Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scintigraphy with technetium-99m methylene diphosphonate (MDP) delineates a wide spectrum of nonosseous disorders. Neoplastic, hormonal, inflammatory, ischemic, traumatic, excretory, and artifactual entities demonstrate abnormal soft-tissue uptake of Tc-99m MDP. Mechanisms leading to increased extraosseous Tc-99m MDP uptake include extracellular fluid expansion, enhanced regional vascularity and permeability, and elevated tissue calcium concentration. The composition of the calcium deposition and the presence of other metallic ions (eg, iron and magnesium) are important. Soft-tissue Tc-99m MDP uptake is seen in benign (tumoral calcinosis, myositis ossificans) and malignant (sarcomas, adenocarcinomas, metastases) neoplastic entities. Hormonal disturbances in calcium metabolism, especially in hyperparathyroidism, can lead to metastatic calcification, visualized with Tc-99m MDP scintigraphy. Tissue damage from inflammation, infection, or physical trauma results in localized hyperemia, edema, or calcium (and hemosiderin) deposition based on their pathophysiologic characteristics. Urinary tract obstruction, anomalies, or dysfunction are demonstrated by Tc-99m MDP imaging. Common artifacts are related to faulty radiopharmaceutical preparation, Tc-99m MDP administration, and imaging technique. Recognition of these modes of extraskeletal Tc-99m MDP uptake can enhance the diagnostic value of bone scintigraphy.
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PMID:Extraosseous Tc-99m MDP uptake: a pathophysiologic approach. 835 64

This study documents dosage to radiation sensitive organs/structures located outside the radiotherapeutic target volume for four treatment situations: (a) head and neck, (b) brain (pituitary and temporal lobe), (c) breast and (d) pelvis. Clinically relevant treatment fields were simulated on a tissue-equivalent anthropomorphic phantom and subsequently irradiated with Cobalt-60 gamma rays, 6- and 18-MV x-ray beams. Thermoluminescent dosimeters and diodes were used to measure absorbed dose. The head and neck treatment resulted in significant doses of radiation to the lens and thyroid gland. The total treatment lens dose (300-400 cGy) could be cataractogenic while measured thyroid doses (1000-8000 cGy) have the potential of causing chemical hypothyroidism, thyroid neoplasms, Graves' disease and hyperparathyroidism. Total treatment retinal (400-700cGy) and pituitary (460-1000 cGy) doses are below that considered capable of producing chronic disease. The pituitary treatment studied consisted of various size parallel opposed lateral and vertex fields (4 x 4 through 8 x 8 cm). The lens dose (40-200 cGy) with all field sizes is below those of clinical concern. Parotid doses (130-1200 cGy) and thyroid doses (350-600 cGy) are in a range where temporary xerostomia (parotid) and thyroid neoplasia development are a reasonable possibility. The retinal dose (4000 cGy) from the largest field size (8 x 8 cm2) is in the range where retinopathy has been reported. The left temporal lobe treatment also used parallel opposed lateral and vertex fields (7 x 7 and 10 x 10 cm). Doses to the pituitary gland (5200-6200 cGy), both parotids (200-6900 cGy), left lens (200-300 cGy) and left retina (1700-4500 cGy) are capable of causing significant future clinical problems. Right-sided structures received insignificant doses. Secondary malignancies could result from measured total treatment thyroid doses (670-980 cGy). Analysis of three breast/chest wall and regional nodal irradiation techniques demonstrated a 25-50% decrease in secondary lung dose with use of independent collimation compared to use of custom alloy blocking material. However, it is unlikely that a reduction in secondary dose of this magnitude would reduce the risk of treatment sequellae. In four-field "box" pelvic irradiation, secondary testes dose may result in temporary (clamshell shield) or permanent azoospermia, but is unlikely to impair androgen production.
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PMID:Doses to radiation sensitive organs and structures located outside the radiotherapeutic target volume for four treatment situations. 840 17

Parathyroid carcinoma occurs in 0.1 to 5% as the cause of primary hyperparathyroidism (HPT). It is difficult to determine the true incidence, because parathyroid carcinoma is diagnosed too often due to unreliable histologic criteria. It is only justified to make the diagnosis, when a local recurrence or metastases with the clinical picture of a recurrent or persistent HPT occurred. Treatment of choice is the initial en-bloc resection, which may result in long disease-free intervals. Pharmacological treatment, chemotherapy, and radiation are mostly ineffective in the treatment of parathyroid carcinoma. A satisfactory long-term palliation can only be achieved with repeated resections of the local recurrences and metastases. Diagnostic efforts should be made to localize the recurrent tumor before every reoperation, whereby ultrasonography of the neck is the most sensitive procedure. Occasionally the parathyroid tissue cannot be identified in spite of preoperative diagnostic studies or hypercalcemia persists after surgery. In these cases forced diuresis and medical treatment with calcitonin, diphosphonates or mithramycine can briefly control hypercalcemia. The clinical courses of 3 patients with metastasizing parathyroid carcinoma are presented and discussed. In these patients 3 to 11 surgical interventions were performed in combination with an intermittent medical treatment. By this regimen we achieved long-term palliations up to 13 years.
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PMID:[Parathyroid gland cancer. Problems in diagnosis and therapy]. 846 48

A retrospective analysis of 93 patients undergoing 128 re-explorations for persistent or recurrent hypercalcaemia is presented. Seventy-six patients (82 per cent) became normocalcaemic after between one and five reoperations. Nine patients had hypercalcaemia caused by sarcoidosis, familial hypocalciuric hypercalcaemia or metastatic disease, and two had parathyroid carcinoma. Fifteen patients (16 per cent) developed permanent hypoparathyroidism requiring vitamin D and/or calcium therapy and nine had permanent recurrent laryngeal nerve paralysis. Undetected adenomas (41 cases) and inadequate resection in hyperplastic disease (28) were the predominant causes of initial failure. Reoperation for persistent or recurrent hyperparathyroidism restored normocalcaemia in the majority of patients. This 'cure' was achieved at the cost of considerable morbidity and a careful risk-benefit analysis of each patient is recommended before performing reoperative parathyroid surgery.
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PMID:Reoperation for suspected primary hyperparathyroidism. 849 8

Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.
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PMID:Plasma chromogranin A in pheochromocytoma, primary hyperparathyroidism and pituitary adenoma in comparison with catecholamine, parathyroid hormone and pituitary hormones. 922 69

Primary anterior mediastinal neoplasms comprise a diverse group of tumors and account for 50% of all mediastinal masses. Thymomas are most common and can be locally invasive and associated with parathymic syndromes. Thymic carcinomas and thymic carcinoids are rare malignancies with a propensity for local invasion and distant metastases. Thymolipomas are benign thymic tumors. The mediastinal germ cell tumors are a heterogeneous group of benign and malignant neoplasms. Mediastinal lymphangiomas are rare tumors and predominantly occur in young children. In contrast, mediastinal goiters are relatively common in adults. Mediastinal parathyroid adenomas are an uncommon cause of persistent hyperparathyroidism and rarely cause a discernible mass. The clinical, radiologic, and therapeutic aspects of the most common masses are reviewed.
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PMID:Primary mediastinal tumors. Part 1: tumors of the anterior mediastinum. 926 92

In recent classifications of gastric endocrine tumors, tumors arising in patients with multiple endocrine neoplasia type 1 (MEN-1) are regarded to be regulated by the concomitant hypergastrinemia resulting from to pancreatic or, most commonly, duodenal gastrinomas and to have a benign behavior. In this article, we report on two cases of MEN-1 gastric neuroendocrine tumors having a fatal course. Case 1 was a young male with hyperparathyroidism and Zollinger-Ellison syndrome and with florid development of multiple gastric carcinoids and multiple duodenal gastrinomas. Metastases occurred in the liver, of exclusive gastric origin, in periduodenal lymph nodes, of exclusive duodenal origin, and in perigastric lymph nodes, of mixed origin. The patient died 48 months after diagnosis. Case 2 was an adult female patient with hyperparathyroidism, adrenocortical disorders, and gastric tumors but no hypergastrinemia. The patient died 3 months after tumor diagnosis. At autopsy, the stomach showed multiple benign carcinoids and two independent neuroendocrine carcinomas not reported before in MEN-1 and massively metastatizing to lymph nodes, liver, and peritoneum. Multiple islet cell tumors mostly producing pancreatic polypeptide were found, whereas gastrinomas were seen in neither the pancreas nor the duodenum. Allelic losses at the MEN-1 gene locus in chromosome 11q13, the mechanism responsible for tumor development in MEN-1 syndrome, were demonstrated in the carcinoid tumors of case 1 and in the neuroendocrine carcinoma of case 2. We conclude that gastric neuroendocrine tumors in patients with MEN-1 may have a poor outcome, they have the same genetic mechanism as MEN-1 tumors in other organs, and they may be independent of the trophic effect of hypergastrinemia.
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PMID:Aggressive forms of gastric neuroendocrine tumors in multiple endocrine neoplasia type I. 929 84

