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Background: Metabolic disorders are common in individuals with Turner syndrome (TS). Hyperuricemia is associated with metabolic syndrome. This study investigated the serum uric acid (SUA) profile in patients with TS. Methods: A retrospective observational study was conducted with 145 patients with TS. A total of 72 normal girls were in the control group from 2015 to 2024: 86 TS patients were treated with growth hormone (GH), 80 with stanozolol, and 52 with estrogen. Results: Hyperuricemia was present in 33.1% (47/145) of patients with untreated TS and in 16.67% (12/72) of the controls (P < 0.001). Multivariable linear regression analysis showed that BMISDS, fasting serum glucose, and eGFR explained 34.4% (model R 2 = 0.344) of the total variation in SUA in the untreated TS group. SUA and SUASDS (SUA standard deviation score) levels generally showed a slow rising tendency with age. SUA increased significantly in the first year of stanozolol initiation (P = 0.032), while adding estrogen and stanozolol improved the lipid profile during the whole assessment period. Conclusion: Girls with TS showed a slow rising tendency in SUA and SUASDS with age and had higher SUA and SUASDS levels and incidence of hyperuricemia compared to their healthy female peers. The independent risk factors for hyperuricemia in pediatric patients with TS were BMISDS, HOMA-IR, glucose, and eGFR. The incidence of hyperuricemia increased in the first year of stanozolol treatment. [ABSTRACT FROM AUTHOR]

Background and Aim: The aim of this study was to determine the effect of 8 weeks of resistance training combined with Tribulus terrestris extract on oxidative stress and pro-inflammatory cytokine markers in the heart tissue of male Wistar rats exposed to stanozolol. Methods: In this experimental study, 48 male Sprague-Dawley rats, aged 8 weeks, were randomly divided into 8 groups of 6 (1. Control, 2. Sham, 3. Stanozolol, 4. Stanozolol + Tribulus 50 mg/kg, 5. Stanozolol + Tribulus 100 mg/kg, 6. Resistance training, 7. Stanozolol + Tribulus 100 mg/kg + Resistance training, 8. Stanozolol + Tribulus 50 mg/kg + Resistance training). For 8 weeks, groups 3 to 8 received 5 mg/kg stanozolol daily via intraperitoneal injection. Groups 6 to 8 performed resistance training three times a week, and groups 4, 5, 7, and 8 received the specified doses of Tribulus terrestris daily via intraperitoneal injection. The expression levels of genes of Interleukin-10 (IL-10), Malondialdehyde (MDA), and Advanced Oxidation Protein Products (AOPP) were measured using Real-Time PCR. Results: Stanozolol significantly increased AOPP and MDA expression and decreased IL-10 expression in the heart tissue of rats (P

BackgroundMetabolic disorders are common in individuals with Turner syndrome (TS). Hyperuricemia is associated with metabolic syndrome. This study investigated the serum uric acid (SUA) profile in patients with TS.MethodsA retrospective observational study was conducted with 145 patients with TS. A total of 72 normal girls were in the control group from 2015 to 2024: 86 TS patients were treated with growth hormone (GH), 80 with stanozolol, and 52 with estrogen.ResultsHyperuricemia was present in 33.1% (47/145) of patients with untreated TS and in 16.67% (12/72) of the controls (P < 0.001). Multivariable linear regression analysis showed that BMISDS, fasting serum glucose, and eGFR explained 34.4% (model R2 = 0.344) of the total variation in SUA in the untreated TS group. SUA and SUASDS (SUA standard deviation score) levels generally showed a slow rising tendency with age. SUA increased significantly in the first year of stanozolol initiation (P = 0.032), while adding estrogen and stanozolol improved the lipid profile during the whole assessment period.ConclusionGirls with TS showed a slow rising tendency in SUA and SUASDS with age and had higher SUA and SUASDS levels and incidence of hyperuricemia compared to their healthy female peers. The independent risk factors for hyperuricemia in pediatric patients with TS were BMISDS, HOMA-IR, glucose, and eGFR. The incidence of hyperuricemia increased in the first year of stanozolol treatment.

