lymphoma, non-Hodgkins-
A group of malignant, solid tumors of lymphoid tissue.
SYM:  Painless lymphadenopathy in 2/3's of patients is the most frequent
presenting symptom.  Others have fever, night sweats, ...In most cases the
cause of NHL is unknown, but PATIENTS WHO HAVE RECEIVED IMMUNOSUPPRESSIVE
AGENTS HAVE A MORE THAN 100 TIMES  GREATER CHANCE OF DEVELOPING NON-HODGKINS
LYMPHOMA...."
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".... THE FINAL STAGING IS MORE OFTEN BASED UPON
CLINICAL FINDINGS ..."

"The Merck Manual--Malignant Lymphomas:  Non-Hodgkin's
Lymphoma"---"Summary:  Clinical staging procedures similar to those for
Hodgkin's disease (see above) are indicated, except that laparotomy and
spenectomy are rarely required.  THE FINAL STAGING IS MORE OFTEN BASED UPON
CLINICAL FINDINGS  than is the case in Hodgkin's disease, in which pathologic
stage is critical for management decisions."   [My question---If a doctor
thinks Lyme is a rare disease due to using some of the self designated "lyme
experts" as a  source of info.-- can a doctor confuse Lyme with
non-Hodgkin's Lymphoma? - both are ultimately clinical disgnoses]  How will
doctors know that Lyme may be in the
differential diagnosis of this type of lymphoma?  If you think something is
rare and don't even know it's different manifestations--in this particular
situation---what happens?  The doctor has to know to rule out possible Lyme in
a case where a patient has been diagnosed with non Hodgkins lymphoma.

  This is an article that appeared in the health section of Vogue magazine in
Dec. of 1996--"Cancer conundrum:  Non-Hodgkin's lymphoma has increased about
75%  over the past 25 years--and doctors aren't sure why.  Both AIDS and organ
transplant patients are susceptible to non-Hodgkin's lymphoma, and these two
groups are growing.  Yet they account for only a small part of the increase.
Some physicians believe that exposure to agricultural herbicides and pesticides
may play a role.  The good news is, while survival rates were once low, now up
to half of patients with lymphoma are cured or go into remission for many
years."

This is from a Miami Herald article I got from the Miami Herald Medical Reports
on line.  It is from Sept.  1994  "Non-Hodgkin's  Lymphoma :  What you should
know-----.....The incidence of non-Hodgkin's lymphoma has increased in the past
few years.  Carlos Dominguez, M.D., an oncologist at Mount Sinai's
Comprehensive Cancer Center, says .......'For example, currently we're finding
in women age 20 to 30 a type of lymphoma that is confined to the chest and
initially manifests itself as a persistent cough or chest discomfort,' "
 "..'in addition, much attention is now being paid to a
non-Hodgkin's lymphoma that starts in the stomach, causing non-specific
symptoms of dyspepsia.  ' This particular lymphoma is notable because of its
association with a BACTERIAthat is commonly found in the stomach.  This is the
first time bacteria has been implicated as a cause of lymphoma, ' Dominguez
notes.  'The eradication of the BACTERIA with antibiotics can result in a CURE
for lymphoma.........' "
?????

from:  California Lyme Disease Symposium 1994
Lyme Disease Resource Center of California
reported by Jean Hubbard

"Dermatologic Manifestations of Lyme Disease------

"Dermatologist Rudy Scrimenti, the first physician to identify EM in the United
States, noted that cutaneous manifestations of Lyme disease have served as
hallmarks of the disease., but agreed with Dr. Katzel  that 'the classical
lesion with central clearing and red bands, although most diagnosable and most
readily recognizable, is far from being the most common lesion of EM, with
triangular lesions being quite common............ There are also
lymphocytomas that remain, sometimes for years, after the more  typical EM rash
resorbs;  these do improve with tetracycline and I am SURE I HAVE SEEN THESE IN
MY PRACTICE IN WISCONSIN,  but thus far I've been unable to obtain a positive
culture.  The most important alternative diagnosis for such lymphocytomas are
malignant lymphoma........"

Another reference:  It is for sypillis but close enough since
there is  so little research in this area for Lyme.

