Dursun Odabas

Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets.

In this study, we compared three different therapy modes (150,000 IU, 300,000 IU, and 600,000 IU vitamin D p.o.) in infants with nutritional vitamin D deficiency rickets (VDR). Our purpose was to determine the most effective dosage of vitamin D with least side effects for treating VDR. The study included 56 patients, 3-36 months of age, with nutritional VDR and 20 age-matched control infants. In all infants, serum calcium, phosphorus, alkaline phosphatase, magnesium, serum 25-hydroxycholecalciferol, plasma intact parathormone levels and urinary Ca/creatine ratio were determined. Of 56 patients, 52 were able to be followed long-term. These patients were reexamined on the 3rd day, 7-10th day, and 25-30th day after treatment. On the 30th day post-treatment, we did not find any difference between the doses in the improvement of rickets. However, hypercalcemia was present in eight infants who had been administered 300,000 IU (two infants) and 600,000 IU (six infants) of vitamin D. In conclusion, our findings showed that 150,000 IU or 300,000 IU of vitamin D was adequate in the treatment of VDR, but 600,000 IU of vitamin D may carry the risk of hypercalcemia.

Deadly nightshade (Atropa belladonna) intoxication: an analysis of 49 children.

Deadly nightshade (Atropa belladonna) intoxication has been infrequently reported in both children and adults in the literature. In this article, the clinical and laboratory findings of 49 children with acute deadly nightshade intoxication are reviewed. Our purpose was to enlighten the findings of deadly nightshade intoxication in childhood. The most common observed symptoms and signs were meaningless speech, tachycardia, mydriasis, and flushing. None of the children required mechanical ventilation or died in our series. The patients were categorized into two groups, mild/moderate and severe intoxication. Children with and without encephalopathy were accepted as severe and mild/moderate intoxication, respectively. While 43 children were placed in the group of mild/moderate intoxication, six were in severe intoxication group. We found that meaningless speech, lethargy, and coma were more common, but tachycardia was less common in the severe intoxication group (children with encephalopathy) (P B-0.05). In the treatment, neostigmine was used in all children because of no available physostigmine in our country. In conclusion, our findings showed that the initial signs and symptoms of acute deadly nightshade intoxication might be severe in some children, but no permanent sequel and death were seen in children. We also showed that meaningless speech, lethargy, coma, and absence of tachycardia were ominous signs in deadly nightshade intoxication in childhood. Lastly, we suggest that neostigmine may be used in cases of deadly nightshade intoxication if physostigmine cannot be available.

Report of Eight Infants with Acute Infantile Hemorrhagic Edema and Review of the Literature

Acute infantile hemorrhagic edema (AIHE) is a cutaneous leukocytoclastic vasculitis, clinically characterized by the symptom triad of fever, large purpuric skin lesions, and edema. The clinical picture has a violent onset, a short benign course, and spontaneous complete recovery. In this article, we present eight patients who were admitted with rashes on the skin and edema on the eyelids and extremities, and were diagnosed with AIHE according to their clinical and histopathological features (immunohistological study was also performed in three of them). Our purpose was to emphasize that, aside from Henoch‐Schönlein purpura, meningococcemia, septicemia, and purpura fulminans, AIHE benign disorder should also be considered in the differential diagnosis to determine the clinical course and treatment protocol in patients with purpuric rashes.

Left Ventricular Function by Echocardiography, Tissue Doppler Imaging, and Carotid Intima-Media Thickness in Obese Adolescents With Nonalcoholic Fatty Liver Disease

