Classification and origin
Tumors of lymphoid tissue are divided into precursor cell neoplasms and mature peripheral cell neoplasms. Neoplasms of mature cells are clinically subdivided into disseminated leukemias, forms with predominant nodal involvement, and primary extranodal variants.
B-cell chronic lymphocytic leukemia is classified as a mature B-cell tumor. Its key markers are CD19, CD20, and CD23 antigens, as well as surface immunoglobulins. Chromosomal aberrations are detected in half of patients, with trisomy 12 being the most common.
Changes in lymph nodes and spleen
At the macroscopic level, lymph nodes in this disease are generalized, enlarged, and fused into massive soft or moderately dense clusters, showing a juicy, pinkish-white, and uniform cut surface. The microscopic picture is characterized by the loss of node architecture and the formation of solid masses of lymphocytes with proliferation centers composed of large prolymphocytes.
The spleen is significantly enlarged, its mass increases, its consistency becomes fleshy, and the cut surface is red. Organ infiltration develops in stages: follicles are affected first, then pathological elements proliferate in the red pulp, involving vessel walls, trabeculae, and the capsule.
Involvement of the liver, kidneys, and bone marrow
In the bone marrow of flat and tubular bones, the red color of the tissue is preserved, and areas of yellow marrow remain in the diaphysis of tubular bones, which distinguishes this condition from myeloid leukemia. In severe cases, diffuse displacement of myeloid tissue is observed.
The liver becomes enlarged and dense, with small grayish-white nodules visible on its cut surface. Microscopically, lymphocytic infiltration along the portal tracts is revealed, and hepatocytes undergo protein or fatty degeneration. The kidneys enlarge, acquiring a moderately dense consistency and grayish-brown color due to pronounced leukemic infiltration.
Complications of the disease
The clinical course of the pathology is complicated by secondary infections, such as pneumonia. Hemolytic states occur, leading to hemolytic jaundice and general hemosiderosis.
Compression syndromes pose a particular danger: compression of the heart, trachea, and esophagus by enlarged mediastinal lymph nodes, as well as impaired blood outflow in the portal venous system due to mesenteric node involvement, leading to portal hypertension and ascites.
CLL is characterized by Clear Lymphadenopathy and Leukocytosis: mature B-cells crowd the nodes, spleen, and liver, forming clusters and proliferation centers.
Class and exam questions
How does the macroscopic picture of the bone marrow in chronic lymphocytic leukemia differ from myeloid leukemia?
In chronic lymphocytic leukemia, small areas of yellow color are preserved among the red bone marrow in the diaphyses of tubular bones, unlike in myeloid leukemia.
What changes occur in the architecture of lymph nodes?
There is a complete loss of the normal architectural pattern of the lymph node, which is replaced by solid masses of lymphocytes with characteristic proliferation centers.
What complications cause compression syndrome in lymphocytic leukemia?
Compression of mediastinal organs (heart, trachea, esophagus) by enlarged lymph nodes, as well as compression of the portal vein by mesenteric nodes, leading to ascites and portal hypertension.
What else to study on this topic
- Acute lymphoblastic leukemias and lymphoblastic lymphomas from precursor cells
- Characteristics of other mature B-cell tumors (hairy cell leukemia, plasmacytoma)
- Pathomorphology of T- and NK-cell tumors
- Histological features of proliferation centers in lymph nodes
- Immunophenotypic markers (CD19, CD20, CD23, SigIgM)
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