Metabolic function and liver histopathology in Reye‐like illnesses

Jw, Hou; Sp, Chou; Tr, Wang

doi:10.1111/j.1651-2227.1996.tb14216.x

Cited by 19 publications

(9 citation statements)

References 17 publications

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“…As previously reported, as well as salycilates, some other drugs are also involved in Reye's syndrome, in valproic acid, an anti-epilectic drug, 39 pivampicilline, tetracycline, zidovudine 22 and various anti-neoplastic drugs. 40 Moreover non-steroidal anti-inflammatory drugs such as sodium diclofenac and mephenamic acid can produce or aggravate Reye's syndrome.…”

Section: Drugs and Chemical Productsmentioning

confidence: 76%

Reye's and Reye's‐like syndromes

Pugliese

Beltramo

Torre³

2008

Cell Biochemistry & Function

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The review reports various questions about Reye's syndrome and Reye's-like syndromes. Although there is a significant decrease in the classic Reye's syndrome cases, because of the reduced employment of salicylates in children (salicylate seems to be the most important inducing factor of the syndrome in paediatric subjects affected by viral infection), the problem is still of interest considering the presence of different Reye's-like forms. All these pathological situations are associated with various aetiologic or predisposing causes that are examined in the text. Particular attention is placed on metabolic disorders, especially of fatty acid metabolism, and also of one amino acid. In fact, a latent form can also be the basis of possible biochemical disturbances induced by various exogenous factors such as viral infections, particularly of the respiratory tract (more rarely of bacterial aetiology), or produced by microbial toxins, or by chemical substances, including some therapeutic drugs. A full discussion of biochemical mechanisms of salicylate-induced Reye's syndrome is reported. Finally a possible diagnostic differentiation from classic Reye's syndrome and Reye's-like syndromes plus therapeutic prospects are briefly examined.

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Section: Drugs and Chemical Productsmentioning

confidence: 76%

Reye's and Reye's‐like syndromes

Pugliese

Beltramo

Torre³

2008

Cell Biochemistry & Function

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“…Many children with metabolic disorders present with Reye-like syndrome episodes, usually at a young age and/or with a positive past or family history suspicious for an inborn error of metabolism [11]. It has been reported as a presenting sign of type I 3-MGC aciduria and in a few cases of mitochondrial cytopathies in older children [12,13]. However in the neonatal period, a Reye-like episode is not a typical presenting feature of a mitochondrial cytopathy.…”

Section: Discussionmentioning

confidence: 99%

Neonatal presentation of ventricular tachycardia and a Reye-like syndrome episode associated with disturbed mitochondrial energy metabolism

et al. 2002

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BackgroundHyperammonemia, hypoglycemia, hepatopathy, and ventricular tachycardia are common presenting features of carnitine-acylcarnitine translocase deficiency (Mendelian Inheritance in Man database: *212138), a mitochondrial fatty acid oxidation disorder with a lethal prognosis. These features have not been identified as the presenting features of mitochondrial cytopathy in the neonatal period.Case presentationWe describe an atypical presentation of mitochondrial cytopathy in a 2 day-old neonate. She presented with a Reye-like syndrome episode, premature ventricular contractions and ventricular tachycardia. Initial laboratory evaluation exhibited a large amount of 3-methylglutaconic acid on urine organic acid analysis, mild orotic aciduria and a nonspecific abnormal acylcarnitine profile. The evaluation for carnitine-acylcarnitine translocase deficiency and other fatty acid oxidation disorders was negative. The patient later developed a hypertrophic cardiomyopathy and continued to be affected by recurrent Reye-like syndrome episodes triggered by infections. A muscle biopsy exhibited signs of a mitochondrial cytopathy. During the course of her disease, her Reye-like syndrome episodes have subsided; however, cardiomyopathy has persisted along with fatigue and exercise intolerance.ConclusionsThis case illustrates that, in the neonatal period, hyperammonemia and ventricular tachycardia may be the presenting features of a lethal carnitine-acylcarnitine translocase deficiency or of a mitochondrial cytopathy, associated with a milder clinical course. This association broadens the spectrum of presenting phenotypes observed in patients with disturbed mitochondrial energy metabolism. Also, the presence of 3-methylglutaconic aciduria suggests mitochondrial dysfunction and mild orotic aciduria could potentially be used as a marker of mitochondrial disease.

