8 research outputs found

    Interventions To Improve Patients' Compliance With Therapies Aimed At Lowering Glycated Hemoglobin (hba1c) In Type 1 Diabetes: Systematic Review And Meta-analyses Of Randomized Controlled Clinical Trials Of Psychological, Telecare, And Educational Interventions

    Get PDF
    Brazilian records on glycemic control in patients with type 1 diabetes show treatment efficacy. Poor patient adherence to therapeutic proposals influences these results and can be associated with social, psychological, and economic aspects, besides others factors. The aim of this study was to evaluate the efficacy of psychological, telecare, and educational interventions to improve treatment compliance among patients with type 1 diabetes. Compliance was assessed indirectly using reduction of glycated hemoglobin (HbA1c) as the principal outcome measure. Methods: Systematic review and meta-analyses of randomized controlled clinical trials (RCTs) were performed using Medline, Embase, Cochrane and Scopus databases up to April 2015. The following medical subject headings were used: Diabetes Mellitus, Type 1, Patient Compliance or Adherence, Hemoglobin A, glycated, and Randomized Controlled Trial. The principal outcome was change in HbA1c between baseline and follow-up. Where appropriate, trials were combined in meta-analysis using fixed effects models. Results: From 191 articles initially identified, 57 were full text reviewed, and 19 articles met the inclusion criteria providing data from 1782 patients (49.4 % males, age 18 years). The RCTs (2 to 24 months in duration) were divided into four groups according to type of intervention: psychology (seven studies; 818 patients), telecare (six studies; 494 patients); education (five studies; 349 patients), and psychoeducation (one study; 153 patients). All studies reported some type of adherence measurement of the interventions. Decrease in HbA1c was observed after psychology (MD -0.310; 95 % CI, -0.599 to -0.0210, P = 0.035) but not after telecare (MD -0.124 %; 95 % CI, -0.268, 0.020; P = 0.090) or educational (MD -0.001; 95 % CI, -0.202, 0.200; P = 0.990) interventions. Conclusion: Psychological approaches to improve adherence to diabetes care treatment modestly reduced HbA1c in patients with type 1 diabetes; telecare and education interventions did not change glycemic control. However, the limited number of studies included as well as their methodological quality should be taken into account. © 2016 Viana et al.17

    Virus C Genotype Predisposes To Primary Hypothyroidism During Interferon-α Treatment For Chronic Hepatitis C

    No full text
    Objective: The treatment of the chronic hepatitis C (HCV) with α-interferon is associated with thyroid dysfunction (TD). The aim of this study was to evaluate thyroid function outcome among patients with chronic HCV under treatment with conventional interferon (IFN) or peguilated interferon (PEG-IFN) in association with ribavirin. Patients and Methods: We studied 293 patients with chronic HCV, submitted to drug therapy for 24 or 48 weeks. Initially, we evaluated FT4, TSH, TPOAb, TgAb, and continued to monitor FT4 and TSH every three months during therapy and six months thereafter. Results: At baseline, TD prevalence was 6.82% (n = 20); 6.14% hypothyroidism; 0.68% hyperthyroidism. TPOAb was present in 5.46% of euthyroid patients. Out of 273 euthyroid patients at baseline, 19% developed TD: 17.2% hypothyroidism; 1.8% hyperthyroidism; 5.1% destructive thyroiditis (DT). 