In Memory of Dr. Bleiweiss: Pt 3 " When to Suspect LD"
JoeGriz
Thanks Rita for the post. It is similar to the one on Donna's wb site.
The essay at her site is dated November, 1992. It will be interesting to
read and compare the 11/92 with this aticle dated 4/94. Do you have a
reference on this article? Was it ever published? Has his personal story
been written or published? He sounds like a true hero that needs to be
remembered.
Thanks
Elizabeth
Lynne Pitcher
Thank you Rita for supplying this. I had heard of Dr. Bleiweiss, but did
not know this story. How sad for us all that his outlook did not prevail
from the start, and what a motivator for us to become more active in our
own behalf. Lynne
Rita Stanley
> . He must have been a very special person. When we get ready to
> give up we need to think of him and the other doctors that have put so
> much on the line to help us. They can't keep doing all this without our
> support! georgia
Yes and yes again.
To know that maybe your doc is laying it all on the line for you; or maybe
he has and is now gone( as in my situation), puts it in perspective that we
need to fight towards common goals especially keeping our treating docs
from being undone by the powers that be.
To remember the fallen and the continuing-to-struggle heroes in this fight
can give us the impetus to carry on when it seems all so overwhelming.
Rita
MHHirsch
Rita,
Thank you so much for reprinting the Bleiweiss article(s). Your
darlin' daughter didn't type all that in, did she? If so, give her a big
hug for me.
I think people do need to know that your doctor, who died so much too
early from cancer, was Dr. Paul LaVoie, a true scientist and physician. I
am sorry I never got to meet him. I still admire his writing and have the
Conn's Current Therapy article he wrote - 1992, wasn't it? I know he was
much respected by his peers and his patients.
Thought I would mention the above, to show that we have lost two
dedicated docs.
Ann
Rita Stanley
Within 72 hours of stopping Motrin use, the wbc rebounded to 4,700 but
by then the patient had developed an acute partial paralysis of her legs
(3/5), with deltoid, biceps and vastus lateralis myositis, a new left VII
neuritis, and the polyarthritis was more ebullient and painful. A fever of
101 degrees F had appeared. Susequently, hypertension (BP = 154/94), a
small posterior pericardial effusion and hypokalemia (K+ = 3.3 mmol/L) were
appreciated. Urine and Blood Cultures were negative. Urine analysis (U/A)
contained 30-35 wbc, but proteinuria and cylindruria were absent. Elevated
LFT's were again encountered. The patientdeclined, at various times: an
MRI of brain, a bone marrow aspiration, spinal tap, EEG, and EMG.
On admission to the hospital, IV Claforan was initiated. At 41 hours,
a crescendo J-H reaction attained a fever apex of 103 degrees F, but the
wbc count again fell to a nadir of 1,800 with neutropenia (67.2% = 1200
PMN's). As the patient gradually defervesced (temp = 100 degrees F at 75
hours), the wbc count slowly ascended to 2,700 (PMN's = 2100) inspite of
continued Claforan, The paralysis remitted over the initial 48 hours.
concommitantly, the LFT's normalized rapidly, the Sjogren manifestations
and cranial neuropathies disappeared, the BP became 120/70, muscle
tenderness was reduced and the U/A was devoid of abnormalities.
By discharge to home on the 6th hospital day, the polyarthritis (as
judged by joint swelling) had resolved in 75% of the involved joints and
was ameliorated in the rest, and the fever = 99.6 degrees F. However, the
knees were still painful and hobbled the patient, and range of motion was
impaired in the knees, shoulders and hips. Biaxin, begun day 6, caused a
transient acute memory loss from day 8-9 without fever.
Features supportive of the SLE diagnosis include: leukopenia, positive
ANA, a high DS-DNA titer, arthritis (R/O erosions).
