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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical or subclinical hyperparathyroidism is one of the most common endocrine disorders. Excessive secretion of parathyroid hormone is most frequently caused by an adenoma of >or=1 parathyroid gland. Unsuccessful surgery with persistent hyperparathyroidism, due to inadequate preoperative or intraoperative localization, may be observed in about 10% of patients. The conventional surgical approach is bilateral neck exploration, whereas minimally invasive parathyroidectomy (MIP) has been made possible by the introduction of (99m)Tc-sestamibi scintigraphy for preoperative localization of parathyroid adenomas. In MIP, the incision is small, dissection is minimal, postoperative pain is less, and hospital stay is shorter. Localization imaging techniques include ultrasonography, CT, MRI, and scintigraphy. Parathyroid scintigraphy with (99m)Tc-sestamibi is based on longer retention of the tracer in parathyroid than in thyroid tissue. Because of the frequent association of parathyroid adenomas with nodular goiter, the optimal imaging combination is (99m)Tc-sestamibi scintigraphy and ultrasonography. Different protocols are used for (99m)Tc-sestamibi parathyroid scintigraphy, depending on the institutional logistics and experience (classical dual-phase scintigraphy, various subtraction techniques in combination with radioiodine or (99m)Tc-pertechnetate). MIP is greatly aided by intraoperative guidance with a gamma-probe, based on in vivo radioactivity counting after injection of (99m)Tc-sestamibi. Different protocols used for gamma-probe-guided MIP are based on different timing and doses of tracer injected. Gamma-probe-guided MIP is a very attractive surgical approach to treat patients with primary hyperparathyroidism due to a solitary parathyroid adenoma. The procedure is technically easy, safe, with a low morbidity rate, and has better cosmetic results and lower overall cost than conventional bilateral neck exploration. Specific guidelines should be followed when selecting patients for gamma-probe-guided MIP.
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PMID:Preoperative localization and radioguided parathyroid surgery. 1296 Jan 91

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.
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PMID:Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism. 1523 58

A 60-year-old Caucasian woman with a 1-year history of pain at the ribs, spine, and pelvis consulted at our Institute in March 1999. She brought a bone densitometry performed using a Lunar DPX densitometer that showed bone mineral density (BMD) measurements in the osteoporotic range at both the lumbar spine and the femoral neck. As a child she had had bowed legs and had been treated with ultraviolet radiation. Results of the laboratory test performed at our institute showed normal total serum calcium, repeated low serum P levels, and a low renal phosphate threshold with elevated total and bone fraction of alkaline phosphatase with normal intact parathyroid hormone (PTH). A diagnosis of hypophosphatemic osteomalacia due to renal phosphate leak was made. She began treatment with neutral sodium phosphate at 1.5 g/day and calcitriol 0.5 microg/day. Her serum P levels normalized, and there was a progressive decrease in alkaline phosphatase levels. The densitometry showed a very rapid increase in BMD values with normalization at the lumbar spine after 10 months of treatment. This case shows the importance of bone densitometry in the follow-up of patients with suspected osteomalacia.
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PMID:Bone densitometry in a patient with hypophosphatemic osteomalacia. 1531 75

Inflammatory bowel disease (IBD) is associated with an increased incidence of osteoporosis. Osteoporosis with osteoporotic pain syndromes, fragility fractures and osteonecrosis accounts for significant morbidity and impacts negatively on the quality of life. It is generally agreed that there is a need to increase awareness for inflammatory bowel disease-associated osteoporosis. However, the best ways in which to identify at-risk patients, the epidemiology of fractures and an evidence-based rational prevention strategy remain to be established. The overall prevalence of IBD-associated osteoporosis is 15%, with higher rates seen in older and underweight subjects. The incidence of fractures is about 1 per 100 patient years, with fracture rates dramatically increasing with age. While old age is a significant risk factor, disease type (Crohn's disease or ulcerative colitis) is not related to osteoporosis risk. Corticosteroid use is a major variable influencing IBD-associated bone loss; however, it is difficult to separate the effects of corticosteroids from those of disease activity. The recommendations in inflammatory bowel disease are similar to those for postmenopausal osteoporosis, with emphasis on lifestyle modification, vitamin D (400-800 IE daily) and calcium (1000-1500 mg daily) supplementation and hormone replacement therapy (oestrogens/selective oestrogen receptor modulators in women, testosterone in hypogonadal men). Bisphosphonates have been approved for patients with osteoporosis (T-score < 2.5), osteoporotic fragility fractures and patients receiving continuous steroid medication. Data on the recently Food and Drug Administration-approved osteoanabolic substance parathyroid hormone and on osteoprotegerin are promising in terms of both steroid-induced and inflammation-mediated osteoporosis, the key elements of inflammatory bowel disease-associated bone disease.
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PMID:Review article: bone disease in inflammatory bowel disease. 1535 93