90% of TPOAb-positive patients at baseline developed hypothyroidism vs 14.5% of TPOAb-negative patients (p < 0.001). On average, TD occurred after 25.8 ± 15.5 weeks of treatment 87.2% of patients who developed hypothyroidism did so during the first therapeutic cycle (p = 0.004; OR = 3.52; 95% CI = 1.36-9.65). Patients infected with genotype 1 virus were 2.13 times more likely to develop hypothyroidism (p = 0.036; 95% CI = 1.04-4.38). Hypothyroid and DT patients presented higher TSH levels before-treatment than patients who had remained euthyroid (p < 0.001; p = 0.002, respectively). DT patients presented lower qALT (p = 0.012) than euthyroid patients. Conclusion: Hypothyroidism was the most frequent TD, especially during the first cycle of α-interferon. Genotype 1 virus was associated with a risk two times higher for developing the illness. There was no need to interrupt or to change HCV treatment. Therefore, approximately 34% of TD was transient. © 2011 Elsevier Editora Ltda.155449456Bellentani, S., Tiribelli, C., The spectrum of liver disease in the general population: lessons from the Dionysos study (2001) J Hepatol, 35, pp. 531-537Poynard, T., Marcellin, P., Lee, S.S., Randomized trial of interferon a2b plus ribavirin for 48 weeks or for 24 weeks versus interferon a2b plus placebo for 48 weeks for treatment of chronic infection with hepatitis C virus (1998) Lancet, 352, pp. 1426-1432Tam, R.C., Pai, B., Bard, J., Ribavirin polarizes human T cell responses toward a type 1 cytokine profile (1999) J Hepatol, 30, pp. 376-382Koh, L.K.H., Greenspan, F.S., Yeo, P.P.B., Interferon-α induced thyroid dysfunction: three clinical presentations and review of the literature (1997) Thyroid, 7, pp. 891-896Dalgard, O., Bjoro, K., Hellum, K., Thyroid dysfunction during treatment of chronic hepatitis C with interferon-α: no association with either interferon dosage or efficacy of therapy (2002) J Int Med, 251, pp. 400-406Carella, C., Mazziotti, G., Amato, G., Interferon-α related thyroid disease: pathophysiological, epidemiological, and clinical aspects (2004) J Clin Endocrinol Metab, 89, pp. 3656-3661Prummel, M.F., Lauberg, P., Interferon-α and autoimmune thyroid disease (2003) Thyroid, 13, pp. 547-551Tomer, Y., Blackard, J.T., Akeno, N., Interferon alpha treatment and thyroid dysfunction (2007) Endocrinol Metab Clin N Am, 36, pp. 1051-1066Blackard, J.T., Kemmer, N., Sherman, K.E., Extrahepatic replication of HCV: insights into clinical manifestations and biological consequences (2006) Hepatology, 44, pp. 15-22Fried, M.W., Side effects of therapy of hepatitis C and their management (2002) Hepatology, 36, pp. 237-244Evon, D.M., Verma, A., Simpson, K., Psychiatric symptoms during interferon treatment for hepatitis C: experiences from a tertiary care hepatology centre (2008) Aliment Pharmacol Ther, 27, pp. 1071-1080Fentiman, I.S., Thomas, B.S., Balkwill, F.R., Primary hypothyroidism associated with interferon therapy of breast cancer (1985) Lancet, 8438, p. 1166Sachithanandan, S., Clarke, G., Crowe, J., Interferon-associated thyroid dysfunction in anti-D-related chronic hepatitis C (1997) J Interf Cytok Res, 17, pp. 409-411Pateron, D., Hartmann, D.J., Duclos-Vallee, J.C., Latent autoimmune thyroid disease in patients with chronic HCV hepatitis (1992) J Hepatol, 16, pp. 244-245Antonelli, A., Ferri, C., Fallahi, P., Thyroid disorders in chronic hepatitis C virus infection (2006) Thyroid, 16, pp. 563-572Tran, A., Quaranta, J.F., Benzaken, S., High prevalence of thyroid autoantibodies in a prospective series of patients with chronic hepatitis C before interferon therapy (1993) Hepatol, 18, pp. 253-257Preziati, D., La Rosa, L., Covini, G., Autoimmunity and thyroid function in patients with chronic active hepatitis treated with recombinant interferon alpha-2a (1995) Eur J Endocrinol, 132, pp. 587-593Fernandez-Soto, L., Gonzalez, A., Escobar-Jimenez, F., Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during, and after discontinuing interferon therapy (1998) Arch Int Med, 158, pp. 1445-1448Antonelli, A., Ferri, C., Pampana, A., Thyroid disorders in chronic hepatitis C (2004) Am J Med, 117, pp. 10-13Muratori, L., Bogdanos, D.P., Muratori, P., Susceptibility to thyroid disorders in hepatitis C (2005) Clin Gastroenterol Hepatol, 3, pp. 595-603Stefanova-Petrova, D.V., Tzvetanska, A.H., Naumova, E.J., Chronic hepatitis C virus infection: prevalence of extrahepatic manifestations