O uso do cloridrato de piridoxina para induzir estro em cadelas / The use of pyridoxine chloridrate to induce estrus in female dogs

Os agonistas dopaminérgicos são utilizados para induzir estro em cadelas, pois atuam na síntese e liberação de prolactina. Objetivou-se avaliar o efeito da piridoxina como indutor de estro em cadelas por agir na neurotransmissão dopaminérgica. Foram selecionadas 40 cadelas em anestro, divididas em quatro grupos experimentais, tratadas com 10mg/kg/dia (G1) e 50mg/kg/dia (G2) de cloridrato de piridoxina, 5µg/kg/dia (G3) de cabergolina e grupo controle/placebo (G4) por até 20 dias. Foram realizadas citologias vaginais a cada 24h para acompanhamento do ciclo estral e análises hormonais (FSH, LH e PRL) no dia zero e 120h do início do tratamento. As cadelas do G3 (100%) manifestaram proestro após 12 dias de tratamento aproximadamente, tempo inferior aos demais grupos (P<0,05). Apenas uma cadela do G1 e uma do G2 ficaram gestantes contra oito fêmeas do G3 e nenhuma do G4 (P<0,05). As concentrações plasmáticas de prolactina foram reduzidas nas fêmeas do G2 e G3 (P<0,05). As demais avaliações hormonais não sofreram influência do tratamento (P>0,05). O cloridrato de piridoxina foi ineficiente para induzir estro em cadelas, mas foi capaz de suprimir a prolactina, de forma semelhante à cabergolina, quando utilizado na dose de 50mg/kg/dia.(AU)

Dopaminergic agonists are used to induce estrus in female dogs as they act in the synthesis and release of prolactin. The objective of this study was to evaluate the effect of pyridoxine as an inducer of estrus by acting on dopaminergic neurotransmission. A total of 40 female dogs in anestrous were divided into four experimental groups treated with 10mg/kg/day (G1) and 50mg/kg/day (G2) of pyridoxine hydrochloride, 5µg/kg/day (G3) of cabergoline and control group/placebo (G4) for up to 20 days. Vaginal cytologies were performed every 24h for follow-up of the estrous cycle and hormonal analyzes (FSH, LH and PRL) on day zero and 120 hours after the start of treatment. The female dogs from G3 (100%) showed proestrus after 12 days of treatment, less time than the other groups (P< 0.05). Only one female from G1 and one from G2 were pregnant against eight from G3 and none from G4 (P< 0.05). Plasma concentrations of prolactin were reduced by treatment in females from G2 and G3 (P< 0.05). The other hormonal evaluations were not influenced by the treatment (P> 0.05). Pyridoxine chloridrate was inefficient to induce estrus in female dogs but was able to suppress prolactin when used at a dose of 50mg/kg/day.(AU)

Convulsiones por isoniazida: una causa toxicológica a considerar / Isoniazid seizures: A toxicological cause to consider

La neurotoxicidad de la isoniazida (INH) frecuentemente no es tenida en cuenta por el pediatra ante un paciente con un cuadro convulsivo agudo. La INH es uno de los fármacos más indicados en el tratamiento y quimioprofilaxis de la tuberculosis. Habitualmente se la indica al grupo familiar, debido a las características epidemiológicas de esta enfermedad, lo cual permite una amplia disponibilidad en los hogares, pudiendo originar intoxicaciones accidentales o intencionales. La intoxicación severa se caracteriza por un cuadro neurotóxico agudo, expresado en un síndrome convulsivo o coma, que no cede con el tratamiento habitual. Se presenta un caso clínico de una paciente intoxicada grave con isoniazida, habiendo sido la anamnesis dirigida ampliada junto con un diagnóstico precoz y el tratamiento específico con el antídoto, la base fundamental para la evolución favorable de la paciente.

