Lupus vulgaris reported in 2 cases

Department of Dermatovenerology, State University of Medicine and Pharmacy "Nicolae Testemitanu", Chișinău, Republic of Moldova, Congresul consacrat aniversării a 75-a de la fondarea Universității de Stat de Medicină și Farmacie „Nicolae Testemițanu” din Republica Moldova, Ziua internațională a științei pentru pace și dezvoltareIntroduction: Cutaneous tuberculosis is a group of polymorphous and varied manifestations of the skin and mucous membranes, produced by infection with some species of Mycobacterium tuberculosis complex. The specific primary lesion is the lupoma, sometimes evolving into mutilating forms. Purpose: Lupus vulgaris particularities reported in two clinical cases. Material and methods: A 68-year-old female, presented for multiple infiltrative, prominent erythematous plaques and placards with various diameter, well contoured by a violaceus halo, with irregular contour on the trunk. A 6-year-old boy presented for brownish-red, soft papules with smooth surface on the face and trunk. The lesions appeared 3 years ago; and 6 months ago after a minor trauma injury, the lesions have spread. Results: Chest X-ray didn’t reveal any abnormalities. During dermascopy the sign of “apple jelly” was found positive. Histopathological exam found caseous necrosis, tuberculoid granulomas composed of epithelioid cells and Langhans giant cells, surrounded by mononuclear and a dense lymphocyte infiltrate localized in the dermis. Mantoux probe was 17 mm in diameter. Clinical examination sustained by the histopathological exam and Mantoux probe inferred the diagnosis of lupus vulgaris (tuberculosis). Conclusions: The particularities of the presented cases with distinct clinical signs, the histopathological presence of granulomatous inflammation with specific cellular appearance, the hyperergic Mantoux test and the lack of characteristic pulmonary changes represent a casuistic interest of lupus vulgaris

Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed

Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature

Mitochondrial Effects of Common Cardiovascular Medications : The Good, the Bad and the Mixed

Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature

Cell‐permeable succinate rescues mitochondrial respiration in cellular models of amiodarone toxicity

Amiodarone is a potent antiarrhythmic drug and displays substantial liver toxicity in hu-mans. It has previously been demonstrated that amiodarone and its metabolite (desethylamioda-rone, DEA) can inhibit mitochondrial function, particularly complexes I (CI) and II (CII) of the elec-tron transport system in various animal tissues and cell types. The present study, performed in human peripheral blood cells, and one liver‐derived human cell line, is primarily aimed at assessing the concentration‐dependent effects of these drugs on mitochondrial function (respiration and cellular ATP levels). Furthermore, we explore the efficacy of a novel cell‐permeable succinate prodrug in alleviating the drug‐induced acute mitochondrial dysfunction. Amiodarone and DEA elicit a con-centration‐dependent impairment of mitochondrial respiration in both intact and permeabilized platelets via the inhibition of both CI‐ and CII‐supported respiration. The inhibitory effect seen in human platelets is also confirmed in mononuclear cells (PBMCs) and HepG2 cells. Additionally, amiodarone elicits a severe concentration‐dependent ATP depletion in PBMCs, which cannot be explained solely by mitochondrial inhibition. The succinate prodrug NV118 alleviates the respiratory deficit in platelets and HepG2 cells acutely exposed to amiodarone. In conclusion, amiodarone severely inhibits metabolism in primary human mitochondria, which can be counteracted by in-creasing mitochondrial function using intracellular delivery of succinate