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Old Mon Aug 15, 2011, 09:36 PM
captpgs captpgs is offline
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Join Date: Aug 2011
Location: Knoxville, TN
Posts: 1
Blessing

Bob, thanks so much for talking with me. I got the same message when I tried to send an e-mail to your wife.

I am a new member and it has been such a blessing to find this website. My husband died in March from Myelofibrosis which had progressed into AML. He was in Vietnam from 1969 to 1970. He was also stationed at New River and received training at Camp Lejeune. All information is so helpful.


Quote:
Originally Posted by Bob Macfarlane View Post
The number one question I am asked concerns what a nexus letter should look like, so I decided since my orginal was a bad scan I would re-entire it and share with you. The attachment contains all (21) of the footnotes that he used. I was successful before the BVA because of this letter. The BVA issued their decision without my ever appearing before them.

NORTHWEST ONCOLOGY AND HEMATOLOGY ASSOCIATES

DIPLOMATES AMERICAN BOARD OF INTERNAL MEDICINE
MEDICAL ONCOLOGY AND HEMATOLOGY

NEAL J. WEINRAB, M.D., F.A.C.P.
STEVEN WEISS, M.D.
TIMOTHY ALIFF, M.D.

April 24, 2006

To whom it may concern:

This letter is written on behalf of Mr. Robert Macfarlane a patient, whom I have evaluated for a diagnosis of myelodysplastic syndrome. I am a medical board certified oncologist currently in practice in Florida. My training in the field of oncology includes significant research and clinical experience in the diagnosis of hematologic malignancies.

Mr. Macfarlane is a 61-year old gentleman who was referred for hematologic evaluation following a several year history of macrocytic anemia. Ultimate work-up for this condition included a bone marrow examination which was performed on July 6, 2005, and led to a diagnosis of myelodysplastic syndrome (MDS) as the etiology of his macrocytic anemia. The key aspect of his bone marrow findings include a hyprocellular marrow, dyserythropiesis , dysmegakaryopiesis, and increased ringed sideroblasts. Because of the prolonged nature of his macrocytic anemia, it is presumed that Mr. Macfarlane’s case of MDS evolved well before he reached 60 years of age.

Myelodysplastic syndrome is generally an idiopathic disease of the elderly and rarely occurs in patients under 60 years of age. In patients like Mr. Macfarlane who develop early onset MDS , their disease is usually due to prior exposure to mutagenic agents, either through treatment with chemotherapy or through environmental/occupational exposure to genotoxins, particularly the aromatic hydrocarbons. Mr. Macfarlane has never received chemotherapy but from an occupational standpoint is it clear that Mr. Macfarlane was exposed to 2,3,7,8-tetrachlorodibenzo-p-dixon (TCDD), a known contaminant of herbicides while employed by the United States in Vietnam War. It is my medical opinion that Mr. Macfarlane’s myelodysplastic syndrome is casually related to exposure to TCDD during his military service in Vietnam on the basis of both epidemiologic and mechanistic data.

From a epidemiologic standpoint, it is established that TCDD exposure is causally related to a variety of clonal bone marrow diseases. In fact, many of these malignancies are already presumed by the Veterans’ Administration to be related to Agent Orange exposure and include all forms of non-Hodgkin’s lymphomas, chronic lymphocytic leukemia, and multiple myeloma. An increased risk has been documented in agricultural workers , an occupation in which exposure to dioxin-contaminated herbicides and pesticides is assumed. Other studies have linked exposure to benzene to elevated risk for MDS. As will be described below, benzene and TCDD are known to exert their toxic effects via common molecular pathways. Further epidemiologic evidence derives from a 1976 industrial accident in Seveso, Italy, in which several thousand residents were exposed to TCDD. Studies of this population have revealed a probable relationship between TCDD exposure and an increased risk of acute myeloid leukemia. Because acute myeloid leukemia (AML) may arise from previously unrecognized antecedent MDS, this finding suggests the possibility that a portion of the increased risk of AML in the residents of Seveso may be due to TCDD-mediated MDS. In conclusion, available epidemiologic data support the possibility of a connection between TCDD exposure and the pathogenesis of MDS.

Beyond the epidemiologic findings, the identification of characterization of the aryl hydrocarbon receptor have provided substantial mechanistic evidence linking TCDD to the pathogenesis if malignant disease. In fact, this evidence was the basis for the 1997 decision of the International Agency for Research on Cancer (a division of the World Health Organization) to upgrade its categorization of TCDD from “possibly carcinogenic to humans” (category 2B) to “known to be carcinogenic to humans” (category 1). The aryl hydrocarbon receptor (AhR) is a highly conserved nuclear receptor and transcription factor stimulated by TCDD, which leads to the induction and suppression of numerous genes. Mutagenic/carcinogenic events occurring downstream of AhR stimulation include changes in cell signaling proteins, calcium mobilization, growth factors, oncogenes, and cell proteins. Members of aromatic hydrocarbon family known to activate AhR include benzene, benzene metabolites, and TCDD (an aromatic hydrocarbon containing two benzene rings). Recent in vivo research molecular epidemiology research involving the victims of the Seveso accident has confirmed that TCDD exposure leads to predictable and consistent changes in the AhR pathway.

This growing body of mechanistic data regarding the aryl hydrocarbon receptor supports the presumption that aryl hydrocarbons, which include benzene and TCDD, act via a final common pathway in exerting their mutagenic effects. Because epidemiological studies correlate benzene exposure and the development of MDS (see foot notes 7-8), it is therefore plausible that TCDD exposure should carry identical risks. In the assessment of Mr. Macfarlane’s case of MDS, it is important to note that it was very early onset, which previously described suggests its relationship to toxic exposures. It is also important to note that with the exception of to TCDD during his military service in the Vietnam War, Mr. Macfarlane has not been known to exposed to any other mutagenic toxins which may lead to MDS, including no know exposure to benzene, chemotherapy or radiation, or even cigarette smoking. Accordingly, it is my firm medical opinion that when Mr. Macfarlane’s medical condition and history are viewed in totality, it is unlikely that anything other than TCDD exposure during his service in Vietnam caused his case of myelodysplastic syndrome.

Sincerely,



Timothy Aliff, M.D.


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Click here to download this letter as a PDF

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