Objective: To compare composite adverse outcome rate of infants <32 weeks gestational age (GA) who were born after preterm premature rupture of membranes (PPROM) at previable gestation to those born without PPROM.Study Design: Retrospective review of prospective collected data for infants discharged between 2004 and 2007 was conducted. Cases were infants with >7 days of PPROM that occurred before 24 weeks. Matched cohort consisted of infants born without PPROM (matched for GA, sex and admission date). Composite adverse outcome was assessed considering death or any of the following three severe morbidities (severe neurological injury, severe retinopathy of prematurity or chronic lung disease).Result: The 29 cases had higher mean severity of illness score compared with 74 matched infants. Mean duration of ROM was 45 vs 2 days and mean GA at the ROM was 21 vs 27 weeks, respectively. Logistic regression confirmed significantly higher risk of composite adverse outcome rates for cases (69 vs 47%; P ¼ 0.02, adjusted odds ratio 4.0, 95% CI 1.2, 13.6). Conclusion:The survival rate for infants born at <32 weeks following PPROM at previable age has improved significantly; however, these infants had a higher rate of adverse composite neonatal outcome.

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Adenosine is a neuromodulator with its level increasing up to 100-fold during ischemic events, and attenuates the excitotoxic neuronal injury. Adenosine is produced both intracellularly and extracellularly, and nucleoside transport proteins transfer adenosine across plasma membranes. Adenosine levels and receptor-mediated effects of adenosine are regulated by intracellular ATP consumption, cellular release of ATP, metabolism of extracellular ATP (and other adenine nucleotides), adenosine influx, adenosine efflux and adenosine metabolism. Recent studies have used genetically modified mice to investigate the relative contributions of intra-and extracellular pathways for adenosine formation. The importance of cortical or hippocampal neurons as a source or a sink of adenosine under basal and hypoxic/ischemic conditions was addressed through the use of transgenic mice expressing human equilibrative nucleoside transporter 1 (hENT1) under the control of a promoter for neuron-specific enolase. From these studies, we conclude that ATP consumption within neurons is the primary source of adenosine in neuronal cultures, but not in hippocampal slices or in vivo mice exposed to ischemic conditions.

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Brucellosis can present initially with its haematological findings including anaemia, leukopenia, and thrombocytopenia and may mimic primary haematological diseases. We present two patients with complaints of severe epistaxis and isolated thrombocytopenia which was initially diagnosed as idiopathic thrombocytopenic purpura but which was finally attributed to brucellosis. Their platelet count reverted to normal within 2-3 weeks of initiating antibrucellosis treatment with recovery from the disease.

BackgroundActivation of adenosine A1 receptors has neuroprotective effects in animal stroke models. Adenosine levels are regulated by nucleoside transporters. In vitro studies showed that neuron-specific expression of human equilibrative nucleoside transporter 1 (hENT1) decreases extracellular adenosine levels and adenosine A1 receptor activity. In this study, we tested the effect of hENT1 expression on cortical infarct size following intracerebral injection of the vasoconstrictor endothelin-1 (ET-1) or saline.MethodsMice underwent stereotaxic intracortical injection of ET-1 (1 μl; 400 pmol) or saline (1 μl). Some mice received the adenosine receptor antagonist caffeine (25 mg/kg, intraperitoneal) 30 minutes prior to ET-1. Perfusion and T2-weighted magnetic resonance imaging (MRI) were used to measure cerebral blood flow (CBF) and subsequent infarct size, respectively.ResultsET-1 reduced CBF at the injection site to 7.3 ± 1.3% (n = 12) in hENT1 transgenic (Tg) and 12.5 ± 2.0% (n = 13) in wild type (Wt) mice. At 48 hours following ET-1 injection, CBF was partially restored to 35.8 ± 4.5% in Tg and to 45.2 ± 6.3% in Wt mice; infarct sizes were significantly greater in Tg (9 ± 1.1 mm3) than Wt (5.4 ± 0.8 mm3) mice. Saline-treated Tg and Wt mice had modest decreases in CBF and infarcts were less than 1 mm3. For mice treated with caffeine, CBF values and infarct sizes were not significantly different between Tg and Wt mice.ConclusionsET-1 produced greater ischemic injury in hENT1 Tg than in Wt mice. This genotype difference was not observed in mice that had received caffeine. These data indicate that hENT1 Tg mice have reduced ischemia-evoked increases in adenosine receptor activity compared to Wt mice.

