Therefore, a lack of testosterone would alter this metabolic process, leading to a decrease in muscle mass.Signs and symptoms of testicular atrophy that are due to a secondary medical condition include:

inflammation
fever
sensitivity or pain of the testicle(s)
nauseaSecondary medical conditions that may cause the signs and symptoms listed above include testicular cancer, chronic alcohol use, sexually transmitted infections, COVID-19, orchitis, varicoceles, or torsion of the testes. Causes
Age
Shrinkage of the testicles is common with advanced age, as overall reproductive function declines. Alcohol use
High alcohol usage lowers testosterone levels by direct damage to the Leydig cells (which produce testosterone) and by affecting hormones involved in signaling to the Leydig cells to produce testosterone. As a result, testicular atrophy is a common feature among individuals with high alcohol use. Testicular malformations and low testosterone levels is also commonly found in people with alcoholic cirrhosis as the negative effect of alcohol use is worsened by the liver damage itself. Excessive alcohol intake can cause inflammation and the degradation of cells in the liver, which can then cause testicular abnormalities (including testicular atrophy). Anabolic steroid use and hormone therapy
Anabolic steroid use and testosterone replacement therapy (TRT) have been found to cause testicular atrophy through similar mechanisms. Anabolic steroids and TRT are both used (either by prescription or illicitly) to mimic the effects of testosterone produced by the body, such as building muscle and maintaining sex drive.
Individuals can get genetic testing done to see if they are a carrier of the trait, and if so may choose to complete genetic counseling to better understand the disorder and help manage family planning. Parents can choose to do prenatal genetic testing for the disorder to determine if their child will have the disease. The only risk factor is if both parents of a child carry the recessive allele linked to the disorder. Mechanism
Individuals with the disorder have a mutation to their fibrinogen gene that prevents the formation of the protein. In normal conditions, fibrinogen is converted to fibrin when it is cleaved by the enzyme thrombin in the blood. The newly formed fibrin forms a fiber-rich network that helps trap red blood cells to start the coagulation process and form a clot. Since there is no fibrinogen present during afibrinogenemia, fibrin can not be formed to aid in this process. Diagnosis
Diagnostic tests
When a problem of fibrinogen is suspected, the following tests can be ordered:

PT
PTT
Fibrinogen level in blood (total and clottable)
Reptilase time
Thrombin timeBlood fibrinogen levels of less than 0.1 g/L and prolonged bleeding test times are indicators of an individual having afibrinogenemia.A suspicion of congenital afibrinogenemia may appear on a platelet aggregation function test. Treatment
The most common treatment is fibrinogen replacement therapy, including cryoprecipitate, blood plasma, and fibrinogen concentration transfusions to help with bleeding episodes or prior to surgery. Although some thrombotic complications have been reported following replacement theory, transfusions of fibrinogen concentrate are widely considered to be the most beneficial.