Primary hyperparathyroidism is a hypercalcemic condition generated as a result of overproduction of parathyroid hormone (PTH) by one or more of the parathyroid glands. The cause is usually an abnormal group of cells forming a benign adenoma and rarely carcinoma. The condition is usually discovered by routine serum chemistry analysis showing hypercalcemia, hypophosphatemia, and elevated PTH levels. Elevated 24-hour urine calcium provides further confirmation. During the last decade, three procedures have been developed to help diagnose the affected parathyroid gland(s) in preparation for surgical intervention: computerized nuclear scanning with technetium-99-m sestamibi performed preoperatively; radio-guided probes; and rapid PTH assay (RPHA), both used intraoperatively. These three techniques have been reported to reduce the need for immediate frozen section diagnosis; shorten the length of the incision, surgical time, and length of hospital stay; produce less pain and discomfort; reduce surgical cost; and produce a quicker return to normal life. This article follows the surgical experience of a patient with a diagnosis of hyperparathyroidism and a history of postoperative nausea and vomiting who was scheduled as 23-hour stay.
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PMID:Primary hyperparathyroidism: a case study. 1547 82

Bone metastasis are a frequent complication of cancer, occurring in up to 70% of patients with advanced breast or prostate cancer. The consequences of bone metastasis are often devastating. Osteolytic metastasis can cause different kinds of skeletal related events including severe pain, pathologic fractures, life-threatening hypercalcemia, spinal cord compression, and other nerve-compression syndromes. These skeletal-related events are the result of the resorption of mineralized bone by osteoclasts. Bisphosphonates are synthetic analogues of naturally occurring pyrophosphate compounds that inhibit bone resorption. Potent bisphosphonates, pamidronate and, more importantly zoledronic acid may cause hypocalcemia, but mostly asymptomatic, mild, transient in most cases. Sufficient calcium and vitamin D intake needs to be ensured in patients with malignancy who have borderline or low levels of calcium when commencing treatment with bisphosphonates. Vitamin D itself induce the formation of osteoclasts by increasing the expression of RANKL on marrow stromal cells. Local calcium also promotes tumor growth and the production of parathyroid hormone-related peptide which in turn stimulates bone resorption. Vitamin D and calcium supplementation during bisphosphonate administration for the purpose of elimination of the side effects related to hypocalcemia in patients with bone metastasis may increase the bone resorption and decrease the efficacy of bisphosphonates. Therefore, vitamin D and calcium supplementation must not be routinely recommended during bisphosphonate administration.
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PMID:Calcium and vitamin D supplementation during bisphosphonate administration may increase osteoclastic activity in patients with bone metastasis. 1569 11

Vitamin D deficiency among hospitalized patients may be more widespread than realized. Vague musculoskeletal complaints in these chronically ill patients may be attributed to multiple underlying disease processes rather than a deficiency in vitamin D. However, the failure to diagnose an underlying deficiency places the patient at risk for continued pain, weakness, secondary hyperparathyroidism, osteomalacia, and fractures. The causes of hypocalcemia and hypophosphatemia in the chronically ill patient are many, and the patient may respond to simple replacement therapy. Elderly hospitalized patients with ionized hypocalcemia and hypophosphatemia, with or without an elevated parathyroid hormone level, are most likely deficient in vitamin D. Initiating treatment during hospitalization is reasonable once the diagnosis has been confirmed by finding a low 25-hydroxyvitamin D level. Treatment with high doses of vitamin D is safe. Unfortunately, some hospital formularies continue to provide multivitamin supplements that contain less vitamin D than currently is recommended.
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PMID:Undiagnosed vitamin D deficiency in the hospitalized patient. 1568 95

