Stanozolol Therapy Research Articles

Hereditary angioedema: Safety of long-term stanozolol therapy

Attenuated androgens control attacks of hereditary angioedema. Short-term studies of such patients treated at our institution with attenuated androgens demonstrated no adverse effects. However, the side-effect frequencies in patients receiving long-term treatment are relatively less well characterized. To assess the frequencies of various side effects of the attenuated androgen stanozolol in a population of patients with hereditary angioedema treated for 20 to 40 years. Data on side effects in patients who continued stanozolol therapy since 1987 were obtained by means of questionnaire. Patients were evaluated by physical examination; biochemical assays of hepatic function, serum lipids, and prostate specific antigen; and liver ultrasound. The minimal initial effective dosage of stanozolol was 0.5 to 2.0 mg daily, although most patients achieved symptomatic control and decreased the dose and frequency as the frequency of attacks decreased. Treatment-related symptoms developed in 10 of 21 patients. No interruption in stanozolol therapy was required because symptoms subsided with a reduction in the stanozolol dosage. Adverse side effects included hirsutism, weight gain, menstrual irregularities or postmenopausal bleeding, acne, and mood changes. Liver enzyme assays revealed no persistent abnormalities. Liver ultrasounds in 8 patients revealed 3 abnormalities deemed unrelated to therapy. Five patients had a reduced high-density lipoprotein, and 2 patients had elevated triglycerides. Stanozolol is a safe and effective drug for the long-term management of hereditary angioedema. Stanozolol may be used in the long-term treatment of patients with hereditary angioedema provided such patients are closely supervised with routine clinical, biochemical, and radiologic assessments.

C1 esterase inhibitor deficiency, airway compromise, and anesthesia.

C1 esterase inhibitor deficiency, airway compromise, and anesthesia.

Leg ulceration due to the antiphospholipid syndrome: successful treatment with intralesional corticosteroids and failure of prolonged stanozolol therapy

AbstractThe clinical manifestations of the antiphospholipid antibody syndrome (APLA) include thrombosis, thrombocytopenia and recurrent fetal loss. Livedo reticularis and leg ulceration may occur as the result of vascular occlusion, and are difficult to treat. We report a patient with a painful leg ulceration and livedo reticularis secondary to APLA in whom intralesional triamcinolone injections induced rapid and complete healing of the ulceration. A year later, the ulcer has not recurred. Initial and prolonged treatment with stanozolol, an androgenic steroid with fibrinolytic properties that has been proposed as a treatment for this condition, seemed to help at first but failed to cause persistent healing. We suggest that intralesional injection of corticosteroids should be the initial treatment of choice in ulcers due to APLA.

THE EFFECT OF STANOZOLOL ON FINAL HEIGHT AND SKELETAL MATURATION IN TURNER'S SYNDROME

<Aims and Methods> The effect of stanozolol on the final height and the skeletal maturation was studied in 35 patients with Turner's syndrome without spontaneous genital bleeding. All patients received stanozolol (1mg/day), estrogen and progesterone therapy. Bone age was evaluated by TW2 RUS method. Height SD score for Japanese Turner standard was used. <Results> The final height (142. 42 = 3.93cm) was significantly higher than that in untreated group (139.1 ± 5.6cm). ΔHeight SD score (Δ HSDS) which means the difference between height SD score at the start of stanozolol therapy and final height SD score was 1.00 ± 0.53. There were no significant differences in final height and Δ HSDS between the patients with 45, X karyotype (n=11) and those with other chromosomal variants (n=24). The final height in SFD group (n=10) was significantly shorter than that in AFD group (n = 19). Δ Bone age/Δ chronological age ratio during stanozolol therapy in patients whose bone ages were above 12 years old (n=27, 0. 31±0.18) was significantly lower than that in patients whose bone ages were below 12 years old (n=7. 1.08±0.23)(p<0. 005). <Conclusions> Stanozolol didn't accelerate bone maturation after 12 years of bone age. The final height was improved by stanozolol.

Fibrinolytic Enhancement with Stanozolol Fails to Improve Symptoms and Signs in Patients with Post-surgical Back Pain

An open trial with the fibrinolytic enchancing agent stanozolol was completed by eighteen patients (14 male) with severe back and radicular pain, despite previous lumbar surgery for prolapsed intervertebral disc. Assessments of their pain, disability and plasma fibrinolytic activity were undertaken before and after 12 or 24 months of therapy. Prior to treatment patients exhibited significant fibrinolytic abnormalities when compared with 84 normal controls; euglobulin clot lysis time (ELT) 442 vs 157 mins and fibrin plate lysis area (FPLA) 61 vs 113 mm2 respectively (p less than 0.01 for both). Stanozolol therapy normalised patients' fibrinolytic activity within three months. Disappointingly there were no concomitant clinical improvements in spinal pain or mobility despite 12 or 24 months of treatment. These results may indicate that perineural fibrosis, once formed, is not amenable to such therapy.

