Outcomes following liver transplantation for seronegative acute liver failure: experience during a 12-year period with more than 100 patients.

Seronegative hepatitis is a common cause of acute liver failure (ALF) requiring liver transplantation. The primary aim of this study was to examine outcomes following transplantation in this group and to identify factors associated with early (<2 months) mortality. Patients studied were 110 consecutive cases of seronegative ALF transplanted at the Queen Elizabeth Hospital, Birmingham, between January 1992 and January 2004. Univariate analysis of 44 pretransplantation recipient, donor, and operative variables was performed initially to identify factors associated with early posttransplantation mortality. Variables identified as significant or approaching significance were analyzed using stepwise multiple logistic regression analysis. Survival following transplantation for seronegative hepatitis was 83%, 81%, and 73% at 2, 12, and 60 months, respectively. The majority (71%) of deaths occurred within the 1st 2 months and sepsis / multiorgan dysfunction was the most common cause of early death. Univariate analysis revealed 9 variables predicting early death. Subsequent multivariate analysis identified high donor body mass index (BMI; a possible surrogate marker for hepatic steatosis) as the most important predictor of early death (P = .009; odds ratio, 1.2; 95% confidence interval, 1.0-1.3). Recipient age >50 (P = .015; odds ratio, 4.2; 95% confidence interval, 1.3-14.1) and non-Caucasian recipient ethnicity (P = .015; odds ratio, 4.9; 95% confidence interval, 1.2-19.2) were other variables associated with early death on multivariate analysis. This study specifically examined factors that determine the early outcome of transplanted seronegative ALF patients. In conclusion, we found that donor and recipient factors identify patients who have a high chance of early death after transplantation.     

Cerebral infarction associated with protein C deficiency following allogeneic bone marrow transplantation.

Hypercoagulable states associated with deficiencies in circulating anticoagulant protein C occur after chemotherapy for a variety of malignant diseases. Protein C deficiency also occurs following bone marrow transplantation (BMT) and may be responsible for a variety of transplantation-associated complications. We report the case of a child who suffered a stroke associated with low protein C antigen and activity occurring 11 months after allogeneic BMT. Protein C levels recovered spontaneously by 18 months after BMT. We speculate that the protein C deficiency and and resultant hypercoagulable state led to the stroke, and the deficiency of this anticoagulant was a sequela of the transplant.     

Screening for sexually transmitted diseases during preparticipation sports examination of high school adolescents.

In an urban school district, 636 students in grades 9-12 were tested for Chlamydia trachomatis and Neisseria gonorrhoeae by ligase chain reaction assays using specimens collected for routine urinalyses during sports physical examinations. Chlamydia and gonorrhea prevalences were 2.8% and 0.7% among males, and 6.5% and 2.0% among females, respectively. Among athletes infected with either sexually transmitted disease (STD), 93.1% reported no symptoms, and treatment was documented for 75.9%. Sports physicals offered a unique opportunity to screen and treat adolescents for STDs and to provide STD-prevention counseling.     

Gliadin antibody detection in gluten enteropathy

Circulating antigliadin antibody has been described in patients with gluten enteropathy although the prevalence varies in different studies. It has been suggested that the investigation for antigliadin antibody might be useful as a screening test. The object of the present study was to evaluate two different techniques for assaying these antibodies — an indirect immunofluorescent method and an enzyme-linked immunosorbent assay (ELISA). Antibodies were assayed in the sera of 102 patients in whom jejunal biopsies were also obtained. The specificity of both tests was greater than 95%, and the correlation between the presence of antibody and histology was significant (p < 0.005), though the sensitivity of each test was less than 70%.     

Molecular interactions during pregnancy: Association between mannan binding protein deficiency and recurrent miscarriage

The distribution of mannan binding protein (MBP) in blood donorsera was determined by enzyme-linked immunosorbent assay toestablish normal concentrations. Abnormally low MBP concentrationswere found in 16% (21 out of 135) of female partners and 14%(15 out of 108) of male partners of couples experiencing recurrentmiscarriage, compared with <5% of obstetrically normal controls(P < 0.005). This relationship was even stronger (9.5 versus1.0%) and more significant (P < 0.002) when only subjectspresumed to be homozygous for the mutant allele responsiblefor MBP deficiency were considered. By immunohistochemistry,MBP could be demonstrated in first trimester placenta. We suggestthat low concentrations of MBP within the feto-placental unitincrease susceptibility to fetal loss, possibly via an infection-inducedplacental cytokine imbalance.     

Role of Eotaxin-1 (CCL11) and CC chemokine receptor 3 (CCR3) in bleomycin-induced lung injury and fibrosis

Eotaxin-1/CCL11 and its receptor CCR3 are involved in recruitment of eosinophils to diverse tissues, but their role in eosinophil recruitment in pulmonary fibrosis is unclear. The present study examined the pulmonary expression of CCL11 and CCR3 during bleomycin (blm)-induced lung injury and determined their importance in the recruitment of inflammatory cells and the development of lung fibrosis. In mice, blm induced a marked pulmonary expression of CCL11 and CCR3. Immunostaining for CCR3 revealed that this receptor was not only expressed by eosinophils but also by neutrophils. CCL11-deficient (CCL11(-/-)) mice developed significantly reduced pulmonary fibrosis. Expression of profibrotic cytokines such as transforming growth factor-beta1 was diminished in the absence of CCL11. Furthermore, increased lung expression of CCL11 significantly enhanced blm-induced lung fibrosis and production of profibrotic cytokines. These effects were also associated with an increase of eosinophil and neutrophil pulmonary infiltration. In contrast, mice treated with neutralizing CCR3 antibodies developed significantly reduced pulmonary fibrosis, eosinophilia, neutrophilia, and expression of profibrotic cytokines. Together, these data suggest that CCL11 and CCR3 are important in the pulmonary recruitment of granulocytes and play significant pathogenic roles in blm-induced lung fibrosis.     

Fibrillar anti-cellular antibody associated with mumps and measles infection

Fibrillar anti-cellular IgM antibody was found in sera of 8/10 children with acute mumps infection and in 8/12 children with acute measles infection. Absorption experiments showed that the antibody was against cellular components in cells of human origin and was unrelated to either viral antibody or to RF. Similar antibody was previously found in patients with MS.