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  1. Home
  2. Browse by Author

Browsing by Author "Evrengul, H"

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    Spectral and time-domain analyses of heart-rate variability during head-upright tilt-table testing in children with neurally mediated syncope
    Evrengul, H; Tavli, V; Evrengul, H; Tavli, T; Dursunoglu, D
    Neurocardiac syncope (NS) is a common cause of syncope in children. The mechanism, though related to abnormalities in autonomic function, has not been fully elucidated, particularly in pediatric patients. This study assessed the heart-rate variability (HRV) response to head-upright tilt-table test (HUT) in children with NS and normal volunteers. Spectral and time-domain analysis of HRV was used to assess changes in autonomic function in 27 children (9 male, mean age 12.3 +/- 1.6 years) with a history of at least one episode of syncope and positive passive HUT and 27 age-matched normal volunteers with negative passive HUT before and during postural tilt and to attempt to relate such changes to specific types of hemodynamic response to tilt. Frequency-domain measurements of the high-(HF) and low-(LF) frequency bands and the ratio LF/HF were derived from Holter recordings and computed by fast Fourier analysis for 5-min intervals. Time-domain measurements of the SDNN, SDNNI, SDANN, RMSSD, and triangular index were derived from 24-h Holter recordings. There were no significant differences between clinical characteristics, time-domain, and basal frequency domain parameters of the groups. Mean values of LF and LF/HF ratio was increased and HF was decreased significantly in response to tilt in both patient and control groups. Mean values of LF and LF/HF ratio were higher and HF was lower compared to controls immediately after tilt. LF and LF/HF ratio showed a statistically significant decrease and a significant increase in HF during syncope in patients. The three subgroups of patients had similar patterns of changes in autonomic activity. The results of this study show that although the basal autonomic function was similar to that of the control group, patients with NS have a different pattern of response to the HUT. In our study, patients with NS demonstrated an exaggerated response to the HUT. This exaggerated response may be the factor that activates the pathological reflexes of NS. The pathological mechanism leading to NS appears to be independent of the specific type of hemodynamic response to HUT.
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    The relationship between urinary tract infection and urine calcium and uric acit excretion in children
    Evrengul, H; Akil, I
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    A Patient with Cystinosis Presenting Like Bartter Syndrome and Review of Literature
    Ertan, P; Evrengul, H; Ozen, S; Emre, S
    Background: Nephropathic cystinosis is an autosomal recessively inherited metabolic disorder presenting with metabolic acidosis, Fanconi syndrome and renal failure. Case Presentation: We present a 6-year-old girl with severe growth failure, hyponatremia and hypokalemia. Her parents were 4th degree relatives. Two relatives were diagnosed as end stage renal failure. She also had persistant hypokalemic hypochloremic metabolic alkalosis. Her renal function was normal at presentation. She was thought to have Bartter syndrome with supporting findings of elevated levels of renin and aldosterone with normal blood pressure, and hyperplasia of juxtaglomerular apparatus. Her metabolic alkalosis did not resolve despite supportive treatment. At 6th month of follow-up proteinuria, glucosuria and deterioration of renal function developed. Diagnosis of cystinosis was made with slit lamp examination and leukocyte cystine levels. At 12th month of follow-up her metabolic alkalosis has converted to metabolic acidosis. Conclusion: In children presenting with persistant metabolic alkalosis, with family history of renal failure, and parental consanguinity, cystinosis should always be kept in mind as this disease is an important cause of end stage renal failure which may have features mimmicking Bartter syndrome.
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    RENAL AGENESIS AND HYOPLASIA IN HUMANS ARE NOT ASSOCIATED GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR
    Evrengul, H; Ertan, P; Serdaroglu, E; Yuksel, S; Mir, S; Ergon, EY; Berdeli, A

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