PubMed · 12349100
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C Stauffer. 1999. Building pyramids.. https://pubmed.ncbi.nlm.nih.gov/12349100/
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BACKGROUND: Although narrative reviews have concluded that there is strong support for familial clustering of prostate carcinoma, the association has never systematically been quantified in reviews. The purpose of this meta-analysis was to summarize and quantify the recurrence risk ratio with emphasis on the degree of relation, the specific relationship of the family member, the number of affected family members, and the age at diagnosis. METHODS: Publications were identified through computerized database searches for epidemiologic studies published up to December 2002. In addition, references cited in original and review papers were examined. Three blinded reviewers extracted both qualitative and quantitative information from each paper. Using random effects meta-regression analyses, the authors calculated summary recurrence risk ratios (S(lambda)). The reviewers also evaluated changes in S(lambda) according to differences in study methodology. RESULTS: Thirty-three epidemiologic studies were included in the current review. S(lambda) was 2.53 (95% confidence interval, 2.24-2.85) for first-degree family members. S(lambda) appeared to be greater for men with an affected brother than for men with an affected father. S(lambda) for men who had second-degree relatives with prostate carcinoma was only slightly elevated. The nature of the familial clustering is such that S(lambda) increases with decreasing age of the patient and family members, with increasing genetic relatedness of the affected relative, and with increasing number of individuals affected within a family. CONCLUSIONS: The studies that were reviewed consistently demonstrate that family history is a significant risk factor for development of prostate carcinoma.
Previous studies reported an association between cortical Lewy body (LB) formation and dementia in Parkinson's disease (PD). However, it is unclear whether cognitive decline in this disorder is related to specific patterns of LB distribution within the cerebral cortex. Moreover, the prediction of cognitive status based on concomitant assessment of LB and Alzheimer's disease lesions has led to conflicting results. We performed a clinicopathological study in 22 elderly PD patients in whom parkinsonism preceded cognitive decline by at least 3 years. Cognitive status was assessed prospectively using the clinical dementia rating scale (CDR); quantitative assessment of LB, neurofibrillary tangles (NFT), and senile plaques (SP) was performed in Brodmann areas 9, 21, 24, 40 and the entorhinal cortex. Statistical analysis was performed using both correlation coefficients and logistic regression models. There was a highly significant correlation between CDR scores and regional LB scores in the entorhinal cortex and area 24. LB and SP densities in the entorhinal cortex accounted for 36.2% and 19.3% of the variability in CDR scores. LB densities in area 24 could explain 25.2% of this variability. NFT densities did not predict cognitive status. In multivariate models only LB densities in the entorhinal cortex and anterior cingulate cortex were significantly associated with CDR scores. These results imply that an assessment of LB pathology limited to the entorhinal cortex and area 24 may be sufficient to predict cognition in PD. They also suggest that LB formation in limbic areas may be crucial for the development of PD dementia.
The authors compared 130 patients treated for cervical dystonia with original botulinum toxin (BTX) type A (Botox; Allergan, Inc., Irvine, CA), 42 of whom were exposed only to the original BTX type A used before 1998 (25 ng protein/100 units), and 119 treated only with the current BTX type A (5 ng of protein/100 units). Blocking antibodies were detected in 4 of 42 (9.5%) patients treated only with original BTX type A but in none of the 119 patients treated exclusively with current BTX type A (p < 0.004). The current preparation decreased the risk of antibody formation by a factor of six. The authors conclude that the low risk of antibody formation after current BTX type A treatment is related to lower protein load.