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Biomedical subjects

J W Hanson

Publications and source records attributed to J W Hanson.

At least 73 records · Page 4Linked to original sources
PubMed1977

Alcohol and the fetus.

Current data clearly point to an association between chronic maternal alcoholism and serious morphological and developmental abnormalities in the fetus. When these abnormalities are severe the condition is recognizable as the fetal alcohol syndrome. However, this represents only the most severe end of a spectrum of abnormalities, some of which may be found in a proportion of infants exposed to lesser amounts of alcohol during pregnancy. Alcohol is an avoidable hazard for the fetus, but only through increased awareness by the medical community and improved education of the lay public may we hope to control this problem.

Abnormalities, Drug-Induced↗
PubMed1976

Fetal alcohol syndrome. Experience with 41 patients.

Forty-one patients with the fetal alcohol syndrome, including 11 whose cases were previously reported, were studied. These children have a pattern of defects including prenatal and postnatal growth deficiency, small head size with mental subnormality, and facial abnormalities allowing for recognition of the disorder in infancy. The same pattern of abnormalities has been independently reported from France in a series of 127 offspring of chronic alcoholics.

Abnormalities, Drug-Induced↗
PubMed1976

Risks to the offspring of women treated with hydantoin anticonvulsants, with emphasis on the fetal hydantoin syndrome.

The fetal hydantoin syndrome is a variable pattern of altered growth and performance which includes unusual facies, distal phalangeal hyoplasia, and other defects occurring in some infants exposed in utero to hydantoins. A prospective study of 35 infants exposed prenatally to this class of anticonvulsants showed that 11% had sufficient features to be classified as having the fetal hydantoin syndrome. An additional 31% displayed some features compatible with the prenatal effects of hydantoins. A case-control study of 104 infants whose mothers received hydantoins during pregnancy supports these conclusions. Reduction of intellectual ability in infants with the fetal hydantoin syndrome is the area of greatest concern. Women being treated with hydantoin anticonvulsants should be told of the nature and magnitude of risks to the developing fetus before considering a pregnancy.

Abnormalities, Drug-Induced↗
PubMed1976

Prominent lateral palatine ridges: developmental and clinical relevance.

Unusually prominent lateral palatine ridges have been found to be a nonspecific feature of a variety of disorders in which there is either neuromotor dysfunction or a malformation which prevents tongue thrust into the palatal vault. Observations of the lateral palatine ridges in 3 fetal specimens and in 260 normal individuals over a wide range of ages revealed that these structures are normally more prominent during prenatal life and infancy. With increasing age these ridges normally become progressively flattened and usually disappear by age 5 years. The observation of unusual prominence of these ridges in infants with neuromuscular dysfunction as well as in those with malformations which limit tongue thrust into the palatal vault suggests that a long-standing deficit of tongue thrust is the common pathogenetic mechanism. Prominent lateral palatine ridges may be misinterpreted as a true "narrow, high-arched palate", which is a much less common anomaly. This distinction is important clinically, since prominent lateral palatine ridges most commonly imply a long-term deficit of neuromuscular function and thus may be an important diagnostic clue to alterations dating back to early prenatal development.

Adolescent↗
PubMed1976

The iduronidase-deficient mucopolysaccharidoses: clinical and roentgenorgraphic features.

Hurler and Scheie syndromes, two of the six clinically distinct mucopolysaccharidoses, are deficient in the same lysosomal enzyme, alpha-L-iduronidase. A third group of iduronidase-deficient patients can now be identified during the pediatric years using clinical and radiographic criteria. Based on inferential evidence for allelism between the Hurler and Scheie genes, the occurrence of genetic compounds which simultaneously carry both mutant alleles may be predicted to occur. This can be considered analogous to the structural gene mutations leading to hemoglobin SC disease. Four patients with phenotypes intermediate between Hurler and Scheie syndromes are flet to represent genetic compounds of this type. Both clinical and roentgenographic features are helpful in distinguishing these patients from those with Hurler syndrome or Scheie syndrome. Fibroblast correction characteristics identical to those of Hurler syndrome and Scheie syndrome and absence of consanguinity are additional features which favor classification as genetic compounds. The possibility of a third mutant allele at the Hurler-Scheie locus or of extreme phenotype variation are not considered likely alternative explantations. Depending on the frequency of the Scheie syndrome and the Hurler syndrome, genetic compounds may occur with an intermediate frequency or may be more common than either homozygous condition.

Adolescent↗
PubMed1975

U-shaped palatal defect in the Robin anomalad: developmental and clinical relevance.

The palatal defect in patients with the Robin anomalad was found to be U shaped. This finding is compatible with the hypothesis that the underlying dysmorphic event is usually early mandibular hypoplasia with secondary extrinsic obstruction of palatal closure by a posteriorly displaced tongue. The more common V-shaped defects of palate closure arise by a different mechanism. Unfortunately, available recurrence risk data for cleft palate do not allow for this distinction. Furthermore, physicians should be alert for instances in which the Robin anomalad is but one feature of a broader pattern of malformation. In the current study, 25% of the 28 patients ascertained as having the Robin anomalad had a recognizable syndrome for which specific, but varying, genetic counsel was indicated.

Child↗
PubMed1975

The fetal trimethadione syndrome.

Three families are described in which each of the mothers took trimethadione during pregnancy. From a comparison of siblings in each family and of others exposed to trimethadione in utero, a specific phenotype is delineated. Features included in the fetal trimethadione syndrome are developmental delay, speech difficulty, V-shaped eyebrows, epicanthus, low-set ears with anteriorly folded helix, palatal anomaly, and irregular teeth. Additional anomalies in some of the patients include intrauterine growth retardation, short stature, microcephaly, cardiac anomaly, ocular anomaly, hypospadias, inguinal hernia, and simian creases.

Abnormalities, Drug-Induced↗