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BACKGROUND
Varenicline (VAR) has demonstrated superior efficacy over other smoking cessation pharmacotherapies, though 50-60% of those treated do maintain abstinence. Some preclinical findings suggest that new nicotine dependence pharmacotherapies should target the glutamatergic system, given its
BACKGROUND
Otosclerosis is a disorder that impairs middle ear function, leading to conductive hearing loss. Surgical treatment results in large improvement of hearing at low sound frequencies, but high-frequency hearing often suffers. A likely reason for this is that inner ear sensory cells are
BACKGROUND
Acetylcysteine prevents hepatic injury when administered soon after acetaminophen overdose. The most commonly used treatment protocols are a 72-hour oral and a 21-hour intravenous (IV) protocol. Between 1984 and 1994, 409 patients were enrolled in a study to describe the outcomes of
BACKGROUND
Nausea and vomiting associated with poisoning can complicate treatment and in some cases delay potential antidote administration. Side effect such as lowering the seizure threshold may at times discourage the use of traditional phenothiazine and butyrophenone antiemetics.
METHODS
We
BACKGROUND
Adverse effects to N-acetylcysteine (NAC) are well recognized, but their etiology and incidence are unclear.
METHODS
The nature and severity of adverse effects were prospectively studied in 169 patients and potential reaction mediators studied in 22 patients.
RESULTS
Adverse effects were
Use-result surveillance was conducted to investigate the safety and efficacy of Acetylcysteine Oral Solution 17.6 % "SENJU" having the indication for the antidote to acetaminophen (Paracetamol) overdose. Ninety six cases (patients) were collected for the safety evaluation, and 13 cases (incidence
Introduction: Anaphylactoid reactions are well-documented adverse events associated with the intravenous administration of N-acetylcysteine (NAC) in patients with acetaminophen overdose. Most reactions are mild, occurring within the first
In the absence of adequate premarketing efficacy and safety evaluations, adverse events from over-the-counter supplements are emerging as a public health concern. Specifically, bodybuilding products are being identified as a frequent cause of drug-induced liver injury. We present a case of a
We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been
We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been
BACKGROUND
Hepatitis A virus can evolve to acute liver failure with a fatal outcome if it is not reversed.
OBJECTIVE
We describe the clinical course of 12 children who presented with hepatitis A acute liver failure and received treatment with oral N-acetylcysteine (NAC).
METHODS
Of the seventy-two
Purpose: Drug-induced liver injury (DILI) that progresses to acute liver failure (ALF) has a high mortality rate, and therapeutic options are limited. Acetylcysteine has a labeled indication for use as an antidote for acetaminophen
Intravenous (IV) acetylcysteine, cysteamine, and methionine treatments were compared in patients with severe acetaminophen poisoning; a control group consisted of patients receiving supportive therapy only. Acetylcysteine proved the safest and most effective mode of treatment. Acetylcysteine was
BACKGROUND
Paracetamol (acetaminophen) is one of the most common agents deliberately ingested in self-poisoning episodes and a leading cause of acute liver failure in the western world. Acetylcysteine is widely acknowledged as the antidote of choice for paracetamol poisoning, but its use is not
The major use of N-acetylcysteine in clinical toxicology is in the treatment of acetaminophen (paracetamol) overdosage. The hepatorenal toxicity of acetaminophen is mediated by a reactive metabolite normally detoxified by reduced glutathione. If glutathione is depleted, covalent binding to