Impact of valproates on haemostasis and blood cell count in children

INTRODUCTION Epilepsy is a highly prevalent disease affecting 0.5-1.5% of the world's population. One of the most frequently used antiepileptics are valproates. These medicines show a negative impact on haemostasis and peripheral blood count. OBJECTIVE The objective of the study was to examine the negative impact of valproates on haemostasis and peripheral blood count in children and to analyse whether these disturbances were dependent on the dosage of valproates and drug level in blood. METHOD A two-year research was conducted. The research included: 35 children using valproates, 12 children using the therapy of both valproates and carbamazepine and 30 healthy children. Complete peripheral blood count, screening tests of haemostasis (bleeding time, prothrombin time, prothrombin ratio, activated partial thromboplastin time, fibrinogen) and capacity of thrombocyte aggregation research were done in all the children. RESULTS We found significantly more common frequency of leukopenia and neutropenia in children using valproates in comparison with the healthy children group. We also found the more common frequency of eosinophilia in comparison with healthy children. The children with the valproate therapy have lower approximate values of the number of platelets, fibrinogen and platelet aggregation in comparison with healthy children, but they have a higher approximate value of bleeding time and prothrombin time. These disturbances are in correlation with the dosage and the level of the medicine in blood. CONCLUSION Valproates have a negative effect on certain blood count parameters and haemostasis in children. Drug dosage and blood drug level are correlated with their negative impact on haemostasis parameters

Report of a newborn with hemimegalencephaly in association with Klippel-Trenaunay-Weber syndrome

Klippel-Trenaunay-Weber syndrome (KTW) is a rare phacomatosis whose main characteristics are: cutaneous angiomas (vascular nevi), varicose veins (arteriovenous fistulae) and hemihypertrophy of bones and soft tissues. This is a case report of KTW syndrome which was diagnosed in the first days of life on the basis of characteristic vascular nevi on the skin of the trunk and extremities in addition to hypertrophy of the left part of the body. Neuroradiologically verified hemimegalencephaly associated with temporal hemangioma represents a special particularity in our case. Measures of monitoring the child as well as stimulating and therapeutic actions were the issues of discussion

Cardiac troponin as biochemical marker of perinatal asphyxia and hypoxic myocardial injury

Background/Aim. Myocardial cell lesion in newborns may be clinically occult. In recent years there has been shown growing interest in the use of cardiac troponin-I (cTnI) in relation to perinatal asphyxia and hypoxic myocardial lesion. The aim of this study was to determine a relationship between high cTnI levels and outcome in critically ill newborns with perinatal asphyxia. Methods. In this study 78 patients were divided into three groups. The group I included 39 newborns (15 term and 24 preterm) with perinatal asphyxia, with no deaths, only full or partial (with some neurological sequels) recovery. The group II included 10 newborns (6 preterm and 4 term), with perinatal asphyxia who died, with critical cardio-respiratory problems and multiorgan dysfunction. The group III included 29 healthy term newborns. A level of cTnI in all three groups was measured within 24-48 hours after delivery. Results. A statistically significant higher value of cTnI (0.082 μg/l ± 0.166) was found in group I than in the group III (healthy newborns). In the group I, 21/39 newborns required respiratory and 16/39 required pressure support. In the group II, the largest average value of cTnI of 0.425 ± 0.307 was found. All of the newborns in the group II required respiratory and pressure support. In the group III the lowest average value of cTnI (0.0186 μg/L ± 0.0286) was found. Conclusions. High cTnI levels could be used as markers of perinatal asphyxia and even as predictors of future outcomes and/or mortality

Clostridium difficile-associated diarrhoea in infants and children

Clostridium difficile (CD) is the most common cause of nosocomial diarrhea in adults with high rates of morbidity and mortality. The epidemiology of CD infection (CDI) has changed in the last few decades associated with increasing severity of the infection rate related to the occurrence of NAP1 hypervirulent strain and the emergence of the disease among ambulatory patients and the wider community. Although little is known about CDI in pediatric patients, CD is surprisingly recognized as an important pathogen in children. In this review article, we direct attention to the recent findings on the incidence and epidemiology of pediatric CDI, including the risk factors for infection, with special emphasis on the importance of CDI in infants and a population of children suffering from chronic gastrointestinal diseases or cancer. Despite recent pharmacotherapeutic protocols successfully used in children with CDI, we would like to draw attention to precautionary and preventive measures in terms of both unnecessary testing and uncritical use of antibiotics as the most important risk factors

