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R Speck

Publications and source records attributed to R Speck.

9 recordsLinked to original sources
PubMed2006

[Risk of infection during treatment with tumor necrosis factor-alpha inhibitors].

Tumor necrosis factor-alpha (TNF) is essential for immune defense. TNF plays a major role in the recruitment of inflammatory cells to the site of infection and in the formation and maintenance of granulomas. In addition, it plays a primary and detrimental role in chronic autoimmune diseases. Drugs that inhibit TNF are effective in the treatment of inflammatory rheumatic and autoimmune diseases. However, the three currently available TNF antagonists (etanercept, infliximab and adalimumab) decrease host resistance to granulomatous diseases such as tuberculosis. The incidence of tuberculosis in patients treated with TNF antagonists is higher than in the general population. There are a number of case reports describing the association of TNF-antagonists and the presentation of other infectious diseases such as histoplasmosis, listeriosis, coccidioidomycosis, candidiasis and aspergillosis. These case reports, however, are anecdotal. Nonetheless, patients treated with TNF antagonists are immunocompromised and infectious diseases are most likely more frequent and may present differently than expected. In this review, we describe the role of TNF in constraining infectious diseases, the difference between the three available TNF antagonists, and we discuss the relevant clinical data published in the literature as related to the risk of anti-TNF therapy for infectious diseases.

Antirheumatic Agents↗
PubMed1999

Resistance mutations to zidovudine and saquinavir in patients receiving zidovudine plus saquinavir or zidovudine and zalcitabine plus saquinavir in AIDS clinical trials group 229.

The relationships among treatment regimens, plasma human immunodeficiency virus (HIV) RNA levels, and resistance mutations to saquinavir (codons 48 and 90) and zidovudine (codon 215) were examined in a cohort of 144 patients from the AIDS Clinical Trials Group 229 study. After 24-40 weeks of therapy, no patients who had received the two-drug combination (zidovudine plus saquinavir) had only codon 48 mutations, 45.8% had only codon 90 mutations, and 8.3% had both codon 48 and 90 mutations. Mutations developed by patients who had received the three-drug combination (zidovudine and zalcitabine plus saquinavir) were codon 48 alone in 1.4%, codon 90 alone in 33.3%, and both codons 48 and 90 in 4.2%. The difference between the groups showed a trend toward reduced mutations with three versus two drugs but did not reach significance (P=.11, two-sided chi2). Higher baseline HIV RNA levels correlated with the development of protease mutations. Mutations at codon 215 were present in 82% of all patients at baseline and in 87% after therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1991

[Determination of alcohol dehydrogenase genotype: no correlation between isoenzyme pattern and liver cirrhosis].

Mounting evidence from various fields of research links the oxidation product of alcohol, acetaldehyde, with the development of alcohol abuse-related pathology. One factor governing the production of acetaldehyde is the genetically determined pattern of class I alcohol dehydrogenase isoenzymes, consisting of "fast" beta 2 and gamma 1 and "slow" beta 1 and gamma 2 subunits. Alcoholics carrying the beta 2 and gamma 1 genes might, therefore, be more susceptible to alcohol-related liver disease. To verify this hypothesis we developed a method based on the polymerase chain reaction and restriction enzyme digestion in order to genotype individuals with respect to their alcohol dehydrogenase isoenzyme pattern. In a total of 100 caucasian individuals the following genotypes were determined: beta 1 beta 1, 92; beta 1 beta 2, 8; beta 2 beta 2 0; gamma 1 gamma 1, 38; gamma 1 gamma 2, 51; gamma 2 gamma 2, 11. No statistically significant differences in the distribution of isoenzymes were detectable between alcoholics with liver disease, patients with non-alcohol abuse-related liver disease, patients with rheumatoid arthritis and healthy controls.

Alcohol Dehydrogenase↗
PubMedDate not supplied

[Not Available].

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Austria↗