Rapid decline of influenza vaccine-induced antibody in the elderly: is it real, or is it relevant?

Advisory committees have cautioned that influenza vaccine-induced antibody declines more rapidly in the elderly, falling below seroprotective levels within 4 months. We conducted a literature review to assess this assertion. The articles that were included in this review reported antibody levels > or =4 months after influenza immunization in persons > or =60 years old, interpretable in the context of annual influenza vaccine-approval criteria (seroprotection/seroconversion) specified by the Committee for Proprietary Medicinal Products (CPMP) for the elderly. The final review included 14 studies; 8 of which reported seroprotection rates. Seroprotection exceeding CPMP criteria was maintained > or =4 months after influenza immunization in all 8 of the studies reporting this for the H3N2 component and in 5 of the 7 studies reporting this for the H1N1 and B components. In determining whether CPMP criteria were met at season's end, primary antibody response appeared to be more relevant than secondary antibody decline. Both studies reporting seroprotection rates that failed CPMP criteria > or =4 months after influenza immunization for each of the H1N1 and B components had also reported failed seroprotection at 1 month after immunization. If initially achieved after immunization, seroprotection rates of 70%-100% were maintained not just at 4 months (2 studies) but also at 5 months (2 studies) and even at >6 months (4 studies), for the H3N2 and H1N1 vaccine components. Seroprotection rates appeared less consistent for the B vaccine component, throughout the postimmunization period. Seroconversion appears to vary substantially and inversely with preimmunization titers but not with age. In 2 of 6 studies reporting seroconversion alone, CPMP criteria were still met at 4 months. In the other 4 studies, the main reason for failure at 4 months was primary failure at 1 month. A total of 6 studies compared antibody persistence by age, and no consistent differences were found on that basis. The historic concern that the influenza vaccine-induced antibody response in the elderly declines more rapidly and below seroprotective levels within 4 months of immunization should be reconsidered.     

Acute hepatitis E complicated by acute pancreatitis: a case report and literature review

The coincidence of viral hepatitis and acute pancreatitis is well described. Most of the cases are related to acute hepatitis A or B. Hepatitis E virus (HEV) infections are rare in Europe, and very few reports describe HEV as a causative agent of acute pancreatitis in areas of endemic hepatitis E prevalence. We report a case of acute pancreatitis in the course of acute hepatitis E in a 28-year-old male patient. The majority of reported cases, including our case, show several common epidemiological and clinical features: young age, male predominance, onset of acute pancreatitis at the early stage of acute hepatitis, and favorable outcome. Acute pancreatitis should be considered in acute hepatitis E, especially in young, male patients presenting with severe epigastric pain early in the course of disease. The pancreatitis in these patients usually runs a benign course. The patients should be closely monitored because life-threatening complications have been reported.     

Participation of Phosphoinositides in Gastric Mucosal Protection by Colloidal Bismuth Subcitrate against Ethanol-Induced Injury

The mechanism of gastric mucosal protection by an antiulcer agent, colloidal bismuth subcitrate (CBS), against ethanol-induced injury was investigated using in vivo and in vitro systems. The experiments in vivo were conducted with groups of rats with and without indomethacin pretreatment, and the animals received either a dose of CBS (100 mg/kg) or a vehicle (saline), followed 30 min later by ethanol. In the in vitro studies, gastric mucosa segments were cultured in the presence of CBS, ethanol, or both. The results of in vivo experiments revealed that in the absence of CBS, ethanol caused extensive gastric hemorrhagic lesions which were significantly reduced following CBS pretreatment and this effect of CBS was not prevented by indomethacin. The data obtained with gastric mucosal culture established that in comparison to the controls, ethanol caused a 27% decrease in mucin synthesis, while mucin synthesis in the presence of CBS increased by 48%. The increase in mucin synthesis evoked by CBS was accompanied by the enhanced metabolism of mucosal phosphoinositides, as reflected by a decrease in PI (15%) and PIP2 (30%), and an increase in IP1 (26%) and IP3 (67%). In contrast, ethanol, which exhibited detrimental effect on mucin synthesis, caused a decrease in PIP (35%), IP2 (47%) and IP3 (38%), and an increase in PIP2 (80%), and IP1 (51%). However, when the mucosal culture was carried out in the presence of both CBS and ethanol, the detrimental changes evoked by ethanol on mucin synthesis were prevented, and the phosphoinositide and inositide phosphate distribution patterns were quite similar to those in the mucosa cultured in the presence of CBS only.(ABSTRACT TRUNCATED AT 250 WORDS)     

