ABSTRACT
Matrix metalloproteinases [MMP] have been associated with neonatal lung morbidity and MMP dysregulation contributes to the pathology of chronic and acute lung disorders. Most of the previous studies were performed in the 1[st] weeks of life of the preterm newborns. There are no data on the serum levels of MMP-2, MMP-9 or tissue inhibitors of matrix metalloproteinases [TIMP-1] from preterm infants recovering from lung morbidities. We aimed to compare MMP-2, MMP-9 and TIMP-1 levels in preterm and term infants hospitalized with their first episode of wheezing. We prospectively evaluated 18 preterm infants with a history of chronic lung disease, respiratory distress syndrome or oxygen therapy and 14 age- and sex-matched term infants who were admitted for a first episode of wheezing. We quantified total serum concentrations of MMP-2, MMP-9 and TIMP-1 to assess whether these serum markers levels were associated with the first episode of wheezing in infants with a history of oxygen therapy during the neonatal period. Upon hospitalization, MMP-2 and TIMP-1 levels were higher in preterm infants than in term infants. In contrast, there was no significant relationship between MMP-9 levels or the MMP-9/TIMP-1 ratio between preterm and term infants. The area under the receiver operating characteristic curve for MMP-2 was 0.70 [95% confidence interval [CI] 0.51-0.89]. The area under the curve for TIMP-1 was 0.78 [95% CI 0.61-0.94]. MMP-9, MMP-2 and TIMP-1 levels did not correlate with gestational age, gender or severity of wheezing. The negative proportion of MMP-9 to TIMP-1 that we detected in term infants was not present in preterm infants. The balance of MMP-9 to TIMP-1 may have been disrupted by lung damage in the premature infants. Overproduction of MMP-2 and TIMP-1 in the serum may be associated with the pathogenesis of wheezing in preterm infants
ABSTRACT
To investigate urinary methylmalonic acid [uMMA] levels and their relationship with markers of myocyte necrosis and inflammation in patients with acute myocardial infarction [AMI]. The study participants consisted of 80 consecutive patients with AMI and 72 age- and sex-matched consecutive controls. Of the patients, 38 had ST segment elevation myocardial infarction [STEMI] and 42 had non-ST segment elevation. All patients with STEMI underwent fibrinolytic therapy. Routine laboratory tests included troponin-I, creatinine phosphokinase MB [CK-MB], high-sensitivity C-reactive protein [hs-CRP], vitamin B12, folate, homocysteine and methylmalonic acid analyses. uMMA measurements were made by a spectrophotometric method. uMMA levels were significantly higher in patients with AMI than in controls [10.1 vs. 5.2 mmol/mol creatinine, p < 0.001] and higher in patients with anterior MI compared to those with non-anterior MI [18.9 vs. 8.7 mmol/mol creatinine, p < 0.001]. In addition, uMMA levels were significantly higher in patients without successful reperfusion compared to those with successful reperfusion. In patients with STEMI, a strong positive association was found between urinary MMA and plasma hs-CRP levels [r = 0.81, p < 0.001], symptom duration [r = 0.91, p < 0.001] and wall motion score [r = 0.60, p = 0.006]. More importantly, a strong positive association was observed between uMMA and the size of myocardial infarction in patients without successful reperfusion [for CK-MB r = 0.81, p = 0.013; for wall motion score r = 0.82, p = 0.012]. uMMA levels were elevated in patients with AMI and, as such, may be a candidate biochemical indicator of larger infarct size and enhanced inflammation in patients with AMI