During the hospital stay, a more thoughtful insurance medical director
rescinded an earlier prohibition for intravenous antibiotics. Had the
first "reviewer" acceded to my initial plan of care, the paralysis and the
hospitalization it prompted could have been avoided. Treatment is
advancing. Repeat DS-DNA, ESR, ANA, CPK, C3, CH50, and X-Ray and MRI
evaluation of joints is anticipated. The anemia is being investigated.
The tabulation of rheumatologic syndromes, either caused by LD or
affiliated with it, is growing. Drs. Weber and Schwartzberg have reported
Polymyalgia Rheumatica apparently caused by LD. As in the case above,
Sjogren's Syndrome with LD has been published. Antibodies to Bb in the
context of Psoriatic arthritis, systemic sclerosis and Reiter's Syndrome
have been documented.
An expanding cohort of patients in my practice appear to have
long-standing LD that dates to their "growth spurt" years and their past
medical history contains the previous development of Osgood-Schlatter's
Syndrome (water on the knee) in their teens. A relationship to LD can't be
excluded.
Arthralgias and bone pain in LD can be excruiating. It is the imprudent
clinician or parent who lackadaisically attributes these symptoms to
"gowing pains" or aging.
Another patient of mine recalled recurrent and migratory polyarthritis
since he was 18 (1966). Monthly Medrol Dose Packs (steroids) failed to
alter the clinical picture. In 1987, he was hospitalized with an acute
exudative synovitis of the knee, whereupon ear lobe biopsy demonstrated the
classic histologic feature of Relapsing Polychondritis, a very rare
disorder with a peak onset in the 5th decade of life. Inspite of continual
high dose steroid treatment, (and later methotrexate with non-steroidal
anti-inflammatory agents), he eventually developed a deforming arthropathy
in his hands which progressed slowly between 6/90 to 12/92. Earlier
physicians had discounted the significance of a positive Lyme Elisa = 1.09
in 4/91 as "low titer". An unsuspected encephalopathy betrayed its
existence as memory and concentration impairment beginning 1/91. The
patient presented for LD evaluation 1/93. Laboratory values include: an
IgG by Elisa = 14.7, IgM by IFA = 80 and the Western Blot had bands at 31
and 41 KDA. the polysynovitis and encephalopathy proved rapidly responsive
to antibiotics for LD. The patient was quickly emancipated from the other
medications although steroids had to be slowly tapered and are now down to
an inconsequential dose without recurrence of rheumatologic complications.
The patient, although symptom free while on antibiotics, has permanent
crippling deformities of the hands.
Cardiac complications arise in 8-12% of LD cases. Conduction defects
and heart block, of which first-degree is the most common, can be
discovered on EKG. A long rhythm strip should be employed to detect
intermittent blocks. Higher degrees of heart block can result in fainting
or death and may require cardiac pacemaker.
Sudden death can also result from arrythmias. Fast and slow heart
rates occur, usually at the time of symptom flares, and sometimes in the
manner of Sick Sinus Syndrome (tachy/brady). Ventricular tachycardia has
been documented to attend LD infection in the heart, confirmed on cardiac
biopsy. The cardiomyopathy may be complicated by congestive heart failure
(CHF) as the following case might illustrate.
I had been treating a white male in his 60's for several years for LD
with (initially IV antibiotics) oral antibiotics and in the main, his
symptoms were controlled. However, he would occasionally complain of
"traveling pains" (arthralgias). I was impressed with mild encepahalopathy
(confusion) and he had a brief monoarticular arthritis of the right knee.
In concert with numerous consultants, our work up over a few years
also uncovered: Diabetes mellitus (non-insulin dependent), COPD;
hypertensive, ischemic and dilated cardiomyopathy (enlarged heart); both
diabetic and hepatitis C related liver involvement confirmed on liver
biopsy (not helped by a prior preference for alcohol); colon cancer for
which he underwent a transverse colectomy (partial removal of the
colon),colonic polyps; and Barrett's esophagus. A fall at work caused a
LