Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amyloidosis primarily involving bone is described in a 59-year-old male pateint. Well circumscribed lytic lesions of the skeleton raised the possibility of myelomatosis. The prolonged insidious course of the disease was uncomplicated by hypercalcemia, pathological fracture, or hematologic abnormalities. The clinical course, together with histological findings and strongly positive bone scan, were the distinguishing features. The osseous manifestations without plasma cell tumor appears to be a rare occurrence in amyloidosis.
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PMID:Bone lesions in primary amyloidosis. 50 49

Intermittent courses of dexamethasone (DEX) were administered to 112 consecutive, previously untreated patients with multiple myeloma (MM). Using criteria based on a 75% or greater reduction of calculated tumor mass, the overall response rate was 43%. Among comparable patients, response rate were approximately 15% less than those observed previously with vincristine-doxorubicin by continuous infusion with intermittent DEX (VAD) and similar to those with melphalan-prednisone. The projected survival times with VAD or DEX were similar. Results indicated that DEX accounted for most of the plasma cell reduction achieved with VAD. Serious complications occurred in 27% of patients treated with VAD, but in only 4% of those who received DEX. In view of the similar outcome with fewer serious complications, DEX provided a simple, effective, and safe primary treatment for a large fraction of patients with MM. Patients who appear most likely to benefit include those with hypercalcemia or pancytopenia, or who require simultaneous radiotherapy for a pathologic fracture.
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PMID:Primary dexamethasone treatment of multiple myeloma. 149 31

Osteolytic bone metastases secondary to breast cancer are extremely common, occurring in more than 50% of breast cancer patients. The resulting increased bone resorption leads to significant symptomatic morbidity caused by bone pain, hypercalcaemia and pathological fracture. Clodronate, an anti-osteolytic agent, inhibits osteoclastic bone resorption and has considerable therapeutic value. Recent studies have shown that clodronate is effective in the treatment of malignancy hypercalcaemia, relief of bone pain and decreases the risk of pathological fracture. The use of clodronate in the future, other than as a palliative therapy, may focus upon the prevention of osteolytic bone metastases at the time of primary diagnosis or later in the disease progression in those patients at risk, for example, those with non-osseous relapse. Since patients with bone metastases secondary to breast cancer often have an increased duration of survival, any agent that would decrease the symptomatic morbidity would have a significant impact upon quality of life, even more so if the actual development of osteolytic bone metastases was delayed or prevented.
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PMID:Clodronate: the potential for the future. 172 14

Pathologic fractures are not commonly described in primary hyperparathyroidism. A 31 year old male with primary hyperparathyroidism developed severe hypercalcemia and cystic osteitis. Bone pains and a fracture of the femur followed. A parathyroid adenoma was demonstrated by ultrasonography. After resection of the tumor, a normalization of serum Ca levels and clinical recovery took place.
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PMID:[Pathologic fracture of the femur due to primary hyperparathyroidism]. 251 66

The search into the way in which skeletal metastases develops has not only shown that there are several mechanisms for the progressive bone destruction and bone formation that occur simultaneously in the majority of skeletal metastases, but also that an understanding of these basic mechanisms has significant therapeutic implications. Our results have shown that there are two main mechanisms for the bone formation: stromal bone formation and reactive bone formation. The former occurs in tumours which tend to be acellular, with a large fibrous stroma, whereas the latter occurs in virtually all metastases. There is no difference in the basic pathological process of sclerotic or lytic metastases, the radiographic appearance purely indicating the net balance between the different types of bone formation and the simultaneous progressive bone destruction. An understanding of the pathophysiological response to skeletal metastases explains why skeletal scintigraphy can be used to diagnose these lesions and the different mechanisms underlying the 'three-phase scintigram'. The first phase indicates the vascularity of the lesion; the second phase or 'blood-pool' image indicates the concentration in the extracellular fluid and the third phase or 'skeletal or delayed image' indicates the uptake in the reactive new bone. The secretion of an osteoblast inhibiting factor by myeloma indicates why there is no reactive bone produced by the majority of lesions in the absence of a fracture, and why scintigraphy is less reliable than plain radiographs for the detection of the lesions. There are two main mechanisms for the bone destruction, the most important being mediated via osteoclasts. An understanding of the humoral mechanisms stimulating the osteoclast proliferation may lead to more effective treatment of malignant hypercalcaemia and lytic metastases. Early results of use of APD are encouraging, and our results also suggest that clinical trials should be established to evaluate the effect of combination therapy with APD or prostaglandin inhibitor combined with the agents normally used in the management of patients with disseminated mammary carcinoma. The development of treatments to inhibit tumour-induced osteolysis will minimise the complications of pathological fracture, spinal instability, etc., and even if these treatments do not affect the primary tumour, its ability to metastasize, or the patient's survival, such treatment will be a major advance in the management of patients with carcinoma, because of the significant morbidity currently associated with the development of skeletal metastases and their complications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The development of skeletal metastases. 279 40

