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• [Effect of fluorine, selenium and cadmium on lipid peroxide and microelements in rat's testicle]
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Example Content from MEDITEXT for 7439-89-6:


Please note: this is an extract of information from a larger document. Full document and details are available by subscription.

ACUTE EXPOSURE INFORMATION

  1. USES: Found primarily as a nutritional supplement in vitamins. Used for the treatment and prevention of iron-deficiency anemia.
  1. PHARMACOLOGY: Iron is required in the function of multiple essential protein and enzyme complexes including hemoglobin, myoglobin, and cytochromes.
  1. TOXICOLOGY: Iron is a general cellular poison and is directly corrosive to the GI mucosa.
  1. EPIDEMIOLOGY: Historically, a common poisoning which was one of the leading causes of pediatric toxicologic deaths. Exposure has been reduced in recent years with improved packaging, but still has the potential for significant morbidity and mortality.
  1. WITH THERAPEUTIC USE
    1. ADVERSE EFFECTS: GI upset, constipation.
  1. WITH POISONING/EXPOSURE
    1. MILD TO MODERATE POISONING: Vomiting and diarrhea may occur within 6 hours of ingestion.
    1. SEVERE POISONING: Severe vomiting and diarrhea, lethargy, metabolic acidosis, shock, GI hemorrhage, coma, seizures, hepatotoxicity, and late onset GI strictures.
    1. CLINICAL COURSE (May Not Occur In All Cases) includes the following:
      1. PHASE I (0.5 to 2 hours) includes vomiting, hematemesis, abdominal pain, diarrhea, hematochezia, lethargy, shock, acidosis, and coagulopathy. Necrosis to the GI tract occurs from the direct effect of iron on GI mucosa. Severe gastrointestinal hemorrhagic necrosis with large losses of fluid and blood contribute to shock.
      1. PHASE II includes apparent recovery; continue to observe patient closely.
      1. PHASE III (2 to 12 hours after phase I) includes profound shock, severe acidosis, cyanosis, and fever. Increased total peripheral resistance, decreased plasma volume, hemoconcentration, decrease in total blood volume, hypotension, CNS depression, and metabolic acidosis have been demonstrated.
      1. PHASE IV (2 to 4 days) includes possible hepatotoxicity. Thought to be a direct action of iron on mitochondria. Monitor liver function tests and bilirubin. Acute lung injury may also occur.
      1. Phase V (days to weeks) includes GI scarring and strictures. GI obstruction secondary to gastric or pyloric scarring may occur due to corrosive effects of iron. Sustained-release preparations have resulted in small intestinal necrosis with resultant scarring and obstruction.
    1. Carbonyl iron (also referred to as "iron carbonyl") appears to be less toxic than other iron formulations because of limited absorption. Please refer to the CARBONYL IRON management for further information.
    1. Case reports suggest that iron-dextran complex overdoses may be associated with high serum iron concentrations without evidence of a corresponding degree of clinical symptoms and signs of toxicity. Please refer to the IRON DEXTRAN management for further information.
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