Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the prevalence of hyperthyroidism and hypothyroidism in giant cell arteritis and polymyalgia rheumatica. The prevalence of thyroid dysfunction in giant cell arteritis and polymyalgia rheumatica patients was determined retrospectively from 1976 through 1984 and prospectively from 1984 through 1991. A control group was composed of patients over 55 years of age consecutively admitted to the same hospital department for another condition. Patients were screened for thyroid dysfunction using a thyrotropin assay. Abnormal results were evaluated by T3 and T4 assays and, if needed, a TRH test. Among the 68 giant cell arteritis patients (mean age 72.6 +/- 7 years), of which 41 were included in the prospective arm of the study, 6 had hypothyroidism and 3 had hyperthyroidism. Corresponding figures were 4 and 4 among the 36 patients with polymyalgia rheumatica (mean age 71.7 +/- 8.3 years), of which 18 were evaluated prospectively. Among the 305 controls (mean age 71.6 +/- 9.4 years), 16 had hypothyroidism and 10 had hyperthyroidism. Prevalences of hypothyroidism, hyperthyroidism, and antithyroid antibodies were not significantly different in the control and case groups. Data fail to support previous suggestions that giant cell arteritis or polymyalgia rheumatica patients may be an increased risk for hypothyroidism or hyperthyroidism. They lend no indirect support to the hypothesis that giant cell arteritis and polymyalgia rheumatica may be autoimmune disorders.
 ...
PMID:[Prevalence of hypothyroidism and hyperthyroidism in temporal arteritis and rhizomelic pseudopolyarthritis. A controlled study of 104 cases]. 814 48

Analysis of TBP gene sequences from a variety of species for clustering of short sequence motifs and for over- and underrepresentation of short sequence motifs suggests involvement of slippage in the recent evolution of the TBP N-terminal domains in metazoans, Acanthamoeba and wheat. AGC, GCA and CAG are overrepresented in TBP genes of other species, suggesting that opa arrays were amplified from motifs overrepresented in ancestral species. The phylogenetic distribution of recently slippage-derived sequences in TBP is similar to that observed in the large subunit ribosomal RNAs, suggesting a propensity for certain evolutionary lineages to incorporate slippage-generated motifs into protein-coding as well as ribosomal RNA genes. Because length increase appears to have taken place independently in lineages leading to vertebrates, insects and nematodes, TBP N-terminal domains in these lineages are not homologous. All gene duplications in the TBP gene family appear to have been recent events despite strong protein sequence similarity between TRF and P. falciparum TBP. The enlargement of the TBP N-terminal domain may have coincided with acquisition of new functions and may have accompanied molecular coevolution with domains of other proteins, resulting in the acquisition of new or more complex mechanisms of transcription regulation.
 ...
PMID:Evolution of sequence repetition and gene duplications in the TATA-binding protein TBP (TFIID). 833 91