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That's why beta blockers sometimes lead to psoriasis
Drugs with the beta blocker class of drugs lower the heart's resting frequency and blood pressure. For this reason, they are often used to treat high blood pressure, irregular heartbeat and coronary artery disease. In some patients, however, these active substances trigger severe inflammatory reactions in the skin, for example in the form of psoriasis. Why this side effect occurs has so far been unclear. A German research team has now been able to decipher the connection.
Researchers at the University of Bonn and the Free University of Berlin were able to identify the causes of a known side effect of hypertension medication with the beta blocker class of active substances. The team found that certain beta blockers interfere with the breakdown of broken cell debris. This leads to the release of messenger substances, which then trigger an inflammatory reaction of the skin. The results were recently presented in the specialist journal "Autophagy".
Focus on propranolol
The research team led by Professor Dr. Günther Weindl took a closer look at the active ingredient propranolol. The active ingredient belonging to the beta blockers is important for the treatment of high blood pressure and other heart diseases. "Propranolol is fat-soluble and at the same time slightly alkaline," explains Professor Weindl. The experiments with cell cultures suggest that these two properties are responsible for the unwanted side effect.
In the cul-de-sac
As the expert reports, thanks to its fat solubility, the active ingredient can cross biomembranes. If it gets into acidic environments, propranolol has a positive charge due to its slightly alkaline pH. After charging, however, the active ingredient loses its ability to cross membranes and is stuck.
Recycling stations in the cells
Cells use a specific recycling process called autophagy. In the broadest sense, this process works like a trash can. Cells use certain bubbles from biomembranes in which they dispose of defective proteins and other cell components. This vesicle then melts into a special membrane bag called a lysosome. There the contents of the “garbage can” are collected, disassembled and converted into reusable building blocks, which are then released to the cells.
Propranolol interferes with cell recycling
As the researchers found, the active ingredient propranolol interferes with the natural process of autophagy. If an alkaline propranolol molecule gets through the membrane into a lysosome, it charges positively because the environment inside the lysosomes is acidic. As a result, the molecule is trapped inside the recycling station. Over time, more and more active substances accumulate in the lysosome, which increasingly disrupts the process. "As a result, inflammatory messengers are released, especially the so-called interleukin-23, which is mainly secreted by immune cells," explains the professor. One consequence of this is the observed skin problems.
Not all beta blockers trigger this effect
This newly discovered mechanism still needs to be examined in more studies. Nevertheless, the scientists believe it is likely that this side effect can only occur in connection with fat-soluble beta blockers. Within the active ingredient group of beta blockers, there are also substances that are less dependent on membranes. "The interleukin-23 release was significantly lower with such substances than after the propranolol administration", sums up Weindl. So far, however, this has only been tested on cell cultures and has yet to be verified in living organisms.
Disrupted autophagy as a cause of disease
Research into autophagy is a high priority in today's science. Connections between an impaired autophagy and serious diseases such as dementia, inflammatory bowel diseases and diabetes are also suspected. (vb)
Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
Graduate editor (FH) Volker Blasek
- University of Bonn: Why beta-blockers cause skin inflammation (accessed: November 1st, 2019), uni-bonn.de
- Gerrit Müller, Charlotte Lübow, Günther Weindl: Lysosomotropic beta blockers induce oxidative stress and IL23A production in Langerhans cells, Autophagy, 2019, tandfonline.com