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The −308G/A polymorphism of TNF-α influences immunological parameters in old subjects affected by infectious diseases (2005)

Cipriano, C. ; Caruso, C. ; Lio, D. ; [et al.]

Oxford, UK : Blackwell Science Ltd

International journal of immunogenetics 32 (2005), S. 0

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ISSN: 1744-313X

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Biology , Medicine

Notes: Abnormal increments of pro-inflammatory cytokines (IL-6 and TNF-α) characterize the outbreak of infectious diseases, which are the major cause of death in the elderly. A counterbalance to the inflammation is exerted by IL-10 with an inhibitory role on TNF-α production. As is well known, some cytokine gene polymorphisms influence the cytokine production, playing a role as susceptibility or resistance factors against immune-mediated and infectious disease. Genetic variations in the −308A/G locus for TNF-α seems to affect the clinical outcome of some infectious diseases. In fact, the −308A allele is associated with severe septic shock and death. On this basis, we have screened healthy old subjects, nonagenarians and old patients affected by the acute phase of chronic obstructive bronchitis and bronchopneumonia of bacteria origin for the −308G/A locus (PCR–RFLP). Subjects are grouped in A+ (AG, AA genotypes) and A– (GG genotype) and data on IL-6, TNF-α, IL-10, NK cell cytotoxicity, zinc and metallothioneins (MTs) gene expression (RT–PCR) were stratified according to different TNF-α genotypes. The frequency of the A allele was increased in infected patients in comparison with healthy old controls. No differences existed between A+ and A– young adult, old and nonagenarian controls in tested parameters. Conversely, A+-infected patients displayed elevated IL-6, TNF-α and MTmRNA, low IL-10 coupled with impaired NK cell cytotoxicity and lower zinc ion than A– patients. However, the data reported are gender independent. Therefore, the −308A polymorphism at the locus of TNF-α may be one of the susceptibility factor for infectious diseases in old persons, particularly considering its association to the increased release of pro-inflammatory cytokines and to the reduction of zinc release and MTs synthesis involved in the control of the inflammatory response. These data strongly suggest that the genetic screening of the −308G/A polymorphism may be a valid tool for identification of subjects needing a more appropriate therapy when affected by acute and/or recurrent infectious diseases.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1744-313X.2005.00490.x

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Liver abnormalities in Turner syndrome (1999)

Salerno, M. ; Di Maio, S. ; Gasparini, N. ; [et al.]

Springer

European journal of pediatrics 158 (1999), S. 618-623

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ISSN: 1432-1076

Keywords: Key words Alanine aminotransferase ; Aspartate aminotransferase ; γ-Glutamyl transferase ; Oestrogens ; Turner syndrome

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract We evaluated whether hepatic abnormalities represent a specific feature in girls with Turner syndrome (TS) or whether they are related to an increased susceptibility to hormonal therapies and/or other factors. Alanine aminotransferase, aspartate aminotransferase and γ-glutamyl transferase were monitored in 70 patients with TS for a mean period of 7.6 ± 4.2 years. An increase in serum liver enzymes was observed in 14 out of 70 girls (20%) at a mean age of 12.7 years; it was present at entry before hormonal therapy in 3 girls and developed thereafter during the follow up in the other 11. The increase in serum liver enzymes was never observed before the age of 7 years. In the majority of cases (10/14) it was drug related: in 50% the liver abnormalities were transient and self-limiting, in the remaining cases they required interruption of hormonal therapy. Hepatotoxicity was more frequently observed in girls treated with oestrogens or oxandrolone than in those treated with growth hormone. In a small number of cases, liver disease was either auto-immunity-related (2/14), or cryptogenic (1/14) with a benign and self-limiting course. Obesity was a frequent finding, but it played a likely pivotal role only in one patient. Conclusion Hepatic abnormalities are relatively frequent in Turner syndrome and surveillance of liver function should be included in the management of these patients independent of initiation of hormonal treatment.