Indication:
For the treatment of chloroquine sensitive falciparum malaria, vivax malaria and three day malaria. It can also be used for the inhibitory prevention of malaria symptoms. It can also be used in the treatment of extraintestinal amoebiasis, connective tissue disease, photosensitive diseases (such as sun erythema), etc.
Adverse reactions:
1. When this product is used in the treatment of malaria, there are few adverse reactions. Generally, the possible oral reactions include dizziness, headache, dizziness, loss of appetite, nausea, vomiting, abdominal pain, diarrhea, pruritus, rash, even exfoliative dermatitis, tinnitus, irritability, etc. Most of the reactions were mild and disappeared spontaneously.
2. In the treatment of paragonimiasis, clonorchiasis and connective tissue diseases, the dosage is large, the course of treatment is long, and there may be severe reactions. The common one is ocular toxicity, because chloroquine can be secreted by lacrimal gland and absorbed by cornea, and diffuse white particles appear on cornea, which can disappear after withdrawal.
3. A considerable part of this product accumulates in the tissue. Long term use can cause mild retinal edema and pigment accumulation, dark spots appear, and affect vision. It is often irreversible.
4. Chloroquine can also damage hearing, pregnant women take a lot can cause children congenital deafness, mental retardation, hydrocephalus, limb defects.
5. Chloroquine can cause inhibition of sinoatrial node, lead to arrhythmia, shock, and even death.
6. This product can also cause drug-induced psychosis, leukopenia, purpura, rash, dermatitis, photosensitive dermatitis, even exfoliative dermatitis, psoriasis, hair whitening, hair removal, neuromuscular pain, mild transient headache, etc.
7. Hemolysis, aplastic anemia, reversible agranulocytosis and thrombocytopenia are rare.
Matters needing attention:
1. Patients with liver and kidney dysfunction, heart disease, severe erythema multiforme, hematoporphyria, psoriasis and psychosis should be cautious.
2. This product can cause fetal hydrocephalus, limb deformity and deafness, so it is forbidden for pregnant women.
3. The effect of chloroquine resistance is not good.
Drug interactions:
1. It is easy to cause allergic dermatitis when used together with butazone.
2. Combined with chlorpromazine, it is easy to increase the burden of liver;
3. This product has direct inhibitory effect on neuromuscular junction, and streptomycin can aggravate the adverse reaction;
4. It is easy to cause heart block after digitalis;
5. It can increase the chance of bleeding when combined with heparin or penicillamine;
6. This product can cure vivax malaria when combined with primaquine.
7. When combined with amine chloride, it can accelerate excretion and reduce blood concentration.
8. Combined with monoamine oxidase inhibitor can increase toxicity.
9. It is easy to cause exfoliative erythroderma when combined with prednisolone.
10. When used together with chloroquine analogues (aminophenquine, hydroxychloroquine, etc.), the blood concentration of chloroquine can be increased.
Pharmacokinetics:
After taking chloroquine orally, the intestinal absorption was fast and sufficient, and the blood concentration was the highest 1-2 hours after taking chloroquine. About 55% of the drugs bind to plasma components in the blood. The T 1 / 2 was 2.5-10 days. The concentration of chloroquine in erythrocytes was 10-20 times higher than that in plasma, and the concentration of chloroquine in erythrocytes invaded by Plasmodium was about 25 times higher than that in normal erythrocytes. The concentration of chloroquine in liver, spleen, kidney and lung was 200-700 times higher than that in plasma. The concentration in brain and spinal cord was 10-30 times of that in plasma. Chloroquine is metabolized in the liver, and its main metabolite is deethylchloroquine, which still has antimalarial effect. A small proportion (10-15%) of chloroquine is excreted in the original form through the kidney. The excretion rate of chloroquine is accelerated by acidification of urine and decreased by alkalization. About 8% of them are excreted with feces, and chloroquine can also be excreted from milk.
Pharmacology and Toxicology:
Chloroquine mainly acted on schizonts in erythrocytic phase. After 48-72 hours, schizonts in blood were killed. This product has no effect on the infrared phase of vivax malaria, so it can not cure vivax malaria. Falciparum malaria can be cured. Chloroquine has no direct effect on Gametophyte and has no effect on infrared phase.
After chloroquine treatment, the nucleus of Plasmodium was broken, vacuoles appeared in the cytoplasm, and the Plasmodium pigment agglomerated. It is known that chloroquine can not kill Plasmodium directly, but can interfere with its reproduction. This product has a strong binding force with nucleoprotein. Through the 7-chloro group on the quinoline ring is close to the 2-amino group on the guanine of DNA, chloroquine is inserted between the two strands of DNA double helix. It forms a complex with DNA to prevent DNA replication and RNA transcription. Chloroquine can also inhibit the incorporation of phosphate into DNA and RNA of Plasmodium, and interfere with the reproduction of Plasmodium due to the reduction of nucleic acid synthesis. The experiment of labeling chloroquine with isotope showed that chloroquine could be accumulated in infected red blood cells, and the food vesicles and lysosomes of protozoa were the concentrated sites. The concentration of chloroquine is related to the pH in the food bubble. The pH in the food bubble is acidic (the optimum pH for decomposing hemoglobin is 4), which can lead to the concentration of chloroquine, an alkaline drug. The concentration of chloroquine consumes hydrogen ions in the food bubble. Therefore, the pH value in the food bubble is increased, and the hemoglobinase digesting hemoglobin is lost. Plasmodium can not digest the ingested hemoglobin, resulting in the loss of hemoglobin The lack of essential amino acids for the growth and development of Plasmodium causes the breakdown of ribonucleic acid. In addition, chloroquine can interfere with fatty acids entering phospholipids, control glutamate dehydrogenase and hexokinase. In recent years, it has been suggested that the early effect of chloroquine on Plasmodium is to cause the agglutination of Plasmodium pigment. Iron protoporphyrin IX (FP), the main component of malaria pigment, can damage red blood cells and form a complex with chloroquine to mediate the chemotherapy effect of chloroquine. It is speculated that there are one or more receptors in protozoa, namely "FP binding complex", which may be a kind of albumin. It can combine with FP to form a non-toxic complex, which can protect protozoa biofilm from FP damage. The mechanism of action of chloroquine may be to separate the "FP conjugate" from FP and form a toxic chloroquine FP complex, thus exerting its antimalarial effect. Because of the change of receptor, chloroquine lost its function, which may be one of the reasons for the resistance of Plasmodium to chloroquine.
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