Injecting steroids
It is among the front line drugs for treatment of endometriosis. injecting steroids Bad side effects of steroids. 39 Plausible mechanisms for which there is evidence for activity in this area include suppression of the midcycle surge of LH/FSH at the hypothalamic level,40 inhibition of the transcription of the gene for the estrogen receptor in monocytes,41 inhibition of estrone sulfatase (required to convert estrone sulfate to estradiol),42 and stimulation of B cells. 43 Danazol therapy is also anti- osteoporotic, whereas many other drugs for endometriosis cause loss of bone mass. 44A disadvantage of danazol therapy is that approximately 10% of patients experience hepatocellular damage, and virilizing side effects are frequent at therapeutic doses for treatment of endometriosis. injecting steroids Bad side effects of steroids. 45 However, application via a vaginal suppository has proven an effective way to target the drug for treatment of endometriosis, which should reduce side effects. Danazol has also been useful for treatment of fibrocystic myopathy of the breast,46 mastalgia,47 idiopathic thrombocytopenic purpurea,47,48 mixed tissue disease with protein S deficiency,49 autoimmune hemolytic anemia,50,51 menorrhagia,52 and "severe PMS. "53,54Danazol binds to low affinity glucocorticoid binding sites (LAGS) in the liver. injecting steroids Bodybuilding-pictures. 55Plasma fibrinogen and lipoprotein (a) levels decrease with danazol treatment, and plasminogen levels rise, thus inhibiting the process of thrombosis. Stanozolol (Oral or I. M. ) "Winstrol"This drug is a potent anabolic, but also binds to the progesterone receptor56 and to LAGS in the liver. 55 In muscle tissue, it has been found to stimulate immediate-early gene expression by a means independent of the AR. 57 Stanozolol can stimulate the production of prostaglandin E2 and the matrix metalloproteases collegenase and stromelysin in skin fibroblasts. It has been found to inhibit growth factor stimulated DNA synthesis and fibroblasts. 56 The drug has substantial fibrinolytic properties, and has been effective in the treatment of urticaria, Raynaud's phenomenon, cryptofibrinogenemia, and lipodermatosclerosis. 58 It has also effected cures of osteonecrosis in cases resistant to all other therapy. 59 Stanozolol has been used successfully in treatment of AIDS wasting syndrome. 60This drug is also useful in treatment of hereditary angioedema. It is somewhat hepatotoxic,61 but less so than many other oral anabolic steroids. It influences some immunological processes. Stanozolol has been found to increase lymphocyte count and CD8+ cell numbers, but to decrease CD4+ and CD3+ in postmenopausal women using it for osteoporosis. 62 This effect would plausibly be useful for treatment of autoimmune disorders. Stanozolol also lowers lipoprotein (a). 63Tibolone (Oral) "Livial"Tibolone shows weak estrogenic, progestogenic, and AR agonist properties. 64 It has been used in postmenopausal women and found to be effective in relieving climacteric symptoms and in maintaining skeletal integrity. It can reduce vasomotor symptoms and reduce vaginal dryness,56 and improve peripheral microcirculation. 65 It has been found to improve sexual desire. 66 Tibolone has been seen to lower lipoprotein (a), triglycerides, and LDL blood lipids. 67It has been argued that, unlike estradiol, tibolone will not stimulate estrogen-sensitive tumors, nor does it stimulate the endometrium, and therefore will not induce vaginal bleeding. (Nonetheless, in some clinical cases vaginal bleeding has been observed. ) Only 2. 5 mg/day is required. Further study of its suitability as a component in hormone replacement therapy for postmenopausal and perhaps elderly women seems called for. Views Regarding Future DevelopmentThis class of drugs has been developed to date without assays that were ever proven to correlate accurately with therapeutic value or side effects of importance in the human, nor with any knowledge of the effects of enzymatic conversion of the drugs within each tissue. Perhaps most seriously, the entire concept of "androgenicity" being a single property of a steroid, in contrast to an "anabolic" property, was fundamentally incorrect. This is not to say that previous workers were incorrect to attempt to maximize the differences in activity which they could measure. It is simply that the means were not then available to adequately understand these drugs, and indeed the means are only developing now. The acquisition of better understanding of structure activity relationships and the development of assays using cultured, differentiated human cells directly demonstrating desired therapeutic activity, as well as specific undesired side effects, should give the drug designer the tools necessary to design a new generation of anabolic/androgenic steroids of superior selectivity and safety. As an illustration, assays measuring ratios between levator ani myotrophic activity versus prostatotrophic activity in the castrated rat (the primary assay used in past development) could not reasonably be expected to of much value in identifying compounds of maximal therapeutic potency with minimal side effects for human female osteoporotic patients, whereas assays with cultured human cells might plausibly be very predictive of clinical properties. Today, rational drug design which accounts for enzymatic biotransformations of steroid drugs is possible. For example, aromatization is generally an undesired side effect, and a number of obvious means may be employed specifically to defeat aromatase. At least several of these possibilities have never been made, but could readily be synthesized today. Organic synthesis techniques today are considerably more versatile than they were in the 1950s and 1960s.
Injecting steroids
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