and association with cryoglobulinemia in Bulgarian patients (2007) World J Gastroenterol, 13, pp. 6518-6528Matsuda, J., Saitoh, N., Gotoh, M., High prevalence of antiphospholipid antibodies and anti-thyroglobulin antibody in patients with hepatitis C virus infection treated with interferon-alpha (1995) Am J Gastroenterol, 90, pp. 1138-1141Custro, N., Montalto, G., Scafidi, V., Prospective study on thyroid autoimmunity and dysfunction related to chronic hepatitis C and interferon therapy (1997) J Endocrinol Invest, 20, pp. 374-380Boadas, J., Rodríguez-Espinosa, J., Enríquez, J., Prevalence of thyroid autoantibodies is not increased in blood donors with hepatitis C virus infection (1995) J Hepatol, 22, pp. 611-615Prentice, L.M., Phillips, D.I., Sarsero, D., Geographical distribution of subclinical autoimmune thyroid disease in Britain: a study using highly sensitive direct assays for autoantibodies to thyroglobulin and thyroid peroxidase (1990) Acta Endocrinol, 123, pp. 493-498Minelli, R., Braverman, L.E., Giuberti, T., Effects of excess iodine administration on thyroid function in euthyroid patients with a previous episode of thyroid dysfunction induced by interferon-alpha treatment (1997) Clil Endocrinol, 47, pp. 357-361Moncoucy, X., Leymarie, F., Delemer, B., Risk factors and long-term course of thyroid dysfunction during antiviral treatments in 221 patients with chronic hepatitis C (2005) Gastroenterol Clin Biolog, 29, pp. 339-345Hsieh, M.C., Yu, M.L., Chuang, W.L., Virologic factors related to interferon-alpha-induced thyroid dysfunction in patients with chronic hepatitis C (2000) Eur J Endocrinol, 142, pp. 431-437Lisker-Melman, M., Di Bisceglie, A.M., Usala, S.J., Development of thyroid disease during therapy of chronic viral hepatitis with interferon alfa (1992) Gastroenterol, 102, pp. 2155-2160Primo, J., Hinojosu, J., Molés, J.R., Development of thyroid dysfunction after alpha-interferon treatment of chronic hepatitis C (1993) Am J Gastroenterol, 88, pp. 1976-1977Reid, I., Sharpe, I., McDevitt, J., Thyroid dysfunction can predict response to immunotherapy with interleukin-2 and interferon-2 alpha (1991) Brit J Cancer, 64, pp. 915-918Watanabe, U., Hashimoto, E., Hisamitsu, T., The risk factor for development of thyroid disease during interferon-alpha therapy for chronic hepatitis C (1994) Am J Gastroenterol, 89, pp. 399-403Vanderpump, M.P., Tunbridge, W.M., French, J.M., The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey (1995) Clin Endocrinol, 43, pp. 55-68Huang, J.F., Chuang, W.L., Dai, C.Y., The role of thyroid autoantibodies in the development of thyroid dysfunction in Taiwanese chronic hepatitis C patients with interferon-alpha and ribavirin combination therapy (2006) J Vir Hepat, 13, pp. 396-401Grossman, C.J., Roselle, G.A., Mendenhall, C.L., Sex steroid regulation of autoimmunity (1991) J Ster Biochem Mol Biol, 40, pp. 649-659Tomer, Y., Davies, T.F., Searching for the autoimmune thyroid disease susceptibility genes: from gene mapping to gene function (2003) Endocr Rev, 24, pp. 694-717Carella, C., Amato, G., Biondi, B., Longitudinal study of antibodies against thyroid in patients undergoing interferon-alpha therapy for HCV chronic hepatitis (1995) Horm Res, 44, pp. 110-114Katabami, S., Kamijo, K., Kodama, T., An episode of silent thyroiditis in a patient with chronic thyroiditis and papillary adenocarcinoma following alpha interferon treatment for hepatitis C (1993) Endocr J, 40, pp. 311-316Simmonds, P., Genetic diversity and evolution of hepatitis C virus - 15 years on (2004) J Gen Virol, 85, pp. 3173-3188Gisslinger, H., Gilly, B., Woloszczuk, W., Thyroid autoimmunity and hypothyroidism during long-term treatment with recombinant interferon-alpha (1992) Clil Exp Immunol, 90, pp. 363-367Nagayama, Y., Ohta, K., Tsuruta, M., Exacerbation of thyroid autoimmunity by interferon alpha treatment in patients with chronic viral hepatitis: our studies and review of the literature (1994) Endocr J, 