Clinical Considerations for Primary Lymphedema and Lymphoma

Cutaneous B-Cell Lymphoma and Lymphedema, Cutaneous T-cell lymphoma and Lymphedema, Hodgkins Lymphoma, Kidney and Renal Cancer, Cervical Cancer, Renal Cell Carcinoma, Breast Cancer, Ovarian Cancer, Testicular, arm swelling, Skin Cancer, angiosarcoma, kaposi's sarcoma, gallium scan, axillary node dissection, gynecological cancer, axillary reverse mapping, lymphatic cancers, inguinal node dissection, cancer treatment, Complete decongestive therapy for arm lymphedema, lymphedema therapy, intensive decongestive physiotherapy, breast cancer related lymphedema, upper limb lymphedema

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Clinical Considerations for Primary Lymphedema and Lymphoma

Postby patoco » Thu Aug 10, 2006 8:16 am

Clinical Considerations for the Diagnosis and Management of Lymphoma with Primary Lymphedema

The key to understanding lymphoma as a secondary condition to primary lymphedema is in the pathophysiology of the lymph system.

Point One

In the situation of primary lymphedema, the lymph system is either incompletely formed or malformed. This means that the spread of and the expression of lymphoma (course of the disease) is going to be different then in an individual with a "normal" lymph system.

The reason is simple. With the lymphatic flow constricted, the malignancy will have a more difficult time spreading to external nodal areas. The incomplete lymph system will act as a "damn" actually helping to contain the lymphoma.

Beause of either the hypoplaysia or hyperplaysia of the lymphatics, it is going to be more difficult to obtain an accurate diagnosis of a lymphtic cancer.

Case in point: The nodes of a person with lymphedema may already be smaller then normal. Therefore, if there is limited nodal enlargment (or even if there is none) you can not assume no malignancy is present.

Furthermore, I have yet to experience really significant lymph node enlargement. But, what I have experienced are nodes that are only slightly larger then "normal" yet have turned hard and rubbery.

Point Two

Standard radiological tests must be viewed carefully in using them to chart lymphatic cancer with lymphedema. MRI's and CAT's are of limited use as the "normal" size node they are picking up, may infact be malignant.

Case in point: When the small needle biopsy of my right inguinal lymph node was performed, the doctor did an ultrasound first. That node looked perfectly normal to the ultrasound. The biopsy came back positive.

Point Three

The use of a PET scan in the staging and diagnosis must be viewed with skepticism. There are important reasons for this. The principle behind the PET is quite simple. Tumor (malignancies) will have a higher metabolic rate then the surrounding nonmalignant tissues. Therefore, the malignancies will have a higher "uptake" of the contrast used.

Because of the dysfuntion of the lymph system, it is going to be more difficult for the contrast to make its way through the body and be absorbed. This will effect the diagnostic effectiveness.

Unfortunately too, there is also no standard uptake value for tissue effected by lymphedema. Therefore, it is going to be difficult to ascertain whether a SUV number indicates a malignancy or not.

On the opposite side, lymphedema patients are faced with constant inflammation and/or chronic low grade infection. Both of these can give a false positive to a PET scan.

Point Four

After the diagnosis of a lymphatic cancer is achieved, the treating physician must carefully monitor changes in the complications experienced by the patient. New complications and changes must not automatically be assumed that they are caused by lymphedema.

Case in point : Before the spread and/or infilitration of lymphoma throughout my system, I did not have lung fluid. Two years ago, I began having fluid accumulate in my right lung. This year, the left lung has also been extensively involved.

Also, my lymphedema has been consistent for decades. Also, during the past two years, I have experienced swelling of my left arm for the first time.

It is important to understand that those of use with a dysfunctional lymph system walk a fine line. In my situation, with an already at risk lymph system, the lymphoma spreading through the chest was enough to "overload" the impaired system resulting in both pleural effusions and swelling of the left arm.

Perhaps the most important point to make is for the physician to "listen" to the patient. Individuals like myself have lived with lymphedema for decades - most for years.