Pediatricians do not usually considered isoniazid (INH) neurotoxicity in cases of patients with severe seizure disorders. INH is one of the most suitable drugs in the treatment and chemoprophylaxis of tuberculosis. It is usually indicated to the family group, due to the epidemiological characteristics of this disease, allowing a wide availability in homes and being able to cause accidental or intentional poisoning. An acute neurotoxic picture, expressed as a convulsive syndrome or coma, which does not improve with the usual treatments, characterized severe intoxication. A case of a patient with severe intoxication with isoniazid is presented. The extended anamnesis, along with an early diagnosis and the specific antidote treatment, set the fundamental basis for the favorable evolution of the patient.

Isoniazid Toxicity Presenting As Status Epilepticus and Severe Metabolic Acidosis.

Isoniazid (INH) is an integral component of treatment of tuberculosis. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents to emergency medical services (EMS) with the triad. We report a patient presenting with multiple generalised tonic clonic (GTC) convulsions with severe metabolic acidosis as a manifestation of INH toxicity. ©

Homocystinuria due to cystathionine beta synthase deficiency.

A two year-old male child presented with cutis marmorata congenita universalis, brittle hair, mild mental retardation, and finger spasms. Biochemical findings include increased levels of homocysteine in the blood-106.62 micromol/L (normal levels: 5.90-16 micromol/L). Biochemical tests such as the silver nitroprusside and nitroprusside tests were positive suggesting homocystinuria. The patient was treated with oral pyridoxine therapy for three months. The child responded well to this therapy and the muscle spasms as well as skin manifestations such as cutis marmorata subsided. The treatment is being continued; the case is reported here because of its rarity. Homocysteinuria arising due to cystathionine beta-synthase (CBS) deficiency is an autosomal recessive disorder of methionine metabolism that produces increased levels of urinary homocysteine and methionine It manifests itself in vascular, central nervous system, cutaneous, and connective tissue disturbances and phenotypically resembles Marfan's syndrome. Skin manifestations include malar flush, thin hair, and cutis reticulata / marmorata.

Pyridoxine for severe metabolic acidosis and seizures due to isoniazid [INH] overdose

Isoniazid [INH] overdose can be effectively treated, only if, suspected. Seizures and coma are due to INH unless proved otherwise in patients with access to the drug. Acute INH intoxication is characterized by a clinical triad consisting of metabolic acidosis resistant to treatment with sodium bicarbonate, seizure which may be fatal and refractory to standard anticonvulsant therapy, and coma. Pyridoxine is the specific antidote for INH overdose. We report a case of a 25-yr-old lady, who in a suicidal attempt ingested a toxic dose of INH resulting in status epilepticus and was successfully treated with pyridoxine [Vit B6]

Potencialização do efeito antiinflamatório e antinociceptivo do diclofenaco e da nimesulida por vitaminas do complexo B / Potentiating effect of pretreatment with some B vitamins on the anti-inflammatory and antinociceptive properties of nimesulide and diclofenac

Investigou-se os efeitos de algumas vitaminas B associadas ao diclofenaco ou nimesulida, na contorção abdominal em camundongos e edema de pata em ratos apenas com a nimesulida ou sua associação com algumas vitaminas B.Verificou-se que o pré-tratamento com as vitaminas tiamina[B1], piridoxina[B6] e cianocobalamina [B12], isoladasou administradas conjuntamente, não inibiu o edema de pata produzido pela carragenina em ratos, nem as contorções abdominais produzidas pelo ácido acético em camundongos. Por outro lado, a nimesulida [5mg/kg]reduziu o edema de pata em ratos, e a associação das três vitaminas à este fármaco, mas não as vitaminas administradas isoladamente, potencializou seus efeitos nos tempos de duas, três e quatro horas após a carragenina. As contorções abdominais em camundongos foram inibidas pelas doses de 25 ou 50mg/kg de diclofenaco. A associação das três vitaminas ou apenas da cianocobalamina, potencializou as duas doses do diclofenaco utilizadas. As contorções abdominais foram reduzidas também pelo nimesulida [5mg/kg] e a associação das três vitaminas, oucada uma das vitaminas administradas isoladamente, foram capazes de potencializar os efeitos do nimesulida. É provável que a diferença no mecanismo de ação destes fármacos sejaresponsável pela diferença dos efeitos das vitaminas. O presente trabalho aponta para a realização de novos estudos com o uso destes antiinflamatórios, combinados com as vitaminas tiamina[B1], piridoxina[B6] e cianocobalamina [B12], em doenças inflamatórias crônicas, na tentativa dereduzir a dose destes fármacos e consequentemente diminuindo seus efeitos colaterais.