41, pp. 565-572Chung, Y.H., Shong, Y.K., Development of thyroid autoimmunity after administration of recombinant human interferonalpha 2b for chronic viral hepatitis (1993) Am J Gastroenterol, 88, pp. 244-247Yamazaki, K., Kanaji, Y., Shizume, K., Reversible inhibition by interferons alpha and beta of 125I incorporation and thyroid hormone release by human thyroid follicles in vitro (1993) J Clin Endocrinol Metab, 77, pp. 1439-1441Hollowell, J.G., Staehling, N.W., Flanders, W.D., Serum TSHm T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III) (2002) J Clin Endocrinol Metab, 87, pp. 489-499Weetman, A.P., Smallridge, R.C., Nutman, T.B., Persistent thyroid autoimmunity after subacute thyroiditis (1987) J Clin Lab Immunol, 23, pp. 1-6Paraná, R., Cruz, M., Lyra, L., Cruz, T., Subacute thyroiditis during treatment with combination therapy (interferon plus ribavirin) for hepatitis C virus (2000) J Vir Hepat, 7, pp. 393-39

    Distribution of HLA-DRB1 alleles in a mixed population with insulin-dependent diabetes mellitus from the Southeast of Brazil

    No full text
    HLA class II genes are strongly associated with susceptibility and resistance to insulin-dependent diabetes mellitus (IDDM). The present study reports the HLA-DRB1 genotyping of 41 IDDM patients and 99 healthy subjects from the Southeast of Brazil (Campinas region). Both groups consisted of an ethnic mixture of Caucasian, African Negro and Amerindian origin. HLA-DRB1*03 and *04 alleles were found at significantly higher frequencies among IDDM patients compared to the controls (DRB1*03: 48.8% vs 18.2%, P&lt;0.005, RR = 4.27; DRB1*04: 43.9% vs 15.1%, P&lt;0.008, RR = 4.37) and were associated with a susceptibility to the disease. DRB1*03/*04 heterozygosity conferred a strong IDDM risk (RR = 5.44). In contrast, the HLA-DRB1*11 allele frequency was lower among IDDM patients (7.3% vs 26.3% in controls), but the difference was not significant. These data agree with those described for other populations and allow genetic characterization of IDDM in Brazi

    Body Composition And Weight Gain In New Users Of The Three-monthly Injectable Contraceptive, Depot-medroxyprogesterone Acetate, After 12 Months Of Follow-up

    No full text
    Objectives: To evaluate weight gain and body composition (BC) in new users of depot-medroxyprogesterone acetate (DMPA) as a contraceptive. Methods: This cohort study followed up 20 DMPA users and 20 copper intrauterine device (TCu380A IUD) users, paired for age (±1 year) and body mass index (BMI±1 kg/m2), during 12-months. Healthy, non-obese women aged 18 to 40 years, unaffected by conditions that could influence their body weight, were enrolled. Socio-demographic variables, habits, weight, BMI, BC using dual-energy X-ray absorptiometry, circumferences, skinfold thickness, body fat percentage and waist-to-hip ratio were evaluated. All participants were encouraged to adopt healthy habits. Results: At baseline, median age was 29 and 30.5 years, and mean BMI was 24.8 and 24.5 kg/m2 in the DMPA and IUD groups, respectively. At 12 months, an increase was observed in waist and hip circumference in the DMPA users and 8/20 of them had a weight gain ≥5% (mean 4.6 kg) with accumulation of fat centrally. Conclusions There were no differences in weight gain or in BC measurements between the groups; nevertheless 40% of women in the DMPA group had larger weight gain and accumulation of fat centrally. The duration of follow-up may have been insufficient to detect differences between the groups.196432438Fraser, I.S., Weisberg, E., A comprehensive review of injectable contraception with special emphasis on depot medroxyprogesterone acetate (1981) Med J Aust, 1 (1), pp. 3-19Mosher, W.D., Martinez, G.M., Chandra, A., Use of contraception and use of family planning services in the United States: 1982-2002 (2004) Advance Data from Vital and Health Statistics, (350), pp. 1-36. , Hyattsville, MD: National Center for Health