Based on the mechanism of pathophysiology, thalassemia major or transfusion-dependent thalassemia patients may have an increased risk of developing organic erectile dysfunction resulting from hypogonadism. However, there have been few studies investigating the association between erectile dysfunction and transfusion-naive thalassemia populations. We constructed a population-based cohort study to elucidate the association between transfusion-naive thalassemia populations and organic erectile dysfunction. This nationwide population-based cohort study involved analyzing data from 1998 to 2010 obtained from the Taiwanese National Health Insurance Research Database, with a follow-up period extending to the end of 2011. We identified men with transfusion-naive thalassemia and selected a comparison cohort that was frequency-matched with these according to age, and year of diagnosis thalassemia at a ratio of 1 thalassemia man to 4 control men. We analyzed the risks for transfusion-naive thalassemia men and organic erectile dysfunction by using Cox proportional hazards regression models. In this study, 588 transfusion-naive thalassemia men and 2337 controls were included. Total 12 patients were identified within the thalassaemia group and 10 within the control group. The overall risks for developing organic erectile dysfunction were 4.56-fold in patients with transfusion-naive thalassemia men compared with the comparison cohort after we adjusted for age and comorbidities. Our long-term cohort study results showed that in transfusion-naive thalassemia men, there was a higher risk for the development of organic erectile dysfunction, particularly in those patients with comorbidities.

BACKGROUND:

Although clinical and immunological studies have shown a possible link between allergy and idiopathic nephrotic syndrome (INS), the nature of the relationship remains unclear. Asthma is the most common chronic allergic airway inflammation. However, no study has used a longitudinal design with a population cohort to investigate INS in children with asthma.

METHODS:

Using nationwide claims data from 2000 through 2007, we randomly selected 251,698 asthma cases and 1,006,791 frequency-matched controls. Incidence rates of INS and hazard ratios (HRs) were calculated.

RESULTS:

The INS incidence was 3.36-fold greater in the asthma cohort than in the nonasthma control (9.26 vs. 2.76 per 100,000 person-years; 95% confidence interval (CI): 2.65-4.26). The HR for INS increased for those with more asthma-related medical visits per year, from 1.49 (95% CI: 1.06-2.11) for <3 visits to 15.7 (95% CI: 11.5-21.5) for ≥6 visits (trend test, P < 0.0001). The HR for INS slightly decreased during the follow-up period, from 3.41 (95% CI: 2.66-4.38) for ≤5.5 y to 2.90 (95% CI: 1.33-6.30) for >5.5 y.

CONCLUSION:

We conclude that children with asthma had an increased incidence rate of INS, and increased incidence rate correlated with asthma-related medical visits.

BACKGROUND:

The association between enterovirus infections in children and risk of leukaemia is unclear. We aimed to assess the risk of leukaemia after enterovirus infection in children.

METHODS:

We did a nationwide retrospective cohort study by analysing data from the National Health Insurance Research Database (NHIRD) in Taiwan. Children with enterovirus infections aged younger than 18 years were identified. With use of computer-generated random numbers, children not infected with enterovirus were randomly selected and frequency matched (1:1) with children infected with enterovirus by sex, age, urbanisation level, parental occupation, and index year of enterovirus infection. We only included children with complete baseline data for age and sex and who had at least three clinic visits with the diagnosis of enterovirus infection. The diagnosis date of the first clinic visit for the enterovirus infection was defined as the index date for initiation of follow-up person-year measurement and participants. All study patients were followed up until they developed leukaemia, were lost to follow-up, withdrew from the NHI programme, or until the end of the study without leukaemia (censored). Our primary endpoint was a diagnosis of leukaemia during follow-up.

FINDINGS:

Insurance claims data for 3 054 336 children younger than 18 years were randomly selected from all insured children in the NHIRD. We identified 282 360 children infected with enterovirus and 282 355 children not infected with enterovirus between Jan 1, 2000, and Dec 31, 2007. The incidence density rates of leukaemia were 3·26 per 100 000 person-years for the enterovirus-infected and 5·84 per 100 000 person-years for the non-enterovirus-infected cohorts. The risk of leukaemia was significantly lower in the enterovirus-infected cohort than in the non-enterovirus-infected cohort (adjusted subhazard ratio [SHR] 0·44, 95% CI 0·31-0·60; p<0·0001). Children infected with enterovirus have a reduced risk of both lymphocytic leukaemia (adjusted SHR 0·44, 0·30-0·65; p<0·0001) and acute myeloid leukaemia (adjusted SHR 0·40, 0·17-0·97; p=0·04). Herpangina and hand-foot-and-mouth disease were the main diseases associated with the reduced risk of leukaemia.

