Common symptoms of diabetic peripheral neuropathy.
Diabetic peripheral neuropathy can occur even in prediabetes. It recommends that patients be screened for diabetic peripheral neuropathy when they are diagnosed with type 2 diabetes. Then patients should also receive relevant screening at least once a year. Common clinical symptoms are as follows:
Distal symmetric polyneuropathy: This lesion begins distally (finger or toe) and progresses proximally (wrist or ankle). Its clinical manifestations are acupuncture, numbness, burning, and ant line feeling in bilateral extremities. Some patients have hypoesthesia, the limbs seem to be wearing gloves or socks, and they are not sensitive to stimuli such as heat, cold, and touch. There are also patients with spontaneous skin acupuncture, burning, and even knife-like pain symptoms.
Autonomic neuropathy:
- Cardiovascular autonomic neuropathy: orthostatic hypotension, resting tachycardia, syncope, etc.
- Gastrointestinal autonomic neuropathy: hiccups, dysphagia, gastroparesis, diarrhea, constipation, etc.
- Urogenital autonomic neuropathy: urinary incontinence, urinary retention, voiding disorders, urinary tract infections, etc.
- Other autonomic neuropathy: Decreased or no sweating. Hands and feet will become dry and cracked, making them prone to infection.
Pathogenesis of diabetic peripheral neuropathy.
Its pathogenesis has not yet been fully elucidated. It is mainly considered to be related to the accumulation of sorbitol, dyslipidemia, hyperglycemia, oxidative stress, and microcirculation disorders.
The accumulation of sorbitol:
Most of the glucose is generally metabolized by the glycolysis and pentose phosphate pathways. Less than 3% of glucose is metabolized via the sorbitol bypass pathway.
When blood sugar rises uncontrollably, the level of glucose in nerve tissue and blood vessels also increases significantly. This condition causes more aldose reductase to be activated, resulting in a marked enhancement of the sorbitol pathway. Sorbitol accumulates in nerve tissue and blood vessels. The accumulation of sorbitol in nerve tissue can damage peripheral nerves.
What medications are commonly used to treat diabetic peripheral neuropathy?
Apart from improving glycemic control in patients, there is currently no effective treatment for the underlying nerve damage. Because some drugs are off-label use, doctors should use with caution.
Methylcobalamin: It is an active vitamin B12 preparation. It can enter nerve cells more easily than inactive vitamin B12 (cyanocobalamin). It promotes nerve myelination and axon regeneration. It is a drug that nourishes the nerves. Oral mecobalamin 3 times a day, 500 ΞΌg each time, for at least 3 months. If there is no effect after taking it for more than three months, there is no need to continue taking it.
Ξ±-lipoic acid: It is an antioxidant factor and acts as an anti-oxidative stress. It inhibits aldose reductase and reduces lipid oxidation in nerve tissue. Oral lipoic acid 3 times a day, 0.2g each time. Or take it orally once a day, 0.6g each time, half an hour before breakfast. The absorption of lipoic acid is affected by food, so it should not be taken with food.
Epalrestat: It is a drug that inhibits aldose reductase activity. It prevents sorbitol from building up in the nerves, improving nerve conduction velocity and symptoms caused by diabetic neuropathy. Epalrestat is taken orally three times a day, 50 mg each time, before meals. If epalrestat is not effective for more than 3 months, it is not necessary to continue taking it. In addition, the patient's urine may appear brownish-red after taking it, which is normal.
Pancreatic kininogenase enteric-coated tablet: Plasmin is activated by it and reduces blood viscosity. It also activates phospholipase A2, preventing thrombosis and platelet aggregation. It can improve the microcirculation of the body. Pancreatic kininogenase enteric-coated tablet is to be taken 120 to 240 units 3 times daily on an empty stomach. Since it is an enteric-coated tablet, it needs to be swallowed whole to prevent it from being destroyed in the stomach.
Pregabalin: It binds to calcium channels in the central nervous system. It reduces the release of calcium channels in the central nervous system, thereby inhibiting central sensitization and hyperalgesia. This can reduce pain. The initial dose of pregabalin is 150 mg daily in 2 to 3 divided doses, with subsequent dose adjustments to 300 to 600 mg daily. Its common side effects are drowsiness and dizziness. In addition, it can cause weight gain and the patient's dosage of antidiabetic drugs may need to be adjusted.
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