StatisticsBakry, S., Merhi, Z.O., Scalise, T.J., Depot-medroxyprogesterone acetate: An update (2008) Arch Gynecol Obstet, 278, pp. 1-12Pelkman, C., Hormones and weight change (2002) J Reprod Med, 47, pp. 791-794Taneepanichskul, S., Reinprayoon, D., Khaosaad, P., Comparative study of weight change between long-term DMPA and IUD acceptors (1998) Contraception, 58, pp. 149-151Clark, M.K., Dillon, J.S., Sowers, M., Weight, fat mass, and central distribution of fat increase when women use depot-medroxyprogesterone acetate for contraception (2005) Int J Obes, 29, pp. 1252-1258Westhoff, C., Jain, J.K., Milsom, I., Changes in weight with depot medroxyprogesterone acetate subcutaneous injection 104 mg/0.65 mL (2007) Contraception, 75, pp. 261-267Berenson, A.B., Rahman, M., Changes in weight, total fat, percent body fat, and central-to-peripheral fat ratio associated with injectable and oral contraceptive use (2009) Am J Obstet Gynecol, 200, pp. 329+e1-8Le, Y.C., Rahman, M., Berenson, A.B., Early weight gain predicting later weight gain among depot medroxyprogesterone acetate users (2009) Obstet Gynecol, 114, pp. 279-284Friendly, M., (1995) SAS System for Statistical Graphics, Version 1.2, 1st Edn., , http://euclid.psych.yorku.ca/SCS/sasmac/, Cary, NC: SAS Institute Inc. Accessed 18 April 2014 from: http://euclid.psych.yorku.ca/SCS/sasmac/fpower.ht(2010) Critério de Classificac¸ão Econômica Brasil The Brazilian Economic Classification Criteria, , http://www.abep.org/novo/Utils/FileGenerate.ashx?id=46, Brazilian Association of Research Companies Accessed 18 April 2014 fromFord, E.S., Kohl, H.W., 3rd, Mokdad, A.H., Sedentary behavior, physical activity, and the metabolic syndrome among U.S. adults (2005) Obes Res, 13, pp. 608-614Lohman, T.G., Roche, A.F., Martorell, R., (1991) Anthropometric Standardization Reference Manual, 1st Edn., , Champaign, IL: Human Kinetics BooksPhysical status: The use and interpretation of anthropometry (1995) Technical Report Series, (854). , http://whqlibdoc.who.int/trs/WHO_TRS_854.pdf?ua=1, Geneva: World Health Organization Accessed 18 April 2014 fromFaulkner, J.A., Physiology of swimming and diving (1968) Exercise Physiology, pp. 415-446. , Falls H, ed. Baltimore: Academic PressAmatayakul, K., Sivasomboon, B., Thanangkul, O., A study of the mechanism of weight gain in medroxyprogesterone acetate users (1980) Contraception, 22, pp. 605-622Vickery, Z., Madden, T., Zhao, Q., Weight change at 12 months in users of three progestin-only contraceptive methods (2013) Contraception, 88, pp. 503-508Pantoja, M., Medeiros, T., Baccarin, M.C., Variations in body mass index of users of depot-medroxyprogesterone acetate as a contraceptive (2010) Contraception, 81, pp. 107-111Bonny, A.E., Ziegler, J., Harvey, R., Weight gain in obese and nonobese adolescent girls initiating depot medroxyprogesterone, oral contraceptive pills, or no hormonal contraceptive method (2006) Arch Pediatr Adolesc Med, 160, pp. 40-45Bonny, A.E., Lange, H.L., Rogers, L.K., A pilot study of depot medroxyprogesterone acetate pharmacokinetics and weight gain in adolescent females (2014) Contraception, 89, pp. 357-360Haider, S., Darney, P.D., Injectable contraception (2007) Clin Obstet Gynecol, 50, pp. 898-90

    Catalase Activity, Allelic Variations In The Catalase Gene And Risk Of Kidney Complications In Patients With Type 1 Diabetes

    No full text
    Aims/hypothesis: Oxidative stress is involved in the pathogenesis of diabetic nephropathy. The antioxidant enzyme catalase plays a key role in redox regulation in the kidney. We investigated associations of catalase gene (CAT) polymorphisms and plasma catalase activity with diabetic nephropathy in type 1 diabetic patients. Methods: We genotyped nine single nucleotide polymorphisms (SNPs) in the CAT region in participants from the Survival Genetic Nephropathy (SURGENE) (340 French participants, 10 year follow-up) and the Génétique de la Néphropathie Diabétique (GENEDIAB) (444 Belgian and French