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)

Antiphospholipid antibodies (APA) were studied in 30 women with a history of recurrent fetal losses. An increased level of anticardiolipin antibodies was found in 7(23.3%) of them, being high and moderate in 4 women. Lupus anticoagulant was present in 9(30.0%) examinees. None cases of SLE were diagnosed. Diagnostically significant APA levels were associated with moderate symptomless thrombocytopenia. 12 of 13 women with antiphospholipid syndrome markers had definite (livedo reticularis, damage of cardiac valves, recurrent thrombophlebitis, leg ulcers, stroke, migraine) and possible (moderate arterial hypertension, proteinuria, retina angiopathy) extragenital features of this disorder. The most serious vascular complications took place in the group with high and moderate levels of anticardiolipin antibodies IgG.
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PMID:[Antiphospholipid syndrome in females with recurrent fetal losses]. 1048 65

Phototherapy has a very long, albeit mostly anecdotal history. Real interest in the use of ultraviolet irradiation in the treatment of various diseases started in the 19th century and reached a climax when Niels Finsen received the Nobel Prize in 1903 for his therapeutic results with lupus vulgaris. This marked the start of modern phototherapy. It was used in thermal stations for treatment of tuberculosis, in the treatment of leg ulcers in wartime, and in the treatment of skin diseases. This article reviews the history of a treatment modality that greatly changed modern dermatologic treatment, although it is as old as mankind.
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PMID:The history of phototherapy: something new under the sun? 1206 93

Primary, isolated deep venous incompetence is rare, difficult to diagnose, and can lead to the development of venous stasis ulcers. We herein report a case demonstrating chronic venous stasis ulcers due to primary, isolated deep venous incompetence, which was misdiagnosed as vasculitis ulcers associated with systemic lupus erythematosus (SLE). Although primary, isolated deep venous incompetence is rare, it is important to bear this possibility in mind when a patient presents with leg ulcers.
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PMID:Venous stasis ulcers due to primary, isolated deep venous insufficiency in a patient with systemic lupus erythematosus: report of a case. 1237 99

We report a 69-year-old Caucasian female with non-Hodgkin's lymphoma who subsequently developed leg ulcers as a manifestation of the antiphospholipid syndrome. Investigations revealed a mixed cryoglobulinaemia with monoclonal IgM-kappa and antiphospholipid activity with anticardiolipin antibodies, antimitochondrial type M5 antibodies and lupus anticoagulant. Significantly increased concentration of anticardiolipin antibodies was detected in the cryoprecipitate. Our case illustrates a connection between cryoglobulinaemia and lymphoproliferative and autoimmune disorders. Both cryoglobulins and anticardiolipin antibodies could participate in the vascular damage. Cutaneous manifestations in the presence of these disorders associated with non-Hodgkin's lymphoma have not been described previously.
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PMID:Purpura and leg ulcers in a patient with cryoglobulinaemia, non-Hodgkin's lymphoma, and antiphospholipid syndrome. 1265 1

The classical clinical picture of the antiphospholipid syndrome (APS) is characterized by venous and arterial thromboses, fetal losses and thrombocytopenia, in the presence of antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), anticardiolipin antibodies (aCL), or antibodies to the protein "cofactor" b2 glycoprotein I. Single vessel involvement or multiple vascular occlusions may give rise to a wide variety of presentations. Any combination of vascular occlusive events may occur in the same individual and the time interval between them also varies considerably from weeks to months or even years. Deep vein thrombosis, sometimes accompanied by pulmonary embolism, is the most frequently reported manifestation in this syndrome. Cerebrovascular accidents-either stroke or transient ischemic attacks-are the most common arterial thrombotic manifestations. Early and late fetal losses, premature births and pre-eclampsia are the most frequent fetal and obstetric manifestations. Additionally, several other clinical features are relatively common in these patients, i.e., thrombocytopenia, livedo reticularis, heart valve lesions, hemolytic anemia, epilepsy, myocardial infarction, leg ulcers, and amaurosis fugax. However, a large variety of other clinical manifestations have been less frequently described in patients with the APS, with prevalences lower than 5%. These include, among others, large peripheral or aortic artery occlusions, Sneddon's syndrome, chorea, transverse myelopathy, intracardiac thrombus, adult respiratory distress syndrome, renal thrombotic microangiopathy, Addison's syndrome, Budd-Chiari syndrome, nodular regenerative hyperplasia of the liver, avascular necrosis of the bone, cutaneous necrosis or subungual splinter hemorrhages. In this article, some of these "unusual" manifestations are reviewed.
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PMID:Unusual manifestations of the antiphospholipid syndrome. 1279 62

