Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brown tumors, focal bony lesions of hyperparathyroidism, result from the direct effect of parathyroid hormone on bone. While such lesions are not uncommon in primary hyperparathyroidism, brown tumors have been associated less frequently with secondary hyperparathyroidism and have rarely been described as involving the orbital bones. We have found only four such cases previously reported in the ophthalmic literature. We report a case of orbital involvement by brown tumor in a child with chronic renal failure and secondary hyperparathyroidism. Use of long-term hemodialysis has increased the life span of individuals with chronic renal failure and produced an increased population of patients with secondary hyperparathyroidism and resultant bony changes. The ophthalmologist should consider brown tumor in the differential diagnosis of a patient with chronic renal failure and ocular symptomatology.
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PMID:Brown tumor of the orbit. Case report and review of the literature. 374 Dec 52

This is a first report of primary hyperparathyroidism (HPT) masquerading as a destructive fibrous sphenoid sinus "Brown tumor" associated with progressive blindness and hypercalcemia. Diagnosis of a Brown tumor was delayed despite serial computerized tomography of the head and repeated transnasal and transethmoid sphenoid biopsies demonstrating diffuse fibrosis. Only detection and medical evaluation of hypercalcemia, demonstrating elevation of both serum calcium and C-terminal parathyroid hormone with an elevated chloride/phosphate ratio, prompted neck exploration, thus confirming a solitary left superior parathyroid adenoma. Postoperative normocalcemia occurred synchronously with the return of light perception and the arrest of sphenoid sinus and parasellar erosion. Although maxillary Brown tumors of secondary HPT have been reported, this is the first report of osteitis fibrosa of the sphenoid sinus. Differential diagnosis of an erosive sphenoid lesion with cranial nerve dysfunction, exclusive of inflammatory or vascular disease, should include sarcoidosis, primary and metastatic sphenoid carcinoma, fibrous dysplasia, giant cell reparative granuloma, midline lethal granuloma, chordoma, and chondrosarcoma. Furthermore, the bony destructive lesions with concomitant hypercalcemia of sarcoidosis and HPT are distinguishable by radiographic and laboratory analyses and by the Dent corticosteroid suppression test. Hypercalcemia of primary HPT is associated with elevated serum C-terminal parathormone, osteitis fibrosa, a negative Dent test, and a chloride/phosphate ratio greater than 33 in 94% of primary HPT patients. Hypercalcemia of sarcoidosis is associated with a normal or decreased C-terminal parathormone assay and a positive Dent test, as well as elevated serum immunoglobulins and erythrocyte sedimentation rate, and a positive angiotensin-converting enzyme assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sphenoid sinus brown tumor, hypercalcemia, and blindness: an unusual presentation of primary hyperparathyroidism. 379 83

The objective of this study was to examine if the Cica clamp technique, sequential citrate and calcium administration sufficient to promote steady-state-blood-ionized calcium concentrations (B-Ca2+) of about 0.20 mmol/l below and above the individual baseline concentrations, was able to produce reciprocal changes in serum intact parathyroid hormone [S-PTH(1-84)] in chronic surgical hypoparathyroidism (HP; n = 10) and chronic idiopathic HP (n = 2). The calcium set point according to Brown [J Clin Endocrinol Metab 1993;56:572-581] was calculated when possible. Data from 22 controls were included for comparison. Within 5-10 min B-Ca2+ lowering in responding patients with surgical HP (n = 7) and controls demonstrated transient S-PTH(1-84) peaks from 1.3 +/- 0.7 to 3.5 +/- 3.2 pmol/l (p < 0.05) and from 3.4 +/- 1.2 to 19.1 +/- 6.7 pmol/l (p < 0.001), respectively. Subsequently S-PTH(1-84) declined to steady-state hypersecretion levels of about 1.9 +/- 1.2 and 8.6 +/- 2.6 pmol/l, respectively. An increase of B-Ca2+ made S-PTH(1-84) unmeasurable in all HP responders except one, while S-PTH(1-84) remained measurable, 0.9 +/- 0.4 pmol/l, in all controls. In responding patients with surgical HP and controls the respective calcium set points averaged 1.05 +/- 0.06 and 1.13 +/- 0.04 mmol/l, respectively (p < 0.001). The remaining nonresponders with surgical and idiopathic HP did not respond at all. To summarize, 7 out of 10 patients with surgical HP demonstrated a normal pattern of parathyroid response to sequential B-Ca2+ decreases and increases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cica clamp evaluation of parathyroid responsiveness in chronic hypoparathyroidism: a sequential citrate and calcium clamp study. 781 2

