Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone pain is one of the most frequent causes of pain in patients with cancer, and the levels of metastases and bone pain are not directly correlated. Nociceptors in the periosteum are probably stimulated by halisteresis or by inflammatory oedema leading to an increase in the intraosseous pressure. Some authors believe that the nociceptors in bone are mediated via intraosseous mechanoreceptors in the bone-matrix. At a low pain level the initial treatment is acetylsalicylic acid, paracetamol or other nonsteroidal antiinflammatory drugs. At increasing pain level initial doses of oral opioids are added. In severe bone pain, where conventional therapy seems difficult, opioids are administered by invasive techniques. In localised bone pain palliative radiation is the first treatment of choice. Corticosteroids induce an analgetic effect indirectly by reducing the inflammatory oedema, inhibiting the synthesis of prostaglandins and may inhibit excitatory nerve fibres. Endocrine treatment, calcitonin and biophosphonates have shown a documented pain-relieving effect in patients with disseminated breast and prostate cancer. Chemotherapy has shown a pain-relieving effect in patients with disseminated breast cancer, surgical intervention is used in stabilizing osteolytic bones before or after a fracture ensuring a reasonable relief of pain.
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PMID:[Malignant bone pain]. 916 11

This prospective nonrandomized trial was performed to evaluate the efficacy of salmon calcitonin (sCT) in controlling pain related to bone metastasis in cancer patients and the relation of sCT's analgesic efficacy with beta-endorphin blood levels. The study group consisted of 22 cancer patients with bone metastases (male 13 and female 9, age range 38-77 years). Pain control was first achieved by continuous subcutaneous (s.c.) morphine administration. The next increase in pain was managed with continuous s.c. administration of 400 IU/day sCT. Beta-endorphin blood levels were measured before and during sCT administration. The first measurement was taken before sCT administration; subsequent measurement occurred at 12, 24, and 48 hours and 7 days after the commencement of treatment. Pain scores were monitored by a visual analogue scale. A complete blood count and a biochemical screening profile were taken before the administration of calcitonin and also on the seventh and the fifteenth day of the administration. The results showed a satisfactory analgesic effect. The mean pain score before the calcitonin administration was 4.43 and the score on the seventh day was 1.17. The gradual reduction of pain score was associated with an increase in beta-endorphin blood levels (increase to 147.2% of baseline on the seventh treatment day). In three cases, no satisfactory analgesic effect was obtained and pain control was achieved by increasing the continuous s.c. morphine dosage. No significant side effects were observed. These data suggest that sCT in high doses may be a useful adjuvant analgesic when combined with low doses of morphine in continuous s.c. administration for the management of metastatic bone pain.
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PMID:Continuous subcutaneous administration of high-dose salmon calcitonin in bone metastasis: pain control and beta-endorphin plasma levels. 1058 55

Bone pain is the most common symptom in osteoporotic patients. To date, there is mounting evidence that calcitonin significantly reduces bone pain in osteoporosis, and that the analgesic effect can be evident as soon as the second week of treatment. The limitations to the use of calcitonin, which are parenteral administration and side effects, can now be overcome by the availability of the nasal spray preparation. At present, controlled studies have demonstrated the analgesic activity of calcitonin given by nasal spray in patients with vertebral crush fractures and bone pain. The mechanism for the analgesic effect of calcitonin is yet to be clarified. In humans, similarities between calcitonin and morphine-induced analgesia, and reports of calcitonin-induced elevation of plasma beta-endorphin levels, suggest the possible involvement of the endogenous opiate system in mediating the analgesic action of calcitonin. However, the demonstration of calcitonin binding sites in areas of the brain involved in pain perception and a series of animal studies have raised the possibility that calcitonin may directly modulate nociception in the central nervous system. In support of this hypothesis are some observations of an analgesic effect obtained by direct epidural or subaracnoidal injection of calcitonin in humans.
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PMID:Analgesic effect of calcitonin in osteoporosis. 1200 61