Hypovitaminosis D is common in patients with peripheral arterial disease (PAD). Subsequent secondary hyperparathyroidism and osteomalacia contribute to bone pain and myalgias, and so aggravate clinical symptoms of claudication. We evaluated 95 out of 297 patients with angiographically confirmed PAD stages II (pain in the calves and/or thighs only during exercise) or IV (history of, or presence of local ulcers) and compared them with 44 matched healthy controls regarding their medical history, bone density measurements of the femoral neck and calcaneal bone ultrasound. Bone pain, myalgias and mobility restriction as well as routine laboratory parameters, serum vitamin D [25(OH)D], crosslaps (CTX), parathyroid hormone (PTH), osteocalcin (OC) and alkaline phosphatase (AP) were recorded and analysed. 25(OH)D was significantly lower in PAD IV patients (9.6+/-4.6 ng/ml, P<0.0001) as compared to PAD II stages and controls (19.0+/-7.6 and 19.1+/-9.1 ng/ml), paralleled by lower serum calcium [2.24+/-0.02 mmol/l, P=0.0002 versus PAD II (2.36+/-0.02) and P<0.0001 versus controls (2.39+/-0.02)] and higher iPTH serum levels (66.3+/-3.6 pg/ml, P<0.0001) as compared to PAD II patients (45.3+/-3.5) and healthy controls (38.5+/-2.4). Alkaline phosphatase and serum crosslaps values were significantly higher and age-adjusted bone density and bone ultrasound measurements significantly lower in PAD IV patients, who were also twice as likely to have bone pain and myalgias as PAD II patients. Bone ultrasound measurements correlated significantly with both clinical severity and pain as well as serological parameters of bone metabolism. Underlying PAD has a significant impact on bone density and metabolism as well as on bone and muscular pain. Patients with PAD are at high risk for osteoporosis and osteomalacia and should be regularly monitored and treated for their vitamin D deficiencies.
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PMID:Hypovitaminosis D, impaired bone turnover and low bone mass are common in patients with peripheral arterial disease. 1572 36

Calciphylaxis is a rare, but life-threatening complication of end-stage renal disease (ESRD) that has been reported mostly in adult patients. The exact etiology is unknown, but the disease is commonly associated with a high calcium-phosphorus product and elevated levels of parathyroid hormone (PTH). We herein review the published reports on calciphylaxis in ESRD patients less than 18 years old and report the case of a patient with severe calciphylaxis who presented with lower extremity pain, muscle tenderness and difficulty in walking. The serum PTH was low, and the calcium-phosphorus product was normal. The diagnosis of calciphylaxis was confirmed by a muscle biopsy. Treatment with low calcium peritoneal dialysate and substitution of calcium-based phosphorus binders with sevelamer (Renagel) was unsuccessful. The patient's clinical condition progressed to extensive soft tissue calcification and ulcerating skin lesions. Nine months after the onset of symptoms, the patient died of cardiopulmonary arrest.
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PMID:Calciphylaxis in pediatric end-stage renal disease. 1613 40

Gastrectomy/gastric bypass has been used for patients with gastric cancer, and its application is now expanding to treating patients with morbid obesity, the prevalence of which is increasing worldwide. It is well known that gastrectomy leads to osteopenia, but the underlying pathophysiology and optimum treatments for this disorder have not been delineated. We followed 13 patients who showed progressive osteopenia (bone mineral density T-score<-2.4 SD) after gastrectomy/gastric bypass due to gastric cancer and who were resistant to long-term treatment (mean, 6 years) of active vitamin D3 and prospectively studied the effects of alendronate, a bisphosphonate, on osteopenia-related parameters for 2 years. Oral administration of alendronate in addition to vitamin D3 led to remarkable improvement within 2 years, not only in clinical symptoms, such as radial bone fractures and lumbar pain, but also in parameters for osteopenia, including decreased bone mineral density of the lumbar spine (P<0.01), decreased concentrations of calcium (P<0.05), increased urine levels of deoxypyridinoline (P<0.01), increased serum levels of bone-specific alkaline phosphatase (P<0.01), increased serum levels of osteocalcin (P<0.01), and increased serum levels of intact parathyroid hormone (P<0.05), although body weight did not alter. These results suggest that bisphosphonate may improve osteopenia after gastrectomy/gastric bypass.
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PMID:Alendronate improves vitamin D-resistant osteopenia triggered by gastrectomy in patients with gastric cancer followed long term. 1613 91


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