As part of the disease-fighting lymphatic system, the spleen is an important, but not vital, organ. Abnormal calcifications are often seen in the spleen, particularly in the elderly.
In the context of disease, calcification is defined as the abnormal deposition of calcium salts in a tissue, along with some iron, magnesium and other mineral salts.
Two types of pathologic (abnormal) calcifications can affect the spleen. "Dystrophic calcification" refers to mineral deposition in dying tissues, in spite of normal blood calcium levels. "Metastatic calcification" describes the deposition of calcium salts in normal tissues, usually in the presence of high blood calcium levels.
Located just under the left side of the rib cage, the spleen is a spongy, fist-sized organ. It is covered with a fibrous capsule and is comprised of a white pulp and a red pulp.
The white pulp of the spleen helps the body fight infections by producing white blood cells called lymphocytes, The main role of the red pulp is to filter the blood to remove unwanted substances.
Splenic calcifications may result from previous infections. In such cases, the calcification is usually diffuse. Possible causes include:
• Histoplasmosis, caused by the soil fungus Histoplasma Capsulatum
• Brucellosis, caused by bacteria of the genus Brucella
• Tuberculosis (TB), caused by Mycobacterium tuberculosis
• Candidiasis (yeast infection) in immunocompromised patients
• Pneumocystis infection, especially Pneumocystis carinii
• Parasitic cysts
Calcification may occur in the parenchyma, or essential tissue, of the spleen. Possible causes include:
• Phleboliths (stony deposits in veins)
• Hemangioma (benign blood vessel tumor)
• Splenic lymphoma (lymph tissue cancer)
• Hematoma (mass of clotted blood in tissue or organ)
Diffuse uniform calcification can result from impaired blood flow to the spleen and tissue death (splenic infarction). This usually happens in sickle cell patients.
- "Robbins and Cotran's Pathological Basis of Disease" (7e Ed.); Vinay Kumar, M.D., et al.; Elsevier; 2004
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