Patients with clinically evident medullary thyroid cancer should have a total extracapsular thyroidectomy with bilateral central neck dissection and an ipsilateral prophylactic or therapeutic modified (functional) radical neck dissection when the primary tumor is greater than 1 cm and when the central neck nodes are positive. A prophylactic contralateral neck dissection should be done when the primary tumor is bilateral and when there is extensive lymphadenopathy on the side of the primary tumor. Patients who have gross, unresectable residual medullary thyroid cancer should receive postoperative external radiotherapy. Patients who are carriers of germ-line RET proto-oncogene point mutations or have an elevated (basal or stimulated) calcitonin levels on screening should have a prophylactic total thyroidectomy before age 6 years. In patients with an elevated basal or stimulated plasma calcitonin level and an intrathyroidal nodule on ultrasound, a total thyroidectomy and central neck lymph node dissection should be done. Patients with persistent or recurrent medullary thyroid cancer should have a complete thyroidectomy (if not done initially) and bilateral central and modified radical neck dissection, including upper mediastinal lymphadenectomy. Patients who are symptomatic from distant medullary thyroid cancer metastases (diarrhea, flushing, weight loss, or bone pain) should be treated with somatostatin analogs. Bone metastases should be resected if possible, and symptomatic lesions that are unresectable should be treated with external radiotherapy. Cytoreductive procedures such as radiofrequency ablation or cryoablation for liver metastases should be considered in symptomatic patients to reduce tumor burden. Localized pulmonary metastases should be resected. Chemotherapy or radioactive immunotherapy (iodine 131 labeled carcinoembryonic antigen monoclonal antibody) protocols should be considered in patients with nonoperative widely metastatic progressing medullary thyroid cancer.
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PMID:Medullary thyroid cancer. 1205 61

Although skeletal pain plays a major role in reducing the quality of life in patients suffering from osteoarthritis, Paget's disease, sickle cell anemia and bone cancer, little is known about the mechanisms that generate and maintain this pain. To define the peripheral fibers involved in transmitting and modulating skeletal pain, we used immunohistochemistry with antigen retrieval, confocal microscopy and three-dimensional image reconstruction of the bone to examine the sensory and sympathetic innervation of mineralized bone, bone marrow and periosteum of the normal mouse femur. Thinly myelinated and unmyelinated peptidergic sensory fibers were labeled with antibodies raised against calcitonin gene-related peptide (CGRP) and the unmyelinated, non-peptidergic sensory fibers were labeled with the isolectin B4 (Bandeira simplicifolia). Myelinated sensory fibers were labeled with an antibody raised against 200-kDa neurofilament H (clone RT-97). Sympathetic fibers were labeled with an antibody raised against tyrosine hydroxylase. CGRP, RT-97, and tyrosine hydroxylase immunoreactive fibers, but not isolectin B4 positive fibers, were present throughout the bone marrow, mineralized bone and the periosteum. While the periosteum is the most densely innervated tissue, when the total volume of each tissue is considered, the bone marrow receives the greatest total number of sensory and sympathetic fibers followed by mineralized bone and then periosteum. Understanding the sensory and sympathetic innervation of bone should provide a better understanding of the mechanisms that drive bone pain and aid in developing therapeutic strategies for treating skeletal pain.
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PMID:Origins of skeletal pain: sensory and sympathetic innervation of the mouse femur. 1212 94

Papillary variant of medullary carcinoma of the thyroid (MCT) is an unusual histologic pattern with some diagnostic difficulties. A case of encapsulated papillary variant of MCT with extensive cystic appearance is reported. A euthyroid, 43-yr-old woman with bone pain was incidentally found to have a 4.0-cm solitary, cold nodule on her left thyroid lobe. Histopathologic examination revealed an encapsulated tumor composed of a large cystic cavity with small papillary projections. The papillae were lined by multiple layers of neoplastic cells with small and regular nuclei containing condensed chromatin and lacking the characteristic "ground glass" appearance of the papillary carcinoma of the thyroid gland. Immunohistochemical studies revealed specific cytoplasmic staining of the tumor cells for calcitonin, chromogranin A, neuron-specific enolase, carcinoembryogenic antigen, and cytokeratin. Specific staining for thyroglobulin was not observed in any neoplastic cell. Staining with Congo red disclosed amyloid deposits within the stroma. The case was diagnosed as papillary variant of MCT. Medullary thyroid carcinomas may show a papillary pattern with a totally cystic gross appearance. Thyroid carcinomas should be classified according to their major immunoreactivity pattern rather than their morphologic pattern. Immunohistochemical and/or histochemical studies should be performed in all thyroid tumors that show unusual histologic features.
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PMID:Encapsulated cystic papillary variant of medullary carcinoma of thyroid gland. 1216 66

A 58-year-old man with a 4-month history of atypical chronic myeloid leukemia (aCML), treated with INF-alpha and hydroxyurea, presented with severe localized bone pain with involvement of upper limbs on July 17, 2000. Cytogenetic analysis of peripheral blood cells showed 46,XY,t(9;22)(p23;q11) and no BCR-ABL fusion gene was detected by fluorescence in situ hybridization (FISH). On October 30,2000, x-rays revealed extended destruction of the bilateral proximal upper limbs; pain in the femoral bones appeared in December, and the patient couldn't walk. Roentgenograms taken on January 4, 2001, showed diffuse lytic changes in bilateral femoral bones. On January 23, 2001, fixation of pending fractures in the bilateral femoral bones with an intramedullary rod had produced good results. The infiltration of immature myeloid cells was diagnosed by the histological findings of a bone specimen from the right femur. Because the serum levels of parathyroid hormone (PTH), PTH related protein, and calcitonin were normal, we considered that the bone destruction was caused by the invasion of immature myeloid cells. Four months later, the patient showed a marked increase in peripheral immature granulocytes. A bone marrow specimen showed blastic marrow, and he died of a brain hemorrhage. This report suggests that aCML might cause destructive bone lesions prior to the disease progression. To our knowledge, this is the first published case of aCML in which the chromosomal abnormality t(9;22)(p23;ql 1) was detected.
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PMID:Translocation t(9;22) (p23;q11) in atypical chronic myeloid leukemia (aCML) presenting osteolytic lesions. 1246 98