The objective of the present study was to compare the calcium set-points of E. M. Brown and A. M. Parfitt obtained by sequential citrate and calcium clamp in patients with primary hyperparathyroidism and healthy controls. Twenty-six patients with primary hyperparathyroidism were investigated and compared to 22 healthy volunteers. All participants were investigated by sequential calcium lowering and raising comprising the following four phases: Phase (1) blood ionized calcium lowering of about 0.20 mmol l-1; phase (2) steady-state (relative) hypocalcaemia of blood ionized calcium 0.20 mmol l-1 below baseline; phase (3) blood ionized calcium is raised to about 0.20 mmol l-1 above baseline; and phase (4) (relative) hypercalcaemia of blood ionized calcium 0.20 mmol l-1 above baseline. Serum parathyroid hormone (1-84) was measured by an immunoradiometric assay. Blood ionized calcium was measured by a calcium selective electrode. We found the calcium set-points of Parfitt to be 1.42 mmol l-1 (SD 0.12, n = 52) vs. 1.25 mmol l-1 (SD 0.04, n = 44) in patients and controls, respectively (P < 0.001). The calcium set-points of Brown were 1.32 mmol l-1 (SD 0.10, n = 26) vs. 1.13 mmol l-1 (SD 0.04, n = 22), respectively (P < 0.001). By comparing the calcium set-points of Parfitt and Brown, a strikingly good correlation was observed, in patients (r = 0.91, P < 0.001) and in controls (r = 0.85, P < 0.001). We demonstrate in this paper in vivo that Brown's and Parfitt's calcium set-points are raised in primary hyperparathyroidism and return to normal following parathyroidectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inter-relations between the calcium set-points of Parfitt and Brown in primary hyperparathyroidism: a sequential citrate and calcium clamp study. 798 43

With the purpose of studying the curve of parathyroid response to variations of serum calcium during dialysis, we studied 20 patients on haemodialysis: 10 women and 10 men, with different forms of bone disease diagnosed by bone biopsy (adynamic bone disease, mild hyperparathyroidism, severe hyperparathyroidism). In all patients, we performed parathyroid stimulation by 4 h dialysis with 1 mEq/l of Ca2+ in the dialysate, and an inhibition test in another dialysis session with 4 mEq/l of Ca2+, with a 48 h interval. Ca2+ and intact parathyroid hormone (iPTH) were measured prior to dialysis and every hour subsequently, to obtain a Ca2+-iPTH for each patient. The analysis of the curves was made using Brown's four-parameter model. Stimulation and inhibition levels were similar in all groups, but basal iPTH and the response profiles obtained varied in the different histological groups. Basal, maximal and minimal iPTH were lower in adynamic forms than in the other two groups (P<0.04), and basal calcium was higher than basal calcium of severe hyperparathyroidism, expressing a basal inhibition status. In severe hyperparathyroidism, basal calcium was lower than the set-point, showing a permanent stimulation, and the slope was higher than in other groups, showing more sensitivity to serum calcium variations. The set-point of severe hyperparathyroidism was significantly higher than the set-point of mild and adynamic forms. In conclusion, the functional parathyroid study showed a different response in the different forms of renal osteodystrophy.
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PMID:Are there any differences in the parathyroid response in the different types of renal osteodystrophy? 958 May 36

