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Background: Recurrent vulvovaginal candidiasis [RVVC] is a common cause of morbidity affecting millions of women worldwide. Patients with RVVC are thought to have an underlying immunologic defect. This study has been established to evaluate cell-mediated immunity defect in response to Candida antigen in RVVC cases
Materials and Methods: Our cross-sectional study was performed in 3 groups of RVVC patients [cases], healthy individuals [control I] and known cases of chronic mucocuta-neous candidiasis [CMC] [control II]. Patients who met the inclusion criteria of RVVC were selected consecutively and were allocated in the case group. Peripheral blood mon-onuclear cells were isolated and labeled with CFSE and proliferation rate was measured in exposure to Candida antigen via flow cytometry
Results: T lymphocyte proliferation in response to Candida was significantly lower in RVVC cases [n=24] and CMC patients [n=7] compared to healthy individuals [n=20, P<0.001], but no statistically significant difference was seen between cases and control II group [P>0.05]. Family history of primary immunodeficiency diseases [PID] differed significantly among groups [P>0.0l], RVVC patients has family history of PID more than control I [29.2 vs. 0%, P=0.008] but not statistically different from CMC patients [29.2 vs. 42.9%, P>0.05]. Prevalence of atopy was greater in RVVC cases compared to healthy individuals [41.3 vs. 15%, P=0.054]. Lymphoproliferative activity and vaginal symptoms were significantly different among RVVC cases with and without allergy [P=0.01, P=0.02]
Conclusion: Our findings revealed that T cells do not actively proliferate in response to Candida antigen in some RVVC cases. So it is concluded that patients with cell-mediated immunity defect are more susceptible to recurrent fungal infections of vulva and vagina. Nonetheless, some other cases of RVVC showed normal function of T cells. Further evaluations showed that these patients suffer from atopy. It is hypothesized that higher frequency of VVC in patients with history of atopy might be due to allergic response in mucocutaneous membranes rather than a functional impairment in immune system components
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Hepatitis B virus [HBV] vaccination is a well-known, safe and effective way for protection against HBV infection; however, non-responders remain susceptible to infection with HBV. This is so important in patients with any kind of chronic liver disease, especially chronic hepatitis C virus [HCV] patients in whom acute HBV infection may lead to decompensation of liver disease. Some of the studies have shown that immunogenicity of HBV vaccination is decreased in these patients. The aim of this study was to evaluate the efficacy and safety of double dose vaccination of HBV in these patients, compared with standard dose vaccination in similar patients and healthy adults. A total of64 patients with chronic HCV infection were randomized into 2 groups of 32. Group A received standard dose HBV vaccine, at 0, 1, 6 months, whereas group B received double dose HBV vaccine. Group C consisted of 32 healthy adults who also received standard dose vaccination. At 1 month after the end of vaccination, Hepatitis B surface antibody [HBsAb] titer was checked in all participants and the results were compared. There was no significant difference in age or sex among three groups. The response rate in groups B and C was 100% [all had HBsAb titer >10 mIU/mL], while in group A, 4 patients [12.5%] were non-responders [HBsAb titer < 10 mIU/mL]. The difference in response rate was statistically significant between Group A and the other two groups [P< 0.05]. The efficacy of standard dose HBV vaccination in patients with chronic HCV infection was suboptimal. Using double dose vaccination in these patients was an effective way to increase the antibody response
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Hepatitis D virus [HDV] is dependent on hepatitis B virus [HBV] infection. Acute infection with HDV can occur simultaneously with acute HBV infection of be superimposed onto a chronic HBV infection. This study aimed to identify cases of HCV and determine its prevalence in patients with chronic HBV infection for the first time study in Isfahan, central Iran. In a cross-sectional study in 2009, 346 who had been diagnosed for at least 6 months with chronic HBV were enrolled consecutively. Anti-HDV was measured by ELISA in the serum of these patients. The study included 245 males [70.8%] and 101 [29.2%] females with a mean age of 39 +/- 12.4 years. Anti-HDV was present in 8 [3.5%] HBe antibody-positive patients [p= 0.36] and in 2 [2.3%] HBe antigen-positive cases [p = 0.68]. No association was found between hepatitis D and probable risk factors. This study demonstrates that the prevalence of HDV infection is higher in patients who are positive for HBeAb compared those who are HBeAg-positive. Therefore, most HDV antibody-positive cases in Isfahan are HBV/HDV superinfections but not coinfections
Assuntos
Humanos , Feminino , Masculino , Fatores de Risco , Estudos Transversais , Hepatite B , Prevalência , Hepatite B CrônicaRESUMO
The aim of this study was to characterize the hepatitis B virus surface protein genotypes and sequence variations among hepatitis B virus surface antigen [HBsAg] positive chronic patients in Hormozgan province, south of Iran. A total of 8 patients enrolled in this study. The surface gene was amplified and directly sequenced. Genotypes and nucleotide/ amino acid substitutions were identified compared to the sequences obtained from the database. All strains belonged to genotype D. Overall 77 "mutations" occurred at 45 nucleotide positions, of them, 44 [57.14%] were silent [no amino acid altering] and 33 [42.86%] were missense [amino acid changing]. A number of 24 [80%] out of 30 amino acid changes occurred in different epitopes within surface protein, of which, 9 [30%] in B cell epitopes in 7 residues [2 occurred in "a" determinant region]; 8 [42.1%] in T helper epitopes in 7 residues and 7 [10%] in 4 residues inside CTL epitopes. Hepatitis B virus genome containing mutated immune epitopes no longer could be recognized by specific T-cells of the host immune surveillance and did not enhance anti-HBs production. This could led to the progression of chronicity B virus infection