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Biomedical subjects

J W Hanson

Publications and source records attributed to J W Hanson.

At least 19 recordsLinked to original sources
PubMed1992

The association of waterborne chloroform with intrauterine growth retardation.

The potential reproductive effects of long-term, low-dose exposure to chloroform have received little attention despite the known, acute toxicity of high exposures and the wide-spread occurrence of low concentrations in drinking water. We studied the association of waterborne chloroform with low birthweight (less than 2,500 gm), prematurity (less than 37 weeks gestation), and intrauterine growth retardation (less than 5th percentile of weight for gestational age). Cases were not mutually exclusive, but each outcome was analyzed independently. Birth certificates from January 1, 1989, to June 30, 1990, were used to identify cases and randomly selected controls. All were live, singleton infants born to non-Hispanic, white women from Iowa towns with 1,000-5,000 inhabitants. Exposures to chloroform and other trihalomethanes were ecologic variables based on maternal residence and a 1987 municipal water survey. After adjustment for maternal age, parity, adequacy of prenatal care, marital status, education, and maternal smoking by multiple logistic regression, residence in municipalities where chloroform concentrations were greater than or equal to 10 micrograms/liter was associated with an increased risk for intrauterine growth retardation (odds ratio = 1.8, 95% confidence interval = 1.1-2.9). The major limitations of this study involve the ascertainment and classification of exposures to trihalomethanes, including such issues as the imprecision of using aggregate municipal measures for classifying exposure at the level of the individual, the potential misclassification due to residential mobility, and the fluctuation of trihalomethane levels.

Adult↗
PubMed1992

Craniofacial development in myotonic dystrophy.

Anthropometric, cephalometric, and dental data from 23 subjects (12 males and 11 females) afflicted with myotonic dystrophy were compared to similar data from normal subjects who participated in the Iowa Facial Growth Study. A two by two analysis of variance showed that myotonic subjects differed from normal subjects in headlength, head breadth, cephalic index, bizygomatic face width, nosebreadth, maxillary arch widths, palatal depth, anterior and posterior face heights, cranial base lengths, cranial base angles, and other cephalometric measures. Sex differences were observed for many of the variables. It is hoped that these findings will assist clinicians who treat patients having this disorder.

Adolescent↗
PubMed1991

Unique phenotype associated with a pericentric inversion of chromosome 6 in three generations.

We observed a pericentric inversion of chromosome 6 in three generations of one family. Carriers had several phenotypic alterations including congenital cataracts, hearing loss, dental anomalies, ear anomalies, premature graying, unilateral strabismus, coloboma, and mild mental retardation. These manifestations may all be explained by a failure or delay in development of tissues derived from neural crest cells and are similar to these seen in the Rieger syndrome. The description of this family extends the known phenotypic abnormalities associated with alterations of chromosome 6.

Abnormalities, Multiple↗
PubMed1991

A five-year statewide experience with congenital diaphragmatic hernia.

Antenatal in utero surgery for congenital diaphragmatic hernia has been justified by reported perinatal mortality rates of 77% to 80%. Such rates may have been subject to bias of ascertainment and may include fetuses with additional severe malformations who would not be surgical candidates. We used the Iowa Birth Defects Registry to conduct a complete population survey to determine the incidence of congenital diaphragmatic hernia, the frequency of associated severe malformations, and the morbidity and mortality of infants with isolated congenital diaphragmatic hernia who were not subjected to antenatal surgery. The incidence of congenital diaphragmatic hernia was 1 in 3715. Twenty-eight percent of affected fetuses had associated severe malformations that were potentially identifiable prenatally and that would have precluded antenatal surgery. Of those with isolated congenital diaphragmatic hernia, 55% survived in spite of delivery (88.5%) and/or surgical repair (44%) in a level I or II hospital. Any decision for in utero surgery to repair congenital diaphragmatic hernia must be based on this or similarly obtained information.

Abnormalities, Multiple↗
PubMed1991

Clinical management issues in males with sex chromosomal mosaicism and discordant phenotype/sex chromosomal patterns.

The recent availability of Y DNA probes has made it possible to identify two forms of 46,XX male syndrome: Y DNA positive and Y DNA negative. The Y DNA positive male results from a X;Y translocation with a low recurrence risk; the Y DNA negative males are due to a mutation with a high recurrence risk. 46,XX males and mosaic forms are phenotypically indistinguishable. A review of the case histories for 11 individuals indicates that affected males have highly variable genital and nongenital phenotypes. Physical findings may be clearly apparent or nonexistent. With the exception of external genitalia, the basis for this variability is unknown. It may be related to differences in Y chromatin expression as the result of variable inactivation of the X chromosomes, or to the existence of minor deletions or point mutations secondary to an exchange of genetic material. Common and uncommon clinical problems in these individuals require evaluation and follow-up care that is provided through a cooperative, interdisciplinary approach.

