The natural course of hepatitis B and hepatitis C virus infection

Chronic hepatitis B and hepatitis C virus infections maintain a significant risk for the development of liver cirrhosis and hepatocellular carcinoma and cause a considerable morbidity in the population. Among patients with chronic HBV infection and histologically confirmed hepatitis the annual incidence of liver cirrhosis is 2%. The risk for hepatocellular carcinoma in chronic HBsAg carriers is elevated about 40-230 fold. 20-30% of patients with chronic HCV infection will develop cirrhosis over 20-30 years. Hepatocellular carcinoma evolves yearly in about 3% of patients with chronic HCV infection and cirrhosis, whereas HCV-carriers without cirrhosis usually do not develop hepatocellular carcinoma. The high incidence of serious sequelae warrants a regular surveillance of chronic virus carriers.     

The course and outcome of viral hepatitis B in drug-addicted patients

In this paper, characterization is given of clinical and biochemical features of VH B course against the background of narcomania. Recordable in such patient populations are high percentage of delta hepatitis (14.2%), unusual severity of the intoxication syndrome, protracted course with exacerbations (12.2%) and recurrences (8%), outcome being a chronic hepatitis (14.2%), slower normalization of biochemical indicators, persistently low ratio of AIAT activity in diluted and whole blood sera. The persistence of viral markers in drug addicts discharged from the hospital (68%) is fraught with danger of spreading viral hepatitis of prophylactic measures are not strictly observed.     

Histologic distribution of hepatitis A, B, C, D, E, and G with concomitant cytokine response in liver tissue

BACKGROUND: Studies focusing on the economic impact of cancer on families have emphasized that costs of chronic disease are substantial for patients and their families. However, little effort has been devoted to measuring the costs of care for families of patients hospitalized with stroke. METHODS: A total of 215 stroke patients and their families from four teaching hospitals in the Taipei metropolitan area were monitored from the date of the patient's admission to hospital until the date of discharge. The value of labor contributed by families was estimated by assigning the current monetary market rate of providing health aide to the time families spent caring for patients in hospital. Lost earnings of patients and families, expenditure for medical care, and expenses for food, clothes, adult diapers, transportation and other miscellaneous items were determined and summed to arrive at the total family cost of providing care. RESULTS: The average cost of care for one family per inpatient day was NT$4,358.20. A total of 98.6% of the families incurred labor costs, which accounted for about half of family costs for providing care. Hospital bills accounted for almost 19% of total family costs. The income loss for families and patients accounted for about 25% of total family costs. Expenses for food, clothes, transportation, diapers and other illness-related miscellaneous items accounted for about 12% of total family costs. Multiple regression analyses demonstrated that the number of family members involved in giving care and the length of stay are important predictors for the total cost of care. Average total family costs per day increased by 24.3% when an additional family member was involved in providing care. Total family costs increased 2.5% for each hospital day. CONCLUSIONS: If direct and indirect nonmedical costs are not included in the total cost calculation for providing hospital care to stroke patients, the economic impact of care on families is likely to be underestimated.     

Hospital-acquired pneumonia: epidemiology, etiology, and treatment

Despite improvements in diagnosis, treatment, and prevention, hospital-acquired pneumonia (HAP) remains the number one cause of nosocomial mortality. This article reviews the current knowledge regarding the incidence, epidemiology, and causes of HAP, with the appreciation that the available information is incomplete and that controversies are common, and thus the authors provide a rational approach to the initial management of HAP in immunocompetent adults. A discussion of therapy and what to do with patients who do not respond to the empiric therapy are included. The American Thoracic Society (ATS) statement on HAP has served as a foundation for this review but has been supplemented by newer literature that was not available when the ATS statement was developed.     

Hantavirus pulmonary syndrome: epidemiology, prevention, and case presentation of a new viral strain

Hantavirus pulmonary syndrome (HPS) is a viral infection from a new strain of Hantavirus. The Hantavirus was first discovered in North America in 1993 after an outbreak of fatal illness on a Navajo Indian reservation in New Mexico. Since then, 122 cases of HPS (with a high mortality rate of more than 50%) have been reported in 23 states, with the highest prevalence in the Four Corners area. The reservoir for Hantavirus is small rodents, mostly field mice, vole, and chipmunks. It is transmitted through inhalation of airborne virus from dry rodent excreta and saliva. A North American strain of Hantavirus, named ain nombre virus (SNV), primarily affects the lungs, causing rapid accumulation of fluids and leading to noncardiogenic pulmonary edema, pleural effusion, and acute respiratory distress syndrome (ARDS). In the prodromal stage, HPS presents with flu-like symptoms, nausea, vomiting, and gastrointestinal pain and is often mistaken on the first visit for other infectious diseases or gastroenteritis. In the second acute stage, rapid respiratory deterioration begins: HPS is often misdiagnosed for pneumonia, idiopathic ARDS, and pulmonary edema. HPS treatment with an experimental antiviral intravenous drug, ribavirin, is under investigation. Practitioners must possess through clinical knowledge on the diagnoses, pathology, treatment, and course of the disease to reduce the mortality and morbidity rate of this rare but serious infection. A case report based on a recent HPS death in New York State on Long island in April 1995 is presented.     