We know how lymphedema effects our bodies, what is (normal) for ourselves and what should or should not be happening.


Listen...care about...communicate with your patient.

Pat O'Connor
October 9, 2005

My Life with Lymphedema Blog

http://mylifewithlymphedema.blogspot.com/

................

Lymphedema People

http://www.lymphedemapeople.com
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Sunlight exposure may increase lymphoma risk

Postby patoco » Fri Jul 06, 2007 11:57 am

Sunlight exposure may increase lymphoma risk

Reuters Health
Last Modified: June 1, 2007

Last Updated: 2007-06-01 17:36:15 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Ultraviolet radiation exposure from time spent in the sun appears to boost the risk of non-Hodgkin's lymphoma in women, according to a population-based study.

Dr. Yawei Zhang of Yale University, New Haven, Connecticut and colleagues note in the May issue of the American Journal of Epidemiology that it has been suggested that increasing exposure to ultraviolet radiation may be responsible at least in part for the observed increase in the incidence of non-Hodgkin's lymphoma.

To investigate, the researchers examined data from a case-control study of women living in Connecticut. The study involved 601 women with histologically confirmed non-Hodgkin's lymphoma and female controls who were also Connecticut residents.

A history of suntan was generally associated with an increased risk of lymphoma. In particular, compared to women who had never had a suntan, those who had had a suntan for less than 3 months per year for more than 60 years were at almost 3 times the risk.

However, there appeared to be no increased risk in women who reported having a suntan for 3 or more months per year. The researchers consider a lower suntan duration to have been indicative of irregular exposure. A regular suntan, they suggest, may have provided protective pigmentation that would reduce ultraviolet radiation absorption.

In addition, women with the greatest exposure to strong sunlight between 9 a.m. and 3 p.m. in the summer had a 70% increased risk compared to those with the lowest exposure.

The investigators, who note that the increased risk of non-Hodgkin's lymphoma appears to vary by lymphoma subtypes, conclude that further studies are warranted "to investigate whether genetic susceptibility may modify the relation between sun exposure and risk of non-Hodgkin's lymphoma."

Am J Epidemiol 2007;165:1255-1264.

http://www.oncolink.upenn.edu/resources ... &year=2007
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HCV infection and development of non-Hodgkin lymphoma

Postby patoco » Fri Jul 06, 2007 11:59 am

HCV infection associated with development of non-Hodgkin lymphoma

Reuters Health
Last Modified: May 8, 2007

Last Updated: 2007-05-08 16:00:38 -0400 (Reuters Health)

NEW YORK (Reuters Health) - The prevalence of non-Hodgkin lymphoma and other lymphoproliferative diseases is increased in patients infected with hepatitis C virus (HCV), investigators report in the Journal of the American Medical Association for May 9.

To provide sufficient power to uncover links between HCV and non-hepatic disorders, a research team based at the Michael E. DeBakey Veterans Affairs (VA) Medical Center in Houston and at the National Cancer Institute in Rockville, Maryland, used data compiled from VA administrative records. VA records are of particular interest, because the prevalence of HCV is nearly three times higher among veterans than in the general population.

The VA's Dr. Thomas P Giordano and colleagues searched for associations with leukemias and other types of lymphomas, including Waldenstrom macroglobulinemia, among 146,000 HCV-infected patients and 572,000 uninfected control subjects. Mean follow-up was 2.3 years.

They found an increased risk for non-Hodgkin lymphoma and for Waldenstrom macroglobulinemia associated with HCV infection. Risk was also higher for cryoglobulinemia and thyroiditis. The p value for all four conditions was < 0.0038.

The risk was also increased for monoclonal gammopathy of undetermined significance (MGUS), but the difference was not significant after adjustment for co-factors.

"We demonstrated that (HCV) infection precedes development of these outcomes," Dr. Giordano and colleagues write. They suggest "the intriguing possibility that chronic immune stimulation by HCV infection can result in progression along a spectrum of IgM monoclonal gammopathy from asymptomatic MGUS to symptomatic cryoglobulinemia to the malignant Waldenstrom macroglobulinemia."

