Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome
We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilb...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nahum Méndez-Sánchez, MD, PhD [verfasserIn] Mariana Martínez [verfasserIn] Verónica González [verfasserIn] Ernesto Roldán-Valadez, MD [verfasserIn] Miguel A Flores, MD [verfasserIn] Misael Uribe, MD [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2002 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Annals of Hepatology - Elsevier, 2021, 1(2002), 1, Seite 40-43 |
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| Übergeordnetes Werk: |
volume:1 ; year:2002 ; number:1 ; pages:40-43 |
| Links: |
|---|
| DOI / URN: |
10.1016/S1665-2681(19)32191-X |
|---|
| Katalog-ID: |
DOAJ069007926 |
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| 520 | |a We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. | ||
| 650 | 4 | |a Bilirubin | |
| 650 | 4 | |a Zinc | |
| 650 | 4 | |a Bile salts | |
| 650 | 4 | |a Cholestasis | |
| 650 | 4 | |a Gilbert´s syndrome | |
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10.1016/S1665-2681(19)32191-X doi (DE-627)DOAJ069007926 (DE-599)DOAJbc4ee02e46a94e4689b92c16a676b676 DE-627 ger DE-627 rakwb eng RC581-951 Nahum Méndez-Sánchez, MD, PhD verfasserin aut Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. Bilirubin Zinc Bile salts Cholestasis Gilbert´s syndrome Pigmented gallstones Specialties of internal medicine Mariana Martínez verfasserin aut Verónica González verfasserin aut Ernesto Roldán-Valadez, MD verfasserin aut Miguel A Flores, MD verfasserin aut Misael Uribe, MD verfasserin aut In Annals of Hepatology Elsevier, 2021 1(2002), 1, Seite 40-43 (DE-627)DOAJ078617936 26595982 nnns volume:1 year:2002 number:1 pages:40-43 https://doi.org/10.1016/S1665-2681(19)32191-X kostenfrei https://doaj.org/article/bc4ee02e46a94e4689b92c16a676b676 kostenfrei http://www.sciencedirect.com/science/article/pii/S166526811932191X kostenfrei https://doaj.org/toc/1665-2681 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_2002 AR 1 2002 1 40-43 |
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10.1016/S1665-2681(19)32191-X doi (DE-627)DOAJ069007926 (DE-599)DOAJbc4ee02e46a94e4689b92c16a676b676 DE-627 ger DE-627 rakwb eng RC581-951 Nahum Méndez-Sánchez, MD, PhD verfasserin aut Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. Bilirubin Zinc Bile salts Cholestasis Gilbert´s syndrome Pigmented gallstones Specialties of internal medicine Mariana Martínez verfasserin aut Verónica González verfasserin aut Ernesto Roldán-Valadez, MD verfasserin aut Miguel A Flores, MD verfasserin aut Misael Uribe, MD verfasserin aut In Annals of Hepatology Elsevier, 2021 1(2002), 1, Seite 40-43 (DE-627)DOAJ078617936 26595982 nnns volume:1 year:2002 number:1 pages:40-43 https://doi.org/10.1016/S1665-2681(19)32191-X kostenfrei https://doaj.org/article/bc4ee02e46a94e4689b92c16a676b676 kostenfrei http://www.sciencedirect.com/science/article/pii/S166526811932191X kostenfrei https://doaj.org/toc/1665-2681 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_2002 AR 1 2002 1 40-43 |
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10.1016/S1665-2681(19)32191-X doi (DE-627)DOAJ069007926 (DE-599)DOAJbc4ee02e46a94e4689b92c16a676b676 DE-627 ger DE-627 rakwb eng RC581-951 Nahum Méndez-Sánchez, MD, PhD verfasserin aut Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. Bilirubin Zinc Bile salts Cholestasis Gilbert´s syndrome Pigmented gallstones Specialties of internal medicine Mariana Martínez verfasserin aut Verónica González verfasserin aut Ernesto Roldán-Valadez, MD verfasserin aut Miguel A Flores, MD verfasserin aut Misael Uribe, MD verfasserin aut In Annals of Hepatology Elsevier, 2021 1(2002), 1, Seite 40-43 (DE-627)DOAJ078617936 26595982 nnns volume:1 year:2002 number:1 pages:40-43 https://doi.org/10.1016/S1665-2681(19)32191-X kostenfrei https://doaj.org/article/bc4ee02e46a94e4689b92c16a676b676 kostenfrei http://www.sciencedirect.com/science/article/pii/S166526811932191X kostenfrei https://doaj.org/toc/1665-2681 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_2002 AR 1 2002 1 40-43 |