The effects of a combination of some B vitamins and diclofenac or nimesulide on chemical nociception in mice or paw edema in rats were investigated. While the vitamins alone had no effect, combination of thiamine (B1), pyridoxine (B6) and cyanocobalamin (B12), given i.p. in doses of 100mg and 5mg/kg, respectively, potentiated the inhibition by nimesulide (5mg/kg) of paw edema induced by carrageenin in rats. Antinociceptive effects of diclofenac and nimesulide (inhibition of abdominal writhing induced by acetic acid in mice) were also potentiated by the combination of the vitamins B1, B6 and B12. Thiamine, pyridoxine and cyanocobalamin given singly were effective in potentiating antinociceptive effects of nimesulide, but only cyanocobalamin potentiated these effects of diclofenac, probably reflecting the differing mechanisms of action of the two drugs. The results document the positive influence of B vitamins on the antinociceptive effects of diclofenac or nimesulide and support the use of B vitamins to shorten the treatment time and reduce the daily dose of anti-inflammatories.

Red cell aspartate aminotransferase saturation with oral pyridoxine intake

CONTEXTO E OBJETIVO: A enzima aspartato aminotransferase apresenta o piridoxal fosfato como coenzima, oriunda da piridoxina existente em alimentos vegetais frescos. A anemia sideroblástica responsiva à vitamina B6, mielofibrose e síndrome de Peyronie respondem a altas doses de piridoxina. O objetivo foi investigar a máxima resposta da aspartato aminotransferase à suplementação oral com piridoxina. TIPO DE ESTUDO E LOCAL: Experimento controlado, na Seção de Hematologia, Instituto Adolfo Lutz. MÉTODOS: A atividade da aspartato aminotransferase eritrocitária foi determinada (antes e após) em voluntários que receberam suplementação por 15-18 dias (30 mg, 100 mg e 200 mg diariamente). Estudo in vitro também foi realizado, com sangue de sete indivíduos. As atividades enzimáticas antes e após a incubação foram determinadas, seguindo o mesmo protocolo do estudo in vivo. RESULTADOS: O estudo in vivo revelou um aumento gradativo da saturação da aspartato aminotransferase com doses crescentes de piridoxina. 83% de saturação foi alcançada com 30 mg diariamente, 88% com 100 mg e 93% com 200 mg. O estudo in vitro não revelou saturação de 100%.CONCLUSÕES: Tanto in vivo quanto in vitro, não se revelou saturação completa da aspartato aminotransferase por sua coenzima piridoxal-5-fosfato nos eritrócitos. Entretanto, a dose de 200 mg diariamente poderia ser empregada com segurança no tratamento da anemia sideroblástica, mielofibrose e síndrome de Peyronie. Embora a saturação máxima nos eritrócitos não seja atingida, os eritroblastos e outras células nucleadas que contenham as organelas citoplasmáticas certamente atingirão a saturação completa, possivelmente à razão dos resultados obtidos nas doenças citadas.

Homocystinuria: a rare cause of megaloblastic anemia.

We present an eight-year-old boy who initially presented to us with megaloblastic anemia and subsequently developed dislocation of lens. The child had a positive sodium nitroprusside test and homocystinuria. He was diagnosed to have homocystinuria type 1. His anemia improved on oral pyridoxine and folic acid therapy. Homocystinuria should be remembered as a cause of megaloblastic anemia.