JAMA 2007;297:2010-2017.

http://www.oncolink.upenn.edu/resources ... &year=2007
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Lymphoma risk with pesticide exposure not modified by atopy

Postby patoco » Fri Jul 06, 2007 12:02 pm

Lymphoma risk associated with pesticide exposure not modified by atopy

Reuters Health
Last Modified: May 7, 2007

Last Updated: 2007-05-07 12:39:10 -0400 (Reuters Health)

NEW YORK (Reuters Health) - The risk of non-Hodgkin's lymphoma is increased with substantial exposure to pesticides, regardless of asthma or atopy history, according to findings from a study published in the May issue of the International Journal of Cancer.

"Occupational exposure to pesticides and a personal history of atopy have been widely examined as risk factors for non-Hodgkin's lymphoma (NHL), a neoplasm arising from cells of the immune system," write Dr. Claire M. Vajdic, of the University of New South Wales, Australia, and colleagues. "These studies have typically found that exposure to pesticides increases risk of NHL, while asthma, or atopy more generally, has been inconsistently protective."

In an Australian population-based, case-control study, the researchers examined the interaction between occupational pesticide exposure and atopy on the risk of NHL. Included in the study were 694 incident cases and 694 randomly selected controls who were matched to cases by age, not allowed, and State of residence.

Participants completed telephone-administered job-specific questionnaires. Expert occupational hygienists used these to determine occupational pesticide exposure. History of atopy (including asthma, hay fever, eczema, and food allergy) was self-reported.

The odds ratio (OR) for NHL with substantial exposure to pesticides and any history of asthma was 3.07. With substantial pesticide exposure and no history of asthma, the OR was 4.23. "The p-value for the interaction was 0.29," the team reports.

The risk of NHL was reduced with non-substantial pesticide exposure and a history of asthma (OR = 0.30), and was close to null with non-substantial pesticide exposure and no history of asthma (OR = 0.99).

"This finding was consistent for several measures of pesticide exposure and asthma, including lifetime pesticide dose, subtype-specific pesticide dose and history of asthma as an adult, teenager, or child," Dr. Vajdic and colleagues report.

Furthermore, "The pattern of risk for a history of hay fever, eczema, food allergy or any type of atopy was similar; risk was increased with substantial pesticide exposure and no history of atopy, but less so when atopy was reported."

Int J Cancer 2007;120:2271-2274.

http://www.oncolink.upenn.edu/resources ... &year=2007
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Family history of hematopoietic cancer increases non-Hodgkin

Postby patoco » Fri Jul 06, 2007 12:05 pm

Family history of hematopoietic cancer increases non-Hodgkin lymphoma risk

Reuters Health
Last Modified: May 2, 2007

Last Updated: 2007-05-02 16:52:27 -0400 (Reuters Health)

NEW YORK (Reuters Health) - A family history of non-Hodgkin lymphoma, Hodgkin lymphoma, or leukemia increases the risk of non-Hodgkin lymphoma, according to a report in the April 15th issue of Blood.

Previous studies have shown an excess risk of non-Hodgkin lymphoma among those whose family members have hematopoietic malignancies, the authors explain, but a detailed pattern of non-Hodgkin lymphoma (NHL) has not been clarified.

Dr. Sophia S. Wang from National Cancer Institute, Rockville, Maryland and colleagues in the International Lymphoma Epidemiology Consortium (InterLymph) evaluated NHL risk among individuals who had first-degree relatives with NHL, Hodgkin lymphoma, leukemia or multiple myeloma. The data included 10,211 NHL cases 11,905 controls.


The risk for NHL was increased 50% among individuals with a first-degree relative with NHL, 60% among those with a first-degree relative with Hodgkin lymphoma, and 40% among those with a first-degree relative with leukemia, the authors report. A family history of multiple myeloma was not associated with a significantly increased risk for NHL.

Among individuals having a first-degree relative with NHL, their NHL risk was higher if the relative was a sibling than a parent, and higher if the relative was male, the results indicate.

