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Biomedical subjects

L W O'Neal

Publications and source records attributed to L W O'Neal.

14 recordsLinked to original sources
PubMed1990

Evaluation of children with multiple endocrine neoplasia type IIb following thyroidectomy.

Medullary thyroid carcinoma (MTC) develops in all patients with multiple endocrine neoplasia type IIb (MEN IIb), a rare syndrome that either occurs sporadically or is inherited in an autosomal dominant pattern. The MTC in patients with MEN IIb has been reported to be biologically aggressive with onset at a young age and rapid progression as evidenced by widespread metastases and death, frequently in the teenage years. Seven children, aged 2 to 11 years (mean, 7 years), from three kindreds with MEN IIb were evaluated for evidence of tumor recurrence 3 to 10 years following thyroidectomy. In one child, age 11, a thyroid mass was palpable preoperatively. However, in the remaining six children (aged 2 to 10 years), the diagnosis of MTC was established by an increased concentration of plasma calcitonin (CT), either basally or following pentagastrin (Pg) stimulation. All patients underwent total thyroidectomy with removal of central lymph nodes from the neck. At the time of surgery, six children were found to have bilateral macroscopic MTC, five without and one with cervical metastases. One child (age 2 years) had C-cell hyperplasia, a premalignant precursor of MTC. Currently, five of the seven children are without evidence of recurrent disease clinically and have normal plasma CT levels (less than 0.3 ng/mL) following calcium (Ca) and Pg stimulation 3, 3, 10, 10, and 10 years after thyroidectomy. Two of the seven children have biochemical evidence of residual MTC.(ABSTRACT TRUNCATED AT 250 WORDS)

Biomarkers, Tumor↗
PubMed1990

Linkage of the multiple endocrine neoplasia type 2B gene (MEN2B) to chromosome 10 markers linked to MEN2A.

The syndrome of multiple endocrine neoplasia type 2B (MEN 2B) resembles that of MEN 2A in that both include medullary carcinoma of the thyroid, pheochromocytoma, and autosomal dominant inheritance, but is distinct in that MEN 2B patients have neuromas of the mucous membranes. MEN2A has been linked to RBP3, D10S5, FNRB, D10S15, and D10Z1 near the centromere of chromosome 10. We examined linkage between MEN2B and RFLPs on chromosome 10 in all available members in two or three generations of 14 kindreds. The centromere marker D10Z1 was linked to MEN2B with a peak lod score of 5.42 at theta = 0.02. One possible recombinant was observed between D10Z1 and MEN2B. Multipoint analysis of RFLPs at FNRB, D10Z1, RBP3, and D10S15 gave a peak lod score of 7.12 at the midpoint between D10Z1 and RBP3 on the long arm (band q11). The most likely gene order FNRB-D10Z1-MEN2B was 27 times more likely than MEN2B-FNRB-D10Z1 and 31/2 times more likely than FNRB-MEN2B-D10Z1. Additional data will be required to establish the order of these loci with confidence.

Chromosomes, Human, Pair 10↗
PubMed1987

Lethal hyperparathyroid crisis: hazards of phosphate administration.

Two patients with hypercalcemia crisis and parathyroid adenoma died as a result of pulmonary insufficiency. The administration of phosphate is believed to have contributed to the deaths, since the pulmonary problems appeared when the blood [Ca] X [PO4] product rose and extensive metastatic calcification was present in the pulmonary alveolar lining. The use of phosphates as calcium-lowering agents in hypercalcemia is discouraged, because phosphate appears to lower calcium levels only by intravascular precipitation.

Adenoma↗
PubMed1981

C-cell hyperplasia developing in residual thyroid following resection for sporadic medullary carcinoma.

Four days following resection of a medullary carcinoma of the thyroid, a 49-year-old man experienced elevated serum calcitonin levels. There was no evidence of metastasis. A re-exploration of the patient's neck demonstrated a histologically normal thyroid remnant that demonstrated C-cell hyperplasia by immunoperoxidase staining. The lack of a familial history, a normal parathyroid, and the absence of C-cell hyperplasia in non-tumorous thyroid of the original resection support the concept that the patient had a sporadic tumor. Patients who had undergone incomplete thyroidectomies for non-familial disease are at risk for developing C-cell proliferation and possibly medullary carcinoma. We conclude that the C-cell hyperplasia in this thyroid remnant is the source of the elevated calcitonin level; this mechanism may also explain postoperatively elevated calcitonin levels in some patients with medullary carcinoma treated by partial thyroidectomy and high calcitonin levels for a variable period after complete thyroidectomy.

Adult↗
PubMed1971

HMO revisited.

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Group Practice↗
PubMed1970

Pheochromocytoma.

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Adrenal Gland Neoplasms↗