Analysis of 194 patients with confirmed Pneumocystis carinii pneumonia in the United States over a 3-year period revealed that P. carinii pneumonia occurred almost exclusively in the immunosuppressed host who had a serious underlying disease. The epidemiologic features of pneumocystis pneumonia primarily reflected those of the underlying disease. P. carinii was identified antermortem in 81% of the cases usually by biopsy or needle aspiration of the lung, procedures associated with considerable morbidity and morbidity and mortality. Laboratory identification of P. carinii was usually accurate, but errors resulting from fault staining tecnique occurred. Most patients had been ill less than 2 weeks with bilateral diffuse interstitial pneumonia. Leukopenia (white blood cell count less than or equal to 3,00/mm3) and probably severe hypoxia were negative prognostic factors. Although treatment with pentamidine was effective, the drug frequently cased adverse reactions, particularly impaired renal function, when given with other nephrotoxic agents.

Pneumocystis carinii Pneumonia in the United States: Epidemiologic, Diagnostic, and Clinical Features

Pneumocystis carinii pneumonia in the United States: epidemiologic, diagnostic, and clinical features.

Down syndrome (DS) is the most frequent cause of mental retardation in man. Immunological changes in DS have been observed since the 1970s. The neurological system appears to be ageing precociously, with early occurrence of Alzheimer disease; until now, the observed immunological differences have been interpreted in the same context. Looking back at past and present results of immunological studies in DS children in relation to the clinical consequences they suffer, we conclude that it is more likely that the DS immune system is intrinsically deficient from the very beginning.

/pdf/intrinsic-defect-of-the-immune-system-in-children-with-down-5fj0l97uec.pdf

Intrinsic defect of the immune system in children with Down syndrome: a review.

We have reviewed the records of the 16,564 cases of childhood cancer diagnosed from 1971 to 1983 which were reported to the National Registry of Childhood Tumours in Great Britain for the presence of underlying genetic disease in order to estimate the proportion which results from inherited mutations. A genetic condition was listed for 509 patients, or 3.07% of the total number of tumours. The most frequently recorded diagnoses were: bilateral retinoblastoma (162 cases); Down syndrome (135); neurofibromatosis (90); hereditary Wilms' tumour (71); and tuberous sclerosis (20). The highest hereditary fractions at individual tumour sites were seen for: retinoblastoma (37.2%); kidney (7.2%); leukaemia (2.6%) and brain and spinal cord (2.0%). When information about family history from published reports was incorporated into the figures calculated from Registry data the total genetic fraction was estimated to be 4.2%. We conclude that there is a clear genetic basis for a small minority of the cancers of childhood, but ethnic variation and the lack of known environmental determinants suggest that the total influence of heredity may be higher.

An estimate of the heritable fraction of childhood cancer.

Cancer may result from a multistage process occurring over a long period of time. Presumably, initial and progressive stages of carcinogenesis may be modified by both genetic and environmental factors. Theoretically, genetic factors may alter susceptibility to the carcinogenic effects of an environmental agent at the initial exposure due to variation in metabolism of the carcinogen or variation in specific target cell response to the active carcinogen, or during the latent phase due to numerous factors that might increase the probability of tumor expression, including growth-promoting factors or immunodeficiency states. Observed genetic and environmental interactions in carcinogenesis include an association between genetically determined inducibility of aryl hydrocarbon hydroxylase and smoking-related cancers, familial susceptibility to certain environmental carcinogens, an association between hereditary disorders of mutagenesis and carcinogenesis, and enhancement of tissue-specific, dominantly inherited tumor predisposition by radiation. Multiple primary tumors occur frequently in genetically predisposed individuals. Specific markers for susceptibility must be sought in order that high-risk individuals be identified and appropriate measures taken for early cancer detection or prevention. Study of the nature of the genetically determined susceptibility and interactions with environmental agents may be revealing in the understanding of carcinogenesis in general.

Genetic and environmental interactions

Acute myelomonocytic leukemia was diagnosed in 73 children at the Children's Cancer Research Foundation and the Children's Hospital Medical Center in Boston, 1949–1971. Although the disorder may occur within the first year of life, no association was found with inherited disorders or with prenatal exposure to potential carcinogens. Three patients had a well-documented history of antecedent aplastic anemia, suggesting that prolonged myelodepression is an etiologic factor or precursor state in myelomonocytic leukemia. In addition, eight others appeared to have antecedent anemia, thrombocytopenia, or pancytopenia for months to years, a finding previously described in adults with myelomonocytic leukemia.

Epidemiology of acute myelomonocytic leukemia in children.

Acute Childhood Leukemia: Epidemiologic Study by Cell Type of 1,263 Cases at the Children's Cancer Research Foundation in Boston, 1947–65

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Epidemiology of acute myelomonocytic leukemia in children.

Acute Childhood Leukemia: Epidemiologic Study by Cell Type of 1,263 Cases at the Children's Cancer Research Foundation in Boston, 1947–65