Hepatitis C virus (HCV) can be transmitted to heart transplant recipients by donor organs. Mid‐term results were reported using HCV‐positive donors in patients at risk of imminent death (group I, n = ...10), or in patients who otherwise would not have been offered heart transplantation (group II, n = 10) because of age (9/10) or associated medical risk (1/10). Medical records pertaining to patients receiving HCV‐positive allografts between July 1994 and December 1999 were reviewed. The recipients consisted of 19 males and one female, with a median age of 54 years for group I and 66 for group II. The HCV RNA level, seroconversion of anti‐HCV antibody, biochemical liver dysfunction, and causes of death were examined. Older recipients received reduced immunosuppression. Two patients in group II were HCV positive and were also retransplants. The hospital mortality rate was 10% in group I and 20% in group II; both hepatitis C‐positive recipients died postoperatively prior to discharge. All predischarge deaths were related to multi‐system organ failure (MSOF). All 17 survivors were HCV negative prior to transplant. Of these, 4/17 seroconverted. HCV RNA was detected in two of them. At a median follow‐up of 26.4 months, 2/11 current survivors continue to test anti‐HCV positive and are RNA negative. Three‐year actual survival was 40% for group I and 70% in group II. Transplant coronary artery disease (TCAD) accounted for one postoperative death in group I. Current data show that four out of 11 survivors had developed TCAD at 3‐year follow‐up, yielding an actual freedom from TCAD rate of 12/17 (70%) at 3‐year follow‐up. Hepatitis C transmission using a donor heart as the reservoir is moderate (25%). Limited use of such donors is justified in selected patients. The risk for hepatic disease may be reduced by tailoring immunosuppression specifically for such recipients, particularly if they are at low risk of rejection. Further studies are necessary to define a possible association between HCV and TCAD.
Summary
Kawasaki disease (KD) is a pediatric systemic vasculitis of unknown etiology wherein genetic influence is suspected. Gene clusters within the HLA region at chromosome 6p21.3 have been linked ...to KD and other autoimmune disorders. As collagen is a strong autoantigen inducing chronic inflammation in patients with vasculitis, this study tests a hypothesis that single‐nucleotide polymorphism (SNP) of a collagen gene, COL11A2, located in this HLA region may affect susceptibility to Kawasaki disease and its arterial sequels. SNP sites rs2294478 (at promoter) and rs2076311 (at intron 19) were genome‐typed on 93 KD patients and 680 healthy subjects. Genotypic and allelic frequencies analyses found A allele at rs2076311 as a risk allele for KD. Clinical association study showed protective potential of C/C genotype at rs2294478 and A/A at rs2076311 for developing coronary artery lesions (CALs) in patients. In addition, C‐A haplotype of COL11A2 gene associates with KD development and can serve as a genetic marker to differentiate KD patients lacking CALs from those with such lesions. Our findings suggest the involvement of genetic variations of COL11A2 in Kawasaki disease and CAL formation.
A total of 317 Klebsiella pneumoniae and 291 Escherichia coli nonduplicate isolates were tested by the VITEK 2 system to evaluate its capability to detect extended-spectrum β-lactamases (ESBLs) among ...putative ESBL-producing isolates, in particular those with the coproduction of AmpC enzymes. β-lactamases produced by the test isolates had been characterised. The sensitivity and specificity for ESBLs were 98.9% and 98.5%, respectively. Ninety of the isolates were AmpC (CMY-2, CMY-8 or DHA-1) and ESBL (SHV and/or CTX-M) coproducers, and 74 isolates (82.2%) of them were flagged as ESBL producers. Our study indicates that the VITEK 2 system is an acceptable tool for ESBL detection among K. pneumoniae and E. coli isolates for laboratories where both imported AmpC and ESBLs are prevalent.
The normal ocular surface is covered by corneal, limbal, and conjunctival epithelial cells that, together with a stable preocular tear film, maintain its integrity. Severe damage to the limbal ...epithelial cells from chemical or thermal burns, the Stevens–Johnson syndrome, ocular cicatricial pemphigoid, contact lenses, severe microbial infection, or multiple surgical procedures or cryotherapy in the limbal region may lead to loss of the limbal epithelial cells.
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Limbal-cell deficiency is usually manifested by vascularization and chronic inflammation of the cornea, ingrowth of fibrous tissue, and corneal opacification.
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Patients with limbal epithelial-cell deficiency in one eye only, or in both eyes . . .