Pseudo-Bartter syndrome in an infant with congenital chloride diarrhoea

Introduction. Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. We are presenting an infant with pseudo-Bartter syndrome caused by congenital chloride diarrhoea. Case Outline. A male newborn born in the 37th gestational week (GW) to young healthy and non-consanguineous parents. In the 35th GW a polyhydramnios with bowel dilatation was verified by ultrasonography. After birth he manifested several episodes of hyponatremic dehydration with hypochloraemia, hypokalaemia and metabolic alkalosis, so as Bartter syndrome was suspected treatment with indomethacin, spironolactone and additional intake of NaCl was initiated. However, this therapy gave no results, so that at age six months he was rehospitalized under the features of persistent watery diarrhoea, vomiting, dehydration and acute renal failure (serum creatinine 123 μmol/L). The laboratory results showed hyponatraemia (123 mmol/L), hypokalaemia (3.1 mmol/L), severe hypochloraemia (43 mmol/L), alcalosis (blood pH 7.64, bicarbonate 50.6 mmol/L), high plasma renin (20.6 ng/ml) and aldosterone (232.9 ng/ml), but a low urinary chloride concentration (2.1 mmol/L). Based on these findings, as well as the stool chloride concentration of 110 mmol/L, the patient was diagnosed congenital chloride diarrhoea. In further course, the patient was treated by intensive fluid, sodium and potassium supplementation which resulted in the normalization of serum electrolytes, renal function, as well as his mental and physical development during 10 months of follow-up. Conclusion. Persistent watery diarrhoea with a high concentration of chloride in stool is the key finding in the differentiation of congenital chloride diarrhoea from Bartter syndrome. The treatment of congenital chloride diarrhoea consists primarily of adequate water and electrolytes replacement

Case report of an infant with severe vitamin D deficiency rickets manifested as hypocalcemic seizures

Introduction. Hypocalcemic seizures are uncommon in the post-neonatal period. We report an infant with hypocalcemic seizures caused by severe deficiency of vitamin D. Case Outline. A five-month-old male infant was admitted to hospital in March 2013 with recurrent generalized afebrile seizures resistant to clonazepam therapy. At the clinical examination, the infant showed characteristic rachitic signs, so that after a blood sample was taken for laboratory testing, the infant was given infusion of 2 ml/kg of 10% of calcium gluconate at a rate of 0.5 ml/min. The treatment resulted in immediate termination of seizures and normalization of the consciousness of the infant. Blood sample analysis showed extremely low levels of free and total calcium (0.36/1.24 mmol/l) and 25(OH)D (<3 ng/ml), elevated alkaline phosphatase (878 U/l) and parathyroid hormone (283 pg/ml), and low calcium/creatinine ratio (mg/mg) in a portion of urine (0.03), while the levels of serum phosphorus, pH, total protein, albumin and creatinine were within the reference range. Wrist X-ray showed typical signs of rickets. In order to fully stabilize calcium homeostasis, along with 2,000 IU of vitamin D3 daily and standard cow’s milk formula, calcium gluconate (80 mg/kg daily) was given orally over a period of two weeks. The treatment resulted in complete stabilization of the infant’s condition and rapid improvement in laboratory, radiological and clinical findings of rickets. Conclusion. Generalized convulsions in the afebrile infant represent a serious and etiopathogenically very heterogeneous problem. Extremely rare, as in the case of our patient, it may be due to severe hypocalcemia caused by a deficiency of vitamin D

Pneumococcal meningitis associated with glomerulonephritis: A case report

Introduction. Streptococcus pneumoniae is the second most common cause of meningitis in children, producing more serious complications than other bacteria. Streptococcus pneumoniae infections are a rare trigger of glomerulonephritis. We presented a case of glomerulonephritis developing concurrently with meningitis in a young male child. Case report. Gross haematuria, significant proteinuria, hypertension and decreased level of C3 alongside the signs of central nervous system involvement occurred in a male patient of 5 years and 3 months of age. Spontaneous resolution of renal affliction parameters followed the successful treatment of meningitis. The disease course was strongly suggestive of postinfectious glomerulonephritis, although it manifested at the same time as meningitis. The absence of the latent period might point to the development of IgA nephropathy, but since the renal function was stable, without any abnormalities in urine tests documented during follow-up, our opinion is that this was rather the case of postinfectious nephropathy. Conclusion. The presented case is a unique clinical form of postinfectious glomerulonephritis. An accurate diagnosis of this entity should ensure the adequate treatment and follow-up of these patients