Glutathione, our body's most powerful weapon.: Toxins in Medications

Wednesday 11 September 2013

Toxins in Medications

Toxins, poisons and chemicals can cause peripheral neuropathy. This can happen through drug or chemical abuse or through exposure to industrial chemicals in the workplace or in the environment (after either limited or long-term exposure). Common causes include: exposure to lead, mercury, arsenic and thalium. Some organic insecticides and solvents can result in neuropathies. Sniffing glue or other toxic compounds can also cause peripheral neuropathy. Certain herbal medicines, especially Chinese herbal medicines, are particularly rich in mercury and arsenic and taking them can lead to peripheral neuropathy.

Because patients may have subtle pain or weakness, it may be difficult to arrive at a specific diagnosis of toxic neuropathy.

SYMPTOMS AND SIGNS

(Not all symptoms and signs may be present.)

In feet:

Pain
Tingling
Numbness

Other symptoms:

Weakness
Difficulty walking

Specific drug or toxin

Acetaminophen

Main article: Acetaminophen toxicity

Acetaminophen (3D structure) overdose is the most common cause of drug-induced liver disease

Acetaminophen (paracetamol, also known by the brand name Tylenol and Panadol) is usually well tolerated in prescribed dose, but overdose is the most common cause of drug-induced liver disease and acute liver failure worldwide.Damage to the liver is not due to the drug itself but to a toxic metabolite (N-acetyl-p-benzoquinone imine NAPQI, or NABQI) produced by cytochrome P-450 enzymes in the liver. In normal circumstances, this metabolite is detoxified by conjugating with glutathione in phase 2 reaction. In an overdose, a large amount of NAPQI is generated, which overwhelms the detoxification process and leads to liver cell damage. Nitric oxide also plays a role in inducing toxicity.The risk of liver injury is influenced by several factors including the dose ingested, concurrent alcohol or other drug intake, interval between ingestion and antidote, etc. The dose toxic to the liver is quite variable from person to person and is smaller in chronic alcoholics.Measurement of blood level is important in assessing prognosis, higher levels predicting a worse prognosis. Administration of Acetylcysteine, a precursor of glutathione, can limit the severity of the liver damage by capturing the toxic NAPQI. Those that develop acute liver failure can still recover spontaneously, but may require transplantation if poor prognostic signs such as encephalopathy or coagulopathy is present (see King's College Criteria).

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Although individual analgesics rarely induce liver damage due to their widespread use, NSAIDs have emerged as a major group of drugs exhibiting hepatotoxicity. Both dose-dependent and idiosyncratic reactions have been documented. Aspirin and phenylbutazone are associated with intrinsic hepatotoxicity; idiosyncratic reaction has been associated with ibuprofen, sulindac, phenylbutazone, piroxicam, diclofenac and indomethacin.

Glucocorticoids

Glucocorticoids are so named due to their effect on the carbohydrate mechanism. They promote glycogen storage in the liver. An enlarged liver is a rare side-effect of long-term steroid use in children.The classical effect of prolonged use both in adult and paediatric population is steatosis.

Isoniazid

Isoniazide (INH) is one of the most commonly used drugs for tuberculosis; it is associated with mild elevation of liver enzymes in up to 20% of patients and severe hepatotoxicity in 1-2% of patients.