The sex steroid 17beta-estradiol (17beta-E2) has a broad range of actions, including effects on calcium and bone metabolism. This study with 3-month-old Brown Norway rats was designed to investigate the role of 17beta-E2 in the regulation of calcium homeostasis. Rats were divided in four groups, sham-operated, ovariectomized (OVX), and OVX supplemented with either a 0.025-mg or 0.05-mg 17beta-E2 pellet implanted subcutaneously. After 4 weeks, in none of the groups was serum calcium, phosphate, or parathyroid hormone altered compared with the sham group, while only in the OVX rats was a significant reduction in urinary calcium found. Bone mineral density and osteocalcin were modified, as can be expected after OVX and 17beta-E2 supplementation. OVX resulted in a nonsignificant increase in serum 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). Supplementation with either one of the 17beta-E2 dosages resulted in an 80% reduction of 1,25(OH)2D3 and only a 20% reduction in 25-hydroxyvitamin D3 levels. OVX, as well as supplementation with 17beta-E2, did not affect serum levels of vitamin D binding protein. As a consequence, the estimated free 1,25(OH)2D3 levels were also significantly decreased in the 17beta-E2-supplemented group compared with the sham and OVX groups. Next, the consequences for intestinal calcium absorption were analyzed by the in situ intestinal loop technique. Although the 1,25(OH)2D3 serum level was increased, OVX resulted in a significant decrease in intestinal calcium absorption in the duodenum. Despite the strongly reduced 1,25(OH)2D3 levels (18. 1 +/- 2.1 and 16.4 +/- 2.2 pmol/l compared with 143.5 +/- 29 pmol/l for the OVX group), the OVX-induced decrease in calcium absorption could partially be restored by supplementation with either 0.025 mg or 0.05 mg of 17beta-E2. None of the treatments resulted in a significant change in calcium handling in the jejunum, although the trends were similar as those observed in the duodenum. 17beta-E2 did not change the VDR levels in both the intestine and the kidney. In conclusion, the present study demonstrates that 17beta-E2 is positively involved in intestinal calcium absorption, and the data strengthen the assertion that 17beta-E2 exerts this effect independent of 1,25(OH)2D3. In general, 17beta-E2 not only affects bone turnover but also calcium homeostasis via an effect on intestinal calcium absorption. (J Bone Miner Res 1999;14:57-64)
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PMID:Evidence for involvement of 17beta-estradiol in intestinal calcium absorption independent of 1,25-dihydroxyvitamin D3 level in the Rat. 989 66

Brown tumors have been reported to take up TI-201 when dual-tracer parathyroid scintigraphy using TI-201 and Tc-99m pertechnetate was performed. With the change to the more favorable Tc-99m sestamibi parathyroid scanning, similar phenomena of tracer uptake in brown tumors have been reported. The authors describe a 44-year-old man with a left maxillary swelling. Laboratory investigations revealed elevated parathyroid hormone levels. Computed tomography of the head showed a left maxillary expansile mass. Subsequently, a Tc-99m sestamibi scan was performed to rule out a parathyroid adenoma. Left inferior parathyroid retention of the tracer was seen, indicating a parathyroid adenoma. An incidental finding was the uptake of Tc-99m MIBI in the left maxillary brown tumor. This case suggests the utility and possible specificity of Tc-99m MIBI uptake in diagnosing brown tumors.
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PMID:Technetium-99m sestamibi uptake in a maxillary brown tumor. 1113 61

Brown tumors represent the terminal stage of the remodeling processes during primary or secondary hyperparathyroidism. During the last three decades primary hyperparathyroidism has been recognized much more commonly and the increase has generally been attributed to the routine determination of calcium by new automated methods and the advent of new and more objective parathyroid hormone radioimmunoassay techniques. Early diagnosis and successful treatment of the disease have made clinical evidence of bone disease uncommon. While, the mandible is the most frequently involved bone in the head and neck region, maxillary involvement is extremely rare. A case of brown tumor on the maxilla associated with primary hyperparathyroidism is reported. This patient presented multiple skeletal lesions, which are uncommonly seen nowadays. The diagnosis was suggested by the clinical history and confirmed by biochemical, radiological and histopathological determinations. Excision of a parathyroid adenoma normalized the metabolic status. Excision of the maxillary mass led both histopathological confirmation of the disease and early masticator rehabilitation.
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PMID:Brown tumor of the maxilla associated with primary hyperparathyroidism. 1169 86