participants, 8 year follow-up) study cohorts. Replication was performed in a Brazilian cross-sectional cohort (n = 451). Baseline plasma catalase activity was measured in SURGENE (n = 120) and GENEDIAB (n = 391) participants. Results: The A allele of rs7947841 was associated with the prevalence of incipient (OR 2.79, 95% CI 1.21, 6.24, p = 0.01) and established or advanced nephropathy (OR 5.72, 95% CI 1.62, 22.03, p = 0.007), and with the incidence of renal events, which were defined as new cases of microalbuminuria or progression to a more severe stage of nephropathy during follow-up (HR 1.82, 95% CI 1.13, 2.81, p = 0.01) in SURGENE participants. The same risk allele was associated with incipient nephropathy (OR 3.13, 95% CI 1.42, 7.24, p = 0.004) and with the incidence of end-stage renal disease (ESRD) (HR 2.11, 95% CI 1.23, 3.60, p = 0.008) in GENEDIAB participants. In both cohorts, the risk allele was associated with lower catalase activity. Associations with incipient and established or advanced nephropathy were confirmed in the replication cohort. Conclusions/interpretation: CAT variants were associated with the prevalence and incidence of diabetic nephropathy and ESRD in type 1 diabetic patients. Our results confirm the protective role of catalase against oxidative stress in the kidney. © 2013 Springer-Verlag Berlin Heidelberg.561227332742Jones, C.A., Krolewski, A.S., Rogus, J., Xue, J.L., Collins, A., Warram, J.H., Epidemic of end-stage renal disease in people with diabetes in the United States population: Do we know the cause? (2005) Kidney Int, 67, pp. 1684-1691. , 15840014 10.1111/j.1523-1755.2005.00265.xOrchard, T.J., Secrest, A.M., Miller, R.G., Costacou, T., In the absence of renal disease, 20 year mortality risk in type 1 diabetes is comparable to that of the general population: A report from the Pittsburgh Epidemiology of Diabetes Complications Study (2010) Diabetologia, 53, pp. 2312-2319. , 20665208 10.1007/s00125-010-1860-3 1:STN:280:DC%2BC3cflsFersw%3D%3DPirart, J., Lauvaux, J.P., Rey, W., Blood sugar and diabetic complications (1978) N Engl J Med, 298, p. 1149. , 643042 1:STN:280:DyaE1c7ls1ejug%3D%3DClustering of long-term complications in families with diabetes in the diabetes control and complications trial (1997) Diabetes, 46, pp. 1829-1839. , The Diabetes Control and Complications Trial Research Group 10.2337/diab.46.11.1829Marre, M., Jeunemaitre, X., Gallois, Y., Contribution of genetic polymorphism in the renin-angiotensin system to the development of renal complications in insulin-dependent diabetes: Genetique de la Nephropathie Diabetique (GENEDIAB) study group (1997) J Clin Invest, 99, pp. 1585-1595. , 9120002 10.1172/JCI119321 1:CAS:528:DyaK2sXitlantLY%3DAl-Kateb, H., Boright, A.P., Mirea, L., Multiple superoxide dismutase 1/splicing factor serine alanine 15 variants are associated with the development and progression of diabetic nephropathy: The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Genetics study (2008) Diabetes, 57, pp. 218-228. , 17914031 10.2337/db07-1059 1:CAS:528:DC%2BD1cXmt1WqtQ%3D%3DMohammedi, K., Maimaitiming, S., Emery, N., Allelic variations in superoxide dismutase-1 (SOD1) gene are associated with increased risk of diabetic nephropathy in type 1 diabetic subjects (2011) Mol Genet Metab, 104, pp. 654-660. , 21963083 10.1016/j.ymgme.2011.08.033 1:CAS:528:DC%2BC3MXhsFertL7KDu, X.L., Edelstein, D., Rossetti, L., Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation (2000) Proc Natl Acad Sci U S A, 97, pp. 12222-12226. , 11050244 10.1073/pnas.97.22.12222 1:CAS:528:DC%2BD3cXnvVSgurs%3DBrownlee, M., Biochemistry and molecular cell biology of diabetic complications (2001) Nature, 414, pp. 813-820. , 11742414 10.1038/414813a 1:CAS:528:DC%2BD38Xhtlyltg%3D%3DBrownlee, M., The pathobiology of diabetic complications: A unifying mechanism (2005) Diabetes, 54, pp. 1615-1625. , 15919781 10.2337/diabetes.54.6.1615 1:CAS:528:DC%2BD2MXltVaisbk%3DNiedowicz, D.M., Daleke, D.L., The