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)

A 51-year-old male patient with chronic renal failure, who had required dialysis for 22 years, presented with a cervical mass. Laboratory data were consistent with secondary hyperparathyroidism due to chronic renal failure. Cervical exploration was performed with excision of four parathyroid glands and autotransplantation of the normal gland into the forearm. The cervical tumor of the right inferior gland demonstrated parathyroid carcinoma histologically. Adenoma of the right superior gland and hyperplasia of the left superior gland were also recognized. The left inferior gland was normal. A few cases of parathyroid carcinoma in patients on maintenance hemodialysis have been previously reported. However, this is the first report in which all four parathyroid glands revealed different pathological findings: carcinoma, adenoma, hyperplasia and normal gland. Chronic stimulation of the parathyroid glands to release parathyroid hormone might have caused the variety of findings in the four parathyroid glands.
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PMID:Different pathological findings in each of four parathyroid glands in a long-standing hemodialysis patient. 1110 5

Parathyroid hormone-related protein (PTHrP), a factor responsible for malignancy associated hypercalcemia, plays a physiological roles such as bone development and placental calcium transport. The expression of PTHrP in adult human parathyroid tissues under normal and pathological conditions was analyzed. By immunohistochemistry, PTHrP expression was detected in 86% of normal parathyroid (12/14 cases), 74% of adenomas (14/19) and 89% of hyperplasia secondary to chronic renal failure (16/18). PTHrP protein was observed mainly in the cytoplasm of oxyphil cells, consistent with the localization of its mRNA demonstrated by in situ hybridization. The rate of PTHrP-positive cells was higher in areas consisting of oxyphil cells than in those of non-oxyphil cells, regardless of whether the parathyroid was normal or pathological. In the normal parathyroid, an age-related increase in PTHrP expression was observed with a relative increase in oxyphil cells, reflecting aging and deterioration of parathyroid tissue. In adenoma, cases with a predominance of oxyphil cells expressed PTHrP, whereas clear cell adenoma did not. In secondary hyperplasia, the rate of PTHrP-expressing cells was higher than in normal parathyroid or adenoma, with varying levels of expression among nodules. We speculate that PTHrP could act through the paracrine/autocrine mechanism to regulate proliferation and differentiation of normal and neoplastic parathyroid cells.
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PMID:Expression of parathyroid hormone-related protein (PTHrP) in parathyroid tissue under normal and pathological conditions. 1181 67

Patients with chronic renal failure (CRF) have a high incidence of malignant tumours. Uremia thus induces a remarkable suppression of immune status. In this study, we report that within the last 20 years, 188 (6.7%) various organ tumours were found in 2817 CRF patients that were hospitalised and treated. 69 (36.7%) of 188 patients with various organ tumours were on hemodialysis and the rest (63.3%) were CRF without hemodialysis. 49 (71%) of the 69 patients with hemodialysis were diagnosed with tumours in the first year of the hemodialysis therapy. In 110 (84%) of 119 CRF patients tumours were detected in less than 10 years after diagnosis of CRF. Localisation of the tumours were: 39 (19%) urologic malignancy, 30 (16%) parathyroid adenoma, 28 (15%) skin malignancy, 19 (10%) gynaecologic malignancy, 18 (9.5%) gastrointestinal tract (GIT) malignancy, 17 (9%) lung malignancy, 17 (9%) larynx malignancy, 13 (7%) thyroid malignancy, 5 (2.6%) multiple myeloma and 5 (2.6%) malignant lymphoma. No patients in the series had received a transplant kidney or were therapeutically immunosuppressed for other reasons and obstructive uropathy. CRF patients have a several times greater risk of developing malignant tumour than the general population.
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PMID:Increased incidence of neoplasia in chronic renal failure (20-year experience). 1209 Mar 17

Ectopic parathyroid adenoma is a frequent cause of persistent or recurrent hyperparathyroidism after parathyroidectomy in patients with chronic renal failure on dialysis. An unusual anatomic localization of parathyroid adenoma may make the diagnosis and surgery difficult. In a 41-year-old woman with chronic renal failure, increased serum level of parathyroid hormone and symptoms of progressive renal osteodystrophy, mediastinal parathyroid adenoma was detected in the aorticopulmonary window by 99m Tc sesta MIBI scintigraphy and transmission computed tomography. Extirpation of adenoma, sized 3 x 2 cm, was performed through a left thoracotomy. Serum parathormone level returned to normal and the patient steadily recovered.
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PMID:Surgical treatment of mediastinal parathyroid adenoma. 1259 27

In primary hyperparathyroidism, calcium homeostasis is disrupted by excessive synthesis and secretion of parathyroid hormone (PTH), which is usually caused by a solitary adenoma, or less often by nodular hyperplasia or carcinoma of the parathyroid glands. So far, the distinction between these forms of primary hyperparathyroidism has been made by histological examination. In this report clinical and histological findings, including PTH immunohistochemistry, are described in five dogs with primary hyperparathyroidism, three dogs with secondary hyperparathyroidism due to chronic renal failure, and eight control dogs. In the dogs with primary hyperparathyroidism, nodular adenomatous hyperplasia was found in two animals and parathyroid adenoma in three. The dogs with chronic renal failure had diffuse parathyroid gland hyperplasia. The parathyroid glands of the control dogs and the inactive cells surrounding the hyperplastic nodules showed slight to moderate, localized, paranuclear PTH immunolabelling. In the primary nodular and secondary diffuse hyperplasia, all parathyroid cells had a diffuse cytoplasmic PTH labelling pattern, sometimes in combination with localized paranuclear labelling. In parathyroid adenoma, areas with either paranuclear labelling or diffuse cytoplasmic labelling were observed. As both parathyroid adenoma and primary nodular parathyroid gland hyperplasia have characteristics of intrinsic autonomy (i.e., suppression of the remaining endocrine tissue), there would seem to be no functional difference between the two abnormalities. It is argued that primary (multi)nodular hyperplasia is a multiple form of parathyroid adenoma.
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PMID:Parathyroid hormone immunohistochemistry in dogs with primary and secondary hyperparathyroidism: the question of adenoma and primary hyperplasia. 1285 9

