Eosinophilia an elevated level of the eosinophils of the body. Eosinophils are the type of immune cell thats job is to fight off parasitic invaders. Jaundice yellowing of the skin, eyes and mucous membranes due to an impaired ability of the body to clear the by product of haem breakdown, bilirubin, most often the result of liver damage as it is the livers responsibility to clear bilirubin.It tends to produce less anticholinergic effects, sedation and weight gain than some of the earlier TCAs (e.g. amitriptyline, clomipramine, doxepin, imipramine, trimipramine). It may also be less cardiotoxic than its predecessors. Overdose
It is considered particularly toxic in overdose, with a high rate of renal failure (which usually takes 2–5 days), rhabdomyolysis, coma, seizures and even status epilepticus. Some believe it to be less cardiotoxic than other TCAs in overdose, although reports of cardiotoxic overdoses have been made. Pharmacology
Pharmacodynamics
Amoxapine possesses a wide array of pharmacological effects. It is a moderate and strong reuptake inhibitor of serotonin and norepinephrine, respectively, and binds to the 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3, 5-HT6, 5-HT7, D2, α1-adrenergic, D3, D4, and H1 receptors with varying but significant affinity, where it acts as an antagonist (or inverse agonist depending on the receptor in question) at all sites. It has weak but negligible affinity for the dopamine transporter and the 5-HT1A, 5-HT1B, D1, α2-adrenergic, H4, mACh, and GABAA receptors, and no affinity for the β-adrenergic receptors or the allosteric benzodiazepine site on the GABAA receptor.
The parents of a child with an autosomal recessive disorder are carriers of one copy of the defective gene, but are usually not affected by the disorder.The prevalence of mutations associated with this condition reach 68% to 81% in certain arctic coastal populations, suggesting that the condition had some adaptive value in those habitats at some time. Fewer than 50 people have been identified with this condition. Diagnosis
Genetic testing is necessary for diagnosis. Differential diagnosis
This condition is sometimes mistaken for fatty acid and ketogenesis disorders such as Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD), other long-chain fatty acid oxidation disorders such as Carnitine palmitoyltransferase II deficiency (CPT-II) and Reye syndrome. Treatment
Treatment for this condition is supportive. There is no cure. Affected people should eat a high-carbohydrate, low-fat diet and avoid fasting. See also
Primary carnitine deficiency
Carnitine palmitoyltransferase II deficiency

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This article incorporates public domain text from The U.S. National Library of Medicine