The aim of our studies on parathyroid hormone dynamics were to establish standardized methods for induction of hypocalcaemia, sequential hypercalcaemia and normocalcaemia and sequential hypocalcaemia and hypercalcaemia suitable for careful and detailed evaluation of the PTH(1-84) secretion in vivo. We found that at least two distinctly different mechanisms of PTH(1-84) secretion serve to protect normal humans against hypo- and hypercalcaemia. First, an initial decrement of B-Ca2+ leads to a large transient release of preformed PTH(1-84) from the cellular depots, whereas, an initial increment of B-Ca2+ leads to almost immediate suppression of PTH(1-84) release. The change in PTH(1-84) release is rate dependent in either direction and demonstrable even at small decrements or increments of B-Ca2+. This mechanism of delta regulation provide a strong homeostatic mechanism for maintaining a stable extracellular calcium level during slow as well as rapid changes in B-Ca2+. Second, a mechanism of steady state regulation for continued secretion takes over, being dependent on the absolute B-Ca2+ concentration, which probably controls the synthesis of PTH(1-84) molecules. Selective investigation of the steady state response to hypocalcaemia demands elimination of preformed PTH(1-84). With this precaution, we described the inverse sigmoidal relationship in vivo between the steady state pairs of B-Ca2+ and S-PTH(1-84) in normal humans. The calcium set-points of Brown measured by this computer method were significantly lower than Parfitt's calcium set-points in normal humans, but strikingly well correlated. This observation supporting the view that Brown and Parfitt describe two different points on the same sigmoidal curve, corresponding to 50% and about 85% inhibition of PTH(1-84) in normal humans.
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PMID:Manipulation of calciumhomeostatic mechanisms in man: what are the possibilities? 1462 91

1alpha,25-Dihydroxy-2beta-(3-hydroxypropoxy)vitamin D(3) (ED-71), an analog of active vitamin D(3), 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], possesses a hydroxypropoxy substituent at the 2beta-position of 1,25(OH)(2)D(3). ED-71 has potent biological effects on bone and is currently under phase III clinical studies for bone fracture prevention. It is well-known that the synthesis and secretion of parathyroid hormone (PTH) is regulated by 1,25(OH)(2)D(3). Interestingly, during clinical development of ED-71, serum intact PTH in osteoporotic patients did not change significantly upon treatment with ED-71. The reason remains unclear, however. Brown et al. reported that 3-epi-1,25(OH)(2)D(3), an epimer of 1,25(OH)(2)D(3) at the 3-position, shows equipotent and prolonged activity compared to 1,25(OH)(2)D(3) at suppressing PTH secretion. Since ED-71 has a bulky hydroxypropoxy substituent at the 2-position, epimerization at the adjacent and sterically hindered 3-position might be prevented, which may account for its weak potency in PTH suppression observed in clinical studies. We have significant interest in ED-71 epimerization at the 3-position and the biological potency of 3-epi-ED-71 in suppressing PTH secretion. In the present studies, synthesis of 3-epi-ED-71 and investigations of in vitro suppression of PTH using bovine parathyroid cells are described. The inhibitory potency of vitamin D(3) analogs were found to be 1,25(OH)(2)D(3)>ED-71> or =3-epi-1,25(OH)(2)D(3)>>3-epi-ED-71. ED-71 and 3-epi-ED-71 showed weak activity towards PTH suppression in our assays.
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PMID:Synthesis and biological evaluation of a 3-positon epimer of 1alpha,25-dihydroxy-2beta-(3-hydroxypropoxy)vitamin D3 (ED-71). 1720 91


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