Liver damage caused by therapeutic vitamin A administration: Estimate of dose-related toxicity in 41 cases

Geubel, André; Galocsy, Chantal de; Alves, Niegia Graciely de Medeiros; Rahier, Jacques; Dive, Caroline

doi:10.1016/0016-5085(91)90672-8

Cited by 212 publications

(99 citation statements)

References 21 publications

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“…44 Several previous A hepatotoxicity. 40 The suppression of stromelysin and colla-studies have shown that both RA and retinol may reduce genase gene promoters by RA 41,42 may partly account for this SC proliferation both in basal conditions, [45][46][47] and following fibrosis-enhancing effect. Previously, we have observed that stimulation with growth factors involved in liver inflammanthe acyclic retinoid used in the current study reduces the tion.…”

Section: Discussionmentioning

confidence: 99%

Retinoids exacerbate rat liver fibrosis by inducing the activation of latent TGF-β in liver stellate cells

et al. 1997

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occurs during hepatic fibrosis and cirrhosis. 1,2,5 TGF-b stim-SEE EDITORIAL ON PAGE 1067 ulates SCs to transform into myofibroblast-like cells, enhances their production of extracellular matrix proteins, [1][2][3][4] Liver stellate cells (SCs) play central roles in both the stor-and alters the degradation of the extracellular matrix. 1,6 TGFage of retinol and the development of liver fibrosis. The pres-b suppresses the growth and function of hepatocytes, at least ent study is aimed to understand the mechanism by which in part, by down-regulating the production of hepatocyte retinoic acid (RA, an active metabolite of retinol) enhances growth factor in SCs. 7 hepatic fibrosis in rats. We tested the effect of 9-cis-RA on Three subtypes of TGF-b (TGF-b 1 , -b 2 , and -b 3 ), whose several aspects in vitro rat SC cultures, including the activity biological properties are nearly identical, are found in mamof cellular plasminogen activator (PA), messenger RNA malians. 8 TGF-bs are synthesized and secreted in a biologi-(mRNA), and protein levels of transforming growth factor-b cally latent form (latent TGF-b: 235-280 kd) which must be (TGF-b) mRNA level of type-I procollagen, and the activity activated before it can bind to receptors and perform biologiof type-I collagenase. Employing the rat liver fibrosis model cal activities. 8,9 Latent TGF-b 1 consists of the following three produced by porcine serum, we also estimated the effect of components: the active TGF-b 1 homodimer, the paired TGForal administration of a stable RA analog on the progression b 1 propeptide (also known as the latency-associated peptide), of the fibrosis, as well as on hepatic TGF-b contents. In vitro and the latent TGF-b 1 binding protein. The 25-kd homodi-SC cultures, 9-cis-RA enhanced cellular PA and plasmin levels meric active TGF-b is noncovalently associated with latencythereby induced plasmin-mediated activation of latent TGF-associated peptide (75 kd), and latency-associated peptide, b. Active TGF-b generated self-stimulated its synthesis as in turn, is disulfide-bonded to latent TGF-b 1 binding protein well as that of collagen and suppressed the production of (range, 135-180 kd). Activation releases the 25-kd TGF-b collagenase in an autocrine manner. In in vivo rat models, an molecule from the large complex. In vitro, the latent TGF-b RA analog accelerated the porcine serum-induced fibrosis by can be activated through physical means, such as transient enhancing TGF-b contents and, thus, collagen levels in the acidification (pH 3), which disrupts the noncovalent interacliver, although the RA analog alone was not fibrogenic. These tions between TGF-b and latency-associated peptide, 8,10 or results suggest that RA exacerbated liver fibrosis, at least in by proteases, especially plasmin, which may cleave latencypart, by inducing the activation and production of latent TGF-associated peptide within its amino-terminal region and reb in liver SCs. (HEPATOLOGY 1997;26:913-921.) lease active TGF-b. 10 Plasmin-mediated activation also occur...

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Section: Discussionmentioning

confidence: 99%

Retinoids exacerbate rat liver fibrosis by inducing the activation of latent TGF-β in liver stellate cells

et al. 1997

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“…Still, it must be remarked however that it is necessary to take a cautious approach regarding the use of liposoluble vitamins, vitamin A particularly, as high doses may have a role for instance in the pathogenesis of idiopathic intracranial hypertension 34,35 or cause liver toxicity in individuals with previous liver conditions or under chronic use of liver-metabolised medication. 36 …”

Section: Discussionmentioning

confidence: 99%

Effectiveness and safety of nutritional supplements in the treatment of hereditary retinal dystrophies: a systematic review

Brito-García

Pino-Sedeño

Trujillo-Martín

et al. 2016

Eye

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“…Protracted treatment with methotrexate 32 and in hypervitaminosis 33 are is shown to be associated with NCPF. Patients receiving irradiation and chemotherapy 34 have also been reported to have an increased risk of developing NCPF.…”

Section: Drugsmentioning

confidence: 98%

Noncirrhotic Portal Hypertension

Rajekar¹,

Vasishta²,

Chawla³

et al. 2011

Journal of Clinical and Experimental Hepatology

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Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained

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Liver damage caused by therapeutic vitamin A administration: Estimate of dose-related toxicity in 41 cases

Cited by 212 publications

References 21 publications

Retinoids exacerbate rat liver fibrosis by inducing the activation of latent TGF-β in liver stellate cells

Retinoids exacerbate rat liver fibrosis by inducing the activation of latent TGF-β in liver stellate cells

Effectiveness and safety of nutritional supplements in the treatment of hereditary retinal dystrophies: a systematic review

Noncirrhotic Portal Hypertension

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