ABSTRACT
Background: Respiratory distress syndrome [RDS] is among the most common diseases of preterm infants. RDS is caused by a decreased production or secretion of pulmonary surfactant. Numerous causes of RDS have been identified, and the factors suspected to be involved in the pathogenesis of RDS are numerous, Carnitine is essential for the fetus and is provided via placental transport. As the gestational age increases, fetal tissues store increasing amounts of carnitine, therefore, preterm infants require exogenous carnitine supplementation for carnitine homeostasis. Treatment with carnitine has shown benefit in the respiratory status of ventilator- dependent adults, as well as stabilization of respiratory parameters and increased physical performance in adult patients with chronic respiratory insufficiency
Objective: The present study was designed to measure the level of free carnitine in preterm neonates with RDS and to evaluate the efficacy of L-carnitine therapy on those neonates
Patients and Methods: Forty preterm infants, including 14 females and 26 males. Study group were divided in to 2 groups, group A: received L-carnitin in a dose of 30 mg/kg/ day for 7 days and group B: did not receive supplementation
Results: our results show non statistically significant difference between group A [with Carnitine supplementation] and group B [no supplementation] at day 1. There was statistically significant higher serum carnitine level in group A compared to group B at day 7 [after supplementation]. Seven neonates [35%] in group A, and 13 [65%] in group B, needed surfactant administration and MV after 24 hours from admission and this difference was statistically significant. Dose of surfactant was statistically significant lower in group A compared to group B [P=0.001] and duration of mechanical ventilation was statistically significant lower in group A compared to group B [p=0.03]
Conclusion: L-carnitine is more deficient in preterm with RDS than preterm without RDS and its supplementation can reduce the need and duration of MV and/ or need and dose of surfactant
ABSTRACT
Extracellular matrix remodeling is thought to play an important role in the progression of heart failure [HF]. Matrix metalloproteinases [MMPs] and tissue inhibitors of metalloproteinases [TIMPs] are matrix-degrading enzymes that have been demonstrated to influence left ventricular properties and serve as targets of potential anti-remodeling agents. It has been reported that MMPs concentration and activity are upregulated in the failing human heart. However, there are few reports describing the role of elevated level of circulating MMPs in severe congestive heart failure [CHF] patients. This study examined whether circulating MMPs are also related to the pathogenesis of CHF. The study involved 50 patients with severe CHF and 20 apparently healthy subjects, with matched age and sex were selected as a control group. Two Dimensional echocardiography, Doppler and colour flow mapping were done for the patients. Left ventricular dimensions [LVD] and cardiac size were measured. LV mass [LVM] was calculated from Interventricular septum [IVS], Left ventricular end diastolic dimensions [LVEDd], Left ventricular wall thickness [LVWT] and Left ventricular end systolic dimension [LVESd]. The serum levels of MMP-2, MMP-9 and TIMP-l as well as IL-18, TNF-alpha as pro-inflammatory cytokines were measured in patients with CHF and control subjects. The serum levels of MMP-2, MMP-9, TIMP-1, IL-18 and TNF-alpha were significantly higher in the CHF patients than control group. Moreover, MMP-2, MMP-9 and TIMP-1 serum levels were positively correlated with the levels of IL-8, TNF-alpha, cholesterol, triglyceride and CRP. Furthermore, MMP-2, MMP-9 andTIMP-1 were positively coffelated with LVM, LVED[d] and LVWT. We conclude that, the increasing serum levels of MMP-2, MMP-9 and TIMP-l were associated with increased LV diastolic dimensions and increased wall thickness in patients with CHF. These observations indicate that MMPs and TIMP- I serum levels may be markers for cardiac extracellular matrix degradation, a process involved in LV remodelling. These findings may open a new avenue for therapy that ameliorating heart failure especially high risk patients