This is a first descriptive, retrospective, observational study aiming to evaluate the changes in bone turnover markers in pregnant women and to assess the effect of a long-term treatment with low-molecular-weight heparin (LMWH), specifically, enoxaparin. Study involved 50 pregnant Caucasian women with thrombophilia. The patients either received prophylactic enoxaparin once daily subcutaneously (N = 35) or were observed without treatment (N = 15). Concentrations of total serum alkaline phosphatase (total AP), bone alkaline phosphatase (bone AP), osteoprotegerin (OPG), and the receptor activator of nuclear factor κB ligand (RANKL) were measured at 15, 25, and 35 weeks of gestation. Total serum AP increased with gestational age. In the group treated with enoxaparin, the percentage of bone AP concentration was lower ( P < .05) than in the control group. Serum OPG also increased with gestational age, but no significant difference was found between the groups with- and without treatment. Despite the OPG increased, RANKL did not change.
<i>Objective:</i> To investigate the effect of long-term catecholamine excess in pheochromocytoma on leukocyte and platelet count and on proteins of acute-phase response. <i>Methods:</i> Fifteen subjects with pheochromocytoma, 16 with primary aldosteronism, 18 with essential hypertension and 17 healthy controls were studied. Sixteen subjects with pheochromocytoma were investigated after tumor removal. Leukocyte, neutrophil and platelet count, as well as C-reactive protein were measured in all subjects, while fibrinogen, α<sub>1</sub>-antitrypsin, α<sub>2</sub>-macroglobulin, orosomucoid, transferrin and prealbumin were only measured in subjects with pheochromocytoma, primary aldosteronism and essential hypertension. <i>Results:</i> Subjects with pheochromocytoma showed significantly higher leukocyte [7.5 ± 0.9 10<sup>9</sup>/l, p < 0.001 vs. primary aldosteronism (5.4 ± 0.9 10<sup>9</sup>/l) and healthy controls (5 ± 0.9 10<sup>9</sup>/l), p = 0.04 vs. essential hypertension (6.3 ± 1.6 10<sup>9</sup>/l)], neutrophil (p < 0.001 vs. primary aldosteronism and healthy subjects) and platelet counts (p < 0.001 vs. primary aldosteronism; p = 0.01 vs. essential hypertension) compared to the other groups of subjects. Similar results were obtained for positive proteins of acute-phase response in subjects with pheochromocytoma [C-reactive protein: 0.62 ± 0.52 mg/dl, p < 0.001 vs. healthy subjects (0.08 ± 0.08 mg/dl), p = 0.001 vs. primary aldosteronism (0.17 ± 0.19 mg/dl), p = 0.04 vs. essential hypertension (0.31 ± 0.26 mg/dl); fibrinogen: p = 0.02 vs. primary aldosteronism; orosomucoid: p = 0.005 vs. primary aldosteronism; α<sub>2</sub>-macroglobulin: p = 0.009 vs. primary aldosteronism]. No significant differences were found in plasma levels of α<sub>1</sub>-antitrypsin, transferrin and prealbumin. Tumor removal led to a significant decrease in leukocyte (p = 0.004), neutrophil (p = 0.007) and platelet count (p = 0.003) and also to a significant decrease in acute-phase proteins (C-reactive protein: p = 0.03, fibrinogen: p = 0.008, α<sub>1</sub>-antitrypsin: p = 0.003, orosomucoid: p = 0.04). <i>Conclusions:</i> Chronic catecholamine excess in pheochromocytoma is accompanied by an increase in inflammation markers which was reversed by the tumor removal.
ABSTRACT Objectives: Adiponectin, adipocyte fatty acid–binding protein (AFABP), and leptin have been shown to be present in human breast milk (BM). We determined intraindividual changes of BM levels of these proteins during 12 months of lactation. Subjects and Methods: Proteins were measured using a high‐sensitivity enzyme‐linked immunosorbent assay method in 72 healthy mothers after delivery (day 0, D0) and after 1, 3, 6, and 12 months of lactation. Results: Adiponectin levels in BM on D0 were 22.8 ± 0.8 (mean ± standard error of the mean), in 1 month (M1) 22.0 ± 0.6, in 3 months (M3) 20.5 ± 0.6, in 6 months (M6) 21.4 ± 0.8, and in 12 months (M12) 25.7 ± 1.4 ng/mL. AFABP levels were 12.3 ± 2.0, 6.2 ± 1.3, 1.3 ± 0.2, 2.5 ± 1.0, and 4.6 ± 1.9 ng/mL, respectively. Leptin levels were 0.3 ± 0.04, 0.2 ± 0.03, 0.1 ± 0.01, 0.1 ± 0.02, and 0.2 ± 0.04 ng/mL, respectively. We found significantly higher levels of adiponectin in M12 in comparison to M3 and M6 ( P = 0.0026), higher levels of AFABP in D0 and M1 when compared with M3, M6, and M12 ( P < 0.0001), and higher levels of leptin on D0 than in M1, M3, M6, and M12 ( P < 0.0001). AFABP levels correlated negatively with infants' body weight in M1, but there was no correlation throughout the lactation period between body weight and other proteins. We found positive correlation between adiponectin, AFABP, and leptin throughout the lactation. Conclusions: All of the hormones were detectable in BM up to 12 months of lactation, with decreasing trend until M3 and subsequent increase till M12. We speculate that higher levels in M6 and M12 may be caused by longer intervals between breast‐feeding due to the introduction of complementary food.