Stanozolol and nandrolone decanoate hormones are mainly used in dogs and horses to strengthen muscle growth, increase of body weight, treatment of anemia and stimulation of appetite; nevertheless, some side effects have been reported, including testicular atrophy, and decrease of spermatozoid count in dogs. The aim of the present study is to evaluate the histopathological changes of testicular and epididymal tissues in dogs treated with stanozolol and nandrolone decanoate. The present survey was performed on sixtheen male dogs. The studied animals were divided into two equal groups of eight. Stanozolol was administered to dogs in group A with dosage of 50 mg per dog intramuscularly for 6 continuous weeks. Group B was similar to group A, but instead of stanozolol, nandrolone decanoate was injected with dosage of 1 mg/kg. To evaluate the possible side effects on the testicles, one of them was surgically removed before the investigation and the second testicle was removed on days 28 (four dogs in each group) and 42 (the remaining four of each group). Before the testes were placed in 10% formalin buffer, sperm quality in the epididymis was evaluated for indicators such as motility, morphology and number in times zero, 28 and 42 days. The results showed that destructive effects were obtained such as hyperplasia of interstitial Leydig cells, vacuolation, the presence of multinucleated cells and different stages of spermatogonia in testicular tissue; also, the destruction of duct covering cells and the detachment of cilia in the epididymal epithelium was observed. These changes were significantly greater in the stanozolol group than nandrolone decanoate. The quantitative changes were more pronounced in the stanozolol group and the qualitative changes in the nanderlone decanoate group. Although both drugs had side effects on testicular and epididymal tissues; the side effects of stanozolol were greater than nandrolone decanoate; therefore, it is recommended minimum dose of nandrolone decanate for therapeutic purposes. [ABSTRACT FROM AUTHOR]

Simple Summary: This study assessed the clinical efficacy of a single intra-articular stanozolol injection in canine knees with degenerative joint disease (DJD) and its correlation with serum IL-1β levels. Thirty dogs were divided into a control group (CG, n = 10) and a study group (SG, n = 20) with DJD. Pain levels were assessed using the Brown query, and radiographs were taken at T0 and T3. IL-1β levels were quantified via ELISA. Apart from 2 patients, all showed reduced pain intensity, with 15 showing improvement at T1 and 3 at T2. A positive correlation (r = 0.84; p < 0.01) was found between pain level and IL-1β in 15 patients. No systemic effects were observed. Most patients (18/20) experienced reduced pain, possibly linked to decreased catabolic IL synthesis and increased TGF-1β levels. This pilot study suggests stanozolol's potential in managing DJD in dogs. Further research is warranted to validate these findings and understand stanozolol's mechanism in DJD treatment. Stanozolol shows promise as an anabolic and anti-catabolic agent for treating degenerative joint disease (DJD). This study assessed the clinical efficacy of a single intra-articular stanozolol injection in canine knees with DJD and its correlation with serum IL-1β levels. Thirty dogs (n = 30) were divided into a control group (CG, n = 10) and a study group (SG, n = 20) with DJD. Pain levels were assessed using the Brown query, and radiographs were taken at T0 and T3. IL-1β levels were quantified via ELISA. Apart from 2 patients, all showed reduced pain intensity, with 15 patients showing improvement at T1 and 3 patients at T2. A positive correlation (r = 0.84; p < 0.01) was found between pain level and IL-1β in 15 patients. No systemic effects were observed. Most patients (18/20) experienced reduced pain. This pilot study suggests stanozolol's potential in managing DJD in dogs. Further research is warranted to validate these findings and understand stanozolol's mechanism in DJD treatment. [ABSTRACT FROM AUTHOR]

Because of the activities and effects they induce, hormones are prohibited for use for anabolic purposes in farm animals intended for slaughter, which is regulated in the European Union by relevant legal provisions. Therefore, there is an obligation to monitor residues of hormones in animals and food of animal origin to ensure consumer safety. A hormone banned but used formerly for fattening cattle, stanozolol, and its metabolite 16β-OH-stanozolol are synthetic compounds that belong to a large group of steroid hormones. This study investigates residues of these compounds in animal urine.

