Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple endocrine neoplasia type 1 (MEN-1) is an autosomal dominant disease involving tumors of the parathyroid, pancreas, and pituitary glands. Over 50% of the patients with this syndrome will have involvement of the pituitary gland. Computed tomography (CT) of the head was performed in 21 of 42 patients with the clinical diagnosis of MEN-1. CT demonstrated pituitary abnormalities in 15 patients, 13 of whom had pituitary endocrine dysfunction. The most common endocrinopathy was hyperprolactinemia, documented in nine patients. Hypopituitarism due to nonfunctional adenoma was found in two patients, and acromegaly and Cushing disease in individual cases. The appearance of the pituitary gland in CT evaluation of the sella in patients with MEN-1 is presented.
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PMID:CT of the pituitary gland in multiple endocrine neoplasia type 1 syndrome. 613 81

Circulating human pancreatic polypeptide (hPP) concentrations in the plasma of 61 patients were determined by radioimmunoassay and compared with concentrations in normal age-matched subjects to assess the role of plasma hPP in diagnosis and detection of pathologic dysplasias in endocrinopathies. Basal fasting plasma hPP concentrations greater than 3.0 times normal values were found in six of six patients with multiple endocrine adenopathy syndrome, type I (MEA I) who had islet cell tumors that contained hPP and in only three of 15 nonfamilial patients with sporadic islet cell tumors. An exaggerated plasma hPP response to meal stimulation that exceeded greater than 4.5 times the basal value was found in 15 of 18 patients with MEA I, which indicated the presence of endocrine cell hyperplasia as the underlying genetic trait. The abnormal plasma hPP response to meal stimulation correlated most strongly with islet cell hyperplasia in both the genetic and sporadic endocrinopathies and to some extent with antral G cell hyperplasia. In patients with primary hyperparathyroidism, an exaggerated plasma hPP response to meal stimulation is highly indicative of genetic parathyroid hyperplasia in MEA I and not of sporadic parathyroid adenoma. Informed consent was obtained from all patients who were subjects of these investigations.
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PMID:Pancreatic polypeptide update: its roles in detection of the trait for multiple endocrine adenopathy syndrome, type I and pancreatic polypeptide-secreting tumors. 613 85

A patient had a parathyroid adenoma and prolactin-secreting pituitary tumor, suggestive of the multiple endocrine neoplasia (MEN) I syndrome. The presence of a marfanoid habitus--found more typically in MEN III syndrome--as well as mitral valve prolapse, mental retardation, and bilateral optic atrophy suggests a new variant of the MEN syndrome, possibly representing widespread dysplasia of endocrine and other tissues.
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PMID:Multiple endocrine neoplasia, type I. Association with marfanoid habitus, optic atrophy, and other abnormalities. 613 88

Two cases of Sipple's syndrome with the typical signs of medullary carcinoma of the thyroid, pheochromecytoma and parathyroid adenoma are presented. Cushing's disease and marfanoid habitus were demonstrated. They are classified as multiple endocrine adenopathy type 2A and 2B according to the modern nomenclature.
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PMID:[Sipple syndrome as a differential diagnosis in recurrent laryngeal nerve]. 614 70

Ultrasonic examination of the parathyroid glands has been used in 50 consecutive patients with surgically verified hyperparathyroidism. It revealed 21 of 32 parathyroid adenomas located in the neck. In 16 patients with primary or secondary (uraemic) hyperplasia, 11 out of 48 hyperplastic glands in the neck were identified by ultrasound. A parathyroid adenoma was revealed in all (3) patients with hypercalcaemic crisis. Enlarged parathyroid glands were correctly located in all (5) patients with adenomas and previous explorations of the neck, whereas two out of three glands were visualized by ultrasound prior to secondary explorations in 3 patients with hyperplasia associated with the multiple endocrine neoplasia syndrome type 1. Undetected parathyroid glands were generally smaller than those visualized by ultrasonic examination. It was often difficult to unequivocally establish that identified lesions represented parathyroid glands. Irregular noduli and cysts of the thyroid as well as lymph nodes could be misinterpreted as parathyroid lesions. A nodular thyroid goitre was present in almost half of the patients with a negative ultrasonic examination of the parathyroid glands.
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PMID:Ultrasound scanning for preoperative location of parathyroid tumours. 646 22

