US therapy is safe but use of US in addition to conventional physical therapy programs seems to have no further significant effect in people with knee OA.
Objective: Brucellosis is still an important infectious disease, being widespread as endemic and sporadic cases in Turkey. The aim of this study was to evaluate clinical and laboratory findings, treatment modalities and final outcomes of brucellosis in children. Material and Methods: This is a retrospective record review of all patients 0-18 years of age with brucellosis admitted during a 8-year period between January 2003 and September 2010. Results: Of the 62 patients, 39 (63%) were male. The mean age and standard deviation of patients was 120±51.7 months (4 months-18 years). Most common symptoms on admission were fever (88%), arthralgia (64%) and dizziness (19%). On physical examination, the findings and percentages were as follows; arthritis (29%), lymphadenopathy (25%), hepatomegaly (24%) and splenomegaly (17%). Fiftyone percent of the patients had high sedimentation rate, 41% had high transaminase levels, and 40% had positivity for C-Reactive Protein. Brucella agglutination tests were positive in all cases. Brucella spp. was isolated from blood cultures in 27% of the cases. All of the cases were given combined drug therapy. Three of the cases (4.8%) had relapses during the follow up period. No mortality was seen in patients with brucellosis. Conclusion: Childhood brucellosis remains an important public health problem in our country. It may cause serious complications in children, and treatment with at least two antibiotics for not less than six weeks appears to be effective. (J Pediatr Inf 2011; 5: 59-62)
Background. Obesity is a significant public health problem worldwide. Vitamin deficiencies, developing due to monotype nutrition, are more likely to be observed in patients than healthy children. The present study evaluates vitamin and micronutrient levels in children and adolescents with obesity and metabolic syndrome compared to healthy controls. Methods. The study included 73 patients with obesity, 64 patients with metabolic syndrome and 71 healthy children (control group) aged 10 to 16 years. Physical examinations were performed, and waist circumference and systolic blood pressure measurements were recorded. Fasting blood glucose, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, insulin, vitamin A, vitamin E, vitamin B1, vitamin B2, vitamin B6, vitamin B12, folic acid and free carnitine levels were analyzed. The homeostatic model of assessment-insulin resistance (HOMA-IR) index was calculated and recorded. Results. The mean age of all patients was 11.9±2.6 years. The serum insulin level and HOMA-IR index were found to be significantly higher in the obesity and metabolic syndrome groups. No significant difference was found between the groups in terms of vitamin A, vitamin B6 and free carnitine levels. Significantly decreased vitamin E, vitamin B2, vitamin B12 and folic acid and increased vitamin B1 levels were observed in the obesity and metabolic syndrome groups. Conclusions. Compared to healthy children, children with obesity and metabolic syndrome may have varying degrees of micronutrient and vitamin deficiency due to poor and unbalanced eating habits. These deficiencies should also be considered in the treatment and follow-up of obesity and metabolic syndrome.
The basic helix-loop-helix (bHLH) transcription factor, neuronal differentiation 1 (NEUROD1) (also known as BETA2) is involved in the development of neural elements and endocrine pancreas. Less than 10 reports of adult-onset non-insulin-dependent diabetes mellitus (NIDDM) due to heterozygous NEUROD1 mutations and 2 cases with permanent neonatal diabetes mellitus (PNDM) and neurological abnormalities due to homozygous NEUROD1 mutations have been published. A 13 year-old female was referred to endocrine department due to hyperglycemia. She was on insulin therapy following a diagnosis of neonatal diabetes mellitus (NDM) at the age of 9-weeks but missed regular follow-up. Parents are second cousin. There was a significant family history of adult onset NIDDM including patient's father. Auxological measurements were within normal ranges. On laboratory examination blood glucose was 33.2 mmol/L with undetectable c-peptide and glycosylated hemoglobin level of 8.9% (73.8 mmol/mol). She had developed difficulty in walking at the age of 4 years which had worsened over time. On further evaluation, a diagnosis of visual impairment, mental retardation, ataxic gait, retinitis pigmentosa and sensory-neural deafness were considered. Cranial magnetic resonance imaging revealed cerebellar hypoplasia. Molecular genetic analysis using targeted next generation sequencing detected a novel homozygous missense mutation, p.Ile150Asn(c.449T>A), in NEUROD1. Both parents and 2 unaffected siblings were heterozygous for the mutation. We report the third case of PNDM with neurological abnormalities caused by homozygous NEUROD1 mutation, the first caused by a missense mutation. Heterozygous carriers of the p.Ile150Asn mutation were either unaffected or diagnosed with diabetes in adulthood. It is currently unclear whether the NEUROD1 heterozygous mutation has contributed to diabetes development in these individuals.
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