The aims of this study were to evaluate left ventricular (LV) systolic and diastolic function in obese adolescents with nonalcoholic fatty liver disease (NAFLD) using conventional echocardiography and pulsed-wave tissue Doppler imaging and to investigate the relations between LV function and carotid intima-media thickness (CIMT). LV remodeling, tissue Doppler-derived LV velocities, and cardiovascular risk profiles in obese adolescents with NAFLD were also studied. One hundred eighty obese adolescents and 68 healthy controls were enrolled in the study. LV end-diastolic and end-systolic and left atrial diameters and LV mass were higher in the 2 obese groups compared with controls. By pulsed-wave Doppler echocardiography and pulsed-wave tissue Doppler imaging, the NAFLD group had normal LV systolic function, impaired diastolic function, and altered global systolic and diastolic myocardial performance. In patients with NAFLD, LV mass was positively correlated with homeostasis model assessment of insulin resistance and serum alanine aminotransferase. CIMT was positively correlated with homeostasis model assessment of insulin resistance, alanine aminotransferase, and LV mass. By multiple stepwise regression analysis, alanine aminotransferase (β = 0.124, p = 0.026), homeostasis model assessment of insulin resistance (β = 0.243, p = 0.0001), LV mass (β = 0.874, p = 0.0001) were independent parameters associated with increased CIMT. In conclusion, insulin resistance has a significant independent impact on CIMT and LV remodeling in the absence of diabetes in patients with NAFLD. Pulsed-wave tissue Doppler imaging is suggested to detect LV dysfunction at an earlier stage in obese adolescents with NAFLD for careful monitoring of cardiovascular risk.

Correlation of insulin sensitivity with bone mineral status in obese adolescents with nonalcoholic fatty liver disease.

Aim  The aim of this study was to investigate the relationships between bone mineral density (BMD) vs insulin resistance and metabolic risk factors in obese adolescents with nonalcoholic fatty liver disease (NAFLD).

Acute amitriptyline intoxication: an analysis of 44 children.

The tricyclic antidepressant agents, particularly amitriptyline and dothiepin, are recognized for their potentially lethal cardiovascular and neurological effects in poisoned patients. In this article, the clinical and laboratory findings of 44 children with amitriptyline intoxication are reviewed. Our purpose was to investigate amitriptyline intoxication in childhood. Of 44 patients, 21 (47.7%) were boys, 23 (52.3%) were girls, and the ages ranged from 12 months to 14 years (mean9 / SD; 4.099 / 2.9 years). All children except one who took an overdose of amitriptyline to decrease his pain accidentally ingested an overdose of amitriptyline. The amount of amitriptyline ingested was between 2 mg/kg and 97.5 mg/kg (mean9 / SD; 13.69 / 17.7 mg/kg per dose) (the drug dosage was not known in 13 children). The most commonly observed clinical and laboratory findings were lethargy, tachycardia, convulsion, hyperglycemia and leukocytosis. In all patients except for two children who died the abnormal clinical and laboratory findings returned to normal within a few days after admission and they were discharged from the hospital in good health within the fourth day of admission. One of the children ingested 97.5 mg/kg amitriptyline and probably died due to status epilepticus and another child who died ingested 36 mg/ kg amitriptyline and died due to cardiopulmonary arrest. In conclusion, our findings showed that initial symptoms and signs of acute amitriptyline intoxication appeared severe, but they disappeared with only supportive care required in most children except for cases that ingested high doses of drug within a few days. In contrast to adults, we infrequently noted respiratory insufficiency, arrhythmia and hypotension in children with acute amitriptyline intoxication.

