Higher thrombin activatable fibrinolysis inhibitor levels are associated with inflammation in attack-free familial Mediterranean fever patients.

BACKGROUND: Coagulation abnormalities have been reported in familial Mediterranean fever (FMF) patients with amyloidosis and nephrotic syndrome; but there is not enough data about the continuity of the thrombogenic activity in FMF patients in clinical remission. The purpose of this study was to assess thrombin activatable fibrinolysis inhibitor (TAFI) levels and its relationship with fibrinolytic activity and also evaluate relationships between mutations and clinical signs in attack-free patients without amyloidosis. METHODS: Seventy-nine FMF patients and 40 healthy adults were included. The study group was divided into five groups as follows: first group, homozygote M694V; second group, homozygote M680I; third group, M694V in one allele, the other allele have other mutations or not; fourth group, other mutations; and fifth group, no mutation. RESULTS: Serum TAFI levels were significantly increased in patients compared with healthy individuals (116.64 ± 21.8 vs. 78.48 ± 19.7 µg/mL, p < 0.001) and a positive correlation was detected between TAFI antigen level and erythrocyte sedimentation rate and C-reactive protein levels (r = 0.247, p = 0.029 and r = 0.252, p = 0.032, respectively). Mean fibrinogen and TAFI levels were significantly higher in Group 1 than the other groups (p = 0.04 and p = 0.001, respectively) and in Group 3 it was higher than Groups 2, 4 and 5 (p = 0.04 and p = 0.001, respectively). CONCLUSIONS: High level of TAFI antigen in attack-free period of FMF disease shows ongoing subclinical inflammation and hypercoagulability. Clinicians should be careful about thrombosis even in patients at clinical remission. Also, genetic tests must be considered to predict clinical outcome and to reduce complications of FMF disease.

High levels of cord serum eosinophil cationic protein predict the risk of atopy.

BACKGROUND: Transient tachypnoea of the newborn is a transient respiratory disturbance characterized by tachypnoea shortly after birth, which resolves within 2 to 5 days. The basic pathogenetic mechanism is the delayed resorption of the alveolar fluid of which the exact triggering mechanism still remains unknown. An etiological link associated with parenteral history of atopy was proposed by several studies. Some laboratory studies also revealed that serum IgE, eosinophil cationic protein (ECP) and cord IgE were higher among infants with maternal history of atopy. OBJECTIVE: The purpose of this study was to investigate the possible association of parental history of atopy with cord blood ECP and IgE concentrations in infants with transient tachypnoea of the newborn. METHODS: ECP and IgE levels were quantified in cord blood samples of 30 infants who were diagnosed as having transient tachypnoea of the newborn. The control group (N=30) was selected among healthy newborns with similar birth weight and gestational age. RESULTS: Cord blood ECP concentrations were significantly higher in the study group (17.6 microg/L) than in healthy control subjects (7.89 microg/L). In addition, transient tachypnoea of the newborn was more frequent in infants with a family history of atopic disease (p<0.01). Cord blood IgE concentrations were also higher in the study group than the controls (4.1 versus 3.28 mg/L) but the difference was not statistically significant (p>0.05). CONCLUSION: Family history of atopy and elevated levels of cord blood ECP are risk factors for transient tachypnoea of the newborn. In addition cord blood ECP level is a useful marker for predicting the risk of atopy.