Drug-induced liver injury (DILI) can be considered in cases of acute hepatitis by the exclusion of any disease-related causes. For several decades, anabolic steroids have been considered not only as drugs for treatment of diseases such as hypogonadism, sarcopenia, hypotrophy in cancer patients, aplastic anemia, etc., but also as risk factor for acute liver failure, that can lead to liver cancer, and even sudden death. Anabolic steroids are known to be increa­singly used not only for legitimate medical uses, but also for enhance physical performance and promote muscle growth for ideal body shape. The article presents a clinical case of acute drug-induced hepatitis after 2 months of using stanozolol, a synthetic testosterone derivative, in a 25-year-old previously healthy man. Thorough etiological investigations ruled out other causes of DILI. The man was treated at the in-patient department and discharged with improvement, but it took several months for the disappearance of hepatic cytolytic and cholestatic changes. Clinicians should be aware of the risk for toxic drug-induced hepatitis in male bodybuilders and collect a thorough history of the patient’s intake of nutritional supplements that may contain androgen derivatives.

Potential scenarios as to the origin of minute amounts of banned substances detected in doping control samples have been a much-discussed problem in anti-doping analysis in recent years. One such debated scenario has been the contamination of female athletes' urine with ejaculate containing doping agents and/or their metabolites. The aim of this work was to obtain complementary information on whether relevant concentration ranges of doping substances are excreted into the ejaculate and which metabolites can be detected in the seminal fluid (sf) and corresponding blood plasma (bp) samples. A method was established to study the concentration and metabolite profiles of stanozolol and LGD-4033—substances listed under anabolic substances (S1) on the World Anti-Doping Agency's Prohibited List—in bp and sf using liquid chromatography high-resolution mass spectrometry (LC-HRMS). For sf and bp, methods for detecting minute amounts of these substances were developed and tested for specificity, recovery, linearity, precision, and reliability. Subsequently, sf and bp samples from an animal administration study, where a boar orally received stanozolol at 0.33 mg/kg and LGD-4033 at 0.11 mg/kg, were measured. The developed assays proved appropriate for the detection of the target substances in both matrices with detection limits between 10 and 40 pg/mL for the unmetabolized drugs in sf and bp, allowing to estimate the concentration of stanozolol in bp (0.02–0.40 ng/mL) and in sf (0.01–0.25 ng/mL) as well as of LGD-4033 in bp (0.21–2.00 ng/mL) and in sf (0.03–0.68 ng/mL) post-administration. In addition, metabolites resulting from different metabolic pathways were identified in sf and bp, with sf resembling a composite of the metabolic profile of bp and urine. [ABSTRACT FROM AUTHOR]

Drug-induced liver injury (DILI) can be considered in cases of acute hepatitis by the exclusion of any disease-related causes. For several decades, anabolic steroids have been considered not only as drugs for treatment of diseases such as hypogonadism, sarcopenia, hypotrophy in cancer patients, aplastic anemia, etc., but also as risk factor for acute liver failure, that can lead to liver cancer, and even sudden death. Anabolic steroids are known to be increasingly used not only for legitimate medical uses, but also for enhance physical performance and promote muscle growth for ideal body shape. The article presents a clinical case of acute drug-induced hepatitis after 2 months of using stanozolol, a synthetic testosterone derivative, in a 25-year-old previously healthy man. Thorough etiological investigations ruled out other causes of DILI. The man was treated at the in-patient department and discharged with improvement, but it took several months for the disappearance of hepatic cytolytic and cholestatic changes. Clinicians should be aware of the risk for toxic drug-induced hepatitis in male bodybuilders and collect a thorough history of the patient’s intake of nutritional supplements that may contain androgen derivatives. [ABSTRACT FROM AUTHOR]

Los antibióticos y analgésicos han sido descritos frecuentemente como las principales causas de toxicidad hepática. Los esteroides anabólicos se han relacionado también con alteraciones en sistemas como el cardiovascular o el hepático; en este último causan colestasis, carcinoma hepatocelular, hiperplasia regenerativa nodular y sangrado de varices, secundario a hipertensión portal. Es importante entonces considerar los esteroides anabólicos como factores de riesgo para hepatotoxicidad. Se presenta el primer caso en Colombia y uno de los pocos en Latinoamérica, de colestasis asociada únicamente al uso de estanozolol. Se trata de un paciente de 21 años, en tratamiento con el medicamento para incrementar la masa muscular, que presentó compromiso hepático de tipo colestásico. Se descartaron otras posibles causas de ictericia, mediante la escala CIOMS/RUCAM se llegó a establecer causalidad entre el consumo de estanozolol y la colestasis. El objetivo de este reporte es hacer una descripción no reportada en la literatura colombiana y poco común en la literatura mundial.

