Nondipper patern has an additional negative effect on endothelial functions in hypertensive patients. Nondippers have enhanced sCD40L levels, which may contribute to their increased susceptibility to develop vascular damage.
ÖZETAmaç: Kliniğimize 8 yıla yakın bir sürede başvuran 57 Brusellozlu çocuğun dosyasını geriye dönük incelemek.
Gereç ve Yöntem: Bu çalışmada Tepecik Eğitim ve Araştırma Hastanesi Çocuk
Findings:The mean age was 8.75±3.54 years and 63.2% of the patients were male. 82.5% of 57 cases had a history of consumption of unpasteurized milk and ingestion of contaminated dairy products, 50.9% of cases had a history contact with infected animal. Complication was found in 18 out of 57(31.6 percent) patient. Osteomyelitis, arthritis and menengitis was presented in 21.1%, 5.3% and 5.3% of the patients, respectively.
Objective. Ectopic posterior pituitary gland (EPP) is usually characterized by an abnormal pituitary stalk and hypoplasia of the anterior hypophysis. The genetic mechanisms involved in the development of EPP remain uncertain. The aim of this study is to determine whether mutations in the three genes, PROP-1, LHX2, and POU1F1, are associated with the risk for and the characteristics of EPP.Methods. In the Endocrinology Outpatient Clinic of "Dr. Behcet Uz" Children's Hospital, 27 patients with EPP were submitted to sequencing analyses of the PROP-1, LHX2, and POU1F1 genes.Results. Growth hormone, thyrotropin, corticotropin, gonadotropin, and vasopressin deficiency were observed in 22 (81.5%), 23 (85.2%), 17 (63%), 14 (51.9%), and two (7.4%) patients. Thirteen patients (48.1%) presented with hyperprolactinemia. Fourteen patients (51%) had a history of birth dystocia, and 12 cases (42.1%) had a history of breech presentation. Central nervous system abnormalities included five cases with corpus callosum agenesis, one case with schizencephaly, and one case with Chiari type 1 malformation. We identified a homozygous p.S109* mutation in exon 2 in one male patient with EPP and two different PROP1 gene polymorphisms (A142T or c.109+3 G>A polymorphism) in thirteen patients.Conclusions. Our results suggest that PROP1 gene abnormalities might explain the genetic mechanisms involved in the development of EPP.
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