In contrast, a parent with Hodgkin lymphoma conferred a higher risk for NHL than did a sibling with Hodgkin lymphoma, especially among men.

For leukemia, the risk was slightly higher if the relative was a sibling, and the risk was highest among women who reported a sister with leukemia.

The risk for different NHL subtypes varied with the particular hematopoietic malignancy and the family member affected, the researchers note.

"Our data support further examination of all sources of familial aggregation, including investigation of common gene variations that alter NHL risk in the search for etiologic mechanisms," the authors state.

"Because family history represents the interaction between shared environmental exposures, behaviors, and genetic susceptibility, a full understanding of NHL heritability can provide clues regarding underlying disease mechanisms, particularly as it relates to disease and subtype-specific heterogeneity," the investigators explain.

"Future efforts in sib-pair or twin studies may further our understanding of the sibling relationships, particularly for the male- and female-specific associations for family history of NHL and leukemia, respectively," the researchers add.

Blood 2007;109:3479-3488.

http://www.oncolink.upenn.edu/resources ... &year=2007
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Mucosa-associated lymphoid tissue lymphoma

Postby patoco » Fri Jul 06, 2007 12:16 pm

Mucosa-associated lymphoid tissue lymphoma: Molecular pathogenesis and clinicopathological significance.

Pathol Int. 2007 Aug

Inagaki H.
Department of Pathology, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Japan.

Mucosa-associated lymphoid tissue (MALT) lymphoma is a low-grade tumor closely associated with chronic inflammation such as that of Helicobacter pylori gastritis, Sjogren's syndrome, and Hashimoto's thyroiditis. Tumor regression by H. pylori eradication alone is well known in gastric MALT lymphoma, but some tumors occur in the absence of pre-existing chronic inflammation. The understanding of MALT lymphoma biology has significantly improved, and recurrent cytogenetic alterations have been detected. These include the trisomies 3 and 18, and the translocations t. At least some of these alterations result in the constitutive activation of the nuclear factor (NF)-kappaB pathway, and may exert anti-apoptotic action. Apoptosis inhibitor 2-MALT lymphoma-associated translocation 1 (API12-MALT1) fusion, resulting from t(q21;q21), is specific to, and is the most common in, MALT lymphomas, and its clinicopathological significance has been studied extensively. The focus of the present review is on the recent progress made in elucidating MALT lymphomagenesis and its clinicopathological impact, especially in terms of the effect of API2-MALT1 fusion on this unique tumor.

PMID: 17610471 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum
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Genetic susceptibility to lymphoma.

Postby patoco » Fri Jul 06, 2007 12:20 pm

Genetic susceptibility to lymphoma.

Haematologica. 2007 Jul;

Skibola CF, Curry JD, Nieters A.
School of Public Health, 140 Earl Warren Hall University of California, Berkeley, Ca. 94720-7360, USA. chrisfs@berkeley.edu.

Genetic susceptibility studies of lymphoma may serve to identify at risk populations and clarify important disease mechanisms. This review considered all studies published through October 2006 on the contribution of genetic polymorphisms in the risk of lymphoma. Numerous studies implicate the role of genetic variants that promote B-cell survival and growth with increased risk of lymphoma. Several reports including a large pooled study by InterLymph, an international consortium of non-Hodgkin lymphoma (NHL) case-control studies, found positive associations between variant alleles in TNF -308G>A and IL10 -3575T>A genes and risk of diffuse large B-cell lymphoma. Four studies reported positive associations between a GSTT1 deletion and risk of Hodgkin and non-Hodgkin lymphoma. Genetic studies of folate-metabolizing genes implicate folate in NHL risk, but further studies that include folate and alcohol intakes are needed. Links between NHL and genes involved in energy regulation and hormone production and metabolism may provide insights into novel mechanisms implicating neuro- and endocrine-immune cross-talk with lymphomagenesis. However, this links will need replication in larger populations. Numerous studies suggest that common genetic variants with low penetrance influence lymphoma risk, though replication studies will be needed to eliminate false positive associations. Key words: lymphoma, genetic susceptibility, SNP, NHL, polymorphisms.