High-dose oral pyridoxin for treatment of pediatric recurrent intractable seizures

Intractable epilepsy is a common clinical problem in pediatrics and approximately 13% of children with epilepsy experience intractable seizures. To determine the efficacy of pyridoxine in treating seizures, 30 infants and children with recurrent seizures were enrolled in the present study. All of them were treated with high-dose oral pyridoxine [40 mg/kg/day], as an adjunct to antiepileptic drugs. Clinical efficacy criteria were based on the daily frequency of seizures after therapy was initiated during the following three weeks. The results indicated that the mean frequency of seizures decreased significantly from the first [16.2 +/- 11] to the fourth visit [7 +/- 6.2] [p<0.001, t=4]. Three patients became completely seizure free. No adverse effects of pyridoxine were apparent during the observation period. We conclude that pyridoxine is a safe, effective, and well-tolerated adjunct to routine antiepileptic drugs for the treatment of recurrent intractable seizures in children

Ictericia causada por hiperemesis gravídica / Ictericia due to hyperemesis gravidarum

Se presentan dos pacientes con hiperemesis gravídica (HG) de varias semanas de evolución y pérdida de peso entre 7 y 11 kg, que presentan ictericia atribuida a la hiperemesis. Se tratan con hidratación parenteral y administración de electrolitos, y el término de los vómitos se acompaña de evolución favorable de los niveles de bilirrubina que se normalizan en cuatro semanas, y de corrección precoz de la cetonuria. Se revisa la literatura

Clinical and biochemical studies in homocystinuria.

Homocystinuria was diagnosed in 15 (0.59%) cases on screening 2560 children for aminoacidopathies. The commonest presenting features were ectopia lentis (95%) and mental retardation (86%). Other features included, dental anomalies (40%), osteoporosis (40%), behavioral problems (33%) and arachnodactyly (13%). Diagnosis was confirmed by iodoplatinate staining of one dimensional paper chromatography of urine. All the 15 cases of homocystinuria were first treated with high dose oral pyridoxine. Only one case responded to pyridoxine therapy. All the other patients were started on a low methionine, High cysteine diet with folate supplementation. Only one patient showed a complete response to dietary therapy. Nonavailability and high cost of the commercially available methionine-free, cysteine-supplemented diet and late diagnosis were responsible for the poor response in the majority of our patients.

Crisis convulsivas de difícil manejo secundarias a dependencia de piridoxina: presentación de un caso

Se presenta el caso de un lactante, con crísis clónicas inicialmente y luego tónicoclónicas que lo llevan finalmente a status epiléptico, secundarias a déficit de piridoxina. El caso debe alertar sobre la posibilidad de procesos infrecuentes, como el de este ejemplo, como causa de cuadros convulsivos de difícil manejo.

Atrofia girata de coróide e retina / Gyrate atrophy of choroid and retina

Os autores tecem comentários a respeito da atrofia girata da coróide e retina, com ênfase para os distúrbios genéticos e metabólicos como a hiperornitinemia. Apresentam um caso bastante avançado e discutem as possibilidades terapêuticas com doses elevadas de piridoxina

Efecto de la suplementación con tiamina, riboflavina y piridoxina en embarazadas del área norte de Santiago / Effect of thiamin, riboflavin and pyridoxin supplementation in pregnant women of the north area of Santiago

Con el propósito de evaluar la situación nutricional de tiamina, riboflavina y piridoxina de la embarazada y medir el impacto de una suplementación, se estudió la alimentación e indicadores bioquímicos en 40 embarazadas con índice de peso normal. En forma aleatoria fueron asignadas a un grupo control (n=21) y uno experimental (n=19) que recibió un suplemento con las vitaminas mencionadas y zinc. El consumo inicial de tiamina, piridoxina y riboflavina estuvo bajo el 75% de las recomendaciones en un porcentaje importante de las madres (22,4, 42,7 y 60,1% respectivamente) mejorando en ambos grupos en el control final. La presencia de signos que podrían atribuirse a deficiencia de vitaminas fue baja y sin diferencia entre los grupos. La deficiencia evaluada por métodos de función enzimática (transkelotasa, glutatión reductasa y glutáminico pirúvico transaminasa del glóbulo rojo) afectó en promedio al 12,5, 22,5 y 45,0% de las embarazadas para B1, B2 y B6 respectivamente. Al término del embarazo hubo una mejoría significativa sólo para B6 en el grupo suplementado (p<0,01). la baja respuesta hace recomendable utilizar un suplemento en mayor dosis y/o por períodos más prolongados