Infection with H. pylori is an up growing public health problem that affects approximately 50% of people in industrialized nations, and up to 80% in developing countries.Helicobacter pylori (H. pylori) infection had been identified as the main causes of peptic ulcer disease (PUD). Blood group A phenotype was associated with gastric ulcer (GU) and gastric carcinoma, while blood group O phenotype found to be associated with duodenal ulcer DU predominantly; however, no explanation for this association was received. This study was conducted to, first, determine the relationship between ABO blood groups and H. pylori infection in peptic ulcer patients, and second, to study the response to the two weeks H. pylori eradication triple therapy in peptic ulcer patients carrying different blood groups. A total of 84 patients who presented with symptoms of PUD and showed positive endoscopic examination of PUD a n d evidence of H. pylori i nfec tion by histology and stool antigen test, were divided into four groups according to ABO blood group phenotype. All H. pylori infected patients received s t a n d a r d H. pylori eradication triple therapy for 14 days duration. Patients were followed up by re-endoscopic examination after 2 months of treatment course. The percentage of H. pylori infection in patients with peptic ulcer disease carrying blood group O was higher than other blood group phenotype. In H.pylori-detnefni peptic ulcer stfdnefp , higher incidence of gastric ulcer (GU) was noticed among blood group A carriers, while higher incidence of duodenal ulcer (DU) was found among blood group O carriers when compare with other blood group phenotypes. neetfnne days triple therapy showed lower eradication rate in H. pylori infected blood group O peptic ulcer patients, while a higher response to the s t a n d a r d H. pylori eradication triple therapy was found among patients with blood group B phenotype.
Objective: This study aimed to examine the pathological changes in gastric mucosa of Helicobacter pylori-infected peptic ulcer patients carrying different ABO phenotypes and to study the response to the 14 days' standard triple therapy and 10 days' quadruple therapy in peptic ulcer patients according to their ABO phenotypes. Methods:Interventional prospective randomized-controlled open-label study was performed on newly diagnosed patients with PUD. The H. pyloripositive patients were allocated into two major study groups in which they are subdivided according to ABO blood group phenotypes: Group 1 received standard H. pylori eradication triple therapy and Group 2 received standard H. pylori eradication quadruple regimen. Patients were monitored after 2 months for successful H. pylori eradication.Results: Chronic active gastritis was significantly high in patients carrying blood Group O phenotype (81.25%), while the atrophic gastritis and intestinal metaplasia were significantly high in patients carrying blood Group A phenotype (25.00% and 16.67%), respectively. 14 days' triple therapy showed significantly lower eradication rate in H. pylori-infected peptic ulcer patients carrying blood Group O phenotype (p<0.01), meanwhile higher response was found among patients with blood Group B. 10 days' quadruple therapy produced a significant high eradication rate in H. pylori-infected patients carrying blood Group O than those with blood Group A (p<0.01), but still both showed lower response compared to that in patients carrying blood Group B and AB phenotypes. Elderly patients showed significantly less healing efficacy than younger patients (p<0.01), and the least healing rate was noticed in female patients after both regimens. Conclusion:Lower eradication rate in H. pylori-infected was noticed in peptic ulcer patients carrying blood Group O mainly than those with other blood groups and particularly those with duodenal Ulceri. 10 days' quadruple therapy showed significant higher eradication rate in H. pylori infection and a better ulcer healing efficacy.
Nrf2 is active protein presents in the cytoplasm in the cells of the body. In the presence of an activators, Nrf2 can enter the nucleus which bind to Antioxidant Responses Elements (ARE) or otherwise named human ARE (hARE) which control the whole antioxidants activity in human cell. Many factors may contribute to defective or overwhelmed cellular antioxidants activities for instances aging and cellular damages. These cellular damages can be produced by free radicals or oxidative stress. In the mechanism, if Nrf2 activated in the nucleus, can caused the production of collaborative antioxidants enzymes especially: catalase, glutathione (GLT) and superoxide dismutase (SOD) as a responsible for detoxification of free radical inside the cells.
Methotrexate is a chemotherapeutic and immunosuppressive drug used in the treatment of cancer, psoriasis, rheumatoid arthritis and several other disorders. Its use predisposes to hepatotoxicity which is a serious side effect. The current study aimed to assess the oxidative-stress-causing potential of methotrexate to liver cells and evaluate the hepatoprotective activity of the potent antioxidant astaxanthin, by affecting the oxidative stress biomarkers GSH (glutathione), SOD (superoxide dismutase), CAT (catalase) and MDA (malondialdehyde). A model of methotrexate-induced liver toxicity was employed on male rats. Thirty-six rats were divided into six groups; a negative control group, methotrexate induction group given (20 mg/kg) I.P. on day 13, three groups pretreated with oral astaxanthin in ascending doses (50, 75 and 100 mg/kg) for 14 days before methotrexate, and a conventional therapy group pretreated with silymarin (200mg/kg). The use of methotrexate significantly decreased liver tissue GSH, SOD and CAT while significantly increasing MDA, compared to the negative control. On the other side, astaxanthin used in all three doses significantly normalized these biomarkers. This study revealed that since astaxanthin significantly increased GSH, SOD and CAT while decreasing MDA that minimizes oxidative stress, it could be used as pretreatment in patients treated with methotrexate to decrease its hepatotoxicity.
