A prevalence survey of ophthalmic disease was conducted among the Turkana tribe in northwest Kenya. Altogether 900 people were examined in different sites of the semiarid and arid Turkana region. The findings show the prevalence of blindness to be 1-1% and the prevalence of blindness in one eye to be 6*8%. The major causes of blindness up to age 35 were corneal disease from xerophthalmia and trachoma and above age 45 cataract. Trauma was a major cause of monocular blindness. The prevalence of trachoma and its complications was 42-8% and the prevalence of cataract 5*2%. Cataract begins to form at an early age (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). The prevalence of xerophthalmia was 44%. These findings are similar to previously reported studies in Africa, especially in semiarid areas. The main remedy lies in improvement of education and the environment.

BACKGROUND The past decade has witnessed a growing frequency of therapy‐related secondary tumors. The authors studied nine children with secondary malignancies. The primary tumors were bilateral retinoblastoma, neuroblastoma, brain tumor, Wilms' tumor, colon adenocarcinoma, and Hodgkin's disease. The secondary tumors were osteosarcoma at the site of previous radiotherapy, myelodysplastic syndrome, acute myelocytic leukemia, glioblastoma, thyroid carcinoma, and B‐cell lymphoma. METHODS DNA was extracted from the primary and secondary tumors and analyzed for genetic alterations in the p53 gene and in 7 separate microsatellites. RESULTS The authors found p53 mutations in 7 patients, loss of heterozygosity in 1 patient, and both mutation and loss of heterozygosity in 1 patient. Mutations were demonstrated in the primary tumors only in two patients and in the secondary tumors only in three patients. Two patients had a mutation in both the primary and the secondary tumor; in both patients the two mutations were in different exons. Microsatellite instability (MIN) was identified in five to seven loci in the secondary tumors of all patients. CONCLUSIONS The observed MIN is compatible with the presence of a mutator phenotype that predisposes these children to the development of secondary malignancies. Cancer 1999;85:504–10. © 1999 American Cancer Society.

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The observed MIN is compatible with the presence of a mutator phenotype that predisposes these children to the development of secondary malignancies.