BACKGROUND: Stanozolol and Nandrolone decanoate are the most commonly used hormones in canine medi-cine. They are mainly administered to strengthen the muscle, gain weight, treatment of anemia and stimulate the appetite. One of the effects of hormones is to enhance the erythropoietin production and eventually an increase in the number of RBCs. OBJECTIVES: Prolonged usage of hormones may be relevant to the liver and renal disorders; therefore, the pre-sent survey was aimed to evaluate the effects of stanozolol and nandrolone decanoate on liver and kidney indices, erythropoietin and testosterone serum concentrations and hematocrit changes in healthy dogs. METHODS: Sixteen dogs were randomly categorized in two groups of A (stanozolol) and B (nandrolone decano-ate). Each group was divided into two subgroups (A1, A2 and B1, B2). The second testicle was removed on day 28 in the first subgroups (A1 and B1), and day 42 in the second subgroups (A2 and B2). The first testicle was removed at time zero. Stanozolol (50 mg per dog) was administered to all dogs of group A as IM once a week for six weeks. Group B was similar to group A with the difference that nandrolone decanoate was injected (1 mg/kg) instead of stanozolol. Blood samples were collected on days 0, 3, 14, 28 and 42. RESULTS: Erythropoietin and testosterone concentrations were virtually increased in both groups A (p 0.05). The liver enzymes of ALP, ALT and AST were increased more significantly in group A than group B (p

Anabolic-androgenic steroids (AAS) are synthetic derivatives of testosterone which are used medically for several diseases. However, misuse is commonly observed by athletes to promote enhancement of strength and performance. AAS are frequently obtained through online black markets from clandestine drug manufacturing laboratories, without any quality standards, being potentially dangerous for users. The purpose of this work was the development and application of a fast and simple procedure for the quantitation of stanozolol by liquid chromatography coupled to quadrupole time-of-flight-mass spectrometry (LC-QTOF-MS) in tablets packs seized in Rio Grande do Sul state, Brazil. The samples of stanozolol were separated considering its dosage form. The internal standard (methyltestosterone) was added to the aliquots of the samples, dissolved in methanol and 5μL were injected into the analytical system. The newly developed method has been validated for lower limit of quantitation (LLOQ), linearity, accuracy, precision and selectivity. The LLOQ was 0.1 µg/mL. The developed method was successfully applied to 31 samples seized by the Secretaria da Receita Federal do Brasil (a Brazilian federal revenue service agency). According to the results, 90.3% of the suspected medicines (n=31) were adulterated, and 65% exhibited higher concentrations of stanozolol than those indicated in the label. This work successfully established a new method for quantification of stanozolol using LC-QTOF-MS. This method aims at contributing to the identification and quantification of this anabolic androgenic steroid frequently seized by federal inspection agencies.

Background: Protective effect of medicinal plants on the heart has been reported, but the effect of resistance training (RT) and Tribulus terrestris (TT) on the heart exposed to anabolic-androgenic steroids (AAS) abuse is still unknown. Objectives: The present study aimed to investigate the effect of RT and TT on androgen receptor-1 (ar-1), Fas ligand (fasl) gene expression and lipid profiles in rats exposed to stanozolol (S). Methods: Thirty-five male rats were selected and divided into 7 groups as follows: (1) sham (normal saline/Sh), (2) stanozolol (S), (3) S+100 mg/kg TT (S+TT100), (4) S+ 50 mg/kg TT (S+TT50), (5) S+RT+TT, (6) S+RT+TT100, and (7) S+RT+TT50. Over a course of eight-week period, groups 3, 4, 6, and 7 received 50 and 100 mg/kg/d doses of TT peritoneally and groups 5-7 performed three sessions of increasing RT per week. Results: RT decreased plasma cholesterol and low-density lipoprotein cholesterol (LDL-C) levels, as well as ar-1 and fasl gene expression in S-exposed rats (P

