Primobolan depot vs masteron

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Pharmacies in Thailand continue to sell performance enhancing drugs, many of which are not regulated by the Thai food and drug administration (FDA) and/or do not appear in the Monthly Index of Medical Specialties (MIMS) drug information. This has attracted attention from the Thai police and the Department of Special Investigations (DSI) who conduct routine inspections for unlicensed and counterfeit medicines that arrive through unauthorized distribution channels produced in underground labs (UGL). Nonetheless, supply and demand remains strong.

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The most serious complication of anabolic steroid use is the development of hepatic tumors, either adenoma or hepatocellular carcinoma. The hepatic tumors arise in patients on long term androgenic steroids, usually during therapy of aplastic anemia or hypogonadism, but occasionally in athletes or body builders using anabolic steroids illicitly. Tumors are typically found after 5 to 15 years of use, but onset within 2 years of starting therapy with testerosterone esters has been described. Many of the case reports have occurred in patients with other risk factors for cancer, such as Fanconi?s syndrome, iron overload or chronic hepatitis C (from blood transfusions). However, hepatic adenomas and hepatocellular carcinoma have also been described in patients taking androgenic steroids who have no other evidence of liver disease and normal histology in the nontumor parts of the liver. The pathology of the tumors is usually hepatic adenoma or ?well differentiated? hepatocellular carcinoma or hepatic adenoma with areas of malignant transformation. Rare instances of cholangiocarcinoma and angiosarcoma have also been described in patients on long term androgenic steroids. Clinical presentation is generally with right upper quadrant discomfort and a hepatic mass found clinically or on imaging studies. Routine liver tests are often normal unless there is extensive spread or rupture or an accompanying liver disease. Alphafetoprotein levels are usually normal. There is often (but not always) spontaneous regression in the tumor when the anabolic steroids are stopped. Hepatocellular carcinoma arising during anabolic steroid therapy is believed to have a better prognosis than that related to cirrhosis or chronic hepatitis B and C; however, deaths from hepatic rupture or tumor spread and metastasis have been reported in patients with anabolic steroid related hepatocellular carcinoma without cirrhosis.

Masteron will significantly suppress natural testosterone production making exogenous testosterone therapy important when using this steroid. Failure to include exogenous testosterone will lead most men to a low testosterone condition, which not only comes with numerous possible symptoms but is also extremely unhealthy.

As most will use Masteron in a cutting cycle, it’s very common not to want to use a lot of testosterone due to the high levels of estrogenic activity it can provide. If this is the case, you will find a low dose of 100-200mg per week of testosterone to be enough to combat suppression and give you the needed testosterone.

Once Masteron is discontinued and all exogenous steroidal hormones have cleared your system, natural testosterone production will begin again. Prior levels will not return to normal over night, this will take several months. Due to the slow recovery, Post Cycle Therapy (PCT) plans are often recommended. This will speed up the recovery greatly; however, it won’t bring your levels back to their peak, this will still take time. A PCT plan will ensure you have enough testosterone for proper bodily function while your levels continue to naturally rise and significantly cut down on the total recovery time. This natural recovery does assume no prior low testosterone condition existed. It also assumes no damage was done to the Hypothalamic-Pituitary-Testicular-Axis (HPTA) through improper supplementation practices.
 

Primobolan depot vs masteron

primobolan depot vs masteron

The most serious complication of anabolic steroid use is the development of hepatic tumors, either adenoma or hepatocellular carcinoma. The hepatic tumors arise in patients on long term androgenic steroids, usually during therapy of aplastic anemia or hypogonadism, but occasionally in athletes or body builders using anabolic steroids illicitly. Tumors are typically found after 5 to 15 years of use, but onset within 2 years of starting therapy with testerosterone esters has been described. Many of the case reports have occurred in patients with other risk factors for cancer, such as Fanconi?s syndrome, iron overload or chronic hepatitis C (from blood transfusions). However, hepatic adenomas and hepatocellular carcinoma have also been described in patients taking androgenic steroids who have no other evidence of liver disease and normal histology in the nontumor parts of the liver. The pathology of the tumors is usually hepatic adenoma or ?well differentiated? hepatocellular carcinoma or hepatic adenoma with areas of malignant transformation. Rare instances of cholangiocarcinoma and angiosarcoma have also been described in patients on long term androgenic steroids. Clinical presentation is generally with right upper quadrant discomfort and a hepatic mass found clinically or on imaging studies. Routine liver tests are often normal unless there is extensive spread or rupture or an accompanying liver disease. Alphafetoprotein levels are usually normal. There is often (but not always) spontaneous regression in the tumor when the anabolic steroids are stopped. Hepatocellular carcinoma arising during anabolic steroid therapy is believed to have a better prognosis than that related to cirrhosis or chronic hepatitis B and C; however, deaths from hepatic rupture or tumor spread and metastasis have been reported in patients with anabolic steroid related hepatocellular carcinoma without cirrhosis.

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