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Query: UMLS:C0700208 (scoliosis)
8,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have reported abnormal platelet morphology and function in patients with adolescent idiopathic scoliosis. These abnormalities include increased platelet size and dense body numbers, abnormal aggregation, thromboxane A2 synthesis, serotonin release to adenosine diphosphate and epinephrine stimulus, and decreased myosin-adenosine-triphosphatase-specific activity. It was postulated that a membrane-specific defect in calcium transport may be partially responsible for the abnormalities found. In response to a suggestion in the literature that platelet screening could be clinically useful in scoliosis evaluation as well as in basic research of its pathophysiology, a study was performed to evaluate platelet morphology, biochemistry, and function in patients with adolescent idiopathic scoliosis. Platelets from nine volunteers with adolescent idiopathic scoliosis were compared with cells from a control group of nine patients. No significant differences in measured platelet parameters were noted between adolescent idiopathic scoliosis patients and control groups. Platelets from both groups demonstrated normal aggregation and release patterns with all agents except for a mild decreased aggregation and secretion response to epinephrine. No significant differences were noted in serotonin or adenine nucleotide levels. No significant ultrastructural differences were noted. Earlier findings of an abnormal aggregation and secretion response to adenosine diphosphate, increased numbers of dense bodies, or increased intracellular calcium could not be confirmed. On the contrary, we found normal, if not slightly decreased, numbers of dense bodies per platelet and calcium levels that were not different from controls.
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PMID:Platelet function in adolescent idiopathic scoliosis. 155 84

Platelet aggregation studies were performed in 22 adolescent girls with idiopathic scoliosis. Impaired ADP-induced platelet aggregation was found in washed platelets of the 22 patients with idiopathic scoliosis when compared with the controls (76.5% of control values; p less than 0.01). Furthermore, platelets from patients with progressive curves showed a greater degree of abnormality than platelets from those with nonprogressive curves, e.g., 57.6 +/- 22% of control values (p less than 0.001). No significant differences in aggregation could be detected when platelets were aggregated with the ionophore A-23187 in either the absence or the presence of calcium. Platelet aggregation studies in patients with other spinal deformities did not differ from the healthy controls. Because platelets share similar contractile proteins as muscles, the present study suggests that a muscle disorder may play an important pathogenic role in idiopathic scoliosis.
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PMID:Platelet aggregation abnormalities in idiopathic scoliosis. 393 May 69

Platelet functions were investigated in 16 patients with idiopathic scoliosis (IS), in seven patients with congenital scoliosis (CS), and in 12 healthy individuals who served as a control group. All were females, aged 11 to 22 years. Platelet aggregation anomalies were observed in all IS patients. These constituted an impaired platelet-release reaction when aggregation was induced with ADP or epinephrine, but not with collagen or arachidonic acid. A decreased thromboxane A2 synthesis and impaired 14C-serotonin release were also observed when platelets were stimulated with ADP or epinephrine. Platelet from CS patients and the controls did not show any functional abnormalities when stimulated with the above four aggregating agents. The platelet function anomaly in IS patients was not associated with prolongation of the bleeding time, spontaneous occurrence of hemorrhagic episodes, or increased bleeding during invasive procedures, including major spinal surgery. The above findings and the recently described platelet structural anomalies in IS may imply that the pathological process operative in idiopathic scoliosis involves not only the axial skeleton, but also cellular blood elements. The similarity between blood platelets and muscle cells, and the anomalies that have been found in both systems in IS, support the notion that a muscle disorder may be involved in the pathogenesis of the disease.
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PMID:Abnormalities of aggregation, thromboxane A2 synthesis, and 14C serotonin release in platelets of patients with idiopathic scoliosis. 662 92

The fundamental similarity between platelets and muscle, suggested the possiblity of a shared defect in idiopathic scoliosis, a genetic disease with lateral deformity of the spine in which there is an elevation of calicum concentration in muscles and platelets. A variety of platelet tests revealed the following abnormalities: (1) Electron microscopic x-ray analysis and x-ray fluorescence spectrometry showed a 2- to 3-fold increase in calcium and phosphorus in whole cells and in individual dense bodies. (2) Electron microscopy morphometry revealed an increase in electron-opaque bodies in air-dried cells; granules and microtubules were unchanged. There were more large cells and membranous complexes. (3) Aggregations with epinephrine and ADP were depressed in some patients. (4) Proteins (total and contractile) and myosin. ATPase activity in centrifuged fractions of platelets were decreased in the cytosol and increased in the fraction containing membranes and granules. The correlated findings suggest that platelets in idiopathic scoliosis have a mild calcium transport defect related to membrane and/or contractile protein metabolism. This investigation also shows that platelets may be used to advantage in diagnosis and research of muscle diseases.
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PMID:Platelet pathology in patients with idiopathic scoliosis: Ultrastructural morphometry, agrregations, x-ray spectrometry, and biochemical analysis. 689 14