COVID-19 interactions with angiotensin-converting enzyme 2 (ACE2) and the kinin system; looking at a potential treatment

The novel coronavirus disease 2019 (COVID-19) is a rapidly expanding infection around the world. The world Health Organization (WHO) in March 2020 announced the Coronavirus pandemic. This infection causes many deaths on daily basis. Therapeutic options are currently limited. It is revealed that COVID-19 binds to human angiotensin-converting enzyme 2 (ACE2) to enter the host cells. One of the activities of ACE2 is hydrolyzing the active bradykinin metabolite [des-Arg973] BK (DABK). A decreased activity or reducing expression of ACE2 by the virus impairs the inactivation of DABK. This enhances its signaling through the bradykinin B1 receptor (BKB1R) and could lead to fluid extravasation and leukocyte recruitment to the lung. Targeting the bradykinin system by either blocking the bradykinin production or blocking bradykinin receptors may open a new potential therapeutic window for the treatment of COVID-19 induced acute respiratory distress syndrome (ARDS) particularly before patients enter the irreversible stages

The footprint of androgen sensitive serine protease (TMPRSS2) in gender mortality with COVID-19

Male gender is an obvious risk factor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and mortality rate is higher in men than women. Undoubtedly, gender-related behavioral factors, such as higher amounts of smoking, alcohol consumption, and biological differences in immune systems could make males more vulnerable. The role of androgen-responsive elements (AREs) of transmembrane serine proteases type II (TMPRSS2) gene as one of the major players of male dominancy in severe COVID-19 infection has been under appreciated and needs to be clarified

Bullous fixed drug eruption following ibuprofen ingestion

Fixed drug eruption (FDE) is a drug reaction involving skin and less commonly mucosal membranes. The common manifestation is localized well-demarcated patches or plaques appeared following receiving of a culprit drug. When re-exposure occurs, the rashes will appear at areas involved in previous episodes. Limited reports on bullous FDE due to ibuprofen have been documented before. Herein, we described an elderly man who experienced multifocal lesions in his oral mucosa, penis, and multiple sites of skin following ibuprofen ingestion confirmed as FDE by pathological studies. The culprit drug had been discontinued. Systemic and topical glucocorticoids as well as supportive care had been instituted. The patient's outcome was favorable and his lesions had been recovered within the next weeks. Patient's follow-up showed that he had received ibuprofen again sometime later resulting in anal mucosal lesion and similar penile involvement. In routine clinical practice, mucocutaneous adverse drug reactions should be considered. A high index of suspicion, the detailed medication history, the course of the symptoms, and distributing pattern of the lesions are essential clues for the diagnosis. However, judicious and prompt pathological studies can help to differentiate multifocal bullous FDE from major skin drug reactions such as Stevens–Johnson syndrome/toxic epidermal necrolysis