Monocyte chemotactic protein-1 and soluble adhesion molecules as possible prognostic markers of the efficacy of antiviral treatment in chronic hepatitis C

AIM: To explain the role of Monocyte chemotactic protein-1 (MCP-1) and soluble adhesion molecules in chronic hepatitis C during the treatment of interferon alpha (IFNα) 2 b and ribavirin (RBV).METHODS: Concentrations of MCP-1, soluble adhesion molecules intercellular adhesion molecule-1 (sICAM-1), sPselectin, interleukin (IL) 6, and ILl0 in serum were estimated in the group of 40 patients with chronic hepatitis C treated with IFNalpha2 b and RBV in 0, 16, 32, 48 wk of the therapy.RESULTS: In chronic hepatitis C, before and during the treatment, the serum levels of MCP-1 and sP-selectin in responders were similar to those of healthy subjects. In nonresponders (NR), MCP-1 increased in the course of IFN(α+RBV treatment, differences were statistically significant as compared to responders. MCP-1 correlated statistically with the activity of periportal inflammation (r= 0.35, P<0.05) but not with staging of liver fibrosis, sICAM-1 positively correlated with inflammatory activity and fibrosis in NR. sP-selectin did not correlate with histological findings in the liver. The MCP-1 correlated with the soluble form of sP-selectin concentrations (r= 6, P<0.001) and with IL-10 level in NR (r = 0.4, P<0.05). There was no correlation observed between the concentration of MCP-1 and sICAM-1, IL-6 during the treatment.CONCLUSION: MCP-1 concentration may be a prognostic marker of the efficacy of IFN+RBV therapy in patients with chronic hepatitis C.     

Massive myocardial hypertrophy in hypertrophic cardiomyopathy: a risk factor for sudden death and high defibrillation threshold during cardioverter-defibrillator implantation

Two cases of hypertrophic cardiomyopathy with massive hypertrophy and high defibrillation threshold (DFT) are described. A 14-year-old boy, whose single risk factor for sudden death was extreme hypertrophy with maximum interventricular septum (IVS) thickness of 43 mm, survived an episode of ventricular fibrillation. During ICD implantation DFT testing showed energy requirements >30 J and the procedure was aborted. Amiodarone and verapamil treatment was discontinued and treatment with oral sotalol was instituted. After a period of amiodarone washout the procedure was repeated and DFT of 24 J was encountered. An 18-year-old female with massive hypertrophy (IVS thickness=35 mm) and other risk factors for sudden death underwent ICD implantation for primary prevention. During the procedure DFT=20 J and ICD with 30 J maximal output was implanted. An increase in DFT to more than 20 J was encountered during pre-discharge test. Lack of 10 J safety margin warranted ICD system revision and upgrade; during the second procedure DFT was 24 J and ICD with 35 J maximal output was implanted. In summary, in both cases ICDs with 35 J maximal output were successfully implanted.     

Microvillous Inclusion Disease: Report of a Case with Atypical Features

Microvillous inclusion disease is a rare lethal disorder characterized by intractable, severe, watery diarrhea beginning in early infancy. The underlying defect is thought to be an autosomal recessive genetic abnormality resulting in defective brush-border assembly and differentiation. Normally, this diagnosis is easily established through the electron microscopic demonstration of characteristic microvilli-lined inclusions lying within the apical cytoplasm of surface enterocytes. In a small number of patients appearing to have microvillous inclusion disease it has not proven possible to demonstrate the typical inclusions. The existence of another entity, termed intestinal microvillous dystrophy, has been proposed to account for such occurrences. This assertion was founded in large part upon the observation that the few subjects studied all displayed a slightly atypical clinical presentation. The case now being presented exhibited the morphologic features ascribed to intestinal microvillous dystrophy but had a clinical presentation that was entirely typical of microvillous inclusion disease. It serves thus to conceptually unite intestinal microvillous dystrophy with microvillous inclusion disease.