role of oxidative stress in diabetic complications (2005) Cell Biochem Biophys, 43, pp. 289-330. , 16049352 10.1385/CBB:43:2:289 1:CAS:528:DC%2BD2MXpsVegurg%3DCeriello, A., Morocutti, A., Mercuri, F., Defective intracellular antioxidant enzyme production in type 1 diabetic patients with nephropathy (2000) Diabetes, 49, pp. 2170-2177. , 11118022 10.2337/diabetes.49.12.2170 1:CAS:528:DC%2BD3cXos1ejsLY%3DCoughlan, M.T., Mibus, A.L., Forbes, J.M., Oxidative stress and advanced glycation in diabetic nephropathy (2008) Ann N y Acad Sci, 1126, pp. 190-193. , 18448815 10.1196/annals.1433.018 1:CAS:528:DC%2BD1cXmtFynsr4%3DForbes, J.M., Coughlan, M.T., Cooper, M.E., Oxidative stress as a major culprit in kidney disease in diabetes (2008) Diabetes, 57, pp. 1446-1454. , 18511445 10.2337/db08-0057 1:CAS:528:DC%2BD1cXnsF2jurs%3DMates, J.M., Perez-Gomez, C., Nunez De Castro, I., Antioxidant enzymes and human diseases (1999) Clin Biochem, 32, pp. 595-603. , 10638941 10.1016/S0009-9120(99)00075-2 1:CAS:528:DC%2BD3cXos12jsQ%3D%3DDeisseroth, A., Dounce, A.L., Catalase: Physical and chemical properties, mechanism of catalysis, and physiological role (1970) Physiol Rev, 50, pp. 319-375. , 4912904 1:CAS:528:DyaE3cXkvVeqtbw%3DBrezniceanu, M.L., Liu, F., Wei, C.C., Catalase overexpression attenuates angiotensinogen expression and apoptosis in diabetic mice (2007) Kidney Int, 71, pp. 912-923. , 17342175 10.1038/sj.ki.5002188 1:CAS:528:DC%2BD2sXksFeksr0%3DBrezniceanu, M.L., Liu, F., Wei, C.C., Attenuation of interstitial fibrosis and tubular apoptosis in db/db transgenic mice overexpressing catalase in renal proximal tubular cells (2008) Diabetes, 57, pp. 451-459. , 17977949 10.2337/db07-0013 1:CAS:528:DC%2BD1cXhvVOktL8%3DHwang, I., Lee, J., Huh, J.Y., Catalase deficiency accelerates diabetic renal injury through peroxisomal dysfunction (2012) Diabetes, 61, pp. 728-738. , 22315314 10.2337/db11-0584 1:CAS:528:DC%2BC38XovFegurY%3DShi, Y., Lo, C.S., Chenier, I., Overexpression of catalase prevents hypertension and tubulo-fibrosis and normalization of renal angiotensin-converting enzyme-2 expression in Akita mice (2013) Am J Physiol Renal Physiol, 304, pp. 1335-F1346. , 23552863 10.1152/ajprenal.00405.2012 1:CAS:528:DC%2BC3sXhtVyjtLbKForsberg, L., Lyrenas, L., De Faire, U., Morgenstern, R., A common functional C-T substitution polymorphism in the promoter region of the human catalase gene influences transcription factor binding, reporter gene transcription and is correlated to blood catalase levels (2001) Free Radic Biol Med, 30, pp. 500-505. , 11182520 10.1016/S0891-5849(00)00487-1 1:CAS:528:DC%2BD3MXht1Oqu7s%3DHadjadj, S., Belloum, R., Bouhanick, B., Prognostic value of angiotensin-I converting enzyme I/D polymorphism for nephropathy in type 1 diabetes mellitus: A prospective study (2001) J Am Soc Nephrol, 12, pp. 541-549. , 11181802 1:CAS:528:DC%2BD3MXitV2ktro%3DVieira, S.M., Monteiro, M.B., Marques, T., Association of genetic variants in the promoter region of genes encoding p22phox (CYBA) and glutamate cysteine ligase catalytic subunit (GCLC) and renal disease in patients with type 1 diabetes mellitus (2011) BMC Med Genet, 12, p. 129. , 21962117 10.1186/1471-2350-12-129 1:CAS:528:DC%2BC3MXhtl2lsr%2FKPimenta, J.R., Zuccherato, L.W., Debes, A.A., Color and genomic ancestry in Brazilians: A study with forensic microsatellites (2006) Hum Hered, 62, pp. 190-195. , 17106202 10.1159/000096872Levey, A.S., Bosch, J.P., Lewis, J.B., Greene, T., Rogers, N., Roth, D., A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of Diet in Renal Disease Study Group (1999) Ann Intern Med, 130, pp. 461-470. , 10075613 10.7326/0003-4819-130-6-199903160-00002 1:CAS:528: DyaK1MXitFChs7k%3DKohner, E.M., The lesions and natural history of diabetic retinopathy (1991) Textbook of Diabetes, pp. 575-588. , J. Pickup G. Williams (eds) Blackwell OxfordNyholt, D.R., A simple correction for multiple testing for single-nucleotide polymorphisms in