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PubMed1992

Use of color Doppler imaging in the distinction between thyroid and parathyroid lesions.

To determine whether the use of color Doppler imaging in conjunction with standard high-resolution 10-MHz ultrasound could increase the screening sensitivity in distinguishing between thyroid and parathyroid lesions in the detection of parathyroid disease, we studied 32 patients with hyperparathyroidism with both modalities who were subsequently treated surgically. Among these 32 patients, parathyroid lesions were predominantly avascular (n = 21, average size 0.9 x 0.6 cm) but with increased size demonstrated some vascularity (n = 9, average size 2.1 x 1 cm, 32%). Of these 32 patients, 46.6% had thyroid lesions as well. Thyroid lesions were avascular when small (n = 26 lesions, average size 0.5 x 0.5 cm) but tended to demonstrate vascularity (n = 14, 35%) at about 1 cm in size or greater. Although the addition of color Doppler imaging enabled the differentiation of vessel from soft-tissue abnormalities and some distinction between parathyroid and thyroid lesions, it had no effect on overall sensitivity (65%) in the detection of parathyroid disease.

Adult↗
PubMed2002

A comparative study of the int-2 gene product in primary and secondary parathyroid lesions.

OBJECTIVE: The family of fibroblast growth factors stimulates proliferation of cells of mesenchymal, epithelial and neuroectodermal origin. One of the members of this family, the product of proto-oncogene int-2, fibroblast growth factor-3, has been found to stimulate mitosis of parathyroid cells in culture. Primary and secondary hyperparathyroidism have no clear differences with regard to the histopathological features of the diseased parathyroid glands. DESIGN: This study was undertaken in order to determine whether int-2 protein is immunohistochemically expressed in normal and abnormal parathyroid glands and to investigate whether there is a differential expression of the int-2 gene product between primary and secondary parathyroid disease. METHODS: A sheep anti-human int-2 antibody was applied to tissue sections from 37 samples of primary parathyroid disease (12 sporadic adenomas, 25 hyperplastic glands), from 30 samples of renal hyperparathyroidism, and from seven normal controls. Int-2 immunostaining was evaluated semi-quantitatively. RESULTS: None of the normal parathyroid glands stained positively. Int-2 immunopositive expression was more frequently detected in specimens of uraemic patients than in those of patients with primary parathyroid growth processes (P=0.029). The reason for this differential expression appears to be the higher proportion of oxyphilic cells growing in hyperplastic glands of patients with secondary hyperparathyroidism; the latter cells were specifically found to be int-2 immunoreactive. CONCLUSION: The int-2 gene product is likely to participate in the proliferation of this parathyroid cell subpopulation.

Adenoma↗
PubMedDate not supplied

Radionuclide imaging of the parathyroid glands: patterns, pearls, and pitfalls.

Optimal parathyroid scintigraphy requires an understanding of (a) the embryologic, anatomic, and physiologic features of the parathyroid glands and (b) the properties of the two common imaging agents, technetium-99m sestamibi and Tc-99m tetrofosmin. Normal parathyroid glands are too small to be visualized, but parathyroid disease often produces visibly enlarged glands. Enlarged parathyroid glands may be found near the thyroid gland or outside their expected locations. Characteristic abnormal scintigraphic patterns may be described as focal or multifocal, usual or ectopic in location, and associated with a normal or abnormal thyroid gland. Patients who are referred for parathyroid imaging should have an abnormal biochemical profile. The first step in evaluating images of a patient suspected to have parathyroid disease is correlating the normal or abnormal scintigraphic patterns with the clinical and surgical history. By integrating the interpretative and technical pearls and pitfalls of parathyroid scintigraphy, the radiologist can be more confident in establishing a correct diagnosis and can precisely guide the surgeon to a single parathyroid adenoma, multiple parathyroid adenomas, or multigland hyperplasia.

Adenoma↗
PubMed1980

[Radiologic aspects of osteopathy in parathyroid gland diseases and their differential diagnosis].

