In recent years, several important studies have shown that testosterone therapy is associated with an increased risk for heart attack, stroke, and even death, especially in older men.  Mainly, these studies have proposed, but not detailed, the biochemical mechanism by which increases in testosterone levels may pose these such risks, and this was not their aim.  Those studies, including the Vigen et al. (2013) report in Journal of the American Medical Association, the Finkel et al. (2014) report in PLoS One, and the  Xu et al. (2013) report in BMC Medicine, work to frame further research: we must first know that testosterone is linked to adverse cardiac events before we may determine how.

Scientists and doctors have found that testosterone therapy increases hemoglobin and hematocrit levels in the blood.  Hemoglobin is an iron-containing molecule in red blood cells that carries oxygen throughout the body, and hematocrit is the percent (by volume) of red blood cells in the blood.

Erythrocytosis, an elevation in red blood cell count, constitutes a serious clinical problem, and if a case becomes one of polycythaemia (highly elevated red blood cell count), can lead to thrombosis (blood clot) which in turn may cause heart attack or stroke. 

In 2013, Guo et al. published results of a study that aimed to determine how testosterone stimulates the production of red blood cells (“erythropoiesis”).  To do this, the team studied the process in mice, and concluded “testosterone inhibits hepcidin transcription through its interaction with BMP/Smad signaling” and that “Testosterone administration is associated with increased iron incorporation into red blood cells.”  To be clear, hepcidin is a hormone that regulates iron levels in the blood.  Without (as much) hepcidin, iron levels in the blood rise; more testosterone leads to more hemoglobin.

In 2014, Bachman et al. confirmed these results using human subjects and a double-blind, randomized placebo-controlled trial in which patients were given either testosterone gel or a placebo drug.  Results showed 7% increase in hemoglobin and 10% increased hematocrit levels among patients in the testosterone therapy group.  Unfortunately, the study stopped prematurely due to an increased rate of adverse cardiovascular events among study patients.

Further, a number of studies have demonstrated that a high hematocrit level is an independent risk factor for stroke.  The normal hematocrit level is between 40.7-50.3% for males.  The study found by following the above hyperlink determined that men whose hematocrit level is above 51% face a risk for stroke increased by more than 2.5 times.  With the Bachman 2014 study finding an increase in hematocrit levels of 10%, normal men using testosterone therapy may easily fall well above the normal range and face excess risk.  Another study showed that men with hematocrit levels above 46% faced a 1.5-fold increased risk for blood clot.  One proposed reason for this is that elevated hematocrit levels increase blood viscosity, thus raising the risk for thrombosis and stroke.

Another study, dubbed “The Framingham Study” linked high hematocrit levels with an increased risk for cardiovascular disease, myocardial infarction, angina pectoris, stroke, and Ischemic cardiomyopathy.

Testosterone Therapy Lawsuits

Due to the fact that the manufacturers of testosterone therapy products, such as AndroGel, have time and again failed to warn users of the risk for adverse cardiac events, stroke, and death, a number of AndroGel testosterone therapy lawsuits have been filed.  If you or a loved one used AndroGel and suffered one of the above-listed side effects, you may be entitled to significant financial compensation.

For a free, no-obligation case consultation, contact our team of AndroGel lawyers at the information provided below.  We have the experience, resources, and skills required to win the justice you deserve.

Call today and see how we can help.

(855) 452 – 5529

Our AndroGel Lawsuit Information page is a great place to start if you have any questions about AndroGel.