Table 1.
Classification methods for adverse drug reactions.
| Thomson and Rawlins | Type A (Augmented) | Type B (Bizarre) | Type C (Continuing) | Type D (Delayed) | Type E (End-of-Use) | Type F (Failure) |
|---|---|---|---|---|---|---|
| Response to drugs administrated at therapeutic doses being the result of an abnormal response of an otherwise normal pharmacological effect. | Unrelated to the pharmacodynamics or the dosage of the drug and are often fatal. These are less common, and so may only be discovered for the first time after a drug has already been made available for general use. |
Related to the cumulative dose of a long-term pharmacological treatment. | Consequence to the timing of a treatment and become apparent sometime after the use of a medicine. | Associated to the withdrawal of a given medicine. | Occurring when a therapy appears futile. | |
| Dose, Time and Susceptibility (DoTS) | Relation to Dose (Do) | Time Course (T) | Susceptibility Factors (S) | |||
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| EIDOS | Extrinsic chemical species (E) | Intrinsic chemical species (I) | Distribution (D) | Outcome (O) | Sequelae (S) | |
| This can be the parent compound, an excipient, a contaminant or adulterant, a degradation product or a derivative of any of these. | This is usually the endogenous molecule with which the extrinsic species interacts; this can be a nucleic acid, an enzyme, a receptor, an ion channel or transporter or some other protein. | A drug will not produce an adverse effect if it is not distributed to the same site as the target species that mediates the adverse effect. Thus, the pharmacokinetics of the extrinsic species can affect the occurrence of adverse effects. | Interactions between extrinsic and intrinsic species in the production of an adverse effect can result in physiological or pathological changes. | The sequela of the changes induced by a drug describes the clinically recognizable adverse drug reaction, of which there may be more than one. | ||