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Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring 5–10 days after exposure. Symptoms often include a rash , joint pain , fever , and lymphadenopathy .
Other markers which may be measured and monitored are a complete blood count, serum liver enzymes, bilirubin levels (usually grossly elevated), kidney function, and electrolytes. Fecal fat measurement is occasionally ordered when symptoms of malabsorption (e.g., gross steatorrhea) are prominent. [citation needed]
Specific antibodies to a pathogen are thought to be the primary driver of clinical benefit from convalescent plasma. [1] In the case of viral pathogens, the subset of antibodies that retain most of the activity is the one that drives viral neutralization, i.e. neutralizing antibodies, which can be quantified in a viral neutralization assay.
Mechanism of competitive inhibition. Certain drugs share the same plasma protein, bilirubin, for transportation in the bloodstream. When drug concentration is high, they may outcompete bilirubin for binding. Bilirubin is displaced out so serum unconjugated bilirubin levels rise, resulting in unconjugated hyperbilirubinemia.
Pathological jaundice in newborns should be suspected when the serum bilirubin level rises by more than 5 mg/dL per day, serum bilirubin more than the physiological range, clinical jaundice more than 2 weeks, and conjugated bilirubin (dark urine staining clothes). Haemolytic jaundice is the commonest cause of pathological jaundice.
In medicine, a biomarker is a measurable indicator of the severity or presence of some disease state. It may be defined as a "cellular, biochemical or molecular alteration in cells, tissues or fluids that can be measured and evaluated to indicate normal biological processes, pathogenic processes, or pharmacological responses to a therapeutic intervention."
In this article, all values (except the ones listed below) denote blood plasma concentration, which is approximately 60–100% larger than the actual blood concentration if the amount inside red blood cells (RBCs) is negligible.
Alanine transaminase (ALT), also known as alanine aminotransferase (ALT or ALAT), formerly serum glutamate-pyruvate transaminase (GPT) or serum glutamic-pyruvic transaminase (SGPT), is a transaminase enzyme (EC 2.6.1.2) that was first characterized in the mid-1950s by Arthur Karmen and colleagues. [1]