INTERPRETATION:

The association between enterovirus infection and the reduced risk of developing leukaemia supports Greaves' delayed infection hypothesis for the cause of childhood leukaemia.

BACKGROUND:

The association between enterovirus infections in children and risk of leukaemia is unclear. We aimed to assess the risk of leukaemia after enterovirus infection in children.

METHODS:

We did a nationwide retrospective cohort study by analysing data from the National Health Insurance Research Database (NHIRD) in Taiwan. Children with enterovirus infections aged younger than 18 years were identified. With use of computer-generated random numbers, children not infected with enterovirus were randomly selected and frequency matched (1:1) with children infected with enterovirus by sex, age, urbanisation level, parental occupation, and index year of enterovirus infection. We only included children with complete baseline data for age and sex and who had at least three clinic visits with the diagnosis of enterovirus infection. The diagnosis date of the first clinic visit for the enterovirus infection was defined as the index date for initiation of follow-up person-year measurement and participants. All study patients were followed up until they developed leukaemia, were lost to follow-up, withdrew from the NHI programme, or until the end of the study without leukaemia (censored). Our primary endpoint was a diagnosis of leukaemia during follow-up.

FINDINGS:

Insurance claims data for 3 054 336 children younger than 18 years were randomly selected from all insured children in the NHIRD. We identified 282 360 children infected with enterovirus and 282 355 children not infected with enterovirus between Jan 1, 2000, and Dec 31, 2007. The incidence density rates of leukaemia were 3·26 per 100 000 person-years for the enterovirus-infected and 5·84 per 100 000 person-years for the non-enterovirus-infected cohorts. The risk of leukaemia was significantly lower in the enterovirus-infected cohort than in the non-enterovirus-infected cohort (adjusted subhazard ratio [SHR] 0·44, 95% CI 0·31-0·60; p<0·0001). Children infected with enterovirus have a reduced risk of both lymphocytic leukaemia (adjusted SHR 0·44, 0·30-0·65; p<0·0001) and acute myeloid leukaemia (adjusted SHR 0·40, 0·17-0·97; p=0·04). Herpangina and hand-foot-and-mouth disease were the main diseases associated with the reduced risk of leukaemia.

INTERPRETATION:

The association between enterovirus infection and the reduced risk of developing leukaemia supports Greaves' delayed infection hypothesis for the cause of childhood leukaemia.

BACKGROUND:

Most of the previous reports found cirrhosis patients with a high risk of subsequent tuberculosis (TB). However, data about the risk of developing liver cirrhosis in TB patients are limited. As a hepatitis endemic area, the risk of liver cirrhosis in patients with TB should be elucidated in Taiwan.

METHODS:

We conducted the study using Taiwan's National Health Insurance Research Database. Patients with TB (n = 9339) were identified as the TB cohort and matched with a control (n = 37 356). Each study participant was followed until diagnosis of liver cirrhosis, loss of follow-up, death, withdrawal from the insurance or until 31 December 2011.

RESULTS:

A cumulative incidence of liver cirrhosis in the TB cohort had a significantly higher risk for liver cirrhosis compared with the control (log-rank test, P < 0·001). The overall incidence of liver cirrhosis was significantly higher in the TB group than in controls [3·83 vs. 2·02 per 1000 person-year; crude hazard ratio (HR) = 1·88; 95% confidence interval (CI) = 1·59-2·23]. After controlling for age, gender and comorbidities, the risk was 1·79-fold (95% CI = 1·50-2·14) higher in the TB group than in the controls. Analysis by Cox proportional hazard regression revealed that TB increased the risk of cirrhosis in patients with either hepatitis B (adjusted HR = 1·91; 95% CI = 1·05-3·47) or hepatitis C (adjusted HR = 2·56; 95% CI = 1·37-4·78).

CONCLUSION:

An increased incidence of liver cirrhosis was observed among TB patients in Taiwan.