Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Telangiectases of the legs occur frequently, with most patients seeking treatment for cosmetic reasons. Sclerotherapy continues to gain popularity as a safe and valuable therapeutic approach; however, deep vein thrombosis as well as pulmonary embolism have been reported even after sclerotherapy of small intradermal venectases. Hoping to uncover anatomic risk factors predisposing a patient to iatrogenic thrombosis, we investigated 15 patients with telangiectases of the legs applying ascending venography concomitantly with direct injection of the telangiectases. A digital radiographic technique was used as an imaging system. In two patients an unrestrained flow of the contrast medium into the venae femorales was noticed. As far as we know this is the first in vivo demonstration of venae communicantes connecting intradermal venectases to the deep veins. That means that particular anatomic conditions favor the spillage of sclerosant into the deep veins, which might contribute to the development of iatrogenic deep vein thromboses in compression sclerotherapy.
J Dermatol Surg Oncol 1992 May
PMID:Do telangiectases communicate with the deep venous system? 160 63

Light reflection rheography has been increasingly used in the last few years to screen for chronic venous insufficiency. It is non-invasive, easy to perform, and well-suited for repetition and standardization. Light reflection rheography is appropriate for the global assessment of calf-pump insufficiency regardless of whether it is caused by varicosis, the postphlebitic syndrome, or deep venous thrombosis. For this reason, it is a good method to use as a pretreatment selection test, especially for varicose veins. With the application of tourniquets, it can help to predict treatment results. When it is used in combination with ultrasound venous Doppler, a simple decision can be made for the treatment of nearly all venous patients.
J Dermatol Surg Oncol 1992 May
PMID:Light reflection rheography. A non-invasive diagnostic tool for screening for venous disease. 160 66

A patient with painful migratory erythematous nodules for 7 years is presented. The nodules, which were localized on the lower and upper extremities, progressed to palpable cords. Multiple venograms showed no evidence of deep vein thrombosis. Skin biopsy specimens were diagnostic of superficial thrombophlebitis. There was no evidence of internal malignancy. Extensive evaluation for an underlying hypercoagulable state was remarkable for a factor XII level 17% of normal. The patient was unresponsive to a wide range of treatments. The recalcitrant nature of his disease and lack of deep venous involvement are unique. An underlying hypercoagulable state should be considered when the diagnosis of superficial migratory thrombophlebitis is considered.
J Am Acad Dermatol 1990 May
PMID:Superficial migratory thrombophlebitis and factor XII deficiency. 211 May 79

Lipodermatosclerosis of the lower extremity, with or without ulceration, is a common manifestation of severe venous disease and the result of sustained venous hypertension. The latter is generally a sequela of deep vein thrombosis. Factors that enhance clot formation or impair fibrinolysis contribute to the pathogenesis of venous disease. It is already established that faulty fibrinolysis may play a pathogenic role in patients with venous disease. We examined the possibility that patients with venous disease have abnormally low plasma levels of proteins C and S, two proteins whose deficiencies have been reported to cause an increased frequency of thromboembolic disease. Using immunologic and functional assays for plasma proteins C and S, we found that 4 (21%) of 19 patients with lipodermatosclerosis and leg ulcers had abnormally low levels of protein C or protein S. One of 7 patients with lipodermatosclerosis without ulceration had a profoundly depressed level of protein C and a history of cerebral stroke at a young age. Plasma levels of protein C were normal in five patients with arterial insufficiency severe enough to cause leg ulceration. We conclude that abnormally low plasma levels of proteins C and S may be found in patients with lipodermatosclerosis and venous ulceration. As with the abnormally low fibrinolytic activity in these patients, our findings indicate a possible propensity for increased thrombotic disease.
Arch Dermatol 1990 Sep
PMID:Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. 203 43

Two patients with the lupus anticoagulant exhibited unusual cutaneous manifestations. They both fulfilled four criteria for systemic lupus erythematosus and had experienced deep venous thrombosis. The first patient suffered from a leg ulcer that resembled a pyoderma gangrenosum. The second patient presented erythematous and purplish macules on the fingertips. The histologic studies showed only microthrombosis in the dermal vessels without vasculitis, although such lesions in systemic lupus erythematosus are usually attributed to vasculitis. The association of these cutaneous lesions with lupus anticoagulant has never been reported. It is likely that this association is not fortuitous. After a review of the literature, it seems possible to individualize a new syndrome characterized by the presence of a subgroup of antiphospholipid antibodies. Thrombosis, spontaneous abortions, neurologic manifestations, pulmonary hypertension, positive results of a Coombs' test, and thrombocytopenia can be included in this syndrome, which overlaps with systemic lupus erythematosus. Certain cutaneous symptoms are associated with the presence of lupus anticoagulant or other antiphospholipid antibodies: leg ulcers, distal cutaneous ischemia, widespread cutaneous necrosis, and livedo. They can be considered as the dermatologic manifestations of this syndrome.
J Am Acad Dermatol 1986 Aug
PMID:Cutaneous manifestations associated with the presence of the lupus anticoagulant. A report of two cases and a review of the literature. 309 56

