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Theonia K Boyd

Publications and source records attributed to Theonia K Boyd.

5 recordsLinked to original sources
PubMed2006

Fatal cephalosporin-induced acute hypersensitivity myocarditis.

A frequently fatal, although rare, side effect of cephalosporin antibiotics is noninfectious myocarditis. We report two cases of hypersensitivity myocarditis secondary to administration of cephalosporin antibiotics. In both cases, acute hypersensitivity myocarditis was not suspected clinically, and the diagnosis was made postmortem. Histology revealed intense eosinophilic infiltration of the endomyocardium with eosinophil degranulation and myocyte damage, Clinically, death in both cases was due to cardiac failure. When suspected early, appropriate management may be lifesaving.

Acute Disease↗
PubMed2005

Association between fetal growth restriction and polymorphisms at sites -1 and +3 of pituitary growth hormone: a case-control study.

BACKGROUND: Fetal growth restriction is associated with significantly increased risks of neonatal death and morbidity and with susceptibility to hypertension, cardiovascular disease and NIDDM later in life. Human birth weight has a substantial genetic component, with at least a quarter of the variation attributable to additive genetic effects. METHODS: One hundred twenty-five subjects (83 control and 42 case) were selected using stringent inclusion/exclusion criteria. DNA sequencing was used to identify 26 single nucleotide polymorphisms in the pituitary growth hormone gene (GH1) at which all subjects were genotyped. Association with fetal growth restriction was tested by logistic regression for all sites with minor allele frequencies greater than 5%. RESULTS: Logistic regression identified significant association with fetal growth restriction of C alleles at sites -1 and +3 (relative to the start of transcription) that are in complete linkage disequilibrium. These alleles are present at higher frequency (6% vs. 0.4%) in fetal growth restricted subjects and are associated with an average reduction in birth weight of 152 g in normal birth weight and 97 g in low birth weight subjects. CONCLUSIONS: There is suggestive association between fetal growth restriction and the presence of C alleles at sites -1 and +3 of the pituitary growth hormone gene.

Journal Article↗
PubMed2005

Childhood asymmetric labium majus enlargement: mimicking a neoplasm.

We report a distinctive lesion of the labium majus resected in 14 girls from 3.9 to 13.2 years of age. All presented with enlargement of 1 or occasionally both labia majora. Radiographic imaging and surgical exploration showed expansion of the labium majus without definable borders. Grossly, specimens consisted of fibro-fatty tissue from 2 to 8 cm in greatest dimension. Microscopic examination revealed the usual constituents of vulvar soft tissue, with expansion of the fibrous component. Sparsely to moderately cellular interconnected bands encircled lobules of fat, blood vessels, and nerves. The bands consisted of plump and occasionally stellate or round fibroblasts immersed in an abundant pale myxoid matrix containing thin collagen fibers. These fibrous bands merged with thinner denser fibrous septa simlar to those seen in the vulva from age-matched controls. Elastic stains showed variably abundant thin parallel elastic fibers. Fibroblasts were immunohistochemically positive for estrogen and progesterone receptors. Electron microscopy showed fibroblasts with dilated rough endoplasmic reticulum cisternae and prominent nuclear fibrous laminae; extracellular matrix contained precollagen, collagen, elastic fibers, and numerous proteoglycan granules. Cytogenetic analysis of 3 lesions revealed a normal karyotype. Recurrence was observed in 7 (50%) patients, and regression was observed in 1 whose recurrence was not reexcised. Over an 11-year period at Children's Hospital (Boston, MA), these lesions represented 22% of all pediatric vulvar soft tissue masses and 3% of all vulvar lesions biopsied. We conclude that "childhood asymmetric labium majus enlargement" is a distinctive clinicopathologic entity of pre- and early puberty. Recognition of this fairly common lesion is important, since it may clinically, radiographically, and histologically mimic an infiltrative neoplasm. Its occurrence at an age roughly coincident with the time of breast budding, capacity for spontaneous regression, histologic architecture and composition of elements native to the vulva, expression of hormone receptors, and normal karyotype suggest that it is an asymmetric physiologic enlargement in response to hormonal surges of pre- and early puberty.

Adolescent↗
PubMed2002

Triplet placentas: reference values for weights.

The occurrence of twins, triplets, and other multiple births increased significantly between 1970 and 2000 in the United States and other industrialized countries. The number of triplet placentas submitted for examination as pathologic specimens has also markedly increased, but no reference values are published for triplet weights. We examined 196 normal triplet placentas. Specimens with associated conditions known to affect the weights of the placentas were excluded. The gestational ages ranged between 20 and 38 weeks. Mean weights for different gestational ages are summarized as follows: 253 g for 20 weeks, 319 g for 22 weeks, 406 g for 24 weeks, 509 g for 26 weeks, 621 g for 28 weeks, 738 g for 30 weeks, 855 g for 32 weeks, 965 g for 34 weeks, 1,065 g for 36 weeks, and 1,147 g for 38 weeks. Weight gain of triplet placentas appears to parallel that of twin placentas. The mean values of placental weights for triplets at each gestational age are less than triple those of singleton weights for the same duration of gestation. The placental weights in multiple gestations do not increase proportionately with the number of fetuses.

Female↗