PFAPA syndrome mimicking familial Mediterranean fever: report of a Turkish child

The PFAPA (Periodic Fever, Aphthous stomatitis, Pharyngitis, Adenitidis) syndrome is characterized by periodic fever, adenitis, pharyngitis, and aphthous stomatitis. Herein, we present a Turkish child with PFAPA syndrome mimicking familial Mediterranean fever because of a rare presentation. A 9-year-old boy was admitted with recurrent fever, aphthous stomatitis, sore throat, headache, and general body pains, lasting 2 to 3 days since 3.5 years of age. He was completely symptom-free between the attacks. He was diagnosed as having familial Mediterranean fever according to the clinical findings when he was 6 years of age and Colchicum tablet was administrated. Despite colchicines therapy for 8 months, his attacks did not subside; therefore, the drug was discontinued. He had high fever, a painful cervical lymphadenopathy, aphthous stomatitis, and tonsillo-pharyngitis. The patient was then diagnosed as having PFAPA syndrome. He was given a single dose of prednisolone (0.35 mg/kg/dose). His complaints dramatically and completely disappeared 3 h after administration of the drug. During the 8th month of follow-up, a similar febrile attack lasting only 1 day was noted and it was controlled with a single dose of prednisolone (0.5 mg/kg/day). At this writing the patient is in the 12th month of follow-up, and there have been no symptoms after the second attack. In conclusion, our patient shows that PFAPA syndrome can be confused with familial Mediterranean fever. We also would like to emphasize that the typical PFAPA syndrome can be easily diagnosed by detailed history-taking and physical findings.

Four children with colchicine poisoning

Colchicine poisoning is a rare event. It is characterized by multiorgan involvement and by poor prognosis associated with overdose. In this article we present four children with colchicine poisoning to emphasize that colchicine poisoning has a large spectrum in childhood. The childrens ages ranged between 1 year and 3.5 years. The ingested dosage of colchicine was between 0.37 and 1.72 mg/kg. Most of the findings of colchicine poisoning such as gastrointestinal symptoms, hepatotoxicity, cardiotoxicity, bone marrow suppression, hypocalcaemia and hair loss were diagnosed in our patients. Two children receiving 0.37 mg/kg and 1 mg/kg colchicine and admitted 13 and 19 hours after poisoning, respectively, died. Our findings suggest that in addition to amounts of the drug, mortality was also related to the duration between drug ingestion and admission to hospital.

Do not overlook acute isoniazid poisoning in children with status epilepticus

A previously healthy 2-year-old girl was admitted with generalized convulsive status epilepticus. She was in a stupor and could respond only to painful stimuli. She also had severe metabolic acidosis. Although initial liver function tests were normal, they were found to be moderately high on the fifth day of admission; however, they dropped to their normal ranges on the twelfth day of admission. Initially, the patient was diagnosed as having idiopathic status epilepticus, and classic anticonvulsant agents, including diazepam, phenytoin, and then phenobarbital, were given. However, her seizures did not subside, and diazepam infusion was initiated. After initiation of diazepam infusion, the seizures were completely controlled. On the fourth day of admission, her parents said that she had accidentally received 20 tablets (a total dose of 2000 mg) of isoniazid just before admission to our hospital. Later, we injected 200 mg of pyridoxine intravenously. During follow-up, her general condition improved, and anticonvulsant agents were discontinued because an electroencephalogram was found to be normal. She was discharged from the hospital on the twelfth day of admission. At the fourth month of follow-up, she was seizure free. Because of this case, we would like to re-emphasize that acute isoniazid poisoning should also be considered in a child with unexplained status epilepticus. (J Child Neurol 2003; 18: 142—143).

No effect of long-term valproate therapy on thyroid and parathyroid functions in children.

In this study, we studied serum calcium, phosphorus, alkaline phosphatase, thyroid hormones (total thyroxine, free thyroxine, thyroid-stimulating hormone), parathyroid hormone, and osteocalcine levels in children with epilepsy who had been receiving long-term valproate (VPA) therapy in order to determine whether there was any effect of VPA therapy on these hormones. The study included 31 patients with epilepsy receiving VPA and 22 healthy age-matched controls. The age ranged from 15 months to 16 years and 18 months to 17 years in the study and control group, respectively. The duration of VPA use was between 12 months and 5 years (1.93 - 1.90 years). When comparing the results, we did not find any significant difference in any of the parameters, including serum calcium, phosphorus, alkaline phosphatase, osteocalcine, and thyroid and parathyroid hormone levels, between the study and control group. We suggest that VPA can safely be used with regard to thyroid and parathyroid dysfunction in childhood epilepsy.