We have experienced 186 patients with proven primary hyperparathyroidism operated on during past 16 years. In this series, 147 patients (79%) had adenoma, 24 patients (12.9%) had carcinoma and only 15 (8.1%) had hyperplasia. Because of a 92% of single gland involvement, the removal of an enlarged gland is adequate, if the remaining gland are grossly normal. Besides, interestingly enough, an incidence of parathyroid carcinoma is rather high in Japan, so that surgeons should be alert to recognize the parathyroid carcinoma on the basis of clinical and operative findings. In an effort to minimize recurrence, en bloc resection of the parathyroid carcinoma is important. When a patient with parathyroid carcinoma has a local recurrence or distant metastases, an aggressive surgical approach is recommended to alleviate hypercalcemic symptoms. The majority of patients with hyperplasia belong to multiple endocrine neoplasia, type 1. Recent development of the non-invasive diagnostic methods is remarkable. The last consecutive 31 patients underwent preoperative localization study by 201Thallium (201TI-CI) scanning and ultrasonography. 201TI-CI scanning gave the most accurate results and 100% correct localization was obtained when the parathyroid tumor was more than 1 g. However, it is noteworthy that the parathyroid tumor was less than 1 g in 64% of patients who had no evidence of generalized fibrous osteitis.
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PMID:[Surgical management of primary hyperparathyroidism]. 650 56

A 61-year-old patient with treated Conn's syndrome due to multiple bilateral adrenocortical adenomata developed primary hyperparathyroidism. At operation, a parathyroid adenoma and a thyroid colloid nodule were found. Although adrenocortical adenomata and hyperplasia are common findings in multiple endocrine adenopathy type I, they are only rarely functional. Hypertension is often associated with primary hyperparathyroidism, but the relationship is usually unexplained.
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PMID:Primary hyperparathyroidism in a patient with Conn's syndrome. 738 50

Analysis of a series of 205 surgically treated cases of primary hyperparathyroidism was carried out to assess the long-term results of the conservative approach of selectively removing the adenoma only. If primary hyperparathyroidism is due to multiple gland involvement in one-third to one-half of patients, an appreciable number of patients with recurrent disease should have been encountered during this study of the results of conservative no instances of permanent tetany, supports the conservative approach to the treatment when only a single enlarged gland is encountered. Subtotal parathyroidectomy should be reserved for those few cases in which multiple enlarged glands are found, especially in association with multiple endocrine neoplasm, familial hyperparathyroidism, and secondary hyperparathyroidism.
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PMID:Primary hyperparathyroidism: the case for conservative surgery. 738 86

A 48 year old man presented with hyperparathyroidism and acromegaly. Although pancreatic tumour was not demonstrated, the diagnosis of MEN-1 syndrome was made. The parathyroid adenoma was removed surgically and investigated by histology and transmission electron microscopy and was diagnosed as large clear cell adenoma with extensive deposition of glycogen. Much of the endoplasmic reticulum was present in two special forms: annulate lamellae and the rare rail-like configurations both of which showed continuity with the conventional RER as well as with each other. No obvious correlation was apparent between presence of special RER formations and growth rate or endocrine activity of tumour; they may be regarded as signs of cellular dedifferentiation.
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PMID:Large clear cell adenoma of the parathyroid in a patient with MEN-1 syndrome. Ultrastructural study of the tumour exhibiting unusual RER formations. 772 22

Primary aldosteronism is the commonest cause of potentially curable hypertension when diagnosed in both florid and less florid forms. Genetic screening, so far available only for glucocorticoid-suppressible hyperaldosteronism, permits diagnosis from birth, before any biochemical or clinical abnormalities appear. Biochemical screening using the aldosterone-to-renin ratio permits diagnosis in the absence of raised aldosterone or of hypokalemia. Primary aldosteronism occurs in several familial forms. As well as the variety described in 1966 which is ACTH-dependent and glucocorticoid-suppressible, and not so far associated with tumors, another variety described in 1991 is not glucocorticoid-suppressible and is frequently associated with aldosterone-producing adenomas (APAs). Primary aldosteronism due to adrenocortical hyperplasia, adenoma, or carcinoma can also occur as part of the multiple endocrine neoplasia syndromes, where normoplasia, hyperplasia, benign neoplasia, and malignant neoplasia can exist in the same patient in the same endocrine gland(s) at the same time. The morphology of adrenocortical hyperplasia causing primary aldosteronism ranges from glomerulosa-like (idiopathic hyperplasia of the adrenals) to fasciculata-like (glucocorticoid-suppressible hyperaldosteronism). The morphology of adrenocortical neoplasia causing primary aldosteronism can also be either predominantly glomerulosa-like or fasciculata-like, in our experience equally often. Varying morphology of APAs is associated with varying responses of aldosterone to angiotensin II. Tumors predominantly fasciculata-like are unresponsive to angiotensin II, whereas those predominantly glomerulosa-like are responsive to angiotensin II. Both subtypes can be seen in a single family. Primary aldosteronism represents a spectrum of genetic disorders resulting in hyperplasia or neoplasia, but all are associated with some degree of autonomy of aldosterone production, independent of the renin-angiotensin system.
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PMID:Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes. 779 13


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