PMID: 17606447 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum
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Duodenal follicular lymphomas

Postby patoco » Fri Jul 06, 2007 12:23 pm

Duodenal follicular lymphomas share common characteristics with mucosa-associated lymphoid tissue lymphomas.

J Clin Pathol. 2007 Jun 29

Sato Y, Ichimura K, Tanaka T, Takata K, Morito T, Sato H, Sato Y, Kondo E, Yanai H, Ohara N, Oka T, Yoshino T.
Dept. of Pathology, Okayama University, Japan.

Backgrounds: Follicular lymphomas occasionally arise in the extra-nodal organs. We previously reported that they rather frequently found in the duodenum. They are often localized tumor with multiple polyps around the ampulla of Vater.

METHODS: We attempted to examine a IgH/bcl-2 hybrid gene and VH-gene usage to know the nature of the lymphoma cells: how difference to nodal follicular lymphomas and to MALT lymphomas. We have experienced 35 patients with duodenal follicular lymphoma after our latest report (40 patients in total), and we examined clinicopathological characters in details.

RESULTS: Out of 40 in total, 37 were determined in clincial stage I (30) or stage II(7). It is quite different from a datum of previous report on nodal follicular lymphomas (p<0.001). PCR analyses, clonal immunoglobulin gene rearrangement was detected in 53.3% of examined cases, and rearrangement of IgH/bcl-2 gene at the major break point was detected by in 27% cases may indicate similar to that of nodal ones. VH usage of them revealed that 3 out of 8 examined cases was VH4 (38%), and 2 out of them were VH4-34. As VH4 deviation is the one of the common characters of MALT lymphomas and two out of three were idential usage, duodenal folliucular lymphomas might arise from responding to a kind of causative agent similar to MALT lymphomas. And it showed very indolent clinical course regardless various therapeutic ways, which also resembled clinical features of MALT lymphomas.

CONCLUSIONS: These data might suggest that duodenal follicular lymphomas have intermediate characteristics of MALT lymphomas and nodal follicular lymphomas.

http://jcp.bmj.com/cgi/content/abstract ... 7.049825v1
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Non-Hodgkin's lymphoma of nasal cavity and paranasal sinuses

Postby patoco » Fri Jul 06, 2007 12:24 pm

Non-Hodgkin's lymphoma of nasal cavity and paranasal sinuses. A clinicopathological and immunohistochemical study.

Acta Otorhinolaryngol Ital. 2007 Feb

Chalastras T, Elefteriadou A, Giotakis J, Soulandikas K, Korres S, Ferekidis E, Kandiloros D.
Department of Otolaryngology, Medical School, University of Athens, Hippokration Hospital, Athens, Greece.

Aim of this study was to investigate the clinical characteristics, management and prognosis of non-Hodgkin lymphomas of the nasal cavity and paranasal sinuses. Overall 12 patients with non-Hodgkin malignant lymphoma, at our Institute, were studied over an eight-year period from 1997 to 2005. Patients' data collected were age, not allowed, presenting signs and symptoms, histology, treatment, complications, and outcome. Also available were computerised tomography findings, and paraffin-embedded tissue bocks. Mean age was 62 years (range: 42-81), with a male dominance (male to female ratio: 7:5). Most patients had not presented any specific symptoms, such as nasal obstruction, headaches, epistaxis and facial swelling. Using immunocytochemistry on paraffin-embedded tissue sections, the predominance of large B-cell subtype was detected. Treatment administered: only radiotherapy (stage IEA) or in combination with chemotherapy (IIE-IVE). Of these patients, 5 died from the disease, 4 survived without disease, 2 survived with the disease, and one died of non-related causes. Non-Hodgkin's lymphomas are relatively rare. Early diagnosis, based mainly on tissue biopsy and computerised tomography, is essential in the management of non-Hodgkin lymphoma.

PMID: 17601204 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entre ... d_RVDocSum
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