Three patients with karyotype XYY who had presented with deep vein thrombosis and leg ulcers (plus pulmonary embolism in two of them) were investigated for: (1) androgens (plasma testosterone measurement, testosterone oestradiol binding globulin (TeBG) assay, GnRH 50 micrograms test), and (2) haemostasis by fibrinolysis tests (euglobulin lysis time and area, antigenic plasminogen activator assay before and after 10 min venostasis). Full evaluation of haemostasis failed to demonstrate the presence of circulating anticoagulant or of antithrombin III, protein C and protein S deficiencies. One patient had neither hormonal nor fibrinolytic abnormality. The other two patients shared some clinical features with male hypogonadism (gynoid morphotype in both, hypotrophy of the testes in one, gynaecomastia in the other). They also had hormonal disorders ("over-response" to the GnRH test in one case, elevated TeGB in the other case) and abnormalities of fibrinolysis (poor response to venostasis, high baseline level of plasminogen activator). Response to venostasis became normal after 3 months of treatment with percutaneous dihydrosterone 125 mg per day in the two patients with initially poor response. The mechanism of venous pathology in XYY subjects is discussed. A genetic defect not involving the fibrinolysis system is possible since fibrinolysis was normal in one patient; however, abnormal fibrinolysis may have been responsible for the venous pathology in the other 2 patients. The role played by abnormalities of fibrinolysis in the pathogenesis of deep vein thrombosis and leg ulcers is recalled, and the possible implication of these abnormalities in patients with XYY karyotype is emphasized.(ABSTRACT TRUNCATED AT 250 WORDS)
Ann Dermatol Venereol 1987
PMID:[Post-phlebitic leg ulcers and XYY karyotype: fibrinolysis and androgenic function tests. Apropos of 3 cases]. 343 47

We describe a family afflicted with striking clinical and serologic autoimmune features. The mother and maternal uncle of a patient with neonatal lupus had rheumatic disease manifestations. All three had Ro antibodies (SS-A) in their sera, as well as La antibody (SS-B). The 17-year-old mother developed postpartum inflammatory monoarthritis of the right knee and had a positive lupus band test. The uncle at the age of 26 developed a fulminant disease most consistent with systemic lupus erythematosus (SLE); initial manifestations were myocardial infarction, deep vein thrombosis, and the nephrotic syndrome. Although it is known that mothers of neonatal lupus infants can develop SLE postpartum, the development of severe disease in the maternal uncle suggests the relevance of identifying seropositive relatives of individuals with neonatal lupus.
J Am Acad Dermatol 1985 Jun
PMID:Neonatal lupus erythematosus, multiple thromboses, and monoarthritis in a family with Ro antibody. 387 15

A patient with pemphigus vulgaris had lesions on the lip that proved to be refractory to intralesional corticosteroid therapy and to treatment with azathioprine and later to daily administration of 250 mg of prednisone. The patient developed marked cushingoid features and deep vein thrombosis, rendering the continuation of the prednisone therapy unadvisable . Total vermilionectomy of the affected lip was performed and the prednisone was gradually tapered, taking care that oral lesions remained under control. Eighteen months after the operation, the patient is receiving a single alternate-daily dose of 20 mg prednisone, and both the lip and oral lesions are in remission.
Int J Dermatol 1984 May
PMID:Surgical approach to the treatment of refractory lesions of pemphigus vulgaris. 673 56

Patients with venous leg ulcers have a readily recognized clinical syndrome of shallow ulcers, oedema, leg pain, venous ankle blush, lipodermatosclerosis, varicose veins, hyperpigmentation, and atrophie blanche, and they are assumed to have venous abnormalities. We examined 43 patients with venous leg ulcers, and compared those with obvious venous abnormalities (defined as historical or clinical evidence of deep venous thrombosis or varicose veins) with those with presumed venous abnormalities (defined as lacking any such evidence), to see if they presented with different clinical features. We found that both groups had similar clinical features, with the exception that lipodermatosclerosis was present more frequently in those patients with obvious venous abnormalities (94 vs. 36%, P < 0.001). Most patients with presumed venous abnormalities had musculoskeletal conditions which might cause calf pump dysfunction (91%). Using air plethysmography, we were unable to confirm that all patients with presumed venous abnormalities did have intrinsic venous abnormalities. We propose that ulcers occurring in this clinical syndrome be designated as calf pump dysfunction ulcers (CPD ulcers), rather than venous ulcers.
Br J Dermatol 1993 Sep
PMID:Venous leg ulcers: an analysis of underlying venous disease. 828 23

A 70-year-old woman developed erythema and induration of the right chest wall, and swelling of her right arm. The provisional diagnosis was deep venous thrombosis and/or cellulitis of the right arm. Skin biopsy showed a poorly differentiated adenocarcinoma within lymphatic vessels, and immunohistochemical staining revealed this to be of breast origin. Inflammatory carcinoma or carcinoma erysipeloides represents < 1% of all cases of breast carcinoma. Our case illustrates the importance of considering this entity in the differential diagnosis of unilateral chest wall erythema and induration.
Br J Dermatol 1993 Sep
PMID:Inflammatory breast carcinoma (carcinoma erysipeloides): an easily overlooked diagnosis. 828 33


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