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21st July 21:02
External User
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lupus/Lyme; NEJM and Steere (lupus fibrositis syphilis dementia smallpox)
The following is an excerpt of a post by Kathy Cavert posted to the
sci.med.diseases.lyme newsgroup.
From: John Haynes (jchco@sprintmail.com)
Subject: lupus/Lyme; NEJM and Steere
Newsgroups: sci.med.diseases.lyme
View complete thread (3 articles)
Date: 1997/07/11
"....... In the New England
Journal of Medicine, 1989, Vol. 321 No. 9 p. 589 it states, and I quote:
there are "circulating immune complexes, and occasionally rheumatoid
factor, antinuclear antibodies, or anticardiolipin antibodies. " Dr. Paul
Lavoie, a known and well-respected rheumatologist and friend of Dr.
Burgdorfer has recently died of cancer but did a study in which some of
his late stage clear-cut lupus patients did, indeed have lupus instead.
They had the speckled pattern and some the double stranded DNA with many
other sophisticated tests postive for lupus. These immunologic
disasters called lupus actually had Lyme disease when Dr. Lavoie saw the
same type symptoms in his Lyme patients and did a PCR(DNA) on their
spinal fluid. And you guessed it. Misdiagnosed 20 year history of
Lupus which had needed antibiotic therapy as they were Lyme cases
instead. The intracellular, occult infection was the culprit again.
In the chart at the bottom of ...... Dr. Steere's article, he goes on to
list some of the "symptoms" of Lyme in our prestigious, peer-reviewed,
NEJM. One which was rather striking as we discuss lupus was the "malar
rash". For those who do not know what this is, it has often been a
marker for lupus, as it is a "butterfly" facial rash which actually gave
the disease its name ..."wolf".
Steere goes on to list symptoms such as pericarditis, dementia, joint
pains, swellings, joint subluxations, myopericarditis, retinal
detachment, retinal hemorrhage, hepatitis, respiratory distress
syndrome, blood and protein in the urine, severe malaise and fatigue,
and on same page mentioned our "Excruciating headache and mild stiffness
of the neck. He mentions, "musculoskeletal pain of Lyme disease is
generally migratory in joints, bursae, tendons, muscle, and bone,
lasting only hours or days in a given location...and they frequently
have debilitating malaise and fatigue, which may be the predominant
symptoms....symptoms are typically intermittent and changing.
He lists "splenomegaly", "meningitis", "sore throat", "myositis", and so
forth. Not only does this implicate lupus, but it also implicates other
autoimmune disorders as well as fibromyalgia syndrome, chronic fatigue
syndrome ad nauseum. ..."
_____________________________
This is an old post of mine from the newsgroup--concerning lupus.
ge****a
source: Taber's Medical dictionary
"antinuclear antibodies- ABBR: ANA. A group of antibodies that react against
normal components of the cell nucleus. These antibodies are present in a
variety of immunologic diseases, including systemic lupus erythematosus,
progressive systemic sclerosis, Sjogren's syndrome, scleroderma, polymyositis,
and dermatomyositis, and in persons taking hydralazine, procainamide, or
isoniazid. In addition, ANA is present in some normal individuals."
4/93 Update to Lyme Disease 1991
pg, 20 "iv): Lupus: "Dr. Paul Lavoie, rheumatologist from San Francisco's
Presbyterian Hospital, reported that he had recovered B. burgdorferi DNA in
the blood of patients with with lupus erythematosis (SLE). .....Other
physicians in the U.S. are also treating lupus and rheumatoid arthritis with
antibiotics. The CDC accepted three of Dr. Lavoie's case studies suggesting
that 'a spirochete might contribute to the immunopathogenesis of SLE (Lupus).
' " (LymeAid Aug./Sept. 92)
Art Doherty's site:
Lyme Disease Misdiagnosed as Lupus
(Includes nine reasons for false negative Lyme disease blood tests.)
http://www.geocities.com/HotSprings/Spa/6772/lupus-index.html
from : The Pathologist's View of Lyme disease
source: Wisconsin Medical Journal 1989;88(11):17-20
authors: Hejka, England, Schmitz, Schell--Madison
"...Skin manifestations
"Quite frequently, patients do not recall being bitten by a tick. Some
develop an erythematous (red) papule (small, red, elevated area on the skin,
solid and cir***scribed; a pimple. Papules often precede vesicular or
pustular formation and may appear in erythema multiform, exzema papulosum,
prurigo, syphilis, measles, smallpox......from Taber's Cyclopedic Medical
Dictionary) within 24 to 48 hours at this bite site which is not the rash of
Lyme disease but a transient reaction to a trauma of the tick bite.
