Related Experiment Videos
[Changes in local humoral immunity during stomach ulcer healing with laser and drug therapy]
G N Sokolova1, T M Tsaregorodtseva, M M Zotina
1Central Research Institute of Gastroenterology, Moscow.
Abstract:
The increase of the contents of serum IgA, IgG, IgM on the edge of long non-cicatrizing gastric ulcer was determined. At the same time the level of SIgA decreased in comparison with unaltered gastric mucosa. It is shown that the immunoglobulin content in the healed ulcer cicatrice depended on treatment method. The medicamentous therapy was accompanied by lowering of the contents of IgG, IgA, SIgA and by some increase of IgM level. The laser therapy is characterized by lowering of IgA, IgG, IgM level on a background of significant increase of SIgA content. The local humoral immunity after laser therapy was the same as in persons with unaltered gastric mucosa.
Related Concept Videos
Peptic Ulcer Disease IV: Management
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
Peptic Ulcer Disease II: Pathophysiology
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Gastritis II: Pathophysiology