Hodgkin's Disease Treatment Information

HODGKIN'S DISEASE TREATMENT INFORMATION

Hodgkin's Disease is a "malignant lymphoma" virtually always starting in lymph nodes, formerly called "reticulum, cell sarcoma". It is a "lympho-reticular disease" that was first recognized by Thomas Hodgkins in 1832, who noted enlarged lymph nodes in patients not attributable to inflammation. Since then, there has been a continual sub-classification of the malignant lymphoma's, most notably into Hodgkin's and Non-Hodgkin's types. The classic binuceated "owi's eyes" cells, termed "Reed-Stemberg" are believed derivedfrom lymphoctyes or the monocyte-macrophage "antigen presenting" cells, and are pathognemonic for Hodgkin's Disease, which comprises 40% of malignant lymphomas.

Epidemiology and Risk Factors for Hodgkin's Disease:

There are 7400 new cases of Hodgkin's in the U.S.A. each year, causing 1500 deaths. The incidence of Hodgkin's has remained fairly constant over the past 50 years. A small male predominance is seen, the male to female ratio is 1:3:1. In childhood cases, 85% are male. A "bimodal" age distribution is seen for Hodgkin's, with one cluster of cases in the 2nd to 3rd decade, and a second cluster in the 7th decade. In industrials countries, the disease tends to occur at a later age than in underdeveloped countries. The disease is rare in children under 10 years old. There are proportionately more cases in the older age group peak than in the younger age group. It accounts for 0.75 of the new cancer cases in the U.S.A./year.

Risk Factors:

While the reason a particular person gets Hodgkin's is unknown, clusters of the disease in certain regions have been noted, and both genetic and infectious processes have are suspected. People at increased risk for developing Hodgkin's include:

1) Inborn immune deficiency diseases, such as Wiscott-Aldrich, Ataxia Teiangectasia, and T-cell function disorders.
2) Acquired immunodeficiency from AIDS or immunosuppressive drugs.
3) Living in Western countries, being of higher social class, more educated.
4) Genetic pre-disposition, clusters are noted in siblings with similar HLA genotypes.
5) Infection with Epstein-Barr Virus (EBV) history is noted in up to 40% of patients developing Hodgkin's. Elevated levels of the IgG and IgA immunoglobulins against the EBV capsid antigen are noted 3 months to 12 years prior to clinical Hodgkin's development. Components of the EBV genome have been noted in the cellular DNA of the Reed-Stemberg cell (Ref. Weiss NEJM 320: 502 1989). However, the EBV is not noted in all patients and may be merely a marker of the poorer cellular immunity (but intact humoral immunity) seen in Hodgkin's patients.

While the pathogenesis of Hodgkin's still remains unknown, it is likely that a combination of enviromental and genetic factors are at work, such as the EBV precipitating the dis- ease in a genetically susceptible individual.

Molecular Biology:

The Reed-Stemberg (RS) cell likely arises from either lymphocytes or antigenpresenting cells of the monocyte-macrophage line. Regarding lymphocytic origin, 60% of RS cells have T or B cell specific antigens, and B cells are the usual target for EBV. Furthermore. RS cells express IL-2 receptors, HLA-DR antigens, and Ki-1, which are all features of activated lymphoctyes.

On the other hand, RS cells have la antigen, and Fc and C3 receptors which are all found in antigen-presenting cells. It is important to note that RS-like cells are found in several infectious, inflammatory and neoplastic conditions including infectious mononucleosis, reactive lymphoid hyperplasia and immunoblastic lymphoma. Thus, diagnosing Hodgkin's depends on finding the RS cells in the appropriate backround millieu. The lymphocytes within Hodgkin's are usually predominantly CD-4 positive T-cells, recall that poorer cellular immunity (but intact humoral immunity) charactizes Hodgkin's. This defective cellular immunity persists even after clinical cure!

The BCL2 Oncogene is found in 1/3 of Hodgkin's patients, and p53 suppressor gene is found in almost all Hodgkin's patient's except those with Lymphocyte predominant disease. The common tl4:18 translocation of B cell lyphomas is rare in RS cells. We Conclude that different subtypes of Hodgkin's may be derived from different immune cells, sothe RS cell may arise from more than one type of precursor (Ref. Devita Clinical Oncology c. 1994 4th ed.p. 1824).

An prime example of the improvement in medical care is the evolution of treatment for Hodgkin's Disease. At one time, this lymph system cancer was incurable, all stricken patients died from it. Fortunately, most patients can now be cured, owing to tremendous research advancements in treating the disease.

Nonetheless, it is crucial not to take a carefree attitude, but to thoroughly understand the disease to help you make the proper treatment choices. Making the right choices can literally mean the difference between life and death. It is important have the peace-of-mind knowing that you have done everything possible to fight Hodgkin's Disease successfully.

CancerAnswers's materials describes, in plain English, the definition, frequency, symptoms, evaluation, conventional treatment and latest effective treatment for Hodgkin's Disease. We describe surgery, radiation and chemotherapy as well as combined therapies and their results. We tell you everything you need to know to help you make the right decisions today for a Hodgkin's Disease problem.

This is just an excerpt of CancerAnswers's report on Hodgkin's Disease. Much more, including latest can be sent to you by mail when you order the complete Hodgkin's Disease transcript at a nominal cost. Thank you for using CancerAnswers as your information resource.