Lactose enemas plus placebo tablets vs. neomycin tablets plus starch enemas in acute portal systemic encephalopathy

Uribe, Misael; Bérthier, Jesús Moreno; Lewis, Hilel; Mata, Juan M.; Sierra, Jose G.; Garcı́a-Ramos, Guillermo; Acosta, Javier Ramírez; Dehesa, Margarita

doi:10.1016/0016-5085(81)90658-2

Cited by 36 publications

(13 citation statements)

References 11 publications

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“…Table I also summarizes the effects of lactose enemas plus placebo tablets versus Neomycin tablets plus starch enemas (8). In this acute study, both treatments were equally effective, but stool acidification was observed only after the administration of lactose, while Neomycin did not modify the stool pH, suggesting a different mechanism of action.…”

Section: In Vivo Studies With Lactose To Treat Hepatic Encephalopathymentioning

confidence: 91%

In Vitro and In Vivo Lactose and Lactulose Effects on Colonic Fermentation and Portal-systemic Encephalopathy Parameters

Uribe¹,

Morán²,

Jl³

et al. 1997

Scandinavian Journal of Gastroenterology

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Lactose intolerance occurs in the majority of human groups, excluding people from Northern Europe. Because its effect is similar to that of lactulose, lactose seems to be an alternative treatment for patients with portal-systemic encephalopathy (PSE) and lactase deficiency. The mechanism of action of lactose is similar to that of lactulose. In vivo, lactose improves PSE parameters and causes acidic diarrhea. We performed in vitro studies in a fecal incubation system to investigate the biochemical and bacteriological effects induced by different substances customarily used for the treatment of patients with PSE (lactose, lactulose and Neomycin). In vitro experiments showed that lactose and lactulose decreased aerobic flora counts and reduced the pH of fecal incubation. Both disaccharides reduced the ammonia concentration in the incubation system.

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Section: In Vivo Studies With Lactose To Treat Hepatic Encephalopathymentioning

confidence: 91%

In Vitro and In Vivo Lactose and Lactulose Effects on Colonic Fermentation and Portal-systemic Encephalopathy Parameters

Uribe¹,

Morán²,

Jl³

et al. 1997

Scandinavian Journal of Gastroenterology

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“…Lactitol is similar to lactulose and, based on small meta-analyses of even smaller trials, it appears to be more effective [84,85]. In populations with a high prevalence of lactose intolerance, the use of lactose has been suggested [86]. Stool-acidifying enemas (lactose and lactulose) were superior to tap-water enemas in a very small study [87].…”

Section: Treatmentmentioning

confidence: 99%

Hepatic encephalopathy

Ferenci

2017

Gastroenterology Report

121

104

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Hepatic encephalopathy (HE) is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases. The precise pathophysiology of HE is still under discussion; the leading hypothesis focus on the role of neurotoxins, impaired neurotransmission due to metabolic changes in liver failure, changes in brain energy metabolism, systemic inflammatory response and alterations of the blood brain barrier. HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations. Minimal HE is diagnosed by abnormal psychometric tests. Clinically overt HE includes personality changes, alterations in consciousness progressive disorientation in time and space, somnolence, stupor and, finally, coma. Except for clinical studies, no specific tests are required for diagnosis. HE is classified according to the underlying disease, the severity of manifestations, its time course and the existence of precipitating factors. Treatment of overt HE includes supportive therapies, treatment of precipitating factors, lactulose and/or rifaximin. Routine treatment for minimal HE is only recommended for selected patients.

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“…Die bislang durchgeführten Studien sind aufgrund ihrer geringen Patientenzahlen und eines problematischen Designs ausnahmslos als fragwürdig angezweifelt worden [79]. Für Lactuloseeinläufe konnte hingegen in der Akuttherapie der HE in verschiedenen Studien eine im Vergleich zu Plazebo eindeutige Wirksamkeit nachgewiesen werden [80,81]. In dieser Phase können Lactuloseeinläufe bis zu dreimal täglich (jeweils 1-1,5 l 20-bis 50%ige Lösung) verabfolgt werden.…”

Section: Reduktion Ammoniagener Substrate Im Darm Und In Der Zirkulationunclassified

Hepatische Enzephalopathie

Hilgard

Gerken

2004

Med Klin

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Hepatic encephalopathy (HE) may develop within the course of acute or chronic liver failure and is characterized by a complex of psychomotor symptoms. In addition, HE can be induced by portocaval shunting even in the absence of any apparent liver disease. HE is caused by substances, which are either reabsorbed from the gut or are a product of the body metabolism. Normally, these substances are effectively eliminated during their first passage through the liver. However, a decreasing number of functional hepatocytes or the presence of portocaval collaterals in liver disease may significantly impair hepatic detoxification. Ammonia seems to take a central position in the pathogenesis of HE, although the exact cerebral effects of this metabolite are still not known in detail. The actual pathogenetic hypotheses are subject of this review. Depending on the underlying liver disease, HE is divided into an acute and a chronic form. Chronic HE may be present as a persistent or an episodic form, the latter being usually induced by defined precipitating factors, such as diet failures, infection and gastrointestinal-bleeding. With regard to the psychomotor symptoms and the coma depth, the clinical picture is classified into five grades (West Haven criteria). Diagnosis is made by clinical examination of the mental status after relevant differential diagnoses have been excluded. The only causal therapeutic option in the presence of acute or chronic liver failure is liver transplantation. Therefore, the indication for transplantation has to be evaluated in all forms of HE. Symptomatic treatment has three principal aims: (1) stabilization of circulation, oxygen supply, blood sugar and nutrition; (2) identification of the precipitating factor and its removal; (3) reduction of ammonia and other potential toxins in the circulation. In the case of acute HE, these therapeutic aims are complemented by an effective prophylaxis or therapy of brain edema.

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Lactose enemas plus placebo tablets vs. neomycin tablets plus starch enemas in acute portal systemic encephalopathy

Cited by 36 publications

References 11 publications

In Vitro and In Vivo Lactose and Lactulose Effects on Colonic Fermentation and Portal-systemic Encephalopathy Parameters

In Vitro and In Vivo Lactose and Lactulose Effects on Colonic Fermentation and Portal-systemic Encephalopathy Parameters

Hepatic encephalopathy

Hepatische Enzephalopathie

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