Methotrexate is used in the treatment of cancer, psoriasis, rheumatoid arthritis and several other disorders. It has a hepatotoxic potential side effect. Patients who have no access to alternative medications face a serious challenge as a result. The current study aimed to assess the apoptotic potential of methotrexate on liver cells and evaluate the hepatoprotective activity of the potent antioxidant astaxanthin, by downregulation of apoptotic biomarkers caspase 9 and caspase 3. A model of methotrexate-induced liver toxicity was employed on male rats. Thirty-six rats were divided into six groups; a negative control group, methotrexate induction group given (20 mg/kg) on day 13, three groups pretreated with astaxanthin in ascending doses (50, 75 and 100 mg/kg) for 14 days before methotrexate, and a conventional therapy group pretreated with silymarin (200mg/kg). The use of methotrexate significantly increased liver tissue caspase 9 and caspase 3 compared to the negative control. On the other side, astaxanthin used in all three doses significantly normalized these biomarkers. This study revealed that since astaxanthin significantly decreased caspase 9 and caspase 3 that are involved in the apoptotic pathway, it could be used as pretreatment in patients treated with methotrexate to alleviate its hepatotoxicity.
Background: Osteoarthritis (OA) is a degenerative joint disease caused by gradual loss of cartilage. Telmisartan is an angiotensin II receptor antagonist, and act as a partial agonist on the nuclear peroxisome proliferator-activated receptor-gamma (PPAR-γ), that has been reported to exert anti-inflammatory effects. Objective: To evaluate the potential anti-inflammatory effect of telmisartan in patients with knee OA. Methods: Forty-two patients with painful knee OA were allocated into 2 groups, group (1): patients treated with naproxen tablets (500 mg/12 hr), telmisartan tablets (40 mg/day) and omeprazole (20 mg/day) for 3 months, while group (2): patients treated with naproxen tablets (500 mg/12 hr) and omeprazole (20 mg/day) for 3 months. The serum levels of IL-1β, high-sensitivity C-reactive protein (hs-CRP), TNF-α and erythrocyte sedimentation rate (ESR) were measured before and after 3 months of treatment. Results: Telmisartan when used in combination with naproxen resulted in significant decrease in serum levels of IL-1β and hs-CRP, higher than that produced by naproxen when used alone. The mean TNF-α level and ESR was decreased non-significantly in both study groups. Conclusion: Administration of telmisartan as an adjuvant therapy to naproxen in knee OA patients produced a significant decrease in the serum levels of IL-1β and hs-CRP, though no clear effect on TNF-α and ESR was noticed after 3 months treatment. Accordingly, many promising preventive strategies emerged from the available results since telmisartan relatively reduce the inflammatory burden in OA patients. The dose and duration of telmisartan treatment in this study did not indicate a risk of hypotension. Keywords: Telmisartan, naproxen, osteoarthritis, cytokines Citation: Hmood SA, Mohammed MM, Kamal YM, Jasim NA. Evaluation of the anti-inflammatory effect of telmisartan as an adjuvant therapy to NSAID in the management of knee osteoarthritis; a clinical prospective study. Iraqi JMS. 2018; Vol. 16(1): 100-110. doi: 10.22578/IJMS.16.1.14
Nefazodone is atypical antidepressant which was manufactured by Bristol-Myers Squibb in 1994 to avoid the adverse effects associated with other antidepressants, including nausea, sedation, insomnia, cardiovascular toxi-city, weight gain and dysfunction. In 2004, nefazodone was withdrawn from USA after its withdrawal from Canada and Europe due to the reports of liver injury in patients treated with this drug. The current study was performed to investigate the cytotoxic and genotoxic effect of nefazodone on HepG2 cell line at different concentrations by using MTT assay and comet assay, respectively. The results showed that nefazodone causes a reduction in cells viability of HepG2 cell line with an IC50 4.682 µg/ml. Comet assay showed a significant increment in the three parameters (tail length, percent of DNA in tail and tail moment) in a concentration-dependent manner, when compared with negative control (p˂0.01), but these results considered as false positive due to cells death.
Nefazodone is atypical antidepressant which was manufactured by Bristol-Myers Squibb in 1994 to avoid the adverse effects associated with other antidepressants, including nausea, sedation, insomnia, cardiovascular toxi-city, weight gain and dysfunction. In 2004, nefazodone was withdrawn from USA after its withdrawal from Canada and Europe due to the reports of liver injury in patients treated with this drug. The current study was performed to investigate the cytotoxic and genotoxic effect of nefazodone on HepG2 cell line at different concentrations by using MTT assay and comet assay, respectively. The results showed that nefazodone causes a reduction in cells viability of HepG2 cell line with an IC50 4.682 µg/ml. Comet assay showed a significant increment in the three parameters (tail length, percent of DNA in tail and tail moment) in a concentration-dependent manner, when compared with negative control (p˂0.01), but these results considered as false positive due to cells death.
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