Gastric syphillis:  endoscopic and histological features mimicking
lymphoma.  (Am J Gastroenterol 1995;90:1504-1507)(Abstract) by Billy W.
Long v274
JAMA The Journal of the American Medical Association Dec 13 1995
p.1745(1)--

"....Gastroenterologists and pathologists must have an
awareness that gastric syphillis can MIMIC lymphocitic gastritis and
GASTRIC LYMPHOMA ....gastric syphillis MUST be carefully considered as
a diagnostic possibility in any patient with endoscopic and histological
findings suggesting lymphocitic gastritis or lymphoma.  The diagnosis of
gastric syphillis should be weighed even when H.Pylori infection is
present..."
Gastric involvement in syphillis. ( Tips from other journals)  
v46
American Family Physician August  1992 p552(1)".....The most common
clinical manifestations of gastric syphilis were abdominal pain, vomiting
and weight loss......"

  The following is an article to keep in mind when considiring the implications
of gastric syphilis.

[Gastrointestinal pathology in children with Lyme disease
Martin D. Fried, MD; Paul H. Duray, MD; and Dorothy Pietrucha, MD.  JSTD  1996;
3:101-104.

Ten children between the ages of 8 and 19 with Lyme disease presented with
chronic gastrointestinal symptoms. Biopsy evidence of inflammation was found in
the stomach, duodenum, and colon. Pathologies included gastritis, duodenitis,
gastric ulcer, colitis, and a histopathology resembling Crohn's disease.
Spirochetes with the microscopic appearance of Borrelia were found in five
patients with chronic inflammatory conditions of the gastrointestinal tract.
The inflammation may have been due to the spirochete itself, a reactive product
related to their presence in the gastroin testinal tract, or a consequence of
medications used to treat Lyme disease.
?????????? JSTD 1996; Volume 3, Number 3/4 (Fall/Winter) ]

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source: Brain (1992), 115, 399-423
The Clinical and Epidemiological Profile of Lyme Neuroborreliosis in
Denmark 1985-1990
  A prospective study of 187 patients with Borrelia burgdorferi specific
intrathecal antibody production
by Klaus Hanson and Anne-Mette Lebech  (from the Borrelia Laboratory,
Department of Infection-Immunology, Statens Seruminstitut, Copenhagen, Denmark)

"We conclude that neuroborreliosis is a common, clinically
characteristic but still underrecognized neurological syndrome.
.....differential diagnosis:  Guillain-Barre syndrome, herpes zoster
radiculitis, lymphocytic meningitis of other aetiologies, meningeal
carcinomatosis (widespread dissemination of carcinoma in the body), CNS
lymphoma, sarcoidosis, multiple sclerosis and other encephalopathies."
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TITLE: Infection by Borrelia burgdorferi and cutaneous B-cell lymphoma
.AUTHOR: Cerroni L; Zochling N; Putz B; Kerl H
AUTHOR AFFILIATION: Department of Dermatology, University of Graz, Austria
.SOURCE: J Cutan Pathol 1997 Sep;24(8):457-61NLM CIT. ID: 97472931

ABSTRACT: In past years, association of primary cutaneous B-cell lymphoma
(CBCL) with infection by Borrelia burgdorferi has been reported in a few
patients. The evidence for a pathogenetic role was based on clinical grounds or
raised titre of antibodies in serum. Both methods, however, do not prove the
association between the micro-organism and the CBCL, especially in countries
where infection by Borrelia burgdorferi is endemic. Moreover, the exact
percentage of Borrelia burgdorferi-positive CBCL is not known. We retrieved
from our files 50 cases of CBCL to perform PCR analysis of Borrelia burgdorferi
DNA on paraffin-embedded tissue sections. Only patients with primary CBCL were
selected. In all cases, monoclonality of the infiltrate was confirmed by
immunohistological pattern of immunoglobulin light chains or molecular analysis
of JH gene rearrangement, or both. Specific DNA sequences of Borrelia
burgdorferi were identified in cutaneous lesions from 9 patients (follicle
center lymphoma: 3/20; immunocytoma: 3/4; marginal zone B-cell lymphoma: 2/20;
diffuse large B-cell lymphoma: 1/6). Specificity was confirmed by Southern blot
hybridisation in all positive cases. We could show that Borrelia burgdorferi
DNA is present in skin lesions from a small proportion of patients (18%) with
various types of CBCL. Our results may have therapeutic implications. In
analogy to Helicobacter pylori-associated MALT-lymphomas, which in some cases
can be cured by eradication of Helicobacter pylori infection, a proportion of
CBCL may be cured with antibiotic therapy against Borrelia burgdorferi.
Although yet speculative, adequate antibiotic treatment for patients with
primary CBCL should be considered before more aggressive therapeutic options
are applied, particularly in countries where infection by Borrelia burgdorferi
is endemic. PCR analysis of Borrelia burgdorferi DNA is a fast test that should
be performed in all patients with CBCL to identify those who more likely could
benefit from an early antibiotic treatment
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