MF59-adjuvanted seasonal trivalent inactivated (ATIV) vaccine licensed since 1997 and MF59-adjuvanted pandemic H1N1 vaccines have been distributed to approximately 80M persons. Addition of the ...emulsion adjuvant to inactivated vaccine formulations provides for higher levels of antibody to the viral hemagglutinin (HA) in less responsive older adults, infants and children which, in the case of the pandemic vaccine, allowed only 3.75 μg of the HA to be immunogenic. The adjuvant also stimulates production of more broadly-reactive antibodies against strains that are mismatched to those in the vaccine, a potential advantage in the face of perennial influenza virus antigenic drift. In a field trial, ATIV was 89% efficacious in preventing laboratory-confirmed influenza in 6-<72 month old children, 81% more efficacious than the unadjuvanted control split vaccine while, in older adults, ATIV reduced community-acquired pneumonia and influenza hospitalizations in adults >65 years old by 23% compared to unadjuvanted vaccine, in an observational study. The effectiveness of MF59 adjuvanted split pandemic H1N1 vaccine was 74% overall. Unadjuvanted pandemic vaccine was poorly immunogenic in HIV-infected persons, whereas their responses to MF59-adjuvanted vaccine were similar to those of healthy controls. Analyses of the clinical trials and pharmacovigilance databases and observational studies have shown that while MF59-adjuvanted influenza vaccines are more locally reactogenic, they have not been associated with an increased risk for various adverse effects (AE) of special interest, including unsolicited neurological or autoimmune events.
The literature search was performed within Medline, the Cochrane library, and Embase from 1966 to April 2001 with the following search terms: pain, local reaction, local inflammation, injection site ...reaction nociception, injection pain, needle pain, vaccines/complications, vaccines/contraindications, vaccines/toxicity, immunization/adverse effects, vaccines/adverse effects, immunization/complications, immunization/toxicity, immunization/contraindications, and humans. ...of the change in the original scope of the case definition, the WG agreed to broaden the original title of this AEFI from "Pain at or near injection site" to "Immunization site Pain."
Summary
Background Although psoriasis vulgaris (PV) is strongly associated with HLA‐Cw*0602, it has been proposed that the association of Cw*0602 is due to linkage disequilibrium and that other ...nearby genes are involved in PV susceptibility. The α‐helix coiled‐coil rod homologue (HCR) gene, located 110 kb telomeric to the HLA‐C locus, is presumed to be one of the PV candidate genes. Recently, a 10‐kb genomic segment, centromeric to HLA‐C, defined by two new single nucleotide polymorphisms (SNPs) n.7*A and n.9*C, was found to have a stronger association with psoriasis than the HCR gene. Until now, no study of the association of the HCR gene, SNPs n.7, and n.9 has been conducted on Chinese patients with psoriasis.
Objectives We aimed to determine whether the genetic polymorphisms of the HCR gene, SNPs n.7*A, and n.9*C were associated with an increased risk of psoriasis in Chinese patients.
Methods Using direct sequencing of the HCR gene and the genomic region containing SNPs n.7 and n.9, we investigated the HCR gene, SNPs n.7, and n.9 for disease association in 115 Chinese patients with psoriasis and 103 control subjects. The HCR SNPs were confirmed by denaturing high performance liquid chromatography. Genotyping for HLA‐Cw*0602 was also carried out using sequence‐based typing.
Results We observed a different allelic distribution between patient and control groups at nucleotide positions 386, 404, 1802 and 2406 of the HCR gene, and SNPs n.7, and n.9. The associations were much stronger in early onset PV patients (for HCR‐386*T and HCR‐404*T, odds ratio = 5·63, Pc < 0·0001). The HLA‐Cw*0602 also displayed a similar association with PV (odds ratio = 5·4, Pc < 0·0001). Moreover, SNP n.7*A, SNP n.9*C, Cw*0602, HCR‐386*T, HCR‐404*T and HCR‐1802*T were in linkage disequilibrium with each other. Haplotype‐based association analysis showed SNP n.7*A–SNP n.9*C–Cw*0602–HCR‐386*T–HCR‐404*T–HCR‐1802*T–HCR‐2406*G as a major susceptibility haplotype in this Chinese population (for early onset patients, odds ratio = 5·15, Pc < 0·0001).
Conclusions Our results indicate that the HCR gene, SNP n.7*A, and SNP n.9*C as well as Cw*0602 are major susceptibility markers for psoriasis in Chinese patients.
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