Treatment of neonatal hyperbilirubinemia with repetitive oral activated charcoal as an adjunct to phototherapy

Amitai, Yona; Regev, Mordehai; Arad, Ilan; Peleg, Ophra; Boehnert, Mark

doi:10.1515/jpme.1993.21.3.189

Cited by 10 publications

(3 citation statements)

References 19 publications

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“…[2][3][4] Many interventions have been done for the treatment and prevention of neonatal hyperbilirubinemia. These includes phototherapy (causes photo isomerization of bilirubin into a water-soluble form Lumirubin that can be excreted by the kidneys and stool), 5 metalloporphyrins (inhibit heme-oxygenase, the rate-limiting enzyme in the catabolism of heme to bilirubin), 6 oral agar (decreases enterohepatic circulation of bilirubin by causing increased absorption of excreted bilirubin by liver and promoting its removal from body), 7 clofibrate (Glucuronosyl transferase inducer that increases the elimination of bilirubin in neonates with hyperbilirubinemia), 8 zinc (decreases enterohepatic circulation of bilirubin), 9 activated charcoal (binds bilirubin in the intestinal lumen and reduce the enterohepatic circulation of unconjugated bilirubin), 10,11 prophylactic phenobarbitone (induction of Glucuronosyl transferase enzyme), [12][13][14] prebiotic supplementation (increases gastrointestinal motility, increases stool frequency and decreases viscosity of stool, decreases enterohepatic circulation, improves feeding tolerance and growth of beneficial bacteria in the gut), 15,16 intravenous immunoglobulin in case of isoimmunisation (blocks the cell receptors of susceptible red blood cells) 17 , fluid supplementation with phototherapy (helps in excretion of J U S T A C C E P T E D photoproducts because of phototherapy through both urine and bile and also overcomes increased insensible water loss and stool water loss) 18,19 and exchange transfusion (removes bilirubin from blood). [20][21][22] With the advent of phototherapy lights the use of other intervention has gone out of use in nurseries.…”

Section: Introductionmentioning

confidence: 99%

Role of oral zinc supplementation for reduction of neonatal hyperbilirubinemia: a systematic review of current evidence

Sharma

Farahbakhsh

Sharma

et al. 2016

The Journal of Maternal-Fetal & Neonatal Medicine

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Role of zinc in the prevention of neonatal hyperbilirubinemia is not supported by the current evidence. Only one study was able to show reduction in the mean TSB level and requirement of phototherapy with zinc, and the remaining studies did not report any positive effect. None of the studies showed any effect on the duration of phototherapy, incidence of phototherapy, age of starting of phototherapy and any serious adverse effect.

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Section: Introductionmentioning

confidence: 99%

Role of oral zinc supplementation for reduction of neonatal hyperbilirubinemia: a systematic review of current evidence

Sharma

Farahbakhsh

Sharma

et al. 2016

The Journal of Maternal-Fetal & Neonatal Medicine

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“…19,20 In Crigler-Najjar patients, however, the effects of CaP treatment were less pronounced. 7 Other capturing agents like agar, 21 activated charcoal, 22 and cholestyramine 23 are no longer used for the treatment of unconjugated hyperbilirubinemia because of inconsistent clinical results and side effects. [24][25][26] More recently, zinc salts were shown to decrease plasma bilirubin levels in patients with Gilbert syndrome, but serum zinc levels increased simultaneously.…”

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confidence: 99%

Effective oral treatment of unconjugated hyperbilirubinemia in Gunn rats†

et al. 2005

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We sought to develop an oral treatment for unconjugated hyperbilirubinemia. In the Gunn rat model of unconjugated hyperbilirubinemia, dietary supplementation with the lipase inhibitor orlistat (Orl) or with calcium phosphate (CaP) decreases plasma unconjugated bilirubin (UCB) levels. We determined whether Orl, CaP, or their combination is superior to phototherapy, the conventional treatment, and whether the effects of Orl and CaP are influenced by dietary fat content. Gunn rats were treated with Orl (200 mg/kg chow), CaP (20 g/kg chow), Orl ؉ CaP, or continuous phototherapy (19 W/cm 2 /nm) during a low-fat (LF) diet (13 energy%) or high-fat (HF) diet (35 energy%). Plasma UCB and fecal fat excretion were measured before, during, and/or at the end of treatment. Orl treatment for 2 weeks (HF diet) reduced plasma UCB concentrations similar to phototherapy (؊34% and ؊28%, respectively); the combination of both was more effective than either treatment alone (؊48%; P < .001). After 3 weeks of a HF diet, plasma UCB was 46% lower compared with the LF diet (P < .001). Plasma UCB concentrations were negatively correlated with fecal fat excretion (r ‫؍‬ ؊0.96; P < .001). Irrespective of dietary fat content, 3 weeks of combined treatment (Orl ؉ CaP) decreased plasma UCB by approximately 50% (P < .01) and was more effective than phototherapy (P < .05) at the intensity provided. C rigler-Najjar disease is characterized by a permanent unconjugated hyperbilirubinemia due to absent (type I) or decreased (type II) activity of the hepatic enzyme bilirubin-UDP-glucuronosyltransferase. 1 Severe unconjugated hyperbilirubinemia can lead to bilirubin encephalopathy, kernicterus, and death. 2,3 Phenobarbital treatment can usually control unconjugated hyperbilirubinemia in Crigler-Najjar type II patients via residual enzyme induction. 4,5 Phenobarbital is not effective in Crigler-Najjar disease type I, however, so these patients have to undergo daily phototherapy, which has considerable disadvantages. Phototherapy becomes less effective with age, probably due to skin alterations, 6,7 a decrease in the surface area to body mass ratio, 8 and a diminishing compliance to the intensive phototherapy regimen, which may take up to 12 hours per day. 6 To prevent irreversible brain damage due to kernicterus, many patients with CriglerNajjar disease type I undergo liver transplantation in their second decade. 9,10 We sought to develop an alternative treatment for unconjugated hyperbilirubinemia based on oral administration and with equal or higher efficacy than phototherapy. The oral treatment strategy used in the present study is based on reducing the reabsorption of UCB 11,12 through intestinal capture. Reabsorption of UCB can contribute substantially to the pathogenesis

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“…Past attempts to decrease the extensive EHC of UCB have involved oral administration of agents that either trap UCB in the intestinal lumen by adsorption to non-absorbable solids (e.g. agar [27], activated charcoal [28] or cholestyramine [29]), or form insoluble bilirubinate salts Ca CC [30] or Zn CC [31]. All these agents have been effective in animal models of unconjugated hyperbilirubinemia, especially if combined with phototherapy.…”

Section: See Article Pages 238-243mentioning

confidence: 99%

Intestinal flora and bilirubin

Tiribelli

Ostrow

2005

Journal of Hepatology

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Treatment of neonatal hyperbilirubinemia with repetitive oral activated charcoal as an adjunct to phototherapy

Abstract: Amitai et al, Charcoal therapy for neonatal hyperbilirubinemia 189 j. Pennai. Med. Treatment of neonatal hyperbilirubinemia with repetitive oral 21 (1993) 189-194 activated charcoal as an adjunct to phototherapy

Cited by 10 publications

References 19 publications

Role of oral zinc supplementation for reduction of neonatal hyperbilirubinemia: a systematic review of current evidence

Role of oral zinc supplementation for reduction of neonatal hyperbilirubinemia: a systematic review of current evidence

Effective oral treatment of unconjugated hyperbilirubinemia in Gunn rats†

Intestinal flora and bilirubin

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