Adolescent↗
PubMed1991

Genetic counseling.

Achieving the clinical goal of genetic counseling continues to be the proper role of all professionals who deal with disorders and conditions that have a genetic component. That group includes the SLP. One major problem is determining when information can be given generally and when referral to a genetic counselor is needed. Another problem is helping the public accept the idea of genetic counseling as one useful part of the health care system. Of special importance now is the development of new methods for identifying the genetic contribution to diseases and disorders. Careful attention is needed for the effective integration of this new technology into our patterns of health care delivery and public health policy in general.

Adolescent↗
PubMed1990

Potential human teratogenicity of frequently prescribed drugs.

Published data regarding the human teratogenic potential of 157 drug components that are frequently prescribed to outpatients in the United States were evaluated according to a protocol developed for TERIS, an automated clinical teratology resource. This protocol stipulates that a bibliographic search be performed on each agent, a brief narrative summary of the available teratologic information prepared, and a risk rating assigned. The ratings are determined by consensus of five clinical teratologists, who independently assess the magnitude of teratogenic risk associated with each agent under usual therapeutic conditions as "none," "minimal," "small," "moderate," "high," and "undetermined." Forty-nine percent of the components of these frequently prescribed drugs had insufficient published information available to assess the risk of human teratogenicity. Of the agents that could be rated, the teratogenic risk in usual therapeutic doses was considered to be minimal or less in 92.5%. Many of these agents have also been assigned Pregnancy Categories by the United States Food and Drug Administration (FDA) according to a system designed to provide therapeutic guidance. There was no more agreement than that expected by chance between TERIS ratings and the FDA Pregnancy Categories for 83 agents that were classified according to both systems. We believe that the FDA Pregnancy Categories should not be used to provide counseling regarding the risk of teratogenic effects to women who have taken medication during pregnancy. Such counseling should be based on a more comprehensive evaluation of the teratologic literature and clinical situation, but need not involve consideration of the therapeutic benefit of the agent.

Information Systems↗
PubMed1990

Prenatal cocaine exposure and fetal vascular disruption.

The question of the potential teratogenicity of cocaine has been raised by the increasing frequency of its abuse in the United States. In previous studies, an increased incidence has been documented of spontaneous abortion, placental abruption, prematurity, intrauterine growth retardation, and neurologic deficits in the infants of women who abused cocaine. More recently, it has been suggested in studies that fetal vascular disruption accompanying maternal cocaine abuse may lead to cavitary central nervous system lesions and genitourinary anomalies. In this article, 10 children born of women who abused cocaine are described, 9 of whom have congenital limb reduction defects and/or intestinal atresia or infarction. The spectrum of anomalies associated with embryonic and fetal vascular disruption accompanying maternal cocaine abuse is thus enlarged. The specific risk for congenital anomalies accompanying maternal cocaine abuse during an individual pregnancy is unknown. However, data from these patients and the available literature suggest that counseling pregnant women concerning cocaine use should incorporate warnings about the possibility of associated embryonic or fetal vascular disruption.

Abnormalities, Drug-Induced↗
PubMed1989

Criteria for identifying and listing substances known to cause developmental toxicity under California's Proposition 65.

Because of the automatic restrictions and warning requirements imposed on substances identified by the state as "known to cause developmental toxicity," the Expert Committee recommends the use of criteria that emphasize human relevancy, biological plausibility, and evidence in support of a selective, adverse developmental effect at non-maternally-toxic doses. In many instances, data for substances of public concern will be insufficient at present to meet these criteria. The fact that a substance is not listed as "known to cause developmental toxicity" does not create a presumption that the substance is safe. The Expert Committee, therefore, urges that these substances be recommended for further testing and that high priority be given to conducting the necessary tests. The Expert Committee reiterates its concern that substances listed by the SAP be identified according to the toxic endpoints (cancer, male reproductive toxicity, female reproductive toxicity, and/or developmental toxicity) that led to listing. Further, the Expert Committee recommends that the state Health and Welfare Agency institute education programs emphasizing appropriate courses of action for citizens informed of exposures to substances known to the state to cause cancer, birth defects, or reproductive toxicity.

Animals↗
PubMed1989

Autosomal recessive cerebellar hypoplasia.