The diagnosis of aldosterone-producing adenoma (APA) is challenging for endocrinologists, as APA does not always present with the typical constellation of clinical and laboratory features, such as hypertension, hypokalemia, suppressed plasma renin activity (PRA), and high plasma aldosterone concentration (PAC). Very recently, several studies have indicated that APA can be discovered even in normokalemic subjects with normal PRA more frequently than previously considered. Here we report a case of APA associated with chronic renal failure, which showed normokalemia and normal PRA. The patient was referred to our clinic for evaluation of an incidentally discovered adrenal mass with abnormally high PAC. After 6 yr, it was found that the right adrenal tumor showed a marked increase in size. Endocrinological examinations indicated normal PRA and markedly high PAC. Aldosterone showed a better response to the upright posture test than that to ACTH stimulation test. The diagnosis of APA was made based on the markedly high PAC to PRA ratio and the adrenocortical scintigraphy, which showed unequivocal uptake into the tumor. Right laparoscopic adrenalectomy was performed, revealing a right adrenocortical adenoma with massive hemorrhage. Histopathological examinations revealed the presence of two independent adrenocortical adenomas, one APA with predominant clear tumor cells and few c17 (17alpha-hydroxylase) immunoreactivity and the other, cortisol producing adenoma with compact cytoplasm and abundant C17 immunoreactivity. This case indicates a difficulty of diagnosis of "normoreninemic APA" with renal failure. This case is in line with the recent concept that APA is a continuous condition in which only a minority of patients have the classical clinical picture of primary aldosteronism such as hypokalemia. It is possible that normokalemic APA constitutes the most common presentation of the disease.
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PMID:A case of normoreninemic aldosterone-producing adenoma associated with chronic renal failure: case report and literature review. 1451 5

We report here a dialysis patient with secondary hyperparathyroidism who had a history of parathyroidectomy for primary hyperparathyroidism 27 years previously. The patient was a 48-year-old male. In 1974, he was diagnosed as having primary hyperparathyroidism and an adenoma was completely resected in the Department of Urology, Osaka University Hospital. In 1997, he started hemodialysis for chronic renal failure by diabetic nephropathy. Since his intact-PTH was high, we started intravenous vitamin-D pulse therapy, but intact-PTH did not decrease. We could not detect any parathyroid glands by ultrasonography and 201TlCl-99mTcO4-scintigraphy around the thyroid gland. Finally, chest-CT and 99mTc-MIBI scintigraphy revealed a ectopic parathyroid gland in the mediastine, and the ectopic parathyroid gland was successfully resected in July, 2001. In order to distinguish whether the resected ectopic parathyroid gland was due to primary adenoma or secondary hyperplasia, we used an immunohistochemical technique to examine the expression of PRAD1/cyclin D1, Ki67, and p27 and sequence analysis of the MEN1 gene. As a result, the labeling index (LI) of PRAD1/cyclin D1 was 4, LI of Ki67 was 36, and LI of p27 was 257. Moreover, germline-mutation and somatic-mutation of MEN1 gene was not detected. These findings suggested that the resected parathyroid gland was a nodular hyperplasia of secondary hyperparathyroidism. In conclusion, immunohistochemical findings of parathyroid tissue and sequence analysis of MEN1 gene could be useful for the differential diagnosis of primary adenoma and secondary hyperplasia.
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PMID:[A hemodialysis patient with secondary hyperparathyroidism in whom primary parathyroid adenoma was resected 27 years previously]. 1463 67

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

Tertiary hyperparathyroidism represents an autonomous proliferation state of the parathyroid glands that takes place in spite of performing a renal transplantation in patients with chronic renal failure due to the illness. We are reporting 5 own clinical cases collected in a 14 years period corresponding to 2 men and 3 women, with ages between 43 and 53, that were sent from Nephrology for surgical intervention. The AP result was hyperplasia in 4 samples and 1 adenoma in the rest. 2 transitory hypocalcemias were registered but not recurrential palsies. After the surgery we got the normalization of hypercalcemia in all of them and improvement of skeletal symptoms.
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PMID:[Tertiary hyperparathyroidism. Report of 5 cases]. 1525 47

We describe the case of a 49-year-old female with chronic renal failure and secondary hyperparathyroidism that not dissapeared after kidney transplant and turned into an autonomous form (tertiary hyperparathyroidism). The xRays and CT showed the presence of multiple brown tumors in iliac bones and tibia. We performed a parathyroidectomy removing a lower left adenoma confirmed in the histological exam the renal. After the surgery the osteoarticular manifestations improved and lithiasis dissapeared. There were not any postoperative complications such as hypocalcemia or recurrential palsy although Nephrology Department had to control her renal function.
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PMID:[Multiple brown tumours in a patient with tertiary hyperparathyroidism]. 1615 62


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