Effect of the treatment of iron deficiency anemia on chronic drug-resistant cough: a rare case report.

BACKGROUND: A persistent difficult-to-treat cough can be exhausting. Iron is an essential element that plays an important role in regulating the production of pro-inflammatory cytokines, and its deficiency may potentiate airway inflammation and dysfunction. There is a paucity of data regarding a link between iron deficiency (ID) and idiopathic cough. OBJECTIVES: In this study, a case of persistent non-productive cough, which was unresponsive to targeted treatment approaches but responsive to iron therapy, is reported. METHODS: A 53-year-old woman came to a medical clinic with complaints of a chronic and progressive non-productive cough. She underwent a complete clinical and paraclinical evaluation. RESULTS: Her vital signs were stable and no abnormalities were found on the physical examination. The results of the spirometry and chest radiography were unremarkable. The laboratory test indicated hypochromic microcytic anemia, with a hemoglobin value of 9.6 g/dL. Her cough was resolved after treatment of iron-deficiency anemia with an oral nutraceutical capsule containing 28 mg of elemental iron (as ferrous bis-glycinate) plus folic acid, vitamin B12, and vitamin C, once daily for six months. CONCLUSION: In the case of unexplained chronic cough, resistant to targeted therapies, investigation and treatment of ID may contribute to the resolution of cough.

Targeting Mitochondrial and Brain Injury Markers in Acquired Brain Injuries: A Randomized, Double-Blind, Placebo-Controlled Study with Melatonin.

Purpose: Oxidative stress-induced mitochondrial damage is the main event in acquired brain injuries (ABI). This study aimed to evaluate the effects of melatonin, a mitochondria-targeted antioxidant, on mitochondrial and brain injury markers, and the clinical outcomes of patients with ABI. Methods: In this randomized controlled trial, intensive care unit (ICU) or neurology patients with ABI (n=60) received melatonin (21 mg/day) or placebo tablets, within the first 72 hours of injury onset for five days. As a primary endpoint, serum levels of malondialdehyde (MDA), S100B and C-reactive protein (CRP) were compared at baseline, and after five days' intervention. Secondary endpoints included assessment of Glasgow Coma Scale and Sequential Organ Failure Assessment (at the end of day 5), Rancho Los Amigos Revised Scale and modified Rankin Scale (at the end of month 3), the duration of mechanical ventilation, the lengths of ICU and hospital stays, and in-hospital and three-month mortality. Results: There were no significant effects of melatonin on the primary and secondary outcomes. However, the subgroup analysis showed a significant reduction in S100B in patients with non-traumatic brain injuries, receiving melatonin versus placebo (p: 0.016). Conclusion: This study showed that melatonin supplementation in the early phase of brain injury had no significant effects on the injury markers and clinical outcomes of patients with ABI. However, it reduced the level of S100B in the non-traumatic subgroup. Further larger-scale studies are needed to determine the effects of melatonin on the ABI and its subgroups.

Oxidative stress and mitochondrial dysfunction following traumatic brain injury: From mechanistic view to targeted therapeutic opportunities.

Traumatic brain injury (TBI) is one of the most prevalent causes of permanent physical and cognitive disabilities. TBI pathology results from primary insults and a multi-mechanistic biochemical process, termed as secondary brain injury. Currently, there are no pharmacological agents for definitive treatment of patients with TBI. This article is presented with the purpose of reviewing molecular mechanisms of TBI pathology, as well as potential strategies and agents against pathological pathways. In this review article, materials were obtained by searching PubMed, Scopus, Elsevier, Web of Science, and Google Scholar. This search was considered without time limitation. Evidence indicates that oxidative stress and mitochondrial dysfunction are two key mediators of the secondary injury cascade in TBI pathology. TBI-induced oxidative damage results in the structural and functional impairments of cellular and subcellular components, such as mitochondria. Impairments of mitochondrial electron transfer chain and mitochondrial membrane potential result in a vicious cycle of free radical formation and cell apoptosis. The results of some preclinical and clinical studies, evaluating mitochondria-targeted therapies, such as mitochondria-targeted antioxidants and compounds with pleiotropic effects after TBI, are promising. As a proposed strategy in recent years, mitochondria-targeted multipotential therapy is a new hope, waiting to be confirmed. Moreover, based on the available findings, biologics, such as stem cell-based therapy and transplantation of mitochondria are novel potential strategies for the treatment of TBI; however, more studies are needed to clearly confirm the safety and efficacy of these strategies.

Has vitamin E any shreds of evidence in cisplatin-induced toxicity.

Cisplatin is one of the highly consumed and effective antitumor agents whose clinical application is accompanied by nephrotoxicity adverse reaction. Also, other complications such as ototoxicity and hepatotoxicity are a matter of concern. Today, it is suggested that cisplatin-associated toxicities are mainly induced by free radicals production, which will result in oxidative organ injury. The evidence is growing over the protective effects of antioxidants on cisplatin-induced adverse reactions especially nephrotoxicity. The possible protective effects of vitamin E and its derivative in cisplatin-induced nephrotoxicity and ototoxicity are reviewed here at the light of pertinent results from basic and clinical research. Administration of vitamin E alone or in combination with other antioxidant agents could cause amelioration in oxidative stress biomarkers such as decreasing the level of malondialdehyde, reducing serum urea and creatinine, and also enhancing the activities of renal antioxidant enzymes including renal catalase, glutathione-S-transferase, and superoxide dismutase. Although the data from most of the studies are in favors of protective effects of vitamin E against cisplatin-induced toxicity, more clinical trials are needed to clarify the clinical importance of vitamin E administration as an antioxidant during cisplatin therapy in cancer condition.