linkage disequilibrium with each other (2004) Am J Hum Genet, 74, pp. 765-769. , 14997420 10.1086/383251 1:CAS:528:DC%2BD2cXivFCntL0%3DCao, C., Leng, Y., Kufe, D., Catalase activity is regulated by c-Abl and Arg in the oxidative stress response (2003) J Biol Chem, 278, pp. 29667-29675. , 12777400 10.1074/jbc.M301292200 1:CAS:528:DC%2BD3sXlvFOns78%3DHodgkinson, A.D., Bartlett, T., Oates, P.J., Millward, B.A., Demaine, A.G., The response of antioxidant genes to hyperglycemia is abnormal in patients with type 1 diabetes and diabetic nephropathy (2003) Diabetes, 52, pp. 846-851. , 12606529 10.2337/diabetes.52.3.846 1:CAS:528:DC%2BD3sXitFajtLw%3DHeistad, D.D., Oxidative stress and vascular disease: 2005 Duff lecture (2006) Arterioscler Thromb Vasc Biol, 26, pp. 689-695. , 16410455 10.1161/01.ATV.0000203525.62147.28 1:CAS:528: DC%2BD28XitlKmtr0%3DMontezano, A.C., Touyz, R.M., Oxidative stress, Noxs, and hypertension: Experimental evidence and clinical controversies (2012) Ann Med, 44 (SUPPL. 1), pp. 2-S16. , 22713144 10.3109/07853890.2011.653393 1:CAS:528:DC%2BC38XptVGrtrw%3DDevi, T.S., Hosoya, K., Terasaki, T., Singh, L.P., Critical role of TXNIP in oxidative stress, DNA damage and retinal pericyte apoptosis under high glucose: Implications for diabetic retinopathy (2013) Exp Cell Res, 319, pp. 1001-1012. , 23353834 10.1016/j.yexcr.2013.01.012 1:CAS:528:DC%2BC3sXitleisLw%3DDe Cavanagh, E.M., Inserra, F., Ferder, L., Fraga, C.G., Enalapril and captopril enhance glutathione-dependent antioxidant defenses in mouse tissues (2000) Am J Physiol Regul Integr Comp Physiol, 278, pp. 572-R577. , 10712274Lazaro, A., Gallego-Delgado, J., Justo, P., Long-term blood pressure control prevents oxidative renal injury (2005) Antioxid Redox Signal, 7, pp. 1285-1293. , 16115034 10.1089/ars.2005.7.1285 1:CAS:528:DC%2BD2MXos1ertrk%3DPortero-Otin, M., Pamplona, R., Boada, J., Inhibition of renin angiotensin system decreases renal protein oxidative damage in diabetic rats (2008) Biochem Biophys Res Commun, 368, pp. 528-535. , 18243127 10.1016/j.bbrc.2008.01.101 1:CAS:528:DC%2BD1cXislahsr8%3DChappell, M.C., Nonclassical renin-angiotensin system and renal function (2012) Compr Physiol, 2, pp. 2733-2752. , 23720263Ewens, K.G., George, R.A., Sharma, K., Ziyadeh, F.N., Spielman, R.S., Assessment of 115 candidate genes for diabetic nephropathy by transmission/disequilibrium test (2005) Diabetes, 54, pp. 3305-3318. , 16249459 10.2337/diabetes.54.11.3305 1:CAS:528:DC%2BD2MXht1Shsr%2FOKottgen, A., Pattaro, C., Boger, C.A., New loci associated with kidney function and chronic kidney disease (2010) Nat Genet, 42, pp. 376-384. , 20383146 10.1038/ng.568Sandholm, N., Salem, R.M., McKnight, A.J., New susceptibility loci associated with kidney disease in type 1 diabetes (2012) PLoS Genet, 8, p. 1002921. , 23028342 10.1371/journal.pgen.1002921 1:CAS:528:DC%2BC38XhsVaktrvOPerianayagam, M.C., Liangos, O., Kolyada, A.Y., NADPH oxidase p22phox and catalase gene variants are associated with biomarkers of oxidative stress and adverse outcomes in acute renal failure (2007) J Am Soc Nephrol, 18, pp. 255-263. , 17151330 10.1681/ASN.2006070806 1:CAS:528:DC%2BD2sXht1KqtL4%3DCrawford, A., Fassett, R.G., Coombes, J.S., Glutathione peroxidase, superoxide dismutase and catalase genotypes and activities and the progression of chronic kidney disease (2011) Nephrol Dial Transplant, 26, pp. 2806-2813. , 21325350 10.1093/ndt/gfq828 1:CAS:528:DC%2BC3MXht1Siu7jKGoth, L., Nagy, T., Kosa, Z., Effects of rs769217 and rs1001179 polymorphisms of catalase gene on blood catalase, carbohydrate and lipid biomarkers in diabetes mellitus (2012) Free Radic Res, 46, pp. 1249-1257. , 22712453 10.3109/10715762.2012.702899 1:CAS:528:DC%2BC38XhtlektLrPGodin, N., Liu, F., Lau, G.J., Catalase overexpression prevents hypertension and tubular apoptosis in angiotensinogen transgenic mice (2010) Kidney Int, 77, pp. 1086-1097. , 20237455 10.1038/ki.2010.63 1:CAS:528:DC%2BC3cXmsF2isrc%3
    corecore