Cerebellar hypoplasia is found in association with a variety of neurologic and systemic disorders. It is the primary finding in the uncommonly reported condition of autosomal recessive cerebellar hypoplasia. We describe two siblings with cerebellar hypoplasia documented in both by magnetic resonance imaging (MRI) and review the clinical features of previously reported cases of autosomal recessive cerebellar hypoplasia. The most common findings in this disorder are nonprogressive ataxia, strabismus, mental retardation, and speech delay with dysarthria. Previously reported cases have been confirmed by autopsy, pneumoencephalography, or computed tomographic (CT) scans. MRI clearly documents diffuse cerebellar hypoplasia and aids in distinguishing autosomal recessive cerebellar hypoplasia from other disorders. The pathophysiology of this disorder is uncertain, however, studies of the weaver mutant mouse (an animal model of autosomal recessive cerebellar hypoplasia) suggest that an abnormality of the Bergmann glia may lead to the observed granule cell layer deficiency in these patients. This diagnosis should be considered for children with nonprogressive ataxia and families should be made aware of the 25% recurrence risk.

Cerebellar Diseases↗
PubMed1988

Independent dysmorphology evaluations at birth and 4 years of age for children exposed to varying amounts of alcohol in utero.

Two groups of 4-year-old children were examined by a dysmorphologist without knowledge of previous examination results or prenatal exposure and categorized as to whether or not they showed fetal alcohol effects. A priori classification of children into the two groups was on the basis of their mothers' self-report of drinking when interviewed during pregnancy. Children born to 108 mothers in a "heavier" drinking group (absolute alcohol concentration greater than or equal to 30 mL/d [1.0 oz/d]) were compared with a matched group of children born to 97 mothers whose average absolute alcohol concentration was less than 0.3 mL/d (0.01 oz/d). The percentage of children with fetal alcohol effects in the heavier drinking v the comparison group was 20.4% v 9.3%. When fetal alcohol effects were studied in relation to only the absolute alcohol concentration scores, there was a significantly greater chance of a child being classified as having fetal alcohol effects with increasing levels of alcohol exposure prior to recognition of pregnancy (P = .013). A logistic regression, run on the absolute alcohol concentration scores and other primary exposures, indicated that fetal alcohol effects classification was not significantly related to nicotine, caffeine, or marijuana but was significantly related to absolute alcohol concentration scores even after statistically adjusting for these other exposures (P = .002). Classification of fetal alcohol effects at 4 years of age was compared to a fetal alcohol effects classification obtained at birth by an independent dysmorphologist in a sample of 75 subjects examined at both ages, and 80% of the infants classified as having fetal alcohol effects at birth were classified as having fetal alcohol effects at 4 years of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Maternal exposure to spermicides in relation to certain birth defects.

Several studies have found no increase in the overall frequency of birth defects in association with the use of spermicides, but the possibility of an increase in specific defects remains. We evaluated this possibility in a large case-control study. Infants with certain malformations (265 with Down's syndrome, 396 with hypospadias, 146 with limb reduction defects, 116 with neoplasms, and 215 with neural-tube defects) were compared with 3442 control infants with a wide variety of other defects. Exposure to spermicides was assessed for three periods: use during the periconceptional period (one month before through one month after the last menstrual period), use during the first trimester (the first four lunar months of pregnancy), and any use during the lifetime. For the five groups of cases and for each interval, the odds ratios were close to 1.0 (range, 0.7 to 1.3); the upper 95 percent confidence bounds were 2.2 or lower. Risks did not increase with the duration of exposure. When each of the active ingredients in currently available spermicides was considered separately, no differences in odds ratios were apparent between the types of spermicides. With the possible exception of a subgroup of cases (limb reduction defects of unknown cause), these results suggest that risks for the five specific birth defects evaluated are not increased by exposure to spermicides.

Abnormalities, Drug-Induced↗
PubMed1987

Dominantly inherited dilated cardiomyopathy.

We describe a family in which there is segregating an autosomal dominant gene determining a cardiomyopathy. The pathodynamics is that of pump failure associated with dilatation of the heart, generally having an overt clinical onset from the fourth through seventh decades. Dysrhythmia is a frequent concomitant feature. There may be an associated skeletal myopathy, either producing a very mild proximal weakness or proving detectable only upon biopsy. This family is similar to other reported cases of familial dominant "idiopathic" dilated cardiomyopathy, but the nature of the heterogeneity within this category remains to be elucidated. The roles of echocardiography, cardiac biopsy, and skeletal muscle biopsy in the presymptomatic detection of the heterozygote are noted.

Adolescent↗
PubMed1986

Further delineation of Weaver syndrome.

Seven new cases of Weaver syndrome are described, including the first reported case in an adult. Overgrowth is usually but not always present. The combination of characteristic facies and developmental delay, with the peculiar radiographic findings of accelerated dysharmonic osseous maturation and splaying of the distal long bones, is diagnostic of Weaver syndrome.

Adult↗