Hypercalcemia is a common, life-threatening metabolic disorder that can be associated with cancer. Its pathophysiology includes enhanced osteoclastic bone resorption and decreased renal excretion of extracellular calcium. Symptoms of hypercalcemia include nausea, vomiting, bone pain, polyuria, renal insufficiency, bradycardia, and arrhythmia. The goals of medical therapy are to inhibit bone resorption and promote renal calcium excretion. Hydration is the first step in management. Treatments for hypercalcemia include phosphates, calcitonin, bisphosphonates, and gallium nitrate. Although intravenous phosphates prevent intestinal calcium absorption and inhibit mineral and bone matrix resorption, serious adverse events include renal failure, hypotension, extraskeletal calcification, and severe hypocalcemia. Calcitonin has a rapid onset of action and can lower serum calcium concentrations within hours, but its usefulness is limited by its short duration of effect and the development of tachyphylaxis. Bisphosphonates are effective inhibitors of bone resorption but appear to have decreased response rates in hypercalcemic patients with high levels of parathyroid-related protein. Gallium nitrate, an antitumor agent noncytotoxic to osteoclasts and bone cells, appears to be more effective than pamidronate, etidronate, and calcitonin in the treatment of cancer-related hypercalcemia. Importantly, unlike bisphosphonates, gallium nitrate is effective in both parathyroid-related protein-mediated and non-parathyroid-related protein-mediated hypercalcemia.
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PMID:Treatment of cancer-related hypercalcemia: the role of gallium nitrate. 1277 55

Calcitonin has been approved for the treatment of osteoporosis and other diseases involving accelerated bone turnover for approximately 25 years. The most commonly studied and prescribed form is salmon calcitonin, which has a greater efficacy in clinical use. A wealth of well-controlled clinical studies have demonstrated that calcitonin preserves or increases bone mineral density (BMD) and reduces the risk of vertebral fractures in osteoporosis. Recent studies have indicated that while a low BMD is correlated with an increase in fracture risk, increases in BMD alone do not explain the antifracture efficacy of antiresorptive therapies such as calcitonin. Therapies that moderately increase BMD may reduce fracture risk by reducing the rate of bone turnover and maintaining the integrity of the trabecular architecture, resulting in the preservation of bone strength and quality in osteoporotic patients. An advantage of calcitonin that is not shared by other antiresorptive therapies is its direct analgesic effect on bone pain. Calcitonin has been demonstrated to be clinically useful in improving pain, not only from the acute vertebral fractures of osteoporosis, but also in Paget's disease, bone malignancies, and other sources of musculoskeletal pain. Drugs containing calcitonin may be approved for additional indications in the near future, and as more convenient routes of administration such as the oral route become available, the demand for the calcitonin peptide is expected to increase.
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PMID:Calcitonin for osteoporosis and bone pain. 1452 39

Paget's disease of bone is a common condition with a strong genetic component, characterized by focal increases in bone turnover, affecting one or more bones throughout the skeleton. Paget's disease can be asymptomatic but is frequently associated with bone pain, bone deformity, pathological fracture, secondary osteoarthritis and deafness. Inhibitors of osteoclastic bone resorption, such as bisphosphonates and calcitonin, suppress bone turnover and improve bone pain in Paget's disease. Many patients also require therapy with analgesics and anti-inflammatory agents, since pain in Paget's disease can arise not only from increased bone turnover but also from complications such as osteoarthritis and nerve compression syndromes, which do not respond well to antiresorptive therapy. Comparative studies have shown that second- and third-generation bisphosphonates, such as tiludronate, alendronate and risedronate, are more effective than etidronate at inhibiting bone turnover in Paget's disease but they have not been found to be significantly more effective in controlling bone pain. Importantly, none of the treatments that are currently available for Paget's disease have been shown to prevent complications such as deafness, fracture or bone deformity, or to alter the natural history of the disease. More research is required to define the long-term effects of antiresorptive treatment on clinical outcomes in Paget's disease, so that clinicians and their patients can make better-informed choices about the risks and benefits of treatment.
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PMID:Management of Paget's disease of bone. 1563 95


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