Objective: Stanozolol is an anabolic androgenic steroid (AAS) that is widely used by teenagers and athletes in bodybuilding, sports, and athletics. The potential effects of stanozolol in kidney functions have not been defined. In this study we investigated the expression of tumor suppressor protein phosphatase and tensin homolog (Pten) and mRNA levels of phosphatidylinositol 4,5-bisphosphate 3 kinase (Pi3k) and the protein kinase B (Akt1) signaling pathway in rat kidneys treated by stanozolol. Materials and Methods: Rats were randomized to 5 groups as control, solvent control, steroid (stanozolol), solvent-exercise, and steroid-exercise. Subcutaneous injection of stanozolol (5 mg/kg) was applied for 28 days and swimming exercise was performed 20 min/day, 5 days/week in exercise groups. Expression of PTEN was evaluated by immunohistochemistry. Also, Pten, Pi3k, and Akt1 mRNA expressions were analyzed via RT-PCR. Results: Mesangial cells and renal tubules in the control, solvent control, and solvent exercise groups showed strong (+++) PTEN reactivity against weak PTEN reactivity in the steroid group. Moderate PTEN reactivity was detected in cells of the steroid exercise group. Pten mRNA expression was significantly decreased, and Pi3k and Akt1 mRNA expression were significantly increased in the steroid group versus other groups (p<0.001). Pten expression showed increase while Pi3k and Akt1 expression showed decrease with exercise treatment (p<0.05). Conclusion: Our findings suggest that AAS usage may inhibit PTEN expression in kidneys, which can be associated with increased Pi3k and Akt1 mRNA levels. Exercise performed with AAS usage can be protective on stanozolol-exposed kidneys due to increased levels of PTEN expression and decreased levels of Pi3k and Akt1. [ABSTRACT FROM AUTHOR]

The exogenous anabolic‐androgenic steroid (AAS) stanozolol stays one of the most detected substances in professional sports. Its detection is a fundamental part of doping analysis, and the analysis of this steroid has been intensively investigated for a long time. This contribution to the detection of stanozolol doping describes for the first time the unambiguous proof for the existence of 17‐epistanozolol‐1′N‐glucuronide and 17‐epistanozolol‐2′N‐glucuronide in stanozolol‐positive human urine samples due to the access to high‐quality reference standards. Examination of excretion study samples shows large detection windows for the phase‐II metabolites stanozolol‐1′N‐glucuronide and 17‐epistanozolol‐1′N‐glucuronide up to 12 days and respectively up to almost 28 days. In addition, we present appropriate validation parameters for the analysis of these metabolites using a fully automatic method online solid‐phase extraction (SPE) method already published before. Limits of identification (LOIs) as low as 100 pg/ml and other validation parameters like accuracy, precision, sensitivity, robustness, and linearity are given. [ABSTRACT FROM AUTHOR]

Stanozolol is an anabolic-androgenic steroid which is commonly abused by athletes for improved energy, appearance, and physical size. It has been previously shown to cause changes in behaviour and has various physical effects. Studies have previously been conducted on its neurotoxic effect on the central nervous system (CNS), which are typically psychological in nature. This study was performed to investigate the apoptotic effect of stanozolol on different parts of the rat hippocampus. Sixteen male Wistar rats were divided randomly into two groups (experimental and control). The experimental group received subcutaneous injections of stanozolol (5mg/kg/day) for consecutive 28 days, whereas the control group received saline using the same dosing schedule and administration route. After routine procedures, coronal sections of rat brain were stained with Toluidine blue and TUNEL for pre-apoptotic and apoptotic cell detection, respectively. In order to compare groups, the mean number of TUNEL-positive and pre-apoptotic neurons per unit area were calculated and analysed. Histopathological examination revealed that the mean number of pre-apoptotic and apoptotic neurons in the CA1, CA2, CA3 and DG areas of the hippocampus were significantly increased in the stanozolol treated group. In conclusion, stanozolol abuse may induce pre-apoptotic and apoptotic cell formation in different regions of the hippocampus.