We present a patient with prostate cancer who developed symptomatic hypocalcemia while taking oral clodronate for painful bony metastases. He had a past history of a bowel resection for Crohn's disease, and, although he was normocalcemic prior to taking clodronate, it is likely that the surgery had caused mild hyperparathyroidism. The addition of clodronate prevented the chronic osteolysis of bony metastases, which would have helped maintain normocalcemia. The case was complicated by hypomagnesemia and hypokalemia resulting from diarrhea. Hypomagnesemia is a cause of refractory hypocalcemia and hypokalemia. This case illustrates two important points. First, care must be taken with bisphosphonates in patients with a previous bowel resection. Second, magnesium plays a key role in the metabolism of both calcium and potassium, and must be considered in the evaluation of the hypocalcemic patient.
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PMID:Symptomatic hypocalcemia with oral clodronate. 949 15

When mutations of the RETproto-oncogene were found in 1993 to account for hereditary medullary thyroid carcinoma (MTC), surgeons obtained the opportunity to operate on patients prophylactically (i. e., at a clinically asymptomatic stage). Whether this approach is justified, and, if so, when and to which extent surgery should be performed remained to be clarified. A questionnaire was sent to all surgical departments in Germany and Austria. All of the patients who fulfilled the following criteria were enrolled: (1) preoperatively proved RET mutation; (2) age </= 20 years, (3) clinically asymptomatic thyroid C cell disease; and (4) TNM classification pT0-1/pNX/pN0-1/M0. Seventy-five patients were identified, and fifteen mutations were detected in six codons. Two adolescents had unilateral pheochromocytomas as part of the multiple endocrine neoplasia II (MEN-II) syndrome. No hyperparathyroidism was noted. All patients underwent total thyroidectomy, and 57 patients went on to have lymph node dissection. Parathyroid glands were removed in 34 patients and autografted in 11. Histopathology revealed MTC in 46 patients (61%, youngest 4 years); C cell hyperplasia (CCH) only was detected in the other 29 patients. Three patients had lymph node metastases (LNMs) the youngest being age 14 years. Calcitonin levels were not useful for differentiating between CCH and MTC, but in all patients with LNMs at least the stimulated calcitonin levels were assayed. After surgery, five patients (6.7%) sustained permanent hypoparathyroidism, and one patient (1.3%) had a permanent unilateral recurrent nerve palsy. All but three patients (96%) were biochemically cured. In conclusion, prophylactic total thyroidectomy can be performed safely in experienced centers. We recommend prophylactic total thyroidectomy at age 6. Cervicocentral lymph node dissection should be included when calcitonin levels are elevated or if patients are older than 10 years. Bilateral lymph node dissection should be performed if LNMs are suspected or when patients with elevated calcitonin are older than 15 years.
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PMID:Prophylactic thyroidectomy in 75 children and adolescents with hereditary medullary thyroid carcinoma: German and Austrian experience. 960 92

Since bone markers may reflect different aspects of bone disorders and cell function, and osteolytic and osteoblastic activities may be individually or concomitantly altered, determination of more than one marker type is generally appropriate. Also, the individual markers of a particular type do not necessarily show parallelism. For example, in osteomalacia from vitamin D deficiency, bone-specific alkaline phosphatase may be grossly elevated because of enhanced osteoblastic activity, whereas the vitamin D dependent osteocalcin may be decreased. With the exception of measurement of the bone enzymes, bone-specific alkaline phosphatase and tartrate-resistant acid phosphatase, bone marker measurements require complex and expensive immunoassays. As a general rule, the simple enzyme measurements can precede other investigation in most bone disorder> Bone-specific alkaline phosphatase measurement alone is generally adequate for the investigation of osteomalacia, Paget's disease and hyperparathyroidism but should be combined with measurement of tartrate-resistant acid phosphatase in suspected metastatic disease, and in multiple myeloma. Determination of both enzymes together may also be of value in the investigation of osteoporosis but in this disorder added benefit may be obtained by the addition of other bone markers, particularly urine deoxypyridinoline and possibly serum collagen telopeptide.
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PMID:Biochemical markers of bone turnover. 974 51


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