Plasma calcitonin measurement following calcium infusion is extremely useful as a screening procedure for the diagnosis of medullary thyroid carcinoma, when the patients are completely asymptomatic and routine thyroid function tests are normal.
The normal iPTH suppressibility in MEN 2b is consistent with the concept that the parathyroid disease in MEN 2a is genetically determined, and not secondary to MTC and high plasma calcitonin concentration.
A black female with inherited medullary thyroid carcinoma and pheochromocytoma was a mosaic for glucose-6-phosphate dehydrogenase types A and B in normal tissues (blood, thyroid, and adrenal gland); both the medullary carcinoma and pheochromocytoma tissue showed a B pattern only.
The main characteristics of medullary carcinoma of the thyroid are its non-follicular histological appearance, resulting from its origin from the parafollicular C cells, its secretion of calcitonin, providing a relatively simple diagnostic test, and its equal sex incidence, in contrast to all other diseases of the thyroid.
Of particular interest, lymphocytes from six of 12 clinically normal family members genetically at risk for medullary thyroid carcinoma exhibited cellular immune reactivity to tumor antigen.
We evaluated in vitro production of macrophage-migration-inhibitory factor and 3H-thymidine uptake by lymphocytes from patients, family members and normal subjects in response to extracts of medullary thyroid carcinoma and normal thyroid tissue.
The two persons with initially elevated values and three of the seven with increased values after pentagastrin injection were found at subsequent operation to have focal medullary carcinoma and parafollicular cell hyperplasia; after the operation immunoreactive calcitonin was undetectable in the plasma, even after stimulation.
Medullary thyroid carcinoma (M.C.T.) is a tumour of the calcitonin-secreting cells of the thyroid gland; it affects both lobes, has a variable malignant potential, and is often familial.
We determined the activity of DBH in the plasma of 8 patients with pheos, secondary to multiple endocrine neoplasia Type 2 (MEN II) (medullary carcinoma of the thyroid [MCT], pheochromocytoma(s), and parathyroid hyperplasia).
We determined the activity of DBH in the plasma of 8 patients with pheos, secondary to multiple endocrine neoplasia Type 2 (MEN II) (medullary carcinoma of the thyroid [MCT], pheochromocytoma(s), and parathyroid hyperplasia).
We determined the activity of DBH in the plasma of 8 patients with pheos, secondary to multiple endocrine neoplasia Type 2 (MEN II) (medullary carcinoma of the thyroid [MCT], pheochromocytoma(s), and parathyroid hyperplasia).
We determined the activity of DBH in the plasma of 8 patients with pheos, secondary to multiple endocrine neoplasia Type 2 (MEN II) (medullary carcinoma of the thyroid [MCT], pheochromocytoma(s), and parathyroid hyperplasia).
Serum carcinoembryonic antigen (CEA) and calcitonin were assayed in 8 patients with medullary carcinoma of the thyroid (MCT) and 14 unaffected family members, from 4 pedigrees of Sipple's syndrome and one pedigree with inherited MCT.
The G-banding analysis showed that th chromosome rearrangements were not random, and site of rearrangements tended to cluster to band p22 of chromosome 1 in the carriers of childhood leukemia gene and to band q23 of chromosome 17 in the patient with medullary thyroid cancer.
The G-banding analysis showed that th chromosome rearrangements were not random, and site of rearrangements tended to cluster to band p22 of chromosome 1 in the carriers of childhood leukemia gene and to band q23 of chromosome 17 in the patient with medullary thyroid cancer.
The G-banding analysis showed that th chromosome rearrangements were not random, and site of rearrangements tended to cluster to band p22 of chromosome 1 in the carriers of childhood leukemia gene and to band q23 of chromosome 17 in the patient with medullary thyroid cancer.
The G-banding analysis showed that th chromosome rearrangements were not random, and site of rearrangements tended to cluster to band p22 of chromosome 1 in the carriers of childhood leukemia gene and to band q23 of chromosome 17 in the patient with medullary thyroid cancer.