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10.1016/S1665-2681(19)32191-X doi (DE-627)DOAJ069007926 (DE-599)DOAJbc4ee02e46a94e4689b92c16a676b676 DE-627 ger DE-627 rakwb eng RC581-951 Nahum Méndez-Sánchez, MD, PhD verfasserin aut Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. Bilirubin Zinc Bile salts Cholestasis Gilbert´s syndrome Pigmented gallstones Specialties of internal medicine Mariana Martínez verfasserin aut Verónica González verfasserin aut Ernesto Roldán-Valadez, MD verfasserin aut Miguel A Flores, MD verfasserin aut Misael Uribe, MD verfasserin aut In Annals of Hepatology Elsevier, 2021 1(2002), 1, Seite 40-43 (DE-627)DOAJ078617936 26595982 nnns volume:1 year:2002 number:1 pages:40-43 https://doi.org/10.1016/S1665-2681(19)32191-X kostenfrei https://doaj.org/article/bc4ee02e46a94e4689b92c16a676b676 kostenfrei http://www.sciencedirect.com/science/article/pii/S166526811932191X kostenfrei https://doaj.org/toc/1665-2681 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_2002 AR 1 2002 1 40-43 |
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10.1016/S1665-2681(19)32191-X doi (DE-627)DOAJ069007926 (DE-599)DOAJbc4ee02e46a94e4689b92c16a676b676 DE-627 ger DE-627 rakwb eng RC581-951 Nahum Méndez-Sánchez, MD, PhD verfasserin aut Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome 2002 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. Bilirubin Zinc Bile salts Cholestasis Gilbert´s syndrome Pigmented gallstones Specialties of internal medicine Mariana Martínez verfasserin aut Verónica González verfasserin aut Ernesto Roldán-Valadez, MD verfasserin aut Miguel A Flores, MD verfasserin aut Misael Uribe, MD verfasserin aut In Annals of Hepatology Elsevier, 2021 1(2002), 1, Seite 40-43 (DE-627)DOAJ078617936 26595982 nnns volume:1 year:2002 number:1 pages:40-43 https://doi.org/10.1016/S1665-2681(19)32191-X kostenfrei https://doaj.org/article/bc4ee02e46a94e4689b92c16a676b676 kostenfrei http://www.sciencedirect.com/science/article/pii/S166526811932191X kostenfrei https://doaj.org/toc/1665-2681 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_2002 AR 1 2002 1 40-43 |
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Nahum Méndez-Sánchez, MD, PhD |
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Zinc sulfate inhibits the enterohepatic cycling of unconjugated bilirubin in subjects with Gilbert’s syndrome |
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We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. |
| abstractGer |
We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. |
| abstract_unstemmed |
We have previously observed that UCB binds to ZnSO4in vitro, and suppresed the biliary bilirubin secretion in the hamster. The aim of this study was designed to investigate whether Zn salts might inhibit the enterohepatic cycling of UCB in subjects with Gilbert´s syndrome. Fifteen patients with Gilbert´s syndrome and 5 normal healthy volunteers were included in this study according to the following criteria: fasting hyperbilirubinemia, no hemolysis, and free of any medication. Patients were randomly assigned to receive acute o chronic treatment. Subjects treated in acute form and normal healthy volunteers were treated with 40 mg of ZnSO4 in a single dose, where as patients treated in chronic form received 100 mg ZnSO4 in a single dose daily for 7 days. The serum UCB levels (mg/dL) decreased from 2.64 ± 1.04 to 2.02 ± 0.87 (p < 0.001) and 1.8 ± 0.36 to 1.48 ± 0.32 (p < 0.005) in subjects treated in acute an chronic form respectively, but not in the control group. Whereas, the serum Zn levels (μg/dL) increased from 96.3 ± 16.8 to 118.8 ± 19. 5, (p < 0.01) and from 117.6 ± 8.5 to 130.7 ± 6.6 (p < 0.03) in subjects treated in acute an chronic form and also in subjects in the control group (98.0 ± 7.3 to 128.0 ± 21.9) p < 0.03. This study showed that acute and chronic oral administration of ZnSO4 decreased serum UCB levels significantly in subjects with Gilbert´s syndrome. Most likely by the inhibition of the “normal” enterohepatic cycling of UCB. |
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