To assess the impact of parental asthma on risk of pre-term birth (PTB) and intrauterine growth restriction, and their subsequent association with childhood asthma. Three sequential cross-sectional surveys were conducted in 1993 (3,746), 1998 (1,964) and 2006 (1,074) in the same 15 schools among 5-11 year old children in Merseyside using the same respiratory health questionnaire completed by parents (sample size in brackets). Between 1993 and 2006, prevalence of PTB varied between 12.4 and 15.2 %, and of small for gestational age (SGA or growth restricted) babies between 2.1 and 4.6 %, and maternal asthma prevalence between 8.1 and 13.4 %. For the combined surveys mothers with asthma were more likely to have a PTB than non-asthmatic mothers (OR 1.39, 95 % CI 1.10-1.95, p < 0.001), and in the 2006 survey were more likely to have an SGA baby. 40.9 % of PTBs of asthmatic mothers developed doctor diagnosed asthma compared to 34.3 % for term babies (adjusted OR 1.65, 1.34-2.04, p < 0.001). The corresponding estimates for the symptom triad of cough, wheeze and breathlessness were 19.4 and 17.6 % (adjusted OR 1.78, 0.79-3.98). Conversely SGA babies were less likely to develop doctor diagnosed asthma (adjusted OR 0.49, 0.27-0.90, p < 0.021), or the symptom triad of cough, wheeze and breathlessness (adjusted OR 0.22, 0.05-0.97, p < 0.043), whether or not the mother was asthmatic. Maternal asthma is an independent risk factor for PTB which predisposes to childhood asthma. Intrauterine growth restriction was protective against childhood asthma.
Aim: To assess the long term efficacy and safety of Entecavir in the treatment of CHB in Asian-Arabic patients with genotype D, for both nucleoside-naïve as well as experienced, comparing HBeAg positive and negative group. Methods:This study included 70 CHB consecutive patients who were maintained on Entecavir for at least 36 months retrospectively and followed up prospectively every 3 months for a total of 18 months, at 2 centers in Kuwait (October 2012 and April 2014).Results: It showed that 23 (32.8%) were HBeAg +ve. All were found to be HBV genotype D, 47.1% naive, 22 (31.4%) females, with a mean age of 42.9 ± (13), 14 (20%) cirrhotic and 1(1.4%) decompensated. There were no significant differences in the pre-treatment HBV-DNA level among HBeAg+ve and HBeAg-ve group, with a mean± SD log 10 of 7.9 ± 5.4 and 7.4 ± 5.0 respectively (P=0.237). There was a significant viral load reduction in both groups after 6 months of treatment with Entecavir. The reduction was more pronounced in the HBeAg-ve compared to HBeAg +ve group. In HBeAg +ve, 19 patients (82.61%) had complete HBV-DNA suppression after a median period of 7 month, while in HBeAg -ve group; all (100%) had complete HBV-DNA suppression after a median period of 5 month duration (P<0.05). None showed primary non response to Entecavir in both groups. In the HBeAg-ve group; one (2.13%) had HBsAg loss at 45 month compared to non in HBeAg+ve group (P<0.001), while in the HBeAg+ve group; 5 (21.74%) showed HBeAg clearance after a median of 16 month during Entecavir treatment. Multivariate analysis identified HBeAg negative status, pre-treatment as the only independent factor affecting complete viral suppression on Entecavir treatment. The drug showed 100% safety, as there were no serious adverse events throughout 54 month of follow up. None showed hepatic decompensation, HCC or need for liver transplantation during follow up. Also, there was no reported death throughout study period in both groups. Conclusions:In real life data; long term Entecavir treatment for up to 54 months in West Asian CHB patients, with genotype D suppressed HBV-DNA to an undetectable level in 100% of HBeAg-ve, compared to 82% in HBeAg +ve group. Entecavir is considered an effective and safe choice on long term use for treatment CHB patients.
Aim: To assess the long-term efficacy and safety of Entecavir in the treatment of CHB. Patients and Methods: This study included 70 CHB consecutive patients on Entecavir for at least 36 months retrospectively, followed prospectively for 18 months. Results: twenty-three (32.8) were HBeAg +ve, 47.1% naive, 22 (31.4%) females, with a mean age of 42.9±13, 14 (20%) cirrhotic and 1 (1.4%) decompensated. There were no significant differences in the pre-treatment HBV-DNA level among HBeAg (+ve) and HBeAg-ve group, with a mean± SD log 10 of 7.9±5.4 and 7.4±5.0 respectively. (P= 0.237). There was a significant viral load reduction after 6 months Entecavir therapy that was more in the HBeAg -ve compared to HBeAg +ve group. In HBeAg +ve, 19 (82.61%) had HBV-DNA suppression after a median of 7 month, compared to 100% in HBeAg -ve with a median of 5 month (P <0.05). In the HBeAg-ve group; one (2.13%) had HBsAg loss at 45 month compared to none in HBeAg (+ve) group (P <0.001), while in the HBeAg (+ve) group; 5 (21.74%) showed HBeAg clearance after a median of 16 month. Multivariate analysis identified HBeAg negative status, as the only independent factor affecting viral suppression. The drug showed 100% safety. None showed hepatic decompensation, HCC or reported death. Conclusions: In real life data; long term Entecavir treatment effectively sup-pressed HBV. Entecavir is considered an effective and safe treatment for CHB patients compared to 82% in HBeAg (+ve) group. Entecavir is considered an effective and safe choice on long term use for treatment CHB patients.
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