Drug toxicity peripheral neuropathy

Introduction to drug-toxic peripheral neuropathy Many drugs are neurotoxic and can cause peripheral neuropathy. The ototoxicity of aminoglycoside antibiotics is one of the most serious toxic peripheral neuropathies, which can cause severe hearing disability and has attracted the attention of the medical community. At present, new drugs are increasing, and the neurotoxic effects of some drugs cannot be confirmed in animal experiments. They need to be closely observed during clinical application, and timely detection and appropriate measures should be taken to prevent them. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: malnutrition, somatosensory disturbance

The cause of drug-induced peripheral neuropathy

(1) Causes of the disease

Most drugs are chemical poisons, mainly through the axoplasmic transport that affects neurons, leading to distal axonal atrophy and degeneration, the so-called anti-death neuronal degeneration, a few drugs such as chloroquine, amiodarone and maleic acid. Perhexiline can damage Schwann (Schwann) cells, leading to demyelinating peripheral neuropathy. The mechanism of action is that these drugs can inhibit the activity of lysosomal enzymes and affect lipid metabolism.

(two) pathogenesis

The pathological mechanism of peripheral nerve injury caused by different drugs is different. Pathological observation shows lysosomes containing fat particles in cells of various tissues, especially in Schwann cells. Peripheral neuropathy caused by drugs containing metal salts may be caused by drugs. The immune response is abnormal, in addition, isoniazid and hydralazine can interfere with the metabolism of vitamin B6, causing peripheral neuropathy similar to vitamin B6 deficiency; thalidomide (hamipazone) can inhibit vitamin B2, affecting three Carboxylic acid cycle; nitrofuran drugs can compete with thiamine phosphate to interfere with pyruvate oxidation; chloramphenicol can cause vitamin B12 deficiency, and energy metabolism and nutrient deficiency caused by these pharmacological effects are related to peripheral nerve damage.

In recent years, significant progress has been made in the study of the pathological mechanism of aminoglycoside antibiotic ototoxicity. In 1993, Fischel-Ghodsian first discovered that the ototoxicity of aminoglycoside antibiotics has genetic susceptibility, and the latter and mitochondrial DNA 1555 site AG point Related to the mutation, the gene is a 12S ribosomal RNA gene. In 1999, domestic researchers reported 48 cases of deaf patients caused by aminoglycoside antibiotics, 6 cases of mtDNA 1555 AG point mutation, screening for aminoglycosides by mtDNA analysis. Susceptibility to antibiotic ototoxicity is of great significance for the prevention and control of deafness caused by aminoglycoside antibiotics.

In addition to chloroquine, amiodarone and perhexiline (maleic acid penicillin) for demyelinating peripheral neuropathy, the remaining drug-toxic peripheral neuropathy is axonal, developing from the distal to the proximal, in retrograde Dead change.

Drug-induced peripheral neuropathy prevention

1. For drugs known to be neurotoxic, vitamins and energy mixtures should be added at the beginning of the treatment to prevent them. For example, isoniazid and vitamin B6 can avoid peripheral neurotoxic damage.

2. Implement clinical blood drug concentration testing and strictly control the dosage.

Drug-toxic peripheral neuropathy complications Complications, malnutrition, somatosensory disturbance

In patients with drug-toxic peripheral neuropathy, there may be clinical manifestations of impaired liver and kidney function and impaired blood system function.

Symptoms of Toxic Peripheral Neuropathy Common Symptoms Muscle Beating Fantasy Loss Time and... Sensory Disorder Peripheral Nerve Damage Muscle Myasthenia

Drug-induced peripheral neuropathy is insidious, most of which are distal symmetric multiple sensory neuropathy or motor-induced neuropathy. Patients present with numbness in the distal extremities and are dull. Physical examination can be seen that the feeling of the glove socks is reduced, and the depth and the sensation are affected. After the sensory disturbance occurs or at the same time, muscle weakness, muscle tension and sputum reflex can be reduced, and very few can be manifested as simple motor neuropathy. When the autonomic nerve is involved, there may be malnutrition of the distal skin, which is characterized by rough skin, thin skin, cold limbs, brittle nails, and loss of normal luster.

Examination of drug-toxic peripheral neuropathy

1. Detection of clinical pharmacy (drug concentration) in blood and urine of suspected patients.

2. Other blood tests include liver function, kidney function, rheumatism series, immunoglobulin electrophoresis and other serological tests related to autoimmunity.

3. Electromyography and neurophysiological examination.

4. Organize biopsy (including skin, sural nerve, muscle and kidney) as necessary to identify other sensory peripheral neuropathies.

Diagnosis and diagnosis of drug-toxic peripheral neuropathy

The diagnosis of this disease is mainly based on the history of medication and the clinical manifestations of peripheral neuropathy.

Differential diagnosis includes distal sympathetic sensory neuropathy and motor neuropathy for other causes.

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