Sunday 23 February 2014

Drug Induced Liver Disease (Hepatotoxicity)-Chapter 12-TREATMENT FOR DILD Part-2

Prevention:-
The Drug-Development Process
The first opportunity to prevent hepatotoxicity arises in the early stages of drug development, when animals are exposed to a drug and assessments with regard to toxicity are made. Preclinical studies in animals are more useful for detecting dose-related, predictable hepatotoxicity than they are for detecting unpredictable hepatotoxicity in humans. Phase 1 safety studies provide the first opportunity to identify drug-related hepatotoxicity in humans. These studies are limited by their small number of participants — 12 to 30 healthy subjects — and the brief exposure of these subjects to low doses of a given drug. During efficacy testing, more patients are exposed to a drug, and the likelihood that hepatotoxicity will become evident is higher; however, the limited number of participants involved in controlled clinical trials means that a 95 percent or greater chance of even one case of a rare event occurring with a true incidence of 1 in 1000 subjects requires that almost 3000 be observed.
The case of troglitazone highlights the importance of recognizing signs of hepatotoxicity during drug development. Troglitazone was the first peroxisome-proliferator–activated receptor γ agonist approved for use in achieving blood glucose control in patients with non-insulin-dependent diabetes. During clinical trials, 12 of 2510 patients treated with troglitazone had alanine aminotransferase levels of more than 10 times the upper limit of the normal range, and 5 had levels of more than 20 times the upper limit of normal; biopsies were performed in 2 patients, including 1 in whom jaundice developed. These observations proved to be predictive of adverse events after troglitazone was marketed, when liver failure developed in 94 of the nearly 2 million patients who used the drug. Ultimately, troglitazone was withdrawn from the market, in March of 2000. This situation highlighted the need to appreciate signals that predict hepatotoxicity while a drug is being developed.
 

Figure.12.1:- A typical strategy used in drug development. A target receptor or enzyme is established on the basis of knowledge about the biology for the disease of interest. Lead compounds are developed, usually by screening procedures (sometimes by rational design). These candidates enter a series of reiterative development loops. Efficacy and selectivity testing involve pharmacological assays based on the target; developing screening and predictions involve the aspects shown at the right; design and synthesis involve more chemistry. The goal of the process is to develop candidates that are less likely to fail in the detailed later studies and the clinical trials.

Post-marketing Surveillance
         Currently, the period after a drug is approved is the most important for identifying hepatotoxicity. At present, the FDA’s MedWatch program is a good way to report suspected drug-related hepatotoxicity. This voluntary reporting system is limited in the use and adequacy of reported clinical details. Case reports that appear in the literature also draw attention to potential hepatotox-ins,  particularly substances that are not studied by the manufacturer or regulated by the FDA, such as herbal and over-the-counter complementary and alternative medications.
Monitoring of Liver tests in Clinical Practice
         There is no evidence to show that, despite instructions and warnings on drug labels, routine monitoring of liver enzymes prevents clinically significant hepatotoxicity, most of which is unpredictable and quite uncommon. Thus, an argument can be made that a more effective and efficient method of detecting and preventing hepatotoxicity would involve vigilance on the part of the patients themselves in recognizing symptoms, followed by prompt medical evaluation. Admittedly, such an approach may not apply to all drugs.
Pharmacogenomics
         Exploitation of the growing body of knowledge of genetic polymorphisms, through the field of pharmacogenomics, should revolutionize our ability to prevent hepatotoxicity. The emerging fields of proteomics and metabonomics also promise insights into the mechanisms of drug-related hep-atotoxicity.
        It has been postulated that tailoring drug therapy to individual patients may maximize therapeutic effects while minimizing hepatotoxicity, but as yet no genetic tests have come into routine clinical use.

Key Guidelines in the Recognition and Prevention of Hepatotoxicity in Clinical Practice.
Do not ignore symptoms   When a drug is being used, even vague symptoms such as nausea, anorexia, malaise, fatigue, and right upper abdominal discomfort as well as specific symptoms such as itching or jaundice should prompt consideration of hepatotoxicity. Testing for liver injury and abnormal function should be performed.
 

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