During the past ten to 20 years, there have been many advances in the understanding of the way in which skeletal metastases develop and great strides in the methods of detection, particularly with the development of the gamma camera and axial or whole-body skeletal scintigraphy. Skeletal metastases may present with pain, hypercalcemia, large lytic lesions, pathologic fracture, spinal cord or cauda equina compression, or spinal instability. Much has been learned about the management of skeletal metastases, and many of these developments have occurred in Great Britain.
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PMID:Skeletal metastases. 375 60

Human breast cancer frequently metastasizes to the skeleton to cause osteolysis and subsequent pain, pathological fracture, and hypercalcemia. Because bone continuously releases growth factors stored in bone matrix by bone resorption during physiological remodeling and, thus, possibly provides a favorable microenvironment for metastatic breast cancer cells to proliferate, inhibitors of bone resorption used either prophylactically or in patients with established disease, therefore, would seem likely to be useful adjuvant therapy in patients with breast cancer. However, the parameters for monitoring progressive osteolytic bone disease in humans are imprecise. We examined the effects of the third generation bisphosphonate, risedronate, which is a specific inhibitor of osteoclastic bone resorption, in a bone metastasis model in nude mice in which intracardiac injection of the human breast cancer cell line MDA-231 leads to osteolytic bone metastases. Risedronate (4 micrograms/animal/day) was given s.c. to animals (a) after radiologically small but defined osteolytic metastases were observed; (b) simultaneously with MDA-231 cell inoculation through the entire experimental period; or (c) by short-term prophylactic administration before inoculation of MDA-231 cells. In all experiments, risedronate either slowed progression or inhibited the development of bone metastases assessed radiographically. Furthermore, mice treated continuously with risedronate showed significantly longer survival than did control mice. Histomorphometrical analysis revealed that osteoclast numbers were diminished at metastatic tumor sites. Unexpectedly, there was also a marked decrease in tumor burden in bone in risedronate-treated animals. In contrast, the growth of metastatic breast cancer in soft tissues surrounding bones was not affected by risedronate. Moreover, risedronate had no effects on the local growth of s.c. implanted MDA-231 breast cancers in nude mice or on MDA-231 cell proliferation in culture. These data demonstrate that risedronate decreases metastatic MDA-231 breast cancer burden selectively in bone, as well as suppresses progression of established osteolytic lesions and prevents the development of new osteolytic lesions; thus, the data suggest that inhibition of osteoclastic bone resorption may be a useful adjunctive therapy for the treatment of cancers that have colonized in bone.
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PMID:Bisphosphonate risedronate reduces metastatic human breast cancer burden in bone in nude mice. 762 63

Complications of cancer that are amenable to treatment with rehabilitation techniques will develop in many patients with skeletal metastases. This treatment can be given safely, with a low prevalence of pathologic fracture. Many patients with skeletal metastases and pathologic fracture have been shown to be good candidates for intensive rehabilitation programs if they do not have hypercalcemia caused by lytic metastases or pain severe enough to require parenteral narcotics.
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PMID:Rehabilitation of cancer patients with skeletal metastases. 763 3

An 84-year-old man with non-Hodgkin's malignant lymphoma presented with a pathological fracture of the femur and also an intra-atrial mass on echocardiography. The patient was given palliative low-dose chemotherapy, but died of tumor dissemination, hypercalcemia, and dehydration. Autopsy revealed diffuse large B-cell lymphoma involving multiple bones and lymph nodes (the latter were not detected during staging), and a solitary mass on the posterior wall of the right atrium. This rare lesion appeared to be due to hematogenous spread, since the myocardium and pericardium were free of tumor infiltration. A literature review indicated that the frequency of cardiac involvement differed between contemporary and earlier reports, mainly due to the availability of increasingly sophisticated diagnostic methods and improvements in chemotherapy.
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PMID:Non-Hodgkin's malignant lymphoma of the bone with intracavitary cardiac involvement. 824 97

Frequent complications of bone metastases include pain, pathologic fracture, hypercalcemia and spinal cord compression. Lytic bone metastases result from excessive activation of osteoclasts by tumor-produced cytokines. Aredia (pamidronate) is a potent bisphosphonate that inhibits osteoclast activation. In two dose-seeking phase I trials in patients with breast cancer and prostate cancer, repeated intravenous infusion of Aredia was shown to be safe and effective in reducing bone resorption and pain. In a randomized phase III trial of 377 patients with multiple myeloma, Aredia was administered in a dosage of 90 mg i.v. every 4 weeks. Compared with placebo, treatment with Aredia was associated with a significant decrease in bone pain and in the incidence and time to development of all skeleton-related events. Data from two phase III breast cancer trials each involving 300 patients are now being analyzed. The newer bisphosphonates can safely be used together with standard anticancer therapy to provide effective palliation of symptoms caused by lytic bone metastases.
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PMID:The role of bisphosphonates in the treatment of bone metastases--the U.S. experience. 873 55


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