cholestasis/seizures

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Seizure susceptibility alteration following reversible cholestasis in mice: Modulation by opioids and nitric oxide.

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There is an increasing body of evidence that the central nervous system is affected by cholestatic liver disorders. Cholestasis has been shown to result in a decreased seizure propensity which is believed to be mediated by an increased opioidergic tone and nitric oxide (NO) signaling pathway. In

Cholestasis and seizure due to lead toxicity: a case report.

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BACKGROUND Lead poisoning is a major public health risk which may involve major organs. Recently, there have been reports of opioid adulteration with lead in Iran. The following case report is the first of its kind in that intrahepatic cholestasis due to lead toxicity has been described. METHODS A

Case reports: cocktail dosing in a premature infant with a history of cholestasis, seizures, and apnea; treatment of labial adhesions in a child.

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Preoperative observations and short-term outcome after partial external biliary diversion in 13 patients with progressive familial intrahepatic cholestasis.

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BACKGROUND Patients with progressive familial intrahepatic cholestasis (PFIC) often require liver transplantation to survive. An alternative approach is surgical diversion of bile, that is, partial external biliary diversion (PEBD). The aim of the study was to describe 13 patients with PFIC who have

Isolated deficiency of glucocorticoids presenting with cholestasis.

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BACKGROUND Isolated deficiency of glucocorticoids is characterized by elevated levels of adrenocorticotropin (ACTH) and normal aldosterone production. It is rare for isolated deficiency of glucocorticoids to be associated with liver involvement. A case of an infant with isolated deficiency of

Elevation of pentylenetetrazole-induced seizure threshold in cholestatic mice: interaction between opioid and cannabinoid systems.

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OBJECTIVE Several studies have reported that endogenous opioid and cannabinoid systems may be involved in some pathophysiological changes occurring in cholestatic liver disease. It is well known that endogenous opioids and cannabinoids alter the susceptibility of experimental animals to different

Effect of metal chelating agents on pentylenetetrazole-induced seizure threshold in cholestatic mice.

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Zinc has been proven to be anticonvulsant in several studies which indicate that diphenylthiocarbazone (dithizone) and diethyldithiocarbamate (DEDTC), zinc chelating agents, enhance seizure activities. There is also evidence that nitric oxide (NO) generators increase zinc concentration in the brain.

The additive effect of opioids and nitric oxide in increasing pentylenetetrazole-induced seizure threshold in cholestatic mice.

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BACKGROUND Accumulation of endogenous opioids and overproduction of nitric oxide has been reported in cholestatic mice. It is well known that endogenous opioids and nitric oxide alter the susceptibility of experimental animals to different models of seizure. METHODS The alterations in clonic seizure

Vitamin K-deficient intracranial hemorrhage as the first symptom of cytomegalovirus hepatitis with cholestasis.

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Since vitamin K2 (VitK2) syrup prophylaxis has become a routine measure for neonates and young infants, the incidence of vitamin K deficiency (VitK-D) in infancy has markedly decreased. However, we recently experienced 2 infantile cases of VitK deficiency, in whom intracranial hemorrhage (ICH) was

[Chronic cholestatic liver disease and grand mal seizures].

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METHODS A 48-year-old woman was hospitalised because of grand-mal seizures. 3 years previously a malignant melanoma had been resected from the skin of the back. She was also known to have chronic cholestasis of unknown cause. On physical examination there were postictal signs, but no neurological

Vitamin D deficiency associated with dilated cardiomyopathy in early infancy caused by maternal cholestasis.

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Breast feeding is known to be a major cause of vitamin D deficiency in infants because the content of vitamin D in breast milk is significantly lower than that in formula. We report a case of a 1-mo-old boy who developed hypocalcemic seizures and dilated cardiomyopathy caused by vitamin D deficiency

Congenital Isolated ACTH Deficiency Caused by TBX19 Gene Mutation: A Family Report.

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Congenital isolated adrenocorticotropic hormone deficiency (CIAD) is a rare disorder that may be conducive to hypoglycemia, cholestasis, and seizures. We reported on two siblings with a homozygous mutation of the TBX19 gene, C.377 (exon2) C>T, p. P126L. Their parents had heterozygous

Novel Melanocortin 2 Receptor Variant in a Chinese Infant With Familial Glucocorticoid Deficiency Type 1, Case Report and Review of Literature.

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Familial glucocorticoid deficiency type 1 (FGD1) is an autosomal recessive disorder caused by mutations in the melanocortin 2 receptor (MC2R) gene, characterized by a low or undetectable serum cortisol level and a high adrenocorticotropic hormone (ACTH) level. Clinical manifestations include

Neuromuscular complication after liver transplant in children: a single-center experience.

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OBJECTIVE Neurologic complications are a significant cause of morbidity in children after liver transplant. In this study, we sought to evaluate the neurologic complications in children after liver transplant. METHODS All children aged younger than 18 years old who had undergone liver transplant

Jaundice and hepatic enzyme induction during lamotrigine therapy in a bipolar II patient.

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Lamotrigine is a novel mood stabiliser as well as an anti-epileptic drug that has already been used for the prevention of convulsions. Despite several known side effects, hepatic dysfunction related to the drug has not been widely reported. A few cases have been observed in neurological, especially

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