Venous lipodermatosclerosis: treatment by fibrinolytic enhancement and elastic compression.

Burnand, K. G.; Clemenson, G; Morland, M; Jarrett, P. E. M.; Browse, N L

doi:10.1136/bmj.280.6206.7

Cited by 191 publications

(57 citation statements)

References 2 publications

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“…The anabolic steroid stanozolol may be helpful in some patients [1, 9], but not in others [10]. It has been reported that antibiotics, various anti-inflammatory agents, antimetabolites and surgery have been used with limited or non success [1].…”

Section: Discussionmentioning

confidence: 99%

Lipodermatosclerosis – Report of Three Cases and Review of the Literature

Demitsu

Okada²,

Yoneda³

et al. 1999

Dermatology

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We report 3 cases of lipodermatosclerosis (LDS) and discuss the nosology of similar disorders caused by venous insufficiency of the legs. These cases are characterized by (1) occurrence in middle-aged or aged woman, (2) painful, indurated erythema with hyperpigmented scleroderma-like hardening on the lower leg, (3) lobular panniculitis with membranocystic fat necrosis and various degrees of septal fibrosis. Although the designation LDS has been used particularly in the UK and in the USA, this entity is not familiar in other countries including Japan. LDS clinically represents a wide spectrum from an acute, inflammatory phase to a chronic, fibrotic state. The clinicopathologic findings of LDS are similar or identical to the disease previously reported as chronic indurated cellulitis, hypodermitis sclerodermiformis, stasis panniculitis or sclerosing panniculitis. These diseases are probably related conditions, which depend upon the various stages.

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Section: Discussionmentioning

confidence: 99%

Lipodermatosclerosis – Report of Three Cases and Review of the Literature

Demitsu

Okada²,

Yoneda³

et al. 1999

Dermatology

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“…Although the healing rate was twice that of the placebo, the results did not reach statistical significance. 107 No adverse clinical effects were noted during the 3-month clinical trial.…”

Section: Drug Therapymentioning

confidence: 99%

Chronic Venous Insufficiency and Venous Ulceration

Alguire

Mathes

1997

J Gen Intern Med

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OBJECTIVE:To review and summarize the literature on the normal venous circulation of the leg, and the epidemiology, pathophysiology, and treatment of chronic venous insufficiency (CVI).DATA SOURCES: English-language articles identified through a MEDLINE search using the terms venous insufficiency or varicose ulcer and epidemiology, pathophysiology, diagnosis, and clinical trial (pt), and selected cross-references. STUDY SELECTION:Articles on epidemiology, pathophysiology, and treatment of CVI. Randomized, controlled studies were specifically sought for treatment efficacy. DATA EXTRACTION:Data were manually extracted from selected studies and reviews; emphasis was placed on information relevant to the general internist. pproximately 5 million people in the United States exhibit some evidence of chronic venous insufficiency (CVI) and between 400,000 and 500,000 of these individuals have or will develop a venous leg ulcer. 1-3 The signs of CVI include engorgement of the cutaneous veins and dependent edema in mildly affected patients to pigmentation, dermatitis, and ulceration in the more severe cases. Although most patients are asymptomatic, others have leg heaviness and aching or recurrent and recalcitrant leg ulcers punctuated by bouts of cellulitis. These more severe cases are associated with recurrent hospitalization, high health-care costs, and disability. 4,5 Venous insufficiency with trophic skin changes or ulceration is a frustrating problem, which many physicians approach with a sense of ennui. This may be due to the chronic and remitting nature of the problem, the need for lifestyle modification, inconvenient therapies, and contradictory information regarding medical and surgical management. Nevertheless, CVI, including ulceration, is a manageable problem. The purpose of this review is to present the normal anatomy and physiology of the venous circulation and to summarize the epidemiology, pathophysiology, and treatment of CVI. DATA SYNTHESIS: METHODSA MEDLINE search for relevant English-language articles published between 1966 and 1996 was completed using the following MeSH terms: venous insufficiency or varicose ulcer and epidemiology, pathophysiology, diagnosis, and clinical trial (pt). When selecting articles on treatment, randomized, controlled trials were reviewed whenever possible. Emphasis was placed on reviewing articles with clinical relevance for internal medicine physicians. ANATOMY AND NORMAL PHYSIOLOGYVenous blood from the skin and subcutaneous fat is collected in a system of superficial venules and veins that drain toward the deep venous system underneath the fascia via three major pathways: (1) through the long or short saphenous veins, which join the deep system at the saphenofemoral and saphenopopliteal junctions; (2) through the perforating veins originating from the long or short saphenous veins or their branches; or (3) directly into the deep venous system or bypass the deep system entirely and enter the pelvis. 6 Deep veins are categorized as either intramuscular or intermuscular; o...

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“…Although its use has been relatively widespread, in [3] and arteriosclerotic disease [4], the exact modes of action of this compound have been unclear. Stanozolol has been shown to stimulate fibrinolytic activity [5] which could explain some of its actions, for example, the increased breakdown of fibrin in conditions such as rheumatoid arthritis [6].…”

Section: Introductionmentioning

confidence: 99%

The differential effects of stanozolol on human skin and synovial fibroblastsin vitro: DNA synthesis and receptor binding

Ellis¹,

Cawston²,

Mackie³

1994

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The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.

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Venous lipodermatosclerosis: treatment by fibrinolytic enhancement and elastic compression.

Cited by 191 publications

References 2 publications

Lipodermatosclerosis – Report of Three Cases and Review of the Literature

Lipodermatosclerosis – Report of Three Cases and Review of the Literature

Chronic Venous Insufficiency and Venous Ulceration

The differential effects of stanozolol on human skin and synovial fibroblastsin vitro: DNA synthesis and receptor binding

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