several pro-inflammatory cytokines genes, such as those encoding tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). Vitamin D(3) compounds are known to influence melanocyte maturation and differentiation and also to up-regulate melanogenesis through pathways activated by specific ligand receptors, such as endothelin receptor and c-kit. In this review we summarize the complex pathogenetic rationale of vitamin D analogs in vitiligo depigmentation. Understanding the cellular and molecular mechanisms through which vitamin D targets the epidermal melanin unit is of great interest for identification of new effective therapeutic combination(s) that might induce repigmentation in vitiligo.
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PMID:Cellular and molecular mechanisms involved in the action of vitamin D analogs targeting vitiligo depigmentation. 1839 27

Spontaneous ruptures of the extensor mechanism of the knee are very rare. They tend to increase considerably in patients with metabolic diseases such as chronic renal failure, hyperparathyroidism, diabetes, gout, and systemic lupus erythematosus. The reported case regards a 48-year-old man with chronic, spontaneous and simultaneous quadriceps, and contra-lateral patellar tendon rupture. The patient suffered from chronic renal failure and for the past year from tertiary hyperparathyroidism. Ruptured tendons were repaired and both knee were evaluated monthly for the next 12 months. Good functional recovery was achieved on both knees without relapse. This case emphasizes the importance of long-term high parathyroid hormone level in the etiology of tendons ruptures.
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PMID:Simultaneous chronic rupture of quadriceps tendon and contra-lateral patellar tendon in a patient affected by tertiary hyperparatiroidism. 1938 13

Painful violaceous skin lesions that progress to non-healing ulceration and gangrene characterize calciphylaxis. These lesions are associated with secondary hyperparathyroidism and generally occur in patients on dialysis for more than one year. Hyperphosphatemia and hypoalbuminemia are the major risk factors for calciphylaxis. It is usually resistant to medical treatment although parathyroidectomy can help in controlling the disease. The mortality rate of calciphylaxis is very high due to uncontrollable sepsis. In our case, a young female with systemic lupus erythematosus (SLE) developed calciphylaxis within a short period after the onset of hemodialysis; she had a short period of hyperphosphatemia prior to dialysis. The serum phosphate was 4.24 mmol/L, calcium was 1.66 mmol/L, parathormone was 38 and calcium-phosphate was 7.0 mmol/L. It is likely that SLE provoked the development of calciphylaxis. The patient was treated medically but unfortunately died secondary to sepsis.
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PMID:Catastrophic calciphylaxis in a patient with lupus nephritis and recent onset of end-stage renal disease. 2022 22


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