Dengue virus infection: epidemiology, pathogenesis, clinical presentation, diagnosis, and prevention

OBJECTIVES: To investigate whether the isolated urinary bladder spontaneously releases substance P (SP) or bradykinin (BK), which can act as potent mediators of pain and inflammation of the urinary bladder, and whether peptidase inhibitors enhance peptide release. MATERIALS AND METHODS: Urinary bladder segments (2 x 10 x 0.8-1 mm) were isolated from guinea pigs and studied in vitro; tissue contraction was assessed using force-displacement transducers and the release of peptides by specific enzyme immunoassays. RESULTS: In the absence of any exogenous agonists, the inhibition of neutral endopeptidase and angiotensin-converting enzyme by phosphoramidon and captopril, respectively, increased the frequency and magnitude of spontaneous motility of isolated bladder strips. Phosphoramidon increased the net release of SP-like immunoreactivity (SP-LI) and captopril increased the net release of SP-LI and BK-LI, concomitant with contraction. Peptide-LI was recovered primarily from bladder mucosa and to a lesser degree from detrusor smooth muscle. Similarly, peptidase inhibitors primarily affected the bladder mucosa; phosphoramidon induced a fourfold increase in SP-LI and captopril induced a significant increase of SP-LI and BK-LI from the mucosa. Tissues contracted in response to peptidase inhibitors in the presence of atropine and indomethacin, but contraction was reduced significantly by in vitro capsaicin desensitization or removal of bladder mucosa. BK stimulated SP-LI release from mucosa but not detrusor. SP stimulated increased BK-LI release from mucosa and detrusor. CONCLUSIONS: These findings indicate the basal release of peptide-like immunoreactivity by isolated bladder and further support the concept that peptidases located in the bladder mucosa are important in terminating the effects of endogenous peptides.     

Alcoholism, hepatitis B and C viral infections, and impaired liver function among Taiwanese aboriginal groups

Viral hepatitis and alcoholism prevail in four major Taiwanese aboriginal groups. To study the relative importance of the acquisition of hepatitis B virus or hepatitis C virus infection and alcoholism to the presence of impaired liver function in these groups, the authors conducted a semistructured clinical interview for alcoholism and test for seromarkers for viral hepatitis among 993 cohort members enrolled in 1990-1992 in an ongoing prospective study (Taiwan Aboriginal Study Project). The subjects' blood specimens were tested for serum alanine aminotransferase/aspartate aminotransferase levels and for the presence of hepatitis B surface antigen and anti-hepatitis C virus antibody. The prevalence of a combination of an alanine aminotransferase level of > 35 IU/liter and an aspartate aminotransferase level of > 40 IU/liter, implying impaired liver function or advanced liver disease, was 4.3% overall. Univariate and multiple logistic regression analysis showed that, rather than chronic hepatitis B virus infection, hepatitis C virus infection and alcoholism were the two dominant risk factors that signalled the risk of liver damage among these Taiwanese aborigines. In addition, these two contributing factors were able to act synergistically to cause impaired liver function.     

Vascular dementia: a contemporary review of epidemiology, diagnosis, prevention, and treatment

The past decade has seen a renewed interest in vascular dementia. Key epidemiologic studies have examined the prevalence, incidence, course and risk factors of vascular dementia. New classification systems have been developed to improve the reliability of the diagnosis, and there have been advances in diagnostic methodology, such as neuroimaging and neuropsychological assessment. New treatments for vascular dementia are being developed to protect the brain from cerebral ischemia and to limit progression of cognitive impairment. Diagnostic criteria for vascular dementia remain to be validated by carefully designed, systematic, clinicopathologic study. Once such criteria are validated, meaningful study of subgroups of vascular dementia can be explored. Until the relationship between vascular dementia and Alzheimer's disease is better defined, the nosology for vascular dementia may be defined best as dementia associated with stroke.