PubMed · 9270690
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T Riise. 1997. Cluster studies in multiple sclerosis.. https://doi.org/10.1212/wnl.49.2_suppl_2.s27
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BACKGROUND: Although tobacco is the primary etiologic factor for oral precancerous lesions in India, evidence from other sources indicates that diet may modify risk. This case-control study was designed to minimize a variety of biases in its attempt to investigate the relation between diet and oral precancerous lesions. METHODS: In a house-to-house survey of 5056 tobacco users in a rural area of Ernakulam district in Kerala, India, 226 individuals (44 females and 182 males) were found to have precancerous lesions (cases), which in 4 cases proved to be cancer. From among the examinees, an equal number of controls who were free of oral mucosal lesions and were matched to the cases regarding age (+/-5 years), gender, ward of residence, and use of tobacco also were enrolled. Dietary data were obtained using a customized interviewer-administered food-frequency questionnaire. All subjects and interviewers were blinded to the disease status of the subject. RESULTS: After controlling for tobacco use, intake of fruits, vegetables, and beta-carotene evinced inverse trends in risk (P<0.05), with an average reduction of over 10% per quartile of exposure. Associations with certain micronutrients appeared to differ according to gender, with an apparent 20% reduction in risk per mg of zinc consumed per day among men and the suggestion of an increased risk among those women in the lowest quartile of iron intake (an increase of approximately 2.5-fold) and ascorbic acid intake (an increase of approximately 70% increase) compared with other women (P<0.10). CONCLUSIONS: Consumption of vegetables, fruits, and several micronutrients may inhibit precancerous lesions of the oral cavity.
A fast and simple method for determination of sulfatides in the urine of patients with metachromatic leukodystrophy (MLD, arylsulfatase A deficiency) has been developed. The procedure consists of two steps: extraction of total urinary lipids by reversed-phase chromatography and their HPTLC separation. Two types of sorbents based on different matrixes were compared, of which the hydroxyethyl methacrylate C-18 type sorbent was found to be superior. Twenty-milliliter aliquots of urine are sufficient for the analysis. The technique is appropriate for simultaneous qualitative identification and semiquantitative densitometric determination and is suitable for routine work. The amount of sulfatides is expressed in relation to sphingomyelin, which copurifies with sulfatides and better reflects the level of membrane lipids in urine than commonly used parameters (creatinine, urine volume, etc.). The ranges were found to be 0.15-0.68 nmol sulfatide/nmol sphingomyelin for control individuals and 3.5-27.2 nmol sulfatide/nmol sphingomyelin for MLD patients. The excretion of sulfatides is pathonognomic for true MLD (due to the accumulation in kidney) and therefore its analysis is important for evaluation of suspected MLD cases including clinically and enzymatically atypical cases. The method is also useful as a complementary analysis for other lipidoses with high excretion of sphingolipids in urine (e.g., Fabry disease).
BACKGROUND: DFNB1, the locus of an autosomal recessive form of deafness due to mutations in the connexin-26 gene (CX26 or GJB2) is one of the most frequent hereditary defects in human beings. To date, no clinical characterisation of the DFNB1 inner-ear defects has been reported, which precludes the provision of prognostic information and genetic counselling. METHODS: We enrolled, in a prospective study, 140 children from 104 families affected by sensorineural deafness with various degrees of hearing loss. The children either belonged to a family affected by autosomal recessive deafness (DFNB family) or represented sporadic cases. We searched for mutations in the 5' non-coding exon and in the coding region of CX26. Audiometric and radiological features were investigated and compared in deaf children with and without CX26 mutations. FINDINGS: CX26 mutations were present in 43 (49%) of the 88 families with cases of prelingual deafness versus none of the 16 families with postlingual forms of deafness (p<0.01). The inner-ear defects of 54 prelingually deaf children with biallelic CX26 mutations were compared with the defects in 57 prelingually deaf children without CX26 mutations. DFNB1 deafness varied from mild to profound, associated with sloping or flat audiometric curves and a radiologically normal inner ear. Hearing loss was not progressive in 11 of 16 cases tested, and variations in the severity of deafness between siblings were common. INTERPRETATION: The characteristic audiometric and radiological features of DFNB1 should be the reference used to guide the investigation, by CX26 molecular diagnostic tests, of deaf children with a compatible phenotype. Prognostic information can now be given to families: the hearing loss in DFNB1 deafness is non-progressive in most cases, at least up to young adulthood. An important element for genetic counselling is that the severity of hearing loss due to DFNB1 is extremely variable and cannot be predicted, even within families.