The different disturbances of these organs resulting from the relative endocrine autonomy of the parathyroid glands obtain a manifold symptomatology often with an only later diagnosing. In increased activity of the parathyroid glands hypercalcaemia as well as generalized osteodystrophy are indicating the target in combination with subperiostal resorptions of the corticalis at the phalanges. As a rule underfunction distinguishes itself by hypocalcaemia, hyperphosphataemia and osteoscleroses due to increased mineral fixation in bones. Pseudoparathyreotic conditions are to be differed from actual pictures of the disease only in typical expression. In the paraneoplastic syndromes appearing within this boundary only the proof of a malignoma allows a secure demarcation. On account of the often uncharacteristic X-ray picture, the variable symptomatology and the in many cases lacking directive paraclinical findings practically all pathological bone processes which are based on deviations in the calcium and phosphate metabolism are to be included in differential-diagnostic considerations.

Alkaline Phosphatase↗
PubMed1996

Familial medullary thyroid carcinoma: not a distinct entity? Genotype-phenotype correlation in a large family.

BACKGROUND: Multiple endocrine neoplasia type 2A (MEN 2A) is a hereditary syndrome characterized by medullary thyroid carcinoma (MTC), pheochromocytoma, and hyperparathyroidism. Familial MTC (FMTC) is characterized by MTC only. Both MEN 2A and FMTC are caused by germline mutations of the RET proto-oncogene. PURPOSE: To assess genotype/phenotype correlations, large families have to be examined periodically over a long period using an extensive screening program. PATIENTS AND METHODS: Since 1973, we screened a large family with hereditary C cell carcinoma for MTC, pheochromocytoma, and parathyroid disease by clinical tests and imaging methods. A germline codon Cys618 to Ser mutation in the RET proto-oncogene was recently identified in this family. The disease phenotype associated with this mutation was compared with that of Cys634 mutations in some other large MEN 2A families. RESULTS: The distinct course of disease in the family described here is similar to that in other FMTC families and MEN 2A families with a Cys618 mutation of the RET gene, but clearly different from that in families with a Cys634 mutation. The frequency of pheochromocytomas and parathyroid disease is clearly lower, whereas cure rates and life expectancy are higher. However, in families with a Cys618 mutation, pheochromocytoma and parathyroid disease do occur. CONCLUSION: In FMTC families with cysteine codon mutations of the RET proto-oncogene, screening for other endocrinopathies is mandatory, since these may not be MTC-only families. Therefore, we suggest that MEN 2A families should not be subclassified into MEN 2A and FMTC, but rather according to their specific mutation in the RET protein (i.e., for this family MEN 2A RET C618S).

Adrenal Gland Neoplasms↗
PubMed1996

Value of ploidy pattern and nuclear texture in the diagnosis of primary hyperparathyroidism.

OBJECTIVE: To determine if there are subvisual differences (quantitation of DNA and study of chromatin texture) that distinguish single-gland parathyroid disease (adenoma) from multiple-gland disease (hyperplasia). STUDY DESIGN: Forty-eight parathyroid glands from 41 patients with primary hyperparathyroidism were studied. Cytometric differences between the chief cells and clear cells were sought. An image cytometer was used to study histologic sections stained with DNA stain reagent. In each case a total of 200 cells were measured in consecutive fields. To distinguish chief cells from clear cells, a sample of 15,600 cells collected in consecutive fields in 78 histologic sections was analyzed. RESULTS: The results indicated that none of the continuous variables differentiated between single-gland and multiple-gland parathyroid disease. The most common ploidy pattern was diploid (25/45), followed by hypodiploid (7/45) and polyploid (5/45). A tetraploid population > 3% was found in 18/45 of the cases and was more frequent in single-gland lesions (15/34) than in multiple-gland lesions (3/11). The most significant discrete variables were growth pattern and binucleation or multinucleation. Clear and chief cells were classified correctly in 61.3% of the crossover validation tests using the standard deviation of nuclear shape karyometric variable and in 76.3% using the standard deviation of maximal correlation coefficient karyometric variable. Although ploidy pattern did not show significant differences, polyploidy, aneuploidy and tetraploidy > 3% were slightly more common in chief cells. CONCLUSION: In primary hyperparathyroidism there are no subvisual differences that can distinguish adenoma from hyperplasia. Nonetheless, by cytometry, most parathyroid cells can be classified correctly as clear or chief cells.

Cell Nucleus↗
PubMed1998

Multiple endocrine neoplasia type 2-associated RET proto-oncogene mutations do not contribute to the pathogenesis of sporadic parathyroid tumors.

