http://Gengle.bio-x.cn/SADR/ a Database Inheriting Google Technology in Presenting Genes Responsible for Serious Adverse Drug Reactions /cgi-bin/SADR/receptor.cgi?topic=rhabdomyolysis In general, the drug-induced muscle complications have been described diagnostically as myalgia (focal or diffuse muscle pain), myopathy (pain in the absence of inflammation), myositis (pain accompanied by a systemic inflammatory response) and rhabdomyolysis (severe muscle damage accompanied by damage in another organ, most notably the kidneys). /cgi-bin/SADR/receptor.cgi?topic=deafness When a medication damages the inner ear — the part of the ear responsible for receiving/sending sounds and controlling balance — it's called ototoxicity or "ear poisoning." The degree of damage to the ear depends on what type of drug is taking, how much, and for how long. Some people may have no or very minimal hearing loss and "ringing in the ears" (tinnitus), while others may experience major problems with balance and/or profound hearing loss (deafness). Factors affecting drug-induced deafness include dose, duration of therapy, concurrent renal failure, infusion rate, lifetime dose, co-administration with other drugs having ototoxic potential, and genetic susceptibility. /cgi-bin/SADR/receptor.cgi?topic=cholestasis Bile is produced in the liver, moved to the gall bladder and excreted into the gut through the biliary tract, to aid in the digestion of fats. Flow from the liver to the gall bladder and ultimately to the gut can be slowed or stopped by certain drugs. When the flow of bile is inhibited, an individual may become jaundiced (yellow coloration to the eyes and skin). Drugs which cause cholestasis (absence of flow of bile) may damage the liver. /cgi-bin/SADR/receptor.cgi?topic=tdp TdP is a potentially life-threatening form of polymorphic ventricular tachycardia. TdP is caused by drugs that prolong cardiac repolarization and is responsible for many drug withdrawals. There are a number of known risk factors for drug-induced TdP, but they currently fail to identify a significant minority of at-risk individuals. Because of the large numbers of drugs associated with TdP, genetic diagnostics could lead to substantial improvements in healthcare. /cgi-bin/SADR/receptor.cgi?topic=longqt When this SADR occurs, there is a prolongation of the QT interval on the surface electrocardiogram (ECG), often most evident on the beat(s) just before the onset of the arrhythmia; and basic scientific studies have implicated abnormal cardiac repolarization represented as the QT interval on the surface ECG. Although a series of clinical factors have been identified, the reaction in an individual patient remains unpredictable. The basic electrophysiological mechanisms in this syndrome have been established and provide a series of candidate genes for initiating genomic analysis of risk, as listed below. /cgi-bin/SADR/receptor.cgi?topic=sjs Stevens-Johnson syndrome — also called erythema multiforme major — is a rare, serious disorder of the skin and mucous membranes. Often, Stevens-Johnson syndrome begins with several days of flu-like symptoms, followed by inflammation of mucous membranes and a painful red or purplish rash that spreads and blisters, eventually causing the top layer of your skin to die and shed. Although the cause isn't always clear, Stevens-Johnson syndrome usually is a specific type of allergic reaction in response to medication or infection.