Effect of platelet count on secretion capacity: formulization and use of the formulae for evaluation of platelet secretion in thrombocytopenic patients.

The correlation between platelet count and bleeding time is nonlinear. The bleeding time prolongs more prominently as platelet count decreases toward 10 000 microl(-1); however, it becomes stable near 100 000 microl(-1). Clinical observations suggest that platelet functional capacity may also play a role in bleeding complications during thrombocytopenia. However, no routine method has been described for evaluation of platelet function during thrombocytopenia. To test if platelet functional capacity is affected by the cell count, as suggested by the platelet count-bleeding time correlation. To evaluate lumiaggregometry as a possible tool for studying platelet functions and prediction of bleeding in thrombocytopenic patients. Collagen-induced ATP release was studied in different dilutions of 22 healthy platelet-rich plasmas. The relationship between platelet count and ATP release was formulized. ATP release was also tested in 24 thrombocytopenic (10 000-50 000 microl(-1). ) patients, and the results were compared with expected levels derived from the formulae. ATP release increased in a cubic fashion as platelet count elevated. ATP secretion values were within normal limits or increased in patients with idiopathic thrombocytopenic purpura. However, some patients with megakaryocyte deficiency had a secretion defect. ATP secretion was decreased in four out of seven patients with bleeding symptoms compared with no persons without bleeding (P = 0.003). Platelet functional capacity is affected by the cell count. Lumiaggregometry is potentially useful in evaluating platelet functions during thrombocytopenia.

Evidence for higher red blood cell mass in persons with unconjugated hyperbilirubinemia and Gilbert's syndrome.

BACKGROUND: The genetic polymorphism responsible from Gilbert's syndrome is not sufficient for the clinical phenotype to occur in many persons. Additional factors are believed to contribute in pathogenesis. Red cell mass may be such a factor. METHODS: We have retrospectively evaluated computer records of all liver function tests assayed between January 2005 and February 2006. The database was screened to find cases with unconjugated hyperbilirubinemia and normal liver enzymes and blood count values on simultaneous assays. The control group for comparison of surrogate markers of total red cell mass comprised of age- and gender-matched persons who had laboratory tests with completely normal results on the same day with the hyperbilirubinemic cases. Gilbert's syndrome cases were found with medical record assessment, and these cases and their control subjects were more strictly assessed. Three different control groups were established for Gilbert's syndrome cases, one of them including healthy blood donors and personnel. RESULTS: In 48,516 otherwise normal laboratory test results, we have found that 491 male subjects and 323 female subjects with unconjugated hyperbilirubinemia had higher hemoglobin, hematocrit, and red blood cell values compared with age- and gender-matched control subjects (P < 0.001 for all comparisons). Twenty-six males who had been followed for Gilbert's syndrome also showed higher hemoglobin, hematocrit and red cell count values in comparison to all control groups. Mean red cell volume value did not differ between the hyperbilirubinemic persons and control groups. CONCLUSIONS: Relatively increased red cell mass probably plays a role in the pathogenesis of Gilbert's syndrome.

Increased mean platelet volume is related to histologic severity of primary biliary cirrhosis.

AIM: To evaluate the main platelet volume (MPV) as a severity marker in patients with primary biliary cirrhosis (PBC). MATERIALS AND METHODS: Thirty-nine patients with biopsy-proven and as yet untreated PBC followed between January 2008 and January 2015 were included in this study. Liver biopsies were categorized as early stage (stage 1 and 2 according to Scheuer's histological stage) and late stage (Scheuer's stage 3 and 4). As part of the routine evaluation, all PBC patients had their full blood count and biochemistry profile determined, where MPV, white blood cell count, hemoglobin, platelet count, red cell distribution width (RDW), alanine aminotransferase, aspartate aminotransferase (AST), gamma glutamyl transferase, alkaline phosphatase, and total bilirubin values were evaluated. Both groups were compared in terms of the RDW/platelet ratio, the AST platelet ratio index, and the neutrophil lymphocyte ratio. RESULTS: Eighteen patients had early-stage disease (46.2%), whereas 21 PBC patients had late-stage disease (53.8%). There were no differences between groups in terms of routine hematological parameters (white blood cell count, platelet count, hemoglobin, RDW) or biochemical parameters (alanine aminotransferase, AST, gamma glutamyl transferase, alkaline phosphatase, total bilirubin, albumin) (P>0.05). Similarly, there were no differences in AST platelet ratio index, RDW/platelet ratio, or neutrophil lymphocyte ratio values between groups (P values 0.08, 0.19, and 0.14, respectively). The MPV and direct bilirubin were significantly higher in the advanced stage group compared with the early-stage group (11.08 vs. 9.73 fl, respectively, P=0.01 and 0.44 vs. 0.28 mg/dl, respectively, P=0.03). The area under the curve, cut-off value, sensitivity, and specificity of MPV and direct bilirubin for detecting advanced stage were 0.721, 10.3, 71%, and 66%, respectively, and 0.698, 0.23, 71%, and 66%, respectively. CONCLUSION: MPV can be used as a noninvasive, simple, and effective parameter in patients with PBC to predict histological severity of the disease.

Predictors of left ventricular thrombus formation in patients with dilated cardiomyopathy: role of activated protein C resistance.

OBJECTIVES: The aim of this study was to investigate the association between left ventricular thrombus formation and natural anticoagulant systems including the protein C, protein S and antithrombin in patients with dilated cardiomyopathy. MATERIALS AND METHODS: Sixty patients with dilated cardiomyopathy who met the inclusion criteria were included in the study. Patients were divided into two groups: group I consisted of 22 patients with left ventricular thrombus and group II consisted of 38 patients without left ventricular thrombus. Our main inclusion criteria were ejection fraction /= 6.0 cm. These two groups were compared for clinical and hematologic parameters (activated protein C resistance, protein S and antithrombin). RESULTS: There were no statistically significant differences between patients with or without left ventricular thrombi with respect to left ventricular end-diastolic and end-systolic dimensions, ejection fraction, fractional shortening and left atrial diameter. There were no statistically significant differences between patients with and without left ventricular thrombus with respect to platelet count (252 +/- 64/mm3 x 10(3) compared with 260 +/- 74/mm3 x 10(3) respectively, P=0.68), prothrombin time (12.94 +/- 1.9 s compared with 12.86 +/- 1.3 s respectively, P=0.82), activated partial thromboplastin time (32 +/- 5 compared with 30 +/- 4 s respectively, P=0.32) and fibrinogen levels (36 +/- 9 mg/dl compared with 34 +/- 8 mg/dl respectively, P=0.41). None of the patients had protein S and antithrombin deficiency. Activated protein C resistance was found in 12 patients (12 out of 22, 54%) in group I and four patients (four out of 38, 9.5%) in group II (P < 0.01). It was also shown to be an independent predictor of left ventricular thrombus (P < 0.05). CONCLUSION: Activated protein C resistance is found to be an independent predictor of left ventricular thrombus in patients with dilated cardiomyopathy who have ejection fractions less then 35% and left ventricular end-diastolic dimensions > 6.0 cm.