Serum IgA-TTG measurement is effective and at least as good as IgA-EMA in the identification of coeliac disease. Due to a high percentage of poor histological specimens, the diagnosis of coeliac disease should not depend only on biopsy, but in addition the clinical picture and serology should be considered.

The mechanism behind the pronounced effect of estrogen on CRP is most likely an effect on gene expression in the liver. Strong support for this assumption that this effect is mediated by estrogen itself and not by a factor stimulated by estrogen comes from the observations that the effect is dose-dependent, is seen in both women and men, and occurs only after oral treatment. It is not clear whether the effect of estrogen on gene expression is mediated by transcriptional activation or RNA stabilization. No hormone response elements have been discovered in the promoter of the CRP gene, but one study has shown that estrogen can stimulate the transcription factor C/EBP-␤, which is involved in CRP transcription (9 ).Our data contradict findings in mice transgenic for human CRP, in which testosterone but not estrogen was essential for expression of both unstimulated and acutephase CRP (10 ). This discrepancy could be explained by the fact that the transgenic mice had the human CRP gene integrated into another chromosomal context. Because of study design, we cannot exclude that testosterone has an effect on expression of the CRP gene.The findings of the present study might be of major relevance because CRP is associated with an increased risk of CHD, and hormone replacement therapy has been shown to increase the risk of CHD (11 ). In addition, in the present study, patients who underwent estrogen therapy had more cardiovascular events (6 ).One limitation of the present study is that participants suffered from prostate cancer, which could possibly, through some unknown mechanism, trigger CRP expression independently of IL-6. However, the randomized design of the study, which produced treatment groups that were balanced regarding severity of disease, should minimize this risk. In this context, it cannot be excluded that estrogen might have pro-inflammatory effects on the prostate itself. However, the correction for IL-6 stimulation of CRP is likely to exclude this reason for the difference in circulating CRP concentrations between the two groups. Another limitation is that the analyses were performed on blood samples that had been frozen for more than 20 years. Such long-term storage might lead to concentration of samples as a result of freeze drying. Speaking against such an effect is the fact that serum CRP concentrations were within the reference interval. Furthermore, freeze-drying effects would most likely affect both treatment groups similarly.In conclusion, we have shown that estrogen treatment in middle-aged and elderly men is associated with increased circulating CRP concentrations, indicating a role for estrogen in the regulation of unstimulated CRP. The results clearly emphasize the need for further molecular studies of hormonal effects on the regulation of CRP expression. Testosterone and IL-6 requirements for human C-reactive protein gene expression in transgenic mice. J Immunol 1998;160:5294 -9. 11. Seed M, Knopp RH. Estrogens, lipoproteins, and cardiovascular risk factors:an update following the randomized...

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