Identification of serum and bronchoalveolar lavage fluid (BALF) biomarkers may facilitate diagnosis and prognostication in various lung disorders.Serum and BALF levels of surfactant protein A (SP-A), surfactant protein D (SP-D), Clara cell protein 16 (CC16), S100 protein, trefoil factor 3 (TFF3), and prostatic secretory protein 94 (PSP94) were evaluated in 94 consecutive patients (idiopathic pulmonary fibrosis (IPF; n=18), sarcoidosis (n=25), chronic obstructive pulmonary disease (COPD; n=51)), and in 155 healthy controls.Biomarkers were measured at diagnosis and compared with disease characteristics. Both uniparametric and multiparametric analyses were used.Seven significant correlations were found: 1) BALF PSP94 level correlated with prognosis of sarcoidosis (P=0.035); 2) BALF SP-D level with pulmonary functions in IPF (P=0.032); 3) BALF SP-D and TFF3 with IPF mortality (P=0.049 and 0.017, respectively); 4) serum TFF3 level with COPD mortality (P=0.006,); 5) serum SP-A with pulmonary functions impairment in IPF (P=0.011); 6) serum SP-D level was associated with HRCT interstitial score in IPF (P=0.0346); and 7) serum SP-A was associated with staging of COPD according to spirometry (P<0.001). Moreover, our analysis showed that some biomarker levels differed significantly among the diseases: 1) BALF SP-D level differed between sarcoidosis and IPF; 2) serum SP-A level differed among IPF, sarcoidosis, COPD and was also different from healthy controls; 3) serum S100A6, S100A11 levels differed among IPF, sarcoidosis, COPD from healthy controls 4) serum SP-D, CC16, TFF-3 levels distinguished IPF patients from healthy controls; and 5) serum CC16, TFF3, PSP94 distinguished COPD patients from healthy controls. Our study shows that some of selected biomarkers should have prognostic value in the analysed lung disorders. On the other hand, these biomarkers do not appear to be unequivocally suitable for differential diagnosis of these disorders.
The objective of our study was to examine the changes in coagulation parameters and inflammatory reaction over the course of 15 days in patients with severe sepsis. We tried to identify mechanisms by which sepsis-induced pathophysiological changes may influence the effectiveness of subcutaneously (SC) administered enoxaparin 40 mg once daily. A total of 16 patients (8 men, 8 women; age 35-83 years) meeting the inclusion criteria of severe sepsis were enrolled in this study. The follow-up was performed on days 1, 2, 3, 6, 9, 12, and 15 of hospitalization at the intensive care unit (ICU). Blood coagulation (activated partial thromboplastin time [aPTT], prothrombin time [PT], fibrinogen, antithrombin (AT), protein C [PC], D-dimer, fragment 1.2 [F1.2], factor Xa [FXa] inhibition) and inflammatory reactants (interleukin 6 [IL-6], C-reactive protein [CRP], orosomucoid, α-1-antitrypsin) were tested. The mean FXa inhibition was 0.17 (±0.17) IU/mL. The arbitrarily established range of FXa inhibition for prophylaxis, 0.2 to 0.4 IU/mL, was reached in 22 cases (20%), while in 74 cases (68%), it was below and in 13 cases (12%) above the aforementioned range. Factor Xa inhibition positively correlated with AT (r = .42; P < .001) and PC (r = .45; P < .001) activities. A negative correlation was found between the FXa inhibition and α-1-antitrypsin concentrations (r = —.33; P = .01) but only in the subgroup with α-1-antitrypsin concentrations ≥2.2 g/L. We confirmed that in most patients with sepsis, the prophylaxis with enoxaparin did not lead to the required FXa inhibition. The inhibition of FXa by enoxaparin depends mainly on the AT and PC activities.
Identification of serum and bronchoalveolar lavage fluid (BALF) biomarkers may facilitate diagnosis and prognostication in various lung disorders. Serum and BALF levels of surfactant protein A (SP-A), surfactant protein D (SP-D), Clara cell protein 16 (CC16), S100 protein, trefoil factor 3 (TFF3), and prostatic secretory protein 94 (PSP94) were evaluated in 94 consecutive patients (idiopathic pulmonary fibrosis (IPF; n=18), sarcoidosis (n=25), chronic obstructive pulmonary disease (COPD; n=51)), and in 155 healthy controls. Biomarkers were measured at diagnosis and compared with disease characteristics. Six significant correlations were found: 1) BALF TFF3 level was associated with HRCT interstitial score in IPF (P=0.052); 2) BALF PSP94 level with prognosis of sarcoidosis (P=0.035); 3) BALF SP-A level with pulmonary functions in IPF (P=0.032); 4) BALF SP-D and TT3 with IPF mortality (P=0.049 and 0.017, respectively); 5) serum TT3 level with COPD mortality (P=0.006,); and 6) serum SP-A was with pulmonary functions impairment in IPF (P=0.011). Moreover, our analysis showed that some biomarker levels have differed significantly among the diseases: 1) BALF SP-D level differed between sarcoidosis and IPF; 2) serum SP-A and S100 differed among IPF, sarcoidosis and COPD; 3) serum SP-D and TFF3 distinguished IPF and COPD patients from healthy controls; and 4) serum PSP94 distinguished COPD patients from healthy controls. Our study shows that some of selected biomarkers should have prognostic value in analyzed lung disorders. On the other hand these biomarkers do not appear to be unequivocally suitable for differential diagnosis of these disorders.
Patients with severe sepsis are at increased risk for developing thrombembolic phenomena. This article aims to clarify the association between systemic inflammation activation and coagulation, pathogenesis of coagulation abnormalities during severe sepsis. The article reviews incidence and deep venous thrombosis risk factors among these patients and summarizes recent evidence-based guidelines for deep venous thrombosis prophylaxis.
