Vancomycin has been used with increased frequency during the past 15 years and the most common toxicity with this drug is the red man syndrome . Other adverse effects include neutropenia, fever, phlebitis, nephrotoxicity, ototoxicity, thrombocytopenia, interstitial nephritis, lacrimation, linear IgA bullous dermatosis, necrotizing cutaneous vasculitis and toxic epidermal necrolysis. Only two cases of vancomycin-induced Stevens-Johnson syndrome and one case of pancytopenia have been reported in the medical literature. The treatment for both situations is based on cessation of the vancomycin therapy; in cases of Stevens-Johnson syndrome, antihistamine and/or steroid agents can be used. This article reports a case of pancytopenia and a case of erythema major associated with neutropenia.

No abstract

The aim of the study was to detect neurological abnormalities in human immunodeficiency virus (HIV) infected children. This was achieved by a prospective evaluation, from November/1995 to April/2000, of 43 HIV infected children (group I) and 40 HIV seroreverters children (group II) through neurological exam and neurodevelopmental tests: Denver Developmental Screening Test (DDST) and Clinical Adaptive Test / Clinical Linguistic and Auditory Milestone Scale (CAT/CLAMS). A control group (III), of 67 children, were evaluated by CAT/CLAMS. Hyperactivity, irritability and hypotonia were the findings on neurological examination, without statistical differences between group I and II. On CAT/CLAMS, the group I developmental quotient (DQ) was significantly lower than the other groups. The same occurred in DDST, with group I presenting significantly more failures than group II. Nineteen HIV children of group I had brain computed tomographic scan, with abnormalities in three of them (basal ganglia calcification, white matter hypodensity and asymmetry of lateral ventricles). We conclude that in HIV infected children a neurodevelopment delay occur early in the disease, and it can be detected by screening tests.

Cat scratch disease (CSD) is an infectious illness caused by a Gram-negative rod namedBartonella henselae. Typical CSD is characterized by a small skin lesion at the site of a scratch or a bite, followed by regional lymphadenopathy, one to two weeks later. Atypical forms may present as ocular manifestations, neurological manifestations, hepatosplenic involvement and vertebral osteomyelitis. Among neurological complications, encephalopathy is by far the most common. Other neurological manifestations are very rare. We report a case of an 11-year-old boy, with a posterior cervical lymphadenopathy and fever. Cat scratch disease was diagnosed and treated after a positive "Whartin-Starry" stain on lymph node biopsy. Two weeks after treatment, the patient was readmitted presenting an acute episode of left hemiplegia. A brain MRI demonstrated a right subcortical fronto-parietal lesion with no contrast enhancement. Complete recovery was observed after corticosteroid treatment.

RESUMO -Relatamos três casos da insuficiência aguda hepática associada ao uso de ácido valpróico (AVP) em crianças epilépticas. A idade variou de 2 anos e 8 meses a 5 anos e 1 mês. Todos os pacientes apresentavam epilepsia de difícil controle e dois deles tinham desenvolvimento psicomotor severamente comprometido. O AVP foi usado em associação com outros antiepilépticos (carbamazepina em dois, fenobarbital em um). Todos os pacientes apresentaram sinais clínicos de insuficiência hepática.Vômitos, edema e icterícia foram os sinais iniciais. Febre ocorreu em dois pacientes. Os exames laboratoriais mostraram transaminases pouco aumentadas (inferiores a 194 U/l) e níveis de bilirrubina entre 5,5 e 19,8 mg%. Um dos pacientes usava a droga há 12 meses e os dois outros, há menos de 6 meses. Dois pacientes apresentaram resolução do quadro hepático após a retirada da droga e um faleceu. Com este relato, salientamos a toxicidade do AVP em crianças epilépticas mesmo acima de dois anos de idade, principalmente em uso de politerapia, com comprometimento neurológico, e que o quadro pode ser reversível com a retirada da droga. PALAVRAS-CHAVE: ácido valpróico, toxicidade, insuficiência hepática.Acute hepatic failure with valproic acid in children: report of three cases ABSTRACT -We report the cases of three epileptic children who developed hepatotoxicity induced by valproic acid. Two patients had developmental delay. Including the one who died, all patients were receiving polytherapy (carbamazepine in two and phenobarbital in one). The patients age ranged from 2 years and 8 months to 5 years and 1 month. The onset of hepatic complications occurred within 6 months of valproate therapy in two patients and 12 months in one. All patients developed the classical clinical signs of hepatotoxicity. Vomiting, edema and jaundice were the initial symptoms. Fever occurred in two patients. The serum levels of glutamic oxaloacetic transaminase were mildly elevated with a maximum of 194 IU. The bilirubin levels ranged from 5.5 to 19.8 mg%. Two patients recovered clinically and showed normalization of the laboratory abnormalities and one had fatal course. The hepatotoxicity must be considered as a side effect of valproic acid mainly in children under two years age, with polytherapy regimen and neurologic damage. The hepatic insufficiency can be reversible.KEY WORDS: valproic acid, toxicity, hepatic failure.O ácido valpróico (AVP) é um antiepiléptico usado há mais de vinte anos, com excelente eficácia. Apresenta, porém, efeitos colaterais importantes, predominando plaquetopenia, hipofibrinogenemia, insuficiência hepática e pancreática 3 -7 -9 . Existem descritos mais de 100 casos de toxicidade fatal 7 -9 , porém nenhum na literatura nacional.

The clinical profile and outcome of TF patients are similar to those with iNTS. Although comorbidities are more often associated with iNTS, the results of our study suggest that clinical management of these two diseases should remain similar.

No abstract

Our objective was to investigate how metabolic changes, the antioxidant system and the accumulation of oxidative damage occur in muscles with different fibre populations during the ageing process of Wistar rats, as well as to try to map the key age at which these changes occur. For this, 30 male Wistar rats were euthanized aged 11, 15 and 19 months. Then, changes in energy metabolism, antioxidant system and oxidative damage in the soleus and extensor digitorum longus muscles were determined. In this sense, it was possible to observe that changes in body characteristics occur after 15 months of age. Regarding muscle biochemical alterations, we can observe that the soleus muscle presents alterations in protein and anaerobic metabolism only at 19 months, while the extensor digitorum longus presents these alterations at 15 months. Even with the different induction of the antioxidant system between the muscles, the damage accumulation is similar between the two muscles. Therefore, it is possible to conclude that at 15 months of age, the metabolic changes that lead to the reduction of muscle mass and strength found in ageing begin, being, therefore, a key age for the application of interventions that seek to curb the reduction of mass and muscle strength, promoting a better quality of life for individuals.