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Rosalind S Brown

Publications and source records attributed to Rosalind S Brown.

4 recordsLinked to original sources
PubMed2006

Update of newborn screening and therapy for congenital hypothyroidism.

Unrecognized congenital hypothyroidism leads to mental retardation. Newborn screening and thyroid therapy started within 2 weeks of age can normalize cognitive development. The primary thyroid-stimulating hormone screening has become standard in many parts of the world. However, newborn thyroid screening is not yet universal in some countries. Initial dosage of 10 to 15 microg/kg levothyroxine is recommended. The goals of thyroid hormone therapy should be to maintain frequent evaluations of total thyroxine or free thyroxine in the upper half of the reference range during the first 3 years of life and to normalize the serum thyroid-stimulating hormone concentration to ensure optimal thyroid hormone dosage and compliance. Improvements in screening and therapy have led to improved developmental outcomes in adults with congenital hypothyroidism who are now in their 20s and 30s. Thyroid hormone regimens used today are more aggressive in targeting early correction of thyroid-stimulating hormone than were those used 20 or even 10 years ago. Thus, newborn infants with congenital hypothyroidism today may have an even better intellectual and neurologic prognosis. Efforts are ongoing to establish the optimal therapy that leads to maximum potential for normal development for infants with congenital hypothyroidism. Remaining controversy centers on infants whose abnormality in neonatal thyroid function is transient or mild and on optimal care of very low birth weight or preterm infants. Of note, thyroid-stimulating hormone is not elevated in central hypothyroidism. An algorithm is proposed for diagnosis and management. Physicians must not relinquish their clinical judgment and experience in the face of normal newborn thyroid test results. Hypothyroidism can be acquired after the newborn screening. When clinical symptoms and signs suggest hypothyroidism, regardless of newborn screening results, serum free thyroxine and thyroid-stimulating hormone determinations should be performed.

Congenital Hypothyroidism↗
PubMed2004

Minireview: developmental regulation of thyrotropin receptor gene expression in the fetal and newborn thyroid.

The TSH receptor plays a pivotal role in thyroid gland growth, function, and differentiation in the mature animal, but only recently has its role in the fetus and neonate been examined. Observational studies comparing the developmental regulation of TSH receptor gene expression, with thyroid morphology, and thyroid-specific gene expression in the rodent model, are reviewed in the context of older literature. Together, these data strongly suggest that the TSH receptor is essential for terminal thyroid maturation and growth but is not involved in early thyroid organogenesis or migration. Consistent with the aforementioned studies in rodents, babies with a loss of function mutation of the TSH receptor as well as babies born to mothers with potent TSH receptor-blocking antibodies have hypothyroidism and hypoplastic, but normally located, thyroid glands. Because the TSH receptor is probably not expressed in human fetuses before 10-12 wk gestation when thyroid organogenesis and migration are complete, these data provide strong evidence that human chorionic gonadotropin, which peaks in the first trimester of human pregnancy, could not play a role in fetal thyroid development. Similarly, these data imply strongly that maternal TSH receptor antibodies, when present in high titer, are of major importance in influencing fetal thyroid function only after mid-pregnancy when, by analogy with rodents, increased TSH receptor expression is likely to occur.

Animals↗