Chronic venous insufficiency is a widespread disease that can often lead to venous leg ulcers. Recent studies report that certain clotting abnormalities, such as anticardiolipin antibodies, are associated with leg ulcers. Although lupus anticoagulant belongs to the antiphospholipid antibodies, its presence in patients with chronic venous insufficiency has not been reported previously. The purpose of our study was to determine the presence of lupus anticoagulant in chronic venous insufficiency patients at a stage with no leg ulcers, and to follow the clinical outcome. In 37 patients with chronic venous insufficiency and in 54 control patients, lupus anticoagulant was evaluated using the Viper Venom Russell's Diluted Test. Lupus anticoagulant was found significantly more often (p < 0.001) in patients with chronic venous insufficiency than in controls. After 4 years, patients with chronic venous insufficiency with lupus anticoagulant were found to develop a venous leg ulceration more frequently compared to those without (p = 0.01), suggesting that lupus anticoagulant may play an important role in the pathogenesis of chronic venous insufficiency.
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PMID:Lupus anticoagulant in patients with chronic venous insufficiency. 1292 1

A 54-year-old man of Persian origin presented to our department with a 1-year history of ulcers on the right leg that had been unresponsive to numerous topical treatments, accompanied by lymphedema of the right leg. Medical history included hypergonadotropic hypogonadism, which had not been further investigated. He was treated for 20 years with testosterone IM once monthly, which he stopped a year before the current hospitalization for unclear reasons. The patient reported no congenital lymphedema. Physical examination revealed two deep skin ulcers (Figure 1) on the right leg measuring 10 cm in diameter with raised irregular inflammatory borders and a boggy, necrotic base discharging a purulent hemorrhagic exudate. Bilateral leg pitting edema and right lymphangitis with lymphadenitis were noted. He had low head hair implantment, sparse hair on the body and head, hyperpigmentation on both legs, onychodystrophia of the toenails (mainly the large toe and less prominent on the other toes), which was atrophic lichen-planus-like in appearance and needed no trimming (Figure 2), normal hand nails, oral thrush, and angular cheilitis. Other physical findings were gynecomastia, pectus excavatum, small and firm testicles, long extremities, asymmetrical goiter, systolic murmur 2/6 in left sternal border, and slow and inappropriate behavior. The patient's temperature on admission was 39 degrees C. Blood cultures were negative for bacterial growth. Results of laboratory investigations included hemoglobin (11.2 g/dL), hematocrit (26.8%), normal mean corpuscular volume and mean corpuscular hemoglobin volume, and red blood cell distribution width (16%). Blood smear showed spherocytes, slight hypochromia, anisocytosis, macrocytosis, and microcytosis. Blood chemistry values were taken for iron (4 micro g/dL [normal range 40-150 micro g/dL]), transferrin (193 mg/dL [normal range 220-400 mg/dL]), ferritin (1128 ng/mL [normal range 14-160 ng/mL]), transferrin saturation (1.5% [normal range 20%-55%]), serum folate (within normal limits), and vitamin B12 (within normal limits). Direct Coombs' test equaled positive 2 + IgG. All these values indicated anemia of chronic diseases combined with hemolytic anemia. Further blood work-up tested antinuclear antibody (positive <1:80 homogeneous pattern), rheumatoid factors (143 IU/mL [positive >8.5 IU/mL]), C-reactive protein (286 mg/L [normal range 0-5 mg/L]), anticardiolipin IgM antibody (9.0 monophosphoryl lipid U/mL [normal range 0-7.00 MPL U/mL]) and antithrombin III activity (135% [normal range 74%-114%]). Results of other blood tests were within normal limits or negative, including lupus anticoagulant, beta2 glycoprotein, anticardiolipin IgG Ab, anti-ss DNA Ab, C3, C4, anti-RO, anti-LA, anti-SC-70, anti-SM Ab, P-ANCA, C-ANCA, TSH, FT4, anti-T microsomal, antithyroglobulin, protein C activity, protein S free, cryoglobulins, serum immunoelectrophoresis, VDRL, hepatitis C antibodies, hepatitis B antigen, and human immunodeficiency virus. Endocrinological work-up examined luteinizing hormone (22.9 mIU/mL [normal range for adult men 0.8-6 mIU/mL]), follicle stimulating hormone (49.7 mIU/mL [normal range for adult men 1-11 mIU/mL]), testosterone (0.24 ng/mL [normal range for adult men 2.5-8.0 ng/mL]), bioavailable testosterone (0.02 ng/mL [normal range for adult men >0.6 ng/mL]), and percent bioavailable test (8.1% [normal value >20%]). These results indicate hypergonadotropic hypogonadism. Plasminogen activator inhibitor 1 was 6 U (normal value 5-20 U/mL). Karyotyping performed by G-banding technique revealed a 47 XXY karyotype, which is diagnostic of Klinefelter's syndrome. Doppler ultrasound of the leg ulcers disclosed partial thrombus in the distal right femoral vein. X-rays and bone scan displayed osteomyelitis along the right tibia. Histological examination of a 4-mm punch biopsy from the ulcer border revealed hyperkeratosis, acanthosis, hypergranulosis, and mixed inflammatory infiltrate containing eosinophils compatible with chronic ulcer. Multiple vessels were seen, compatible with a healing process. Direct immunofluorescence of the biopsy revealed granular IgM in the dermo-epidermal junction. Indirect immunofluorescence was negative. Thyroid function tests showed normal thyroid stimulating hormone and free throxine4. Multinodular goiter was seen on thyroid scan and ultrasound. Thyroid fine needle aspiration was compatible with multinodular goiter (normal follicular cells, free colloid, macrophages with pigment). IV treatment with amoxicillin-clavulanic acid 1 g t.i.d. was administered for 2 weeks, with a decrease in temperature and normalization of the leukocyte level. Oral antibiotic treatment with amoxicillin-clavulanic acid was continued for 10 more days, followed by 25 days of ciprofloxacin for the osteomyelitis. Local treatment included saline soakings followed by application of Promogran (Johnson & Johnson, New Brunswick, NJ) and Kaltostat (ConvaTec Ltd., a Bristol-Myers Squibb Company, New York, NY) with slight improvement. At the same time, the patient was treated with warfarin sodium due to deep vein thrombosis under international normalized ratio 2-3. The patient was treated with IM testosterone once monthly for 1 year, which resulted in a reduction in the diameter and depth of the leg ulcers (Figure 3). Blood tests were not performed for follow-up of the immune state.
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PMID:Klinefelter's syndrome presenting with leg ulcers. 1536 65