BACKGROUND: Parathyroid disease occurs sporadically or as part of hereditary multiple endocrine neoplasia (MEN) syndrome. The aim of this study was to evaluate the possible role of the RET proto-oncogene not only in hereditary MEN 2-associated hyperparathyroidism but also in different forms of sporadic hyperparathyroidism. METHODS: We investigated 22 patients with parathyroid disease whose family history and results of laboratory and clinical examinations excluded MEN 2 syndrome. DNA extractions of histologically confirmed tumor tissue of patients with primary hyperparathyroidism (n = 18), renal hyperparathyroidism (n = 2), and parathyroid carcinoma (n = 2) were performed. Using solid phase DNA sequencing, mutation analysis of polymerase chain reaction amplified products focused on exons 10, 11, and 16 of the RET proto-oncogene. Parathyroid tissue from four patients with known MEN 2A served as positive controls. RESULTS: No mutations of the codons 609, 611, 618, 620, 634, and 918 were found in the sporadic parathyroid tumors analyzed. DNA sequencing revealed heterozygous mutations in codon 634 of the RET proto-oncogene in four parathyroid glands from four patients with MEN 2A. CONCLUSIONS: Mutations of the RET proto-oncogene contributing to MEN 2 syndromes are absent in sporadic parathyroid tumors. Our data in conjunction with the literature suggest at least three different modes of tumorigenesis in parathyroid disease.

Adenoma↗
PubMed1979

Control of hypercalcaemia in thyrotoxicosis.

Two thyrotoxic patients with significant hypercalcaemia are described. The hypercalcaemia failed to suppress with hydrocortisone, propranolol and calcitonin but serum calcium fell rapidly to normal with carbimazole treatment. Both patients were subsequently treated surgically and at operation no evidence of parathyroid disease was found. Thyroid disease must be controlled before co-existing parathyroid disease is diagnosed in hypercalcaemic thyrotoxic patients.

Adult↗
PubMed1984

Hyperparathyroidism, hypercalcemia and the otolaryngology head and neck surgeon.

Ability to successfully accomplish parathyroid surgery, as well as to understand the pathophysiology of parathyroid disease and hypercalcemia, is essential to the Otolaryngology Head and Neck surgeon (who must treat parathyroid disease), because of the more frequent identification of parathyroid adenomata and parathyroid hyperplasia (with their inherent hypercalcemia). Today many more cases are recognized because of hypercalcemia identified by now routine multiphasic biochemical screening tests. The etiology of hypercalcemia is discussed in considering the differential diagnosis of pseudohyperparathyroidism, and true hyperparathyroidism of parathyroid hyperplasia and parathyroid adenomata. Pseudohyperparathyroidism, secondary to ectopic elaboration of parathormone-like substance is treated medically. Parathyroid hyperplasia can sometimes be controlled medically, but the only definitive treatment for hyperplasia and parathyroid adenomata is surgery, to the extent indicated, in these often critically ill patients with this multisystem disease. Medical, as well as surgical treatment, is described. A patient is described who demonstrated in a slowly moving montage all the classic history and findings of severe hyperparathyroidism in successive phases to her ultimate demise, manifesting neurological, renometabolic , skeletal, cardiovascular and gastrointestinal multisystem symptoms which are described. The complete relief of the acute symptoms following excision of a massive parathyroid adenomata is described and the spectacular pathologic specimen is demonstrated. This patient's course is compared with that of a typical case of pseudohyperparathyroidism.

Adenoma↗
PubMedDate not supplied

Giant mediastinal parathyroid adenoma with hypercalcemia.

Parathyroid disease is uncommon, but when found it is always of interest to the physician. Most patients with parathyroid disease also have hypercalcemia. Benign adenomatous disease is the most frequent surgical parathyroid lesion seen. Most of these lesions occur in the neck and are usually <2 cm in diameter. We report the case of a 50-year-old patient with familial neurofibromatosis, a serum calcium of 19 mg/dl, nephrocalcinosis, and renal failure. Evaluation revealed a large (5.7 x 4.5 x 2.9-cm) mediastinal adenoma. At resection, the tumor weighed 39.5 g. Symptomatology rapidly improved postoperatively.

Adenoma↗