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“…We noticed that the clinical history of LCMV-induced steatosis has several features in common with virus-induced microvesicular steatosis in humans, i.e., classical Reye's syndrome, an apparently virus-triggered, acute liver failure and encephalopathy in children hallmarked by similar light and electron microscopical findings in the liver (16,24). Indeed, the requirement for CCR5 also seems to vary according to age in a herpes simplex model of liver inflammation (3).…”

Section: Fig 8 Elimination Of Cd8mentioning

confidence: 99%

“…6B). This sign of mitochondrial dysfunction is often found under conditions of microvesicular steatosis associated with inflammation (16,24,25).…”

Section: Profound Microvesicular Steatosis In Infected Ccr5mentioning

confidence: 99%

CCR5 and CXCR3 Are Dispensable for Liver Infiltration, but CCR5 Protects against Virus-Induced T-Cell-Mediated Hepatic Steatosis

Holst

Ørskov

Qvortrup

et al. 2007

J Virol

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CCR5 and CXCR3 are important molecules in regulating the migration of activated lymphocytes. Thus, the majority of tissue-infiltrating T cells found in the context of autoimmune conditions and viral infections express CCR5 and CXCR3, and the principal chemokine ligands are expressed within inflamed tissues. Accordingly, intervention studies have pointed to nonredundant roles of these receptors in models of allograft rejection, viral infection, and autoimmunity. In spite of this, considerable controversy exists, with many studies failing to support a role for CCR5 or CXCR3 in disease pathogenesis. One possible explanation is that different chemokine receptors may take over in the absence of any individual receptor, thus rendering individual receptors redundant. We have attempted to address this issue by analyzing CCR5 ؊/؊ , CXCR3 ؊/؊ , and CCR5/CXCR3 ؊/؊ mice with regard to virus-induced liver inflammation, generation and recruitment of effector cells, virus control, and immunopathology. Our results indicate that CCR5 and CXCR3 are largely dispensable for tissue infiltration and virus control. In contrast, the T-cell response is accelerated in CCR5 ؊/؊ and CCR5/CXCR3 ؊/؊ mice and the absence of CCR5 is associated with the induction of CD8 ؉ T-cell-mediated immunopathology consisting of marked hepatic microvesicular steatosis.Chemokines play a key role in virus-induced inflammation and virus clearance, acting as regulators of leukocyte trafficking (18,49). Among the chemokine receptors, CCR5 has drawn considerable attention as the main coreceptor for human immunodeficiency virus and CXCR3 is a promising target for antiinflammatory therapeutics (41, 52). Notably, both receptors have been associated with type 1 cytokine T-cell responses and the majority of tissue-infiltrating T cells in several human inflammatory diseases are found to coexpress these receptors (7,42,48). During viral infection, CCR5 and CXCR3 are expressed on NK cells and activated CD4 ϩ and CD8 ϩ T cells and the ligands are generally expressed in virus-infected tissues (30,38,50). Further support for the important role of CCR5 and CXCR3 comes from the existence of virally encoded chemokine receptor antagonists targeting these receptors (23,27). In this context, it is not surprising that CXCR3 or its ligands have been experimentally demonstrated to be important for immune-mediated virus control in the central nervous system (CNS), the lungs, the ovaries, and the islet of Langerhans in the pancreas (9,15,20,26,51). In contrast, despite the suggestive expression patterns, several studies have indicated that CCR5 or CCR5 ligands are less important in antiviral immunity (30, 37). The positive findings suggest a role for CCR5 in macrophage and CD4 ϩ T-cell recruitment, but the receptor appears not to be required for CD8 ϩ T-cell migration except in young mice, in which the immune system has not yet reached full maturity (3, 17). The reason for this difference between the two receptors could lie in a difference in biological redundancy.Thus, several CCR5 ...

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Metabolic function and liver histopathology in Reye‐like illnesses

Cited by 19 publications

References 17 publications

Reye's and Reye's‐like syndromes

Reye's and Reye's‐like syndromes

Neonatal presentation of ventricular tachycardia and a Reye-like syndrome episode associated with disturbed mitochondrial energy metabolism

CCR5 and CXCR3 Are Dispensable for Liver Infiltration, but CCR5 Protects against Virus-Induced T-Cell-Mediated Hepatic Steatosis

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