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2.
Int J Pediatr Otorhinolaryngol ; 73(4): 555-9, 2009 Apr.
Article in English | MEDLINE | ID: mdl-19150138

ABSTRACT

OBJECTIVE: In this study, our aim was to determine presence of dysfunction in the efferent auditory system of children with type-I diabetes mellitus (DM) presenting no evidence of symptomatic neuropathy. METHODS: Thirty children with type-I DM (DM group) and 31 age matched healthy children (control group) with normal hearing and middle ear function were entered to the study. Distortion product otoacoustic emissions (DPOAE), transiently evoked otoacoustic emissions (TEOAE), and spontaneous otoacoustic emissions (SOAE) measurements were performed. Then, the TEOAE recording was repeated while a continuous broadband white noise (bandwidth: 50-8000 Hz) presented at 40 dB SL was delivered to the contralateral ear for efferent auditory system suppression. RESULTS: We found that contralateral stimulation (CS) with white noise resulted in significantly more pronounced suppression of the TEOAE response amplitude in healthy controls compared to DM group at 2000 and 4000 Hz frequencies. Further, a relatively higher percentage of the controls had suppression in at least three frequencies compared to DM group. SOAE prevalence was found to be higher in the DM group. CONCLUSIONS: Our findings suggest presence of a dysfunction in medial olivocochlear efferent system in diabetic children. This may be regarded as an early central manifestation of diabetic neuropathy.


Subject(s)
Audiometry, Pure-Tone/methods , Diabetes Mellitus, Type 1/physiopathology , Hearing Disorders , Otoacoustic Emissions, Spontaneous/physiology , Acoustic Impedance Tests , Acoustic Stimulation/methods , Adolescent , Audiometry , Auditory Threshold , Case-Control Studies , Child , Hearing Disorders/diagnosis , Hearing Disorders/physiopathology , Humans , Male , Prospective Studies , Statistics, Nonparametric
3.
Pediatr Neurol ; 39(4): 266-71, 2008 Oct.
Article in English | MEDLINE | ID: mdl-18805365

ABSTRACT

This study evaluated the effects of oxcarbazepine monotherapy on bone turnover in prepubertal and pubertal children. Thirty-four newly diagnosed pediatric patients with normal bone mineral density, serum biochemical markers of bone formation, and hormonal markers participated. Levels of 25-hydroxyvitamin D were significantly decreased after therapy compared with baseline values. Levels of gamma-glutamyl transferase, phosphorus, alkaline phosphatase, osteocalcin, parathyroid hormone, and calcitonin had increased. However, only changes in osteocalcin and gamma-glutamyl transferase levels were statistically significant compared with baseline values. Drug-induced osteopenia was evident in 3 patients with z scores of bone-mineral density less than -2.0, whereas these patients had z scores of less than -1.5 before treatment. Although 18 months of oxcarbazepine treatment exerted slightly adverse effects on bone metabolism, the effect seems insignificant in children with normal bone-mineral density. Although alterations in bone metabolism do not always suffice to explain the decrease in bone-mineral metabolism, we think that patients with osteopenia before the initiation of oxcarbazepine therapy should be followed carefully, especially in long-term treatment.


Subject(s)
Bone Density/drug effects , Bone Diseases, Metabolic/chemically induced , Carbamazepine/analogs & derivatives , Osteogenesis/drug effects , Administration, Oral , Adolescent , Alkaline Phosphatase/blood , Anticonvulsants/administration & dosage , Anticonvulsants/adverse effects , Anticonvulsants/therapeutic use , Biomarkers/blood , Bone Diseases, Metabolic/metabolism , Calcitonin/blood , Carbamazepine/administration & dosage , Carbamazepine/adverse effects , Carbamazepine/therapeutic use , Child , Epilepsy , Humans , Osteocalcin/blood , Oxcarbazepine , Parathyroid Hormone/blood , Phosphorus/blood , Vitamin D/analogs & derivatives , Vitamin D/blood , gamma-Glutamylcyclotransferase/blood
4.
J Trop Pediatr ; 51(3): 166-9, 2005 Jun.
Article in English | MEDLINE | ID: mdl-15855306