Infrequently a biopsy is performed on the site and if the tick is still
attached and burrowed into the tissue it may appear in stained tissue sections
surrounded by inflammatory cells." remember that many times the tick is no
bigger than a sesame seed or the period at the end of this sentence.
"Microscopic examination may reveal inflammation and disruption of the
epidermis along with adjacent epithelial hyperplasia.(3) Cases wherein
patients with Lyme disease undergo unrelated operations , during which tissue
is removed, are rare, but can be valuable in studying the systemic
histopathology of Lyme disease.
"Usually, within thirty days of after exposure, erythema migrans (EM) may
develop near the site of the initial tickbite or on the same extremity but may
occur in unrelated sites and be multiple.(4) ................Biopsies of the
skin
lesion shows non-specific inflammation, especially around the blood vessles.
B. burgdorferi has been cultured from these lesions, (5) however, because of
the low number of spirochetes present in the tissues and the complexity of the
culturing system, it is not a technique sensitive enough to be routinely used
in clinical settings...."
"Rarely necrotizing splenitis can be caused by B. burgdorferi. (10).....
"The heart may be a target organ in Lyme disease....
" Lyme arthritis is FREQUENTLY mistaken clinically for rheumatoid
arthritis, systemic lupus erythematous, or Reiter's syndrome. Synovial
biopsies are probably the most frequent tissue examined microscopically from
patients with Lyme disease. The histopathological spectrum ranges from chronic
hyperplastic synovitis with effusions to erosive ostearthritis. (20)..."
http://www.jersey.net/~joebur/
the full article can be found at this address
source:
WHEN TO SUSPECT LYME DISEASE
John D. Bleiweiss, MD
Trenton, NJ 4/94
"........... Among untreated patients with LD, arthritis can ultimately
develop in
up to 60%. The joint swelling, which may or may not be painful, frequently
is episodic, recurrent and migratory if multiple joints are involved. Any
joint can be affected including the TMJ (temperomandibular) and small joints
of the fingers (contrary to earlier reports). Up to 10% of untreated LD
arthritis can develop into destructive/deforming synovitis almost identical
to Pheumatoid Arthritis (RA). Dr. Lavoie has published the coincident
findings of LD with RA, and SLE (lupus) with LD. The SLE was associated
with positive DS-DNA (double stranded DNA) which is considered diagnostic
for lupus. This marker improved with antibiotic treatment for the LD. The
author felt that the LD might be causing/aggravating the SLE.........."
I would like to present a case of a 38 y.o. white female who, 24 days
postpartum, presented with Seropositive LD. She had a prior history of a
round rash 6" diameter in 6/90, DS-DNA =320 in 12/90 and previously treated
Lyme (seronegative)by various physicians (including myself) from 12/90 to
12/92 with eradication of all symptoms. The patient became pregnant 7/93
and her former Lyme symptoms were revived. She declined to take amoxil
prescribed by her OB-GYN until 11/93. this was followed by 10 days of
Zithromax with minimal results. The exacerabation accelerated about 2 weeks
prior to her 3/28/94 visit to me. In addition to Lyme, her contemporary
problems included SLE, episodic Sjogren's Syndrome (dry mouth/eyes,
parotiditis), anticardiolipin antibodies without thrombotic events,
polyarthritis (in ankles, knees, hips, shoulders and PIP's of the fingers),
a left IX neuritis, a right Bell's Palsy, ptosis of the left upper eyelid,
myositis of the rectus abdominus muscle, generalized fibrositis and
periostitis, degenerative changes in several finger joints and a few
costochondral joints, and fibrocystic breast disease. Encephalopathy was
absent!
The lab findings included: Lyme Elisa IgG = 1.4 (+), Lyme IgM = 320
(++), Lyme LgM by IFA = 640 (+++), a NEGATIVE Western Blot (only 41 KDA) and
IgG by IFA for LD, positive Lyme IgG Antibody in synovial fluid (Class II
exudate) obtained from the right knee = 1.94, DS-DNA = 5, 120 (less than 10
is normal), ANA = 2,560 ( (+++), positive Sjorgren antibody (SSB = 33),
positive anticardiolipin antibodies (IgG = 66, IgM = 44.9), leukopenia (wbc
= 2,800), and anemia (Hgb = 11.4), 10 bands and 1736 PMN's on CBC
differential, ESR = 32, slightly depressed complement levels: C3 = 55, C4 =
14 Lyme PCR (a test for the DNA of Bb) in synovial fluid was negative......"
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