Taking anavar and winny together should be fine. go with 40mg anavar and 50mg winny.
Ill thank Nimrod for this info...........
Here is a very interesting study I dug about Anavar. We all knew Ox was great, but now it is being said to reverse liver damage caused by 17-aa steroids, this article talks of winstrol.
Lipodermatosclerosis is a clinical disorder that includes acute inflammatory and chronic fibrotic stages.1 The chronic form is characterized by unilateral or bilateral hyperpigmented induration of the distal lower extremities, primarily in female patients with venous insufficiency. The indurated plaques are often painful and the legs frequently have a characteristic “inverted wine bottle” appearance. In addition, ulceration may develop and healing is often delayed. Therapeutic options for lipodermatosclerosis include elevation, compression stockings, ultrasound therapy, and oral stanozolol.
Stanozolol is a synthetic testosterone derivative with primarily anabolic (and few androgenic) effects that also has potent fibrinolytic properties.2 Presumably, it is the latter property that explains its successful use in the treatment of lipodermatosclerosis.3 However, major systemic side effects of stanozolol include sodium retention, hepatotoxicity, and lipid profile abnormalities.4 We describe a patient with chronic lipodermatosclerosis whose symptoms abated after treatment with stanazolol, but hepatotoxicity developed and the patient required alternative therapy.
The patient was a 54-year-old African American woman with a 15-year history of severe pain and discoloration of the lower extremities, from below the knee to the ankles, circumferentially. Her history was significant for rheumatoid arthritis, hypertension, and hypothyroidism; there was no history of deep vein thromboses. Her medications included prednisone (10 mg daily), levothyroxine (0.5 mg daily), fluvoxamine (25 mg daily), acetylsalicylic acid (650 mg twice daily), hydromorphone as needed, and multivitamins daily.
Approximately 10 years earlier, she underwent an empiric trial of potassium iodide for presumed erythema nodosum, without benefit. Subsequently, she was diagnosed as having lipodermatosclerosis and was treated with compression stockings, elevation, and ultrasound therapy, all without benefit. Clinically and symptomatically, she continued to progress, with increased hyperpigmentation, induration, and pain. At the time of presentation to us, there was symmetric induration and hyperpigmentation of the distal lower extremities, from the mid calf to the ankle. Involvement of both the anterior and posterior aspects of the legs resulted in an “inverted wine bottle” appearance. There was tenderness but no erythema or varicosities. Peripheral pulses (dorsal pedal and posterior tibial) were 2+ and symmetric. The clinical diagnosis was lipodermatosclerosis.
Her worsening pain and extension of the induration prompted a trial of stanozolol (2 mg daily), which resulted in marked alleviation of symptoms within 2 weeks of its initiation. Unfortunately, within 2 months her liver enzyme levels rose from normal baseline levels (alanine aminotransferase, 38 U/L; aspartate aminotransferase, 38 U/L) to 257 U/L (alanine aminotransferase) and 562 U/L (aspartate aminotransferase). Although the patient did not exhibit signs or symptoms of hepatotoxicity, the stanozolol was immediately discontinued, with full resolution of the enzyme abnormalities. A newer anabolic steroid was then started, oxandrolone (10 mg twice daily), because it had been reported to be less hepatotoxic.5 Within 2 weeks, she experienced a reduction in pain (from a score of 7/10 to 3/10) as well as subjective softening of the skin. After 3 months of oxandrolone therapy, her symptoms had continued to abate, and she decided to discontinue the medication. No abnormalities in liver enzymes were noted. Incidentally, several months later she was diagnosed as having an idiopathic cardiomyopathy (a literature search failed to find any reports of oxandrolone-induced cardiomyopathy).
Prolonged venous hypertension is postulated to facilitate the leakage of macromolecules, such as fibrinogen, into the dermis, where fibrin polymerization around capillaries can lead to a decrease in oxygen and nutrient delivery to the dermis. The use of fibrinolytic agents, such as stanozolol, is thought to alleviate lipodermatosclerosis through modulation of fibrin production. The newer anabolic steroid oxandrolone also has known fibrinolytic activity,5 but unlike the majority of oral anabolic steroids it undergoes limited hepatic metabolism and is associated with a lower incidence of hepatotoxicity. In our opinion, oxandrolone represents a therapeutic option for those patients with stanozolol-responsive lipodermatosclerosis in whom hepatic toxicity develops.
16/8/106517
doi:10.1067/mjd.2000.106517
Samantha Segal, MDa
Department of Dermatology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshirea
Jane Cooper, MDb
Department of Internal Medicine, Waterbury Hospital, Waterbury, Connecticutb
Jean Bolognia, MDc
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticutc E-mail:
[email protected]
References
1. Kirsner RS, Pardes JB, Eaglstein WH, Falanga V. The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol 1993;28:623–7.MEDLINE
2. Davidson JF, Lochhead M, McDonald GA, McNicol GP. Fibrinolytic enhancement by stanozolol: a double-blind trial. Br J Hematol 1972;22:543–59.
3. Burnand K, Clemenson G, Morland M, Jarrett PE, Browse NL. Venous lipodermatosclerosis: treatment by fibrinolytic enhancement and elastic compression. Br Med J 1980;280:7–11.MEDLINE
4. Helfman T, Falanga V. Stanozolol as a novel therapeutic agent in dermatology. J Am Acad Dermatol 1995;33:254–8.MEDLINE
5. Ferraresi RW. Clinical profile of Oxandrinr. BTG Pharmaceuticals Drug Monograph. 1995.
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