Clinical significance of occult hepatitis B virus infection in chronic hepatitis C patients

Background/Aims

We investigated the frequency of occult hepatitis B virus (HBV) infection in anti-hepatitis C virus (HCV)-positive individuals and the effects of occult HBV infection on the severity of liver disease.

Methods

Seventy-one hepatitis B virus surface-antigen (HBsAg)-negative patients were divided according to their HBV serological status into groups A (anti-HBc positive, anti-HBs negative; n=18), B (anti-HBc positive, anti-HBs positive; n=34), and C (anti-HBc negative, anti-HBs positive/negative; n=19), and by anti-HCV positivity (anti-HCV positive; n=32 vs. anti-HCV negative; n=39). Liver biopsy samples were taken, and HBV DNA was quantified by real-time PCR.

Results

Intrahepatic HBV DNA was detected in 32.4% (23/71) of the entire cohort, and HBV DNA levels were invariably low in the different groups. Occult HBV infection was detected more frequently in the anti-HBc-positive patients. Intrahepatic HBV DNA was detected in 28.1% (9/32) of the anti-HCV-positive and 35.9% (14/39) of the anti-HCV-negative subjects. The HCV genotype did not affect the detection rate of intrahepatic HBV DNA. In anti-HCV-positive cases, occult HBV infection did not affect liver disease severity.

Conclusions

Low levels of intrahepatic HBV DNA were detected frequently in both HBsAg-negative and anti-HCV-positive cases. However, the frequency of occult HBV infection was not affected by the presence of hepatitis C, and occult HBV infection did not have a significant effect on the disease severity of hepatitis C.     

The immunoreactivity and activity of adenylate cyclase type I are changed in the hippocampal CA1 region after transient forebrain ischemia in gerbils

Adenylate cyclase (AC) has a specific sensitivity to Ca²⁺/calmodulin. AC-I, one of the mediator of learning and memory, plays an important role in signal transduction underlying learning and memory function. In the present study, we found ischemia-related changes of AC-I in the hippocampal CA1 region, but not in the CA2/3 region, after 5 min of transient forebrain ischemia in gerbils. In the sham-operated group, AC-I immunoreactive neurons were detected in pyramidal and non-pyramidal cells in the hippocampus proper. AC-I immunoreactivity was significantly increased at 3 h in the CA1 region after ischemic insult. Thereafter, AC-I immunoreactivity was gradually decreased. Four days after ischemic insult, AC-I-immunoreactive CA1 pyramidal cells in the stratum pyramidale were very few due to delayed neuronal death. The results of Western blot analysis showed that changes of AC-I protein contents were similar to immunohistochemical data after ischemic insult. Gpp(NH)p-dependent AC-I activity in hippocampal CA1 region was not changed in all groups, while Ca²⁺/calmodulin-dependent AC-I activity in hippocampal CA1 region was significantly decreased 24 h after ischemia–reperfusion. These results suggest that the decrease of AC-I activity may be associated with impairment of neurodevelopment and neuroplasticity including learning and memory although the AC-I immunoreactivity was maintained 24 h postischemic group compared to that of the sham-operated group.     

Computer-aided detection (CAD) of lung nodules and small tumours on chest radiographs

Detection of focal pulmonary lesions is limited by quantum and anatomic noise and highly influenced by variable perception capacity of the reader. Multiple studies have proven that lesions - missed at time of primary interpretation - were visible on the chest radiographs in retrospect. Computer-aided diagnosis (CAD) schemes do not alter the anatomic noise but aim at decreasing the intrinsic limitations and variations of human perception by alerting the reader to suspicious areas in a chest radiograph when used as a ‘second reader’.Multiple studies have shown that the detection performance can be improved using CAD especially for less experienced readers at a variable amount of decreased specificity. There seem to be a substantial learning process for both, experienced and inexperienced readers, to be able to optimally differentiate between false positive and true positive lesions and to build up sufficient trust in the capabilities of these systems to be able to use them at their full advantage. Studies so far focussed on stand-alone performance of the CAD schemes to reveal the magnitude of potential impact or on retrospective evaluation of CAD as a second reader for selected study groups. Further research is needed to assess the performance of these systems in clinical routine and to determine the trade-off between performance increase in terms of increased sensitivity and decreased inter-reader variability and loss of specificity and secondary indicated follow-up examinations for further diagnostic workup.     

Old people reporting childhood AD/HD symptoms: Retrospectively self-rated AD/HD symptoms in a population-based Swedish sample aged 65–80

Our knowledge of attention deficit/hyperactivity disorder (AD/HD) has increased in recent years. Little is still known about the course and manifestations in later parts of life and whether elderly persons who once presented childhood AD/HD symptoms can be identified. The aim of the study was to explore the occurrence to which elderly individuals retrospectively report symptoms that may indicate childhood AD/HD. The 25-item Wender Utah Rating Scale (WURS) was administered in a population-based sample of 2500 persons aged 65–80. Demographics, self-ratings of problems in childhood, current health and memory were also investigated. A total of 1599 individuals participated, which corresponds to a response rate of 64%. The prevalence of self-rated childhood AD/HD symptoms was 3.3% using a cut-off score of 36 or more in the WURS. Men rated significantly more AD/HD symptoms. Those who reported more childhood AD/HD symptoms also claimed general problems in childhood as well as worse current health. The proportion of individuals among 65–80-year-olds, who report childhood AD/HD symptoms is slightly lower but comparable with recent prevalence rates of childhood AD/HD. The study encourages further studies of AD/HD using a lifespan perspective.     

How heritable is Alzheimer's disease late in life? Findings from Swedish twins

Although genetic effects are known to be important for early onset Alzheimer's disease, little is known about the importance of genetic effects for late-onset disease. Furthermore, previous studies are based on prevalent cases. Our purpose was to characterize the relative importance of genetic and environmental factors for incident Alzheimer's disease late in life, and to test for differences in the importance of genetic effects at different ages. A cohort of 662 pairs of Swedish twins 52 to 98 years of age who were without symptoms of dementia was followed up for an average of 5 years. Incident dementia cases were detected through follow-up at 2 to 3-year intervals using either cognitive testing or telephone screening followed by dementia workups. A physician, psychologist, and nurse gave consensus diagnoses. During the follow-up period, 5.8% of the sample was diagnosed with Alzheimer's disease. Average age of onset was 83.9 years (standard deviation, 6.3). Of the 26 monozygotic pairs in which at least one twin developed Alzheimer's disease, 5 were concordant (probandwise concordance, 32.2%). The concordance rate for dizygotic pairs was 8.7% (2 of 44 pairs). Structural model fitting indicated that 48% of the variation in liability to Alzheimer's disease could be attributed to genetic variation. Estimates did not differ significantly between twins younger than age 80 years and those older than age 80 years at baseline. Although these genetic estimates for incident disease are lower than those for prevalent disease, the importance of genetic factors for liability to Alzheimer's disease is considerable even late in life.