Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic Sclerosis is a multisystemic disease characterized by sclerosis of the skin and visceral organs, vasculopathy (Raynaud's phenomenon) and autoantibodies. The criteria for the classification of the disease requires either proximal scleroderma (major criteria) or the presence of 2 of the 3 minor features namely sclerodactyly, digital pitting scars and bibasilar pulmonary fibrosis. There are 3 subsets of this condition--diffuse variant, limited variant (CREST syndrome) and Overlap Syndrome (where patients have features of other rheumatic diseases). There are localized forms of scleroderma and pseudoscleroderma states. The presenting features of Systemic Sclerosis are usually Raynaud's, skin changes and arthralgia. Systemic complaints like breathlessness, dyspepsia, etc depending on the organ involved may be present. Management starts with patient education regarding the disease, skin care, exercises and regular medical check-up. There is no miracle cure but much can be done to improve the quality of life of the patient. Nifedepine and other drugs may improve Raynaud's phenomenon. Drugs can be used to treat other complications. Various medication have been tested as disease modifying drugs for scleroderma. These include drugs which inhibit collagen like D-penicillamine, colchicine, and immunosupressive drugs like cyclosporin. Ketotifen, a mast cell stabilizer has been reported to be effective in scleroderma. As it is a relatively safe drug, clinical trials are underway.
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PMID:Systemic sclerosis. 162 Nov 27

Solitary dermatofibromas are a common occurrence, especially on the lower limbs of young women, while multiple dermatofibromas (MDF) are rare, accounting for less than 0.3% of all dermatofibromas and may suddenly develop in immunosuppressed patients. We report a patient with systemic lupus erythematosus (SLE) who developed MDF while she was taking oral prednisone. A 46-year-old woman presented in 1989 complaining of photosensitivity, arthralgias, fatigue, malaise and dyspepsia. The patient denied fever, Raynaud's phenomenon, oral ulcer and hair loss. On examination she presented a typical SLE malar rash. Erythrocyte sedimentation rate (ESR) was elevated (54 mm/h). Speckle patterned IgG/IgM antinuclear antibodies were present at 1/1280 titer. Antibodies anti Ro/SSA were detected by counterimmunelectrophoresis up to 1/8 titer. Other laboratory findings were negative or within normal limits. Systemic lupus erythematosus was diagnosed and the patient given 50 mg/day prednisone. After a few months, both clinical symptoms and immunologic parameters improved. Eighteen months later, prednisone was replaced by 500 mg/day hydroxychloroquine. In 1994, she presented again with malar rash, arthralgias and facial hyperpigmentation. Prednisone 15 mg/day was reintroduced and hydroxychloroquine stopped being a possible cause of the facial hyperpigmented macules. In 1996, while she was taking 5 mg/day prednisone, several nodules developed on her limbs within a few months. On examination we observed 16 firm, slightly elevated 3-15-mm wide brown nodules on her arms, legs and trunk. A biopsy specimen of a lesion of the trunk revealed an epidermal seborrheic-keratosis-like hyperplasia with dermal fibrosis and fibroblastic proliferation (Fig. 1). Dermatofibroma was diagnosed.
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PMID:Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus treated with prednisone. 1210 Jul 3

Although infectiological stimuli, environmental factors and genotypic features are known to contribute to the initiation and perpetuation of systemic sclerosis (SSc), its etiology still remains to be enigmatic, and less elusive insights are to be achieved by ongoing and future investigations. Being characterized, however, as chronic autoimmune disease with excessive collagen accumulation in skin, synovia and visceral organs such as lung, heart, and digestive tract along with obliterating angiopathy, the pathophysiology of SSc can be summarized as being based on imbalances of the cellular and humoral immune system, vascular dysfunction and activation of resident connective tissue cells. A complex interplay between these major components manages to establish and maintain the inability of the vasculature to adequately react to the need for dilatation, constriction and growth of new vessels, to cause the increased deposition of extracellular matrix constituents as well as to facilitate immunological disarrangement. Despite parallels to the chicken and egg causality dilemma, all of these account for what later clinicians observe in patients suffering from Raynaud's phenomenon, digital ulcers, sclerodactyly, rigidity of the face, microstomia, sicca syndrome, dyspnea, dry cough, pulmonary hypertension, palpitations, syncopes, renal insufficiency, dysphagia, gastroesophageal reflux, dyspepsia, generalized arthralgias, but also dyspareunia, or erectile dysfunction.
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PMID:The pathogenesis of systemic sclerosis revisited. 2008 91