ABSTRACT

An association between Helicobacter pylori infection and iron deficiency anemia has been reported in children, and it has been proposed that H. pylori infection needs to be eradicated to treat absolutely iron deficiency anemia (IDA). We investigated whether there was any correlation between H. pylori infection and iron deficiency (ID) and IDA in children, and whether the eradication of H. pylori infection without iron treatment would lead to the resolution of ID. Hemoglobin and ferritin levels, H. pylori stool antigen test and (14)C urea breath test were measured in 140 children aged 6--16 years (median 9.5 years). Children with H. pylori infection were divided into three groups on the basis of hemoglobin, mean corpuscular volume (MCV), and serum ferritin levels: groups of IDA, ID, and control. All the children received anti-H. pylori combination therapy consisting of amoxicillin, clarithromycin, and lansoprazole. Hemoglobin and MCV values rose significantly compared with baseline values after H. pylori eradication without iron supplementation in children with IDA (p=0.002 and p=0.003, respectively). Ferritin values increased significantly after H. pylori eradication in children with ID (p<0.001). We conclude that complete recovery of ID and IDA can be achieved with H. pylori eradication without iron supplementation in children with H. pylori infection.


Subject(s)
Anemia, Iron-Deficiency/diagnosis , Anemia, Iron-Deficiency/epidemiology , Helicobacter Infections/diagnosis , Helicobacter Infections/epidemiology , Helicobacter pylori/isolation & purification , Adolescent , Age Distribution , Analysis of Variance , Anemia, Iron-Deficiency/drug therapy , Anti-Bacterial Agents/therapeutic use , Case-Control Studies , Child , Comorbidity , Enzyme-Linked Immunosorbent Assay , Female , Ferritins/therapeutic use , Helicobacter Infections/drug therapy , Humans , Incidence , Male , Probability , Reference Values , Risk Assessment , Severity of Illness Index , Sex Distribution , Treatment Outcome , Turkey/epidemiology
5.
Turk J Pediatr ; 44(3): 248-50, 2002.
Article in English | MEDLINE | ID: mdl-12405439

ABSTRACT

Minor blood group hemolytic disease is extremely rare, since the overall potency of minor blood groups in inducing antibodies is significantly lower when compared with that of Rh (D) antigen. We hereby report a very rare case of severe neonatal anti-E hemolytic disease due to E minor blood group incompatibility. A term newborn born to a 27-year-old, gravida 3, para 3 mother was referred due to a high and increasing serum bilirubin level despite phototherapy on the 4th day of life. On admission physical examination was normal except for the jaundice, and results of the laboratory investigation demonstrated a moderate-to-severe anemia (hemoglobin 7.8 g/dl) and a severe hemolytic hyperbilirubinemia (serum total and indirect bilirubin levels 36 mg/ dl and 32.8 mg/dl, respectively; reticulocyte count 15%; and a positive direct antiglobulin test). As there was no apparent cause of the hemolytic disease such as Rh or ABO incompatibilities, further investigation (a positive indirect antiglobulin test and a positive irregular anti-E antibody in both the patient and mother, and minor blood group antigen profiles in family members compatible with E minor blood group isoimmunization) revealed the presence of anti-E hemolytic disease due to E minor blood group incompatibility. Two exchange transfusions with a 12-hour-interval were performed with minor blood group compatible fresh whole blood, and the patient was discharged in a healthy condition on the 10th postnatal day. If the most common causes of severe neonatal hemolytic disease such as Rh and ABO incompatibilities cannot be demonstrated in a newborn with significant hemolytic hyperbilirubinemia, anti-E hemolytic disease should strongly be considered in differential diagnosis. It should be kept in mind that a very severe from of minor group antibody hemolytic disease characterized by anemia and severe hyperbilirubinemia many exchange transfusions may be encountered during the course of the disease.


Subject(s)
Erythroblastosis, Fetal/immunology , Rh Isoimmunization , Humans , Infant, Newborn , Male
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