Background: Stanozolol and danazol are widely used in the treatment of aplastic anemia; however, their mechanisms of action are unclear.Methods: Bone marrow mononuclear cells from 10 patients newly diagnosed with aplastic anemia and 10 healthy volunteers were collected and cultured together with stanozolol, danazol, or blank control separately for marrow colony assays. K562 cell lines that had been incubated with stanozolol, danazol, or blank control were tested for erythroid or megakaryocytic differentiation. Meanwhile, CB6F1/Crl mice were injected with 1 × 106 C57BL/6 donor-originated lymphocytes after irradiation with 5 Gy total body irradiation to establish a model for immune-mediated bone marrow failure (aplastic anemia mouse model). Mice with aplastic anemia were treated with cyclosporin A monotherapy, cyclosporin A in combination with stanozolol, and cyclosporin A in combination with danazol for 30 days. Peripheral blood cell counts once a week and bone marrow colony assays at the end of 1 month were performed. The proportion of T cell subsets, level of inflammatory factors, erythropoietin, and thrombopoietin were detected before and after treatment. The levels of erythropoietin receptors on bone marrow mononuclear cells after treatment were tested using western blotting.Results: In the ex vivo experiments, the number of burst-forming units-erythroid; colony-forming units-granulocyte and macrophage; and colony-forming units-granulocyte, erythrocyte, monocyte, and megakaryocyte in the patients with aplastic anemia were significantly lower than that in the normal controls (P < 0.05). However, the number of colonies and mean fluorescence intensity of CD235a or CD41 expression in the harvested cultured cells were not significantly different among the different treatment groups in the patients with aplastic anemia, normal controls, and K562 cell lines. These results show that stanozolol and danazol produce no direct hematopoiesis-stimulating effects on progenitor cells. In the in vivo experiment, the mice with aplastic anemia treated with cyclosporin A and danazol exhibited the most rapid recovery of platelet; the platelet count returned to normal levels after 3 weeks of treatment, which was at least 1 week earlier than in the other groups. In contrast, mice treated with cyclosporin A and stanozolol exhibited the highest hemoglobin level at the end of treatment (P < 0.05). Bone marrow colony assays at 30 days showed that the number of burst-forming units-erythroid was the highest in mice treated with cyclosporin A and stanozolol, while the number of colony-forming units-granulocyte and macrophage was the highest in those treated with cyclosporin A and danazol. Compared to cyclosporin A monotherapy, additional stanozolol and danazol can both increase the level of regulatory T cells and upregulate interleukin-10, inhibiting the expression of tumor necrosis factor-α (P < 0.05). However, IL-2 was more effectively reduced by danazol than by stanozolol (P < 0.05). The cyclosporin A- and stanozolol-treated mice showed higher serum erythropoietin (corrected by hemoglobin level) and higher erythropoietin receptor levels in bone marrow mononuclear cells than the other groups (P < 0.05).Conclusions: Neither stanozolol nor danazol directly stimulated hematopoiesis in vitro. However, in vivo, stanozolol may exhibit an advantage in improving erythropoiesis, while danazol may induce stronger effects on platelets. Both danazol and stanozolol exhibited immunosuppressive roles. Stanozolol could enhance the secretion of erythropoietin and expression of erythropoietin receptor in bone marrow mononuclear cells.

The study aimed to find the histopathological and morphological effects of stanozolol, with different concentrations and periods on the aorta in the male rats. The study comprised 80 white males which set into four groups, with 20 rats for each group. First group set as control group and was left only on tap water and fed with pellets. Second group was injected with stanozolol 25 mg / kgbw and the third group was injected with stanozolol 25 mg / kgbw with vit.E 600 mg / kgbw while fourth group was treated with vit.E 600 mg / kgbw. The period of treatment was extend for 8 weeks, animals were euthanized at fourth, eighth and twelfth week after starting treatment. Histological sections of the aorta in the second group showed the presence of histological changes in the aorta represented by the placement of the fat droplets in all layers of the aortic wall accompanied by the enlarged nuclei of the smooth muscle cells. It was observed that the intensity of histopathological changes increased in week 8 and even at 12 weeks despite of the treatment was interrupted. The proliferation of smooth muscle cells toward the endothelium was observed with endothelial cell enlargement. In the third group, after four and eight weeks, thickening of the aorta lining was found with the deposition of the fat droplets as well as elastic fibers degeneration. The fibers replaced by fat droplets in the middle layer. In the fourth group, no histopathological changes were observed for all periods. The micro morphometric measurements of the all groups presented a significant increment in aortic diameter at a level p≤ 0.05 when compared with the control group. [ABSTRACT FROM AUTHOR]

