Tinnitus can cause extreme morbidity. Despite many attempts to fi nd a treatment for idiopathic cases, they remain diffi cult to manage. Because nerve injury is one of the suspected etiologies of tinnitus and because gabapentin has been found to be eff ective in treating nerve injuries, some authors have attempted to determine if gabapentin has a role in treating tinnitus. Although gabapentin was found to be ineff ective for tinnitus in these previous studies, to the best of our knowledge no studies have been performed that took into consideration the presence of various accompanying factors and concomitant diseases that might infl uence its eff ect. We conducted a prospective, randomized, double-blind, placebo-controlled clinical trial of gabapentin for idiopathic tinnitus. We treated 40 patients with gabapentin and measured its eff ectiveness by comparing diff erences between pre-and post-treatment Tinnitus Severity Index (TSI) values and tinnitus loudness scores. We also compared these outcomes with those of a group of 40 matched placebo controls. At study's end, we found no signifi cant diff erences between the gabapentin and control groups in mean decreases in TSI value and loudness score (p = 0.85 and p = 0.12, respectively). However, we did fi nd that patients with hypertension, diabetes, and/or dyslipidemia showed a better response to gabapentin than did those with tinnitus alone (p = 0.01). We conclude that although there was no statistically signifi cant diff erence between gabapentin and placebo in treating isolated tinnitus or tinnitus overall, patients with concomitant hypertension, diabetes, and/or dyslipidemia may benefi t from gabapentin.
IntroductionCopper (Cu) and zinc (Zn) are important trace elements that are also structural ions of superoxide dismutase (SOD), which reduce oxidative stress. Zinc deficiency and excess copper have been reported to be associated with inflammation. The human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus, which is believed to cause systemic inflammation. The aim of this study is to measure levels of Zn, Cu, SOD, and prooxidant–antioxidant balance (PAB) in HTLV-1-positive patients and investigate the association between serum Zn and Cu concentrations and levels of oxidative stress in them.MethodsThe serum samples of 1,116 subjects who had participated in the “Mashhad Stroke and Heart Atherosclerotic Disorder” study, including 279 HTLV-1-positive and 837 HTLV-1-negative patients, were used. Levels of Zn, Cu, SOD, and PAB were measured.ResultsZinc and SOD levels were lower in the HTLV-1-positive group; however, the difference was statistically significant only for the level of SOD (P=0.003). On the other hand, levels of copper and PAB were significantly higher in HTLV-1 positive subjects; P=0.004 and P=0.002, respectively.ConclusionIn HTLV-infected patients, serum Zn concentration is lower and Cu concentration is higher than healthy controls. This altered situation might be either primary or secondary to HTLV-1 infection, which should be investigated in larger studies. We showed that SOD is significantly lower in HTLV-1-infected subjects. As in some other viruses that evolve different mechanisms to potentiate virus replication by changing the physiologic condition of host cells, HTLV-1 too probably decreases the activity of copper–zinc SOD1 by suppressing its gene.
Osteoarthritis (OA) is a progressive joint disease. The etiology of OA is considered to be multifactorial. Currently, there is no definitive treatment for OA, and the existing treatments are not very effective. Hypercholesterolemia is considered a novel risk factor for the development of OA. Statins act as a competitive inhibitor of the β‐hydroxy β‐methylglutaryl‐CoA (HMG‐CoA) reductase and are widely used to manage hypercholesterolemia. Inhibition of HMG‐CoA reductase results in reduced synthesis of a metabolite named mevalonate, thereby reducing cholesterol biosynthesis in subsequent steps. By this mechanism, statins such as atorvastatin and simvastatin could potentially have a preventive impact on joint cartilage experiencing osteoarthritic deterioration by reducing serum cholesterol levels. Atorvastatin can protect cartilage degradation following interleukin‐1β‐stimulation. Atorvastatin stimulates the STAT1‐caspase‐3 signaling pathway that was shown to be responsible for its anti‐inflammatory effects on the knee joint. Simvastatin had chondroprotective effects on OA in vitro by reducing matrix metalloproteinases expression patterns. In this study, we tried to review the therapeutic effects of statins on OA.
High-density lipoprotein (HDL) is thought to be protective against cardiovascular disease (CVD), and HDL dysfunction is considered to be a risk factor for CVD. It is unclear whether there is an association between Human T lymphotropic virus type 1 (HTLV1) infection and CVD risk. We have assessed HDL lipid peroxidation (HDLox) as a marker of HDL dysfunction and CVD risk in a subgroup of the MASHAD cohort study. One hundred and sixty two individuals including 50 subjects positive for HTLV1 infection and 112 individuals negative for HTLV1 infection were recruited. Anthropometric and biochemical parameters including serum hs-CRP, fasted lipid profile (HDL-C, LDL, triglycerides, and cholesterol), and fasting blood glucose were determined. Serum HDLox was also measured in the study participants. Multivariate analyses were used to evaluate the association between serum HDLox and HTLV1 infection. None of the traditional CVD risk factors were associated with HTLV1 infection, including serum HDL-C. However, serum HDLox was independently associated with the presence of HTLV1 infection. Logistic regression analysis showed that subjects who were positive for HTLV1 infection were also significantly more likely than uninfected individuals to have higher HDLox (odds ratio 9.35, 95%CI: 3.5–24.7; P < 0.001). HDLox was increased approximately 20% (P < 0.001) in infected subjects compared to the uninfected group. Serum HDLox is a marker of CVD risk factor and increased in individuals affected by HTLV1 infection compared to healthy subjects.
Background: Herpes simplex viruses have been implicated as a cause of cardiovascular disease (CVD) due to their widespread distribution and ability to infect human vascular endothelial cells. Objectives: The present study aimed to evaluate the link between Herpes simplex infections and cardiovascular disease. Methods: This case-control study involved 236 patients aged 35 - 65, 118 with known cardiovascular disease and 118 controls. Patients’ cardiovascular disease evaluation was based on data from questionnaires, a specialist’s physical examinations, and paraclinical tests. Herpes simplex viruses (HSV)-antibodies (IgM, IgG) were determined using ELISA in serum samples, and the biochemical blood indicators were analyzed to examine their relationship to the level of HSV antibodies. All the data were analyzed using SPSS software version 20. Results: IgM antibodies against herpes simplex were negative among all 236 patients. The positivity rate of IgG antibodies against herpes simplex was 58.8 and 51.2% in the case and control groups, respectively with no significant difference (P = 0.253). Patients with cardiovascular disease had a 0.587-fold higher positive rate of IgG antibodies than patients in the control group (odds ratio (OR) = 0.587). The mean age of patients with positive IgG antibodies was significantly lower than patients with negative IgG antibodies (P = 0.012). IgG positivity among men and women (P = 0.670) and different job statuses (P = 0.866) were not significantly different. Conclusions: The positivity rate of IgG antibodies against herpes simplex was not significantly different among the study groups. Although patients with positive IgG antibodies’ mean age was lower than those with negative IgG antibodies, the gender and job status were not different.
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