Hemodynamic instability is frequent in high-risk infants admitted to neonatal intensive care units. However, monitoring and treatment strategies of those conditions might show variations among the units. Different factors can compromise hemodynamic status in preterm/ term infants. Treatment options mostly include volume replacement, inotropes and/or vasopressors (dopamine, dobutamine, epinephrine and milrinone) and hydrocortisone. In general, these treatments are driven by predetermined protocols, which are not patient-based. According to the current knowledge, a physiology-driven approach that takes the individual characteristics of the newborn into consideration is accepted to be more suitable. In neonatal hemodynamics, important determinants are cardiac output, systemic vascular resistance, blood pressure, regional tissue perfusion and oxygenation. The novel technological methods, “targeted neonatal echocardiography” and “near-infrared spectroscopy” can help to delineate the underlying pathophysiology better, when added to the clinical assessment. In this review, strategies for the assessment of neonatal hemodynamics, as well as etiology, monitoring, and treatment of hemodynamic instability in preterm and term infants are presented.

Prune-belly syndrome (PBS) is a rare and complicated condition affecting mainly the abdominal wall and the genitourinary system. 1 In addition, respiratory, cardiovascular, gastrointestinal and orthopedic anomalies may accompany PBS. 2 Early recognition and treatment of PBS may prevent serious complications that may lead to fatalities. Herein, we report on a typical case of PBS in an infant, with a complex of genitourinary, respiratory, orthopedic and gastrointestinal anomalies, who died due to respiratory failure following a common respiratory infection. Case ReportA 4-month-old male infant presented to Turgut Ozal Medical Center, Clinic of Pediatrics, with fever, cough and respiratory difficulty. The complaints were noticed 8 days before admission and they gradually increased despite antibacterial treatment and oxygen support.He was delivered at full term and after an uncomplicated pregnancy. Due to the low socioeconomic status of the parents, the patient had no pre-or postnatal medical follow up. However, relative oligohydramnios was noted by an obstetrician in the delivery room.On physical examination, the child was febrile with a poor general condition. His pulse rate was 148 /min and his respiratory rate was 54 breaths/min with peripheral saturation of O 2 at 88% on 8 L/min of facemask oxygen. In addition to his dyspneic and grunting respiration, intercostal, supra-and substernal retractions were noted. Cracking rales were heard in both lungs. Kyphoscoliosis, abdominal distention and easily notable bowel loops secondary to a lack of abdominal wall muscles were determined. An enlarged liver, non-palpable testis and a right clubfoot deformity were determined. The body percentiles were within the normal ranges.Initial investigations were as follows: hemoglobin 9.9 g/dL, leukocyte count 27 200 /mm 3 (82% polymorphonuclear leukocytes, 12% band forms and 8% lymphocytes), erythrocyte sedimentation rate 60 mm/h, blood urea nitrogen (BUN) 10 mg/dL and serum creatinine 0.4 mg/dL. Liver function tests, serum total protein, albumin and electrolytes were within the normal ranges. Echocardiography and electrocardiography were also interpreted as normal. Although >10 5 /mm 3 Proteus vulgaris was grown in culture, microscopic examination of the urine was normal. Blood gas analysis upon admission revealed pH 7.32, PO 2 76 mmHg, PCO 2 45 mmHg and HCO 3 26 mmol/L.Plain chest X-ray showed thoracolumbal scoliosis, decreased right lung volume and ipsilateral displacement of the heart, an elevated right diaphragm, a compensatory increase of left lung volume, protruding liver secondary to an absence of abdominal wall muscles, dilated intestines and a consolidation from the middle lobe to the basal area on the right lung (Fig. 1). The computed chest tomography (CT) showed right lung hypoplasia, shifting of the trachea, mediastinal structures and the heart to the right hemithorax, a pneumonic parenchymal infiltration with air bronchograms on the hypoplastic lung and a compensatory expansion of the opposite lung ( Fig. 2a,b).Abdomina...