A rapidly enlarging leg ulcer appeared in a 54-year-old woman with systemic lupus erythematosus receiving aggressive immunosuppressive therapy. Skin biopsy revealed proliferation of hyphae in the midst of a neutrophilic abscess. Culture yielded Rhizopus azygosporus. As no organ involvement was detected by thorough examination, the patient was diagnosed as having primary cutaneous mucormycosis. Although intravenous amphotericin B therapy seemed to be very effective, it had to be discontinued due to nephrotoxicity. She unfortunately died of subsequent disseminated fungal infection and cerebral infarction in which the primary cause could not be determined. Minimum inhibitory concentrations of several antifungal drugs to the isolate were examined and amphotericin B proved to be the only agent that may potentially reach the effective plasma concentration. This is the first case report of cutaneous mucormycosis caused by R. azygosporus.
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PMID:The first case of cutaneous mucormycosis caused by Rhizopus azygosporus. 1608 61

Leg ulcerations can occur in systemic lupus erythematosus (SLE) patients with antiphospholipid (aPL) antibodies and/or vasculitis, and it has been suggested that aPL antibodies may play a pathogenetic role in skin manifestations of SLE. To our knowledge, there is only one report of an aPL antibody-negative patient who developed pyoderma gangrenosum (PG) several years before the diagnosis of SLE. We describe a case of a young male affected by SLE who developed leg ulcers diagnosed as PG in the absence of aPL antibodies, where the onset of PG was associated with reactivation of SLE. Effective treatment led to significant improvement in skin lesions and SLE activity.
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PMID:Lupus and leg ulcers--a diagnostic quandary. 1663 6

Lipomembranous changes are histological findings without specific clinical correlations, and are thought to be related to vascular impairment in fatty tissue. We describe a case of systemic lupus erythematosus (SLE) in which subcutaneous induration of the lower leg showed lipomembranous changes and calcification. This patient showed thrombophilia with thrombosis of the femoral and iliac veins, and cerebellar and myocardial infarction. A biopsy specimen from the subcutaneous tissue surrounding the multiple leg ulcers revealed degeneration of fat cells, lipomembranous changes in the fatty tissues, and calcification. Another biopsy specimen from the outer edges of the ulcers showed microthrombi and fibrinoid changes in the vessel walls, and mononuclear cell infiltrates in the dermis. Lipomembranous changes have been seen in connective tissue disorders such as lupus profundus, morphoea, systemic sclerosis, and panniculitis associated with dermatomyositis, but rarely associated with SLE. We speculate that ischaemic changes due to the vascular disturbance of the lower legs may have induced lipomembranous changes and calcification in the subcutaneous tissues in the present case.
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PMID:Lipomembranous changes and calcification associated with systemic lupus erythematosus. 1726 29


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