Effect of Stanozolol on Factors VIII and IX and Serum Aminotransferases in Haemophilia

The treatment of haemophilia has been dramatically improved since the introduction of factor VIII and IX concentrates, however these concentrates have brought new problems such as hepatitis and A.I.D.S. An oral agent which could raise endogenous levels of factor VIII and IX would be of great benefit. Danazol, an anabolic steroid, has recently been shown to increase levels of factors VIII and IX in haemophilia. We therefore studied the effect of stanozolol, a closely related anabolic steroid, in 15 patients with haemophilia A or Christmas disease over a 2-4 week period. There was no consistent change in factor VIIIc or factor IX, and fibrinolysis was significantly enhanced. No effect was apparent on the incidence of spontaneous bleeds. However serum aminotransferases which were abnormal in 11 of the 15 patients at the start of the study fell significantly with stanozolol therapy. This raises the interesting possibility that anabolic steroids may be beneficial in patients with chronic liver diseases.

Alteration of hormone levels in normal males given the anabolic steroid stanozolol.

Anabolic steroids have widespread metabolic effects but, to date, their proven clinical indications have been limited. Recently the 17 alpha-alkylated steroid, stanozolol, has been shown to be of value in a variety of commonly occurring vascular diseases. Its endocrine effects have received little attention and we have investigated the effect of administering a 14 d course of stanozolol (10 mg orally per day) on a variety of important hormonal pathways in nine healthy male subjects. Significant changes occurred as follows: a 55% reduction in serum testosterone levels was noted and was accompanied by reductions in 'derived' free testosterone, sex hormone binding globulin and LH levels; total T4 and T3 levels fell in association with a decrease in thyroxine binding globulin, but no alteration was detected in TSH or free T4 levels. Changes in vitamin D status, with falls in 25-hydroxycholecalciferol and vitamin D binding globulin were also observed. These effects were reversible on stopping treatment. Stanozolol therapy therefore leads to a number of hormonal changes, probably by an action at both pituitary and hepatic levels.

Stanozolol in postmenopausal osteoporosis: Therapeutic efficacy and possible mechanisms of action

To assess the efficacy of the anabolic steroid stanozolol in the treatment of osteoporosis, a 29-month double-blind study was performed with 23 treated and 23 control postmenopausal osteoporotic women. Drug efficacy was assessed by serial determinations of total body calcium (TBC—total bone mass) by neutron activation analysis, regional bone mass (RBM) by single-photon absorptiometry, and by spinal roentgenograms. Total body calcium increased 4.4% from baseline values ( P < 0.01) in the treated group and remained unchanged in the control group; the difference in the change in TBC between the treated and control groups was significant ( P = 0.03). The effect of the drug on TBC persisted throughout the 29-month period. In contrast to TBC, measurements of RBM indicated no signficant difference between the treated and placebo groups, suggesting a possible differential response to therapy at various skeletal sites. No new spinal compression fractures were noted in the treated group (compared with three new fractures in the control group). Assessment of serum and urine values indicated a decrease in the level of urinary calcium and an increase in the level of total urinary cyclic AMP in the treated group. These changes were observed even though the level of serum iPTH was significantly decreased during the study. An analysis of changes in bone biopsy specimens revealed no significant differences between the treated and control groups. Seventy-six percent of the treated subjects developed SGOT elevations or other side effects from the stanozolol therapy; at no time were these effects sufficiently severe to cause termination of medication. The data suggest that long-term use of stanozolol increases the net total bone mass above pretreatment levels.

Preoperative stanozolol therapy in patients with hereditary angioedema

Preoperative stanozolol therapy in patients with hereditary angioedema

Clinical and biochemical effects of stanozolol therapy for hereditary angioedema

Stanozolol, an inexpensive anabolic steroid with a 30: 1 anabolic: androgenic ratio, was administered to 12 male and 15 female patients with biochemically proven hereditary angioedema over a 2-yr period to obtain a systematic assessment of the relationship between drug dosage and clinical response, incidence of side effects, and amelioration of complement abnormalities. All 27 patients attained the minimal effective dose, ranging from 0.5 to 2 mg daily, which controlled the frequency and intensity of symptoms with minimal side effects. At daily maintenance doses of 2, 1, and 0.5 mg the frequencies of attacks per weeks of therapy were 1 14.6 , 1 7.2 , and 1 8.2 wk, respectively. Side effects with maintenance therapy included menstrual abnormalities and virilization in four females and elevation of serum creatinine phosphokinase (CPK) in five males. In six patients on maintenance doses of stanozolol, serum levels of testosterone, free thyroxin (T4), and thyroxin binding globulin (TBG) (four males), and of estradiol, progesterone, T4, and TBG (two females) were normal. Slightly low serum levels of progesterone and TBG were found in two females who had normal menstrual cycles. Statistically significant elevations above pretherapy levels of serum inhibitor to the activated first component of complement function and C4 protein and function occurred when patients were on maintenance therapy, but these measurements remained below the lower limit of normal range. Higher doses of stanozolol (4 mg/day), which caused greater immunochemical responses, were unnecessary for control of clinical disease and were unjustified for chronic therapy because of more frequent side effects.