Modulation of prostaglandin activity, part 1: prostaglandin inhibition in the management of nonrheumatologic diseases: immunologic and hematologic aspects.
Prostaglandins (PGs) are active biologic substances that are involved in a wide range of physiologic processes; when their production is out of balance, they are factors in the pathogenesis of illness. Modulation of PGs by inhibition or stimulation is promising for the management of various conditions. PG inhibitors are widely used to relieve pain and inflammation in patients with rheumatologic disease. Interest in the use of PG inhibitors to prevent cancer and cardiovascular events is growing. More than 27 y ago, investigators found that PG depresses antibody production in vivo; reduces serum iron, hemoglobin, and leukoid series in bone marrow during acute and chronic blood loss; reduces albumin during antigenic stimulation; suppresses hypercalcemia after bleeding; and reduces fasting blood sugar and hyperglycemia after ether anesthesia and bleeding. Chronic conditions that produce large quantities of PGs are associated with immunosuppression and secondary anemia. Investigators in the present study hypothesized (1) that the overproduction of PGs is responsible for immunosuppression and secondary anemia in conditions associated with increased PG synthesis, such as pathologic inflammation, malignancy, trauma, and injury, and (2) that PG inhibitors reverse immunosuppression and secondary anemia, thereby enhancing the immune response. This is supported by many reports that show the immunosuppressive effects of PGs and their role in the immunosuppression associated with pathologic inflammation, burns, trauma, and tumors. Inhibition of PGs can be achieved through the use of synthetic medicines and natural products. This article reviews the effects of PGs and inhibition of increased synthesis of PGs on the lymphoid system, hematologic indices, and bone marrow elements in trauma, injury, burns, and tumors. The Medline database (1966-2006) was used in this study. Investigators in the present study and others have provided evidence that shows the involvement of PGs in immunosuppression and secondary anemia, as well as the efficacy of inhibited overproduction of PGs in many pathologic conditions other than rheumatologic disease.
Al-Waili
Noori S
NS
Al-Waili's Charitable Foundation for Science and Trading, New York City, NY, USA. noori786@yahoo.com
Saloom
Khelod Y
KY
Al-Waili
Thia
T
Al-Waili
Ali
A
Al-Waili
Hamza
H
D000740:Anemia / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology; D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007107:Immune System / Q000187:drug effects* / Q000378:metabolism; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D008221:Lymphoid Tissue / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D020030:Nitric Oxide Donors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D011448:Prostaglandin Antagonists / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D011453:Prostaglandins / Q000096:biosynthesis / Q000378:metabolism*; D014947:Wounds and Injuries / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism
D000970:Antineoplastic Agents; D052246:Cyclooxygenase 2 Inhibitors; D005609:Free Radicals; D020030:Nitric Oxide Donors; D011448:Prostaglandin Antagonists; D011453:Prostaglandins