Gold compounds

Pharmacokinetic features and application status

Traditionally, many drugs for treating severe joint pathologies require injection, but auranofin (Auranofinum) is intended for oral administration (per os). This makes its use more convenient for the patient in an outpatient setting, but this is where its pharmacokinetic advantages end.

The main clinical feature of gold compounds is an extremely long latent period. After starting regular administration of the drug, the therapeutic effect develops very slowly. The patient and the attending physician have to wait on average from four to six months before the first objective signs of reduced inflammatory activity and decreased joint pain become noticeable.

Due to this delayed action, as well as the emergence of safer alternatives, the drug's status has been revised today. Currently, auranofin is not registered in the State Register of Medicines of the Russian Federation, which makes its official prescription in routine domestic medical practice impossible.

Mechanism of action: how gold protects the joint

The mechanism by which Auranofinum exerts its pharmacological effect is a sequential cascade of reactions aimed at suppressing the aggressive immune response directly at the site of inflammation.

1. Penetration into the joint cavity. After absorption in the gastrointestinal tract, the active substance purposefully migrates to the affected joints, penetrating into the synovial fluid.
2. Macrophage uptake. In the joint cavity, the drug encounters key inflammatory cells — macrophages. These cells actively engulf (uptake) gold compounds inside themselves.
3. Inhibition of cellular activity. Once inside the macrophage, the drug blocks the process of phagocytosis. In addition, it specifically inhibits the activity of lysosomal enzymes — aggressive molecules that, during autoimmune inflammation, are released outward and begin to destroy the body's own tissues.
4. Reduction of destruction. The result of such intracellular intervention is a sharp drop in the destructive potential of macrophages. The inhibition of lysosomal enzyme release leads to a significant slowing down of the destruction of the cartilage and bone tissue of the joint.

Safety profile and high toxicity

The abandonment of the widespread use of gold compounds in modern medicine is dictated by their high toxicity. Adverse effects affect several vital body systems at once, making therapy potentially hazardous.

• Hematological toxicity: The drug is capable of suppressing hematopoiesis, which clinically manifests as severe anemia. A decrease in red blood cell levels leads to tissue hypoxia.
• Gastrointestinal tract damage: The mucous membranes of the digestive tract are extremely sensitive to gold compounds. Patients often develop stomatitis (painful inflammation of the oral mucosa) and enterocolitis (inflammation of the intestine accompanied by digestive disorders).
• Organ toxicity: The drug delivers a serious blow to the main excretory and metabolic organs. Against the background of gold therapy, pronounced dysfunctions of the kidneys and liver are recorded. The development of renal or hepatic failure is a life-threatening condition and requires immediate discontinuation of the drug.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• The role of macrophages and lysosomal enzymes in the pathogenesis of joint destruction.
• Mechanisms of drug-induced anemia during the intake of heavy metal compounds.
• Pathophysiology of hepato- and nephrotoxicity of disease-modifying antirheumatic drugs.
• Comparative characteristics of gold compounds and modern DMARDs (why gold was excluded from the Register of Medicines).

Other topics in the "Analgesics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.