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BACKGROUND: Stanozolol and Nandrolone decanoate are the most commonly used hormones in canine medicine. They are mainly administered to strengthen the muscle, gain weight, treatment of anemia and stimulate the appetite. One of the effects of hormones is to enhance the erythropoietin production and eventually an increase in the number of RBCs. OBJECTIVES: Prolonged usage of hormones may be relevant to the liver and renal disorders; therefore, the present survey was aimed to evaluate the effects of stanozolol and nandrolone decanoate on liver and kidney indices, erythropoietin and testosterone serum concentrations and hematocrit changes in healthy dogs. METHODS: Sixteen dogs were randomly categorized in two groups of A (stanozolol) and B (nandrolone decanoate). Each group was divided into two subgroups (A1, A2 and B1, B2). The second testicle was removed on day 28 in the first subgroups (A1 and B1), and day 42 in the second subgroups (A2 and B2). The first testicle was removed at time zero. Stanozolol (50 mg per dog) was administered to all dogs of group A as IM once a week for six weeks. Group B was similar to group A with the difference that nandrolone decanoate was injected (1 mg/kg) instead of stanozolol. Blood samples were collected on days 0, 3, 14, 28 and 42. RESULTS: Erythropoietin and testosterone concentrations were virtually increased in both groups A (P<0.05) and B (P<0.05). The effect of stanozolol on erythropoietin (subgroup A1) (11.35±1.31 ng/mL) was significantly higher than nandrolone decanoate (subgroup B1) (8.02±0.55 ng/mL) (P<0.05); nevertheless, the changes in testosterone levels, was not significant between groups A and B (P>0.05). The liver enzymes of ALP, ALT and AST were increased more significantly in group A than group B (P<0.05). CONCLUSIONS: Erythropoietin and testosterone levels were virtually increased in both groups A and B; however, stanozolol had more significant effect than nandrolone decanoate in increment of erythropoietin; nevertheless, it had more side effects on liver indices. It is suggested that nandrolone decanoate to be administered for the therapeutic goals. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the clinical effect of different doses of recombinant human growth hormone (rhGH)combined with small dose of stanozolol in the treatment of non-growth hormone deficient dwarfism. METHODS: Totally 99 children with non-growth hormone deficient dwarfism admitted into the Affiliated Hospital of Hebei University from Jan. 2017 to Jan. 2018 were selected and divided into group A, group B and group C via random number table, with 33 cases in each group. Group A was treated with small dose of stanozolol, group B was given small dose of rhGH based on group A, while group C was given large dose of rhGH based on group A. The clinical efficacy after 1-year treatment, height (Ht) before and after treatment, growth velocity (GV), height standard deviations (HtSDS), increment of bone age (ΔBA), increment of height age (ΔHA), ΔHA/ ΔBA and incidences of adverse drug reactions were compared among three groups. RESULTS: The total effective rates of group A, group B and group C were respectively 69. 70% (23/33), 81. 82% (27/33) and 93. 94% (31/33), with statistically significant differences (P<0. 05). After treatment, the Ht, GV and HtSDS of three groups were significantly increased, those of group C were significantly higher than those of group B, and those of group B were significantly higher than those of group A, with statistically significant differences (P<0. 05). After treatment, there were no statistical significance in differences in ΔBA, ΔHA and ΔHA/ ΔBA among three groups (P>0. 05). During treatment, the incidences of adverse drug reactions of group A, group B and group C were respectively 6. 06% (2/33), 12. 12% (4/33) and 15. 15% (5/33), the differences among groups were not statistically significant(P>0. 05). CONCLUSIONS: The efficacy of rhGH combined with small dose of stanozolol in the treatment of non-growth hormone deficient dwarfism in children is remarkable, which can rapidly improve the GV and height of children, and the combination of large-dose rhGH with small-dose stanozolol is more effective. rhGH does not accelerate skeletal maturation, does not affect the growth potential, and has a good therapeutic safety. [ABSTRACT FROM AUTHOR]

Objective: Nowadays, the use of energetic substances has become a complex problem in sports, such that the role of anabolic-androgenic steroids is undeniable. This study aimed to investigate the antiapoptotic effect of resistance training and Tribulus terrestris in the heart tissue of rats exposed to stanozolol. Materials and Methods: 35 rats divided into 7 groups including (1) sham, (2) stanozolol-treated, (3) stanozolol+50 mg/kg Tribulus terrestris-treated, (4) stanozolol+100 mg/kg Tribulus terrestris-treated, (5) stanozolol+resistance training-treated, (6) stanozolol+resistance training+50 mg/kg Tribulus terrestris-treated, and (7) stanozolol+resistance training+100 mg/kg Tribulus terrestris-treated. During 8 weeks, groups 2-7 received 5 mg/kg stanozolol per day peritoneally; groups 5-7 performed resistance training for 3 sessions per week; and groups 3, 4, 6 and 7 received daily doses of Tribulus terrestris peritoneally. Results: Stanozolol administration significantly increased the BAX, BCL-2, P53, and caspase 3 and BAX/BCL- 2 ratio (P < .001). Resistance training, 100 mg/kg Tribulus terrestris administration, 50 mg/kg Tribulus terrestris administration, resistance training+100 mg/kg Tribulus terrestris administration, and resistance training+50 mg/kg Tribulus terrestris administration significantly decreased BAX, BCL-2, P53, and caspase 3 levels and BAX/BCL-2 ratio (P < .001); however, stanozolol+resistance training+100 mg/kg Tribulus terrestris administration caused more decrease than stanozolol+resistance training+50 mg/kg Tribulus terrestris administration in BAX (P < .001). Conclusion: Resistance training and Tribulus terrestris administration alone appear to have antiapoptotic effects; however, resistance training combined with Tribulus terrestris administration, especially at higher doses, have more desirable effects than resistance training or Tribulus terrestris administration alone on the apoptosis markers. [ABSTRACT FROM AUTHOR]

Options for anemic lower-risk myelodysplastic syndromes (MDS) without del(5q) after failure of erythropoiesis-stimulating agents (ESAs) are very limited. The effectiveness of second-line treatments is uncertain. We retrospectively reviewed the clinical effectiveness and overall survival (OS) of lower-risk MDS without del(5q) patients exclusively treated with stanozolol (STZ) after failure of epoetin alfa. The response was defined according to the 2006 International Working Group (IWG) criteria. Fifty-six patients were included. The median follow-up time was 55 months (range: 5-156 months). Twenty-seven patients (48.2%) achieved hematologic improvement-erythroid response (HI-E). Higher response rates were observed in patients with lower IPSS-R scores (≤3.5, P = 0.008) and hypocellular bone marrow (P = 0.002). In univariate Cox analysis, HI-E was the strongest factor associated with better OS (P = 0.0003). In multivariate Cox, HI-E, age ≤ 50, and transfusion independence (TI) at the onset of STZ were factors associated with better OS. The estimated 5-year OS was 88.6% (68.7-96.2%) and 33.8% (14.9-54.0%) in responders and non-responders (P < 0.01), respectively. The most common side effects included masculinization and liver damage, but they were manageable with supportive measures and dose adjustments. STZ may be considered an alternative treatment in lower-risk MDS after failure of epoetin alfa. [ABSTRACT FROM AUTHOR]

It is unknown whether adding stanozolol to decitabine for maintenance can further improve progression-free survival (PFS) and overall survival (OS) after effective decitabine treatment in patients with high-risk myelodysplastic syndrome (MDS). Patients newly diagnosed with high-risk MDS who achieved at least partial remission after 4 cycles of decitabine (20 mg/m2 days 1-5) were selected. In total, 62 patients (median age 66 years) were enrolled, of whom 21 were treated with stanozolol and decitabine for maintenance, and 41 were treated with decitabine alone. The median number of cycles for maintenance treatment was 6 (2-11) and 5 (2-12) for the stanozolol and control groups, respectively (p > 0.05). PFS in the stanozolol group was significantly longer than in the control group (15.0 vs 9.0 months, hazard ratio [HR] = 0.35, 95%CI: 0.19-0.63, p = 0.0005), whereas OS was not significantly prolonged in the stanozolol group (21.0 vs 15.0 months, HR = 0.73, 95%CI: 0.39-1.37, p = 0.33). The proportion of patients with severe neutropenia during maintenance treatment in the stanozolol group was lower than in the control group (76.2% vs 95.1%, p = 0.039). In conclusion, adding stanozolol to decitabine after effective decitabine treatment can prolong PFS and reduce the severity of neutropenia for patients with high-risk MDS. [ABSTRACT FROM AUTHOR]