| LEF | leukokinesis-enhancing factor; lupus erythematosus factor; lymphoid-enhanced binding factor |
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| LES | Lambert-Eaton syndrome; Lawrence Experimental Station [agar]; local excitatory state; Locke egg seru... |
| NLE | neonatal lupus erythematosus |
| SCLE | subacute cutaneous lupus erythematosus |
| SLAM | scanning laser acoustic microscope; systemic lupus erythematosus activity measure |
| hypertrophic osteoarthropathy | <radiology> Pulmonary, malignancy (bronchogenic carcinoma, lymphoma, metastasis), abscess, COPD / bronchiectasis, pleural, pleural fibroma (highest incidence of HOA, tho' rare itself), mesothelioma, cardiac, cyanotic congenital heart disease, GI, inflammatory disease (Crohn, UC), malabsorption (dysentery, lue, cirrhosis), ** causes symmetrical periosteal reaction (12 Dec 1998) |
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| hypertrophic pyloric stenosis | <radiology> Not seen until 3 weeks, projectile vomiting, palpable olive in RUQ/epigastrium (12 Dec 1998) |
| hypertrophic rhinitis | Chronic rhinitis with permanent thickening of the mucous membrane. (05 Mar 2000) |
| hypertrophic rosacea | A manifestation of severe acne rosacea resulting in significant enlargement of the nose and occurring primarily in men. It is caused by hypertrophy of the sebaceous glands and surrounding connective tissue. The nose is reddened and marked with numerous telangiectasias. (12 Dec 1998) |
| hypertrophic scar | An elevated scar resembling a keloid but which does not spread into surrounding tissues, is rarely painful, and regresses spontaneously; collagen bundles run parallel to the skin surface. (05 Mar 2000) |
| idiopathic hypertrophic subaortic stenosis | <cardiology> A congenital heart disease that results in abnormal thickening of the ventricular septum and left ventricular wall. Enlargement of the ventricular septum can result in ventricular outflow obstruction (subaortic stenosis) and eventual cardiomyopathy. (27 Sep 1997) |
| osteoarthropathy, primary hypertrophic | A conditioned chiefly characterised by thickening of the skin of the head and distal extremities, deep folds and furrows of the skin of the forehead, cheeks, and scalp, seborrhoea, hyperhidrosis, periostosis of the long bones, digital clubbing, and spadelike enlargement of the hands and feet. It is more prevalent in the male, and is usually first evident during adolescence. It is believed to be inherited as an autosomal dominant trait. (12 Dec 1998) |
| osteoarthropathy, secondary hypertrophic | Symmetrical osteitis of the four limbs, chiefly localised to the phalanges and the terminal epiphyses of the long bones of the forearm and leg, sometimes extending to the proximal ends of the limbs and the flat bones, and accompanied by dorsal kyphosis and joint involvement. It is often secondary to chronic conditions of the lungs and heart. (12 Dec 1998) |
| familial hypertrophic cardiomyopathy | Familial occurrence of hypertrophic cardiomyopathy exhibiting an autosomal dominant pattern of inheritance. Familial cardiomyopathy of various kinds occurs with autosomal dominant inheritance. There is also an asymmetrical form affecting the ventricles and the interventricular septum. (05 Mar 2000) |
| chilblain lupus | Skin lesions seen in patients with lupus erythematosus, resembling the small, hardened nodular areas of a cold injury called chilblains. Synonym: chilblain lupus. (05 Mar 2000) |
| neonatal lupus | Lupus erythematosus occurring in newborn children of mothers who had lupus during pregnancy; anti-SSA antibodies usually should be screened for; 50% have anti-nuclear antibodies. A variety of skin lesions are seen, which can resolve or leave scarring; the syndrome usually resolves; however cardiac manifestations can be fatal. Some children develop systemic lupus later in life. (05 Mar 2000) |
| drug-induced lupus | <dermatology> An inflammatory autoimmune disorder, similar to lupus, that develops in response to the use of a particular medication. It is characterised by anti-histone antibodies. More benign than the usual disease, with less renal involvement. The syndrome clears after stopping the offending drug. Drugs that are known to cause this reaction include procainamide, isoniazid, sulphasalazine, hydralazine, methyldopa, phenytoin, chlorpromazine and penicillamine. The arthritis, cardiac, pulmonary and systemic features may be present, but the kidney involvement (nephritis) and neurologic disease are rare. Symptoms generally resolve spontaneously after stopping the medication. Complications include myocarditis, pericarditis, thrombocytopenic purpura and infections. (18 Jul 2002) |
| lupus | A systemic disease that results from an autoimmune mechanism. Individuals with lupus will produce antibodies to their own body tissues. The resultant inflammation can cause kidney damage, arthritis, pericarditis and vasculitis. (27 Sep 1997) |
| lupus anticoagulant | An immunoglobulin that interferes with blood coagulation and has antithromboplastin activity. This immunoglobulin can prolong blood clotting and occurs in approximately 25% of people with lupus. (27 Sep 1997) |
| lupus anticoagulants | Lupus anticoagulants are a common cause of a prolonged activated partial thromboplastin time (APTT) which is corrected by the addition of platelet -rich plasma (or phospholipids) and not by platelet-poor plasma. The methods of choice for detection of lupus anticoagulants are the kaolin clotting time using the rabbit brain neutralisation procedure and the dilute Russell viper venom test (dRVVT). Current data suggest that lupus anticoagulants and antibodies to negatively charged phospholipids (cardiolipin, phosphatidylserine, phosphatidic acid and phosphatidylinositol) are risk factors for arterial and venous thrombosis and for recurrent abortions in populations of patients which are distinct but overlapping. Drug-induced lupus anticoagulants are also associated with increased risk of thrombosis. Current testing for lupus anticoagulants and phospholipid antibodies (cardiolipin plus phosphatidylserine) may be useful for assessing risk in patients with systemic lupus erythematosus. Some data indicate that lupus anticoagulants assays are more reliable predictors of thrombosis, foetal loss and thrombocytopenia than are cardiolipin antibody (ACA) assays. Although the technology is in many ways more reliable, the rush to describe associations of lupus anticoagulants with various disorders has been much less scientifically unseemly than has been that of ACAs with their bewildering variety of clinical associations. The contribution of one serious study must, it seems, render tolerable the excess of trivia recently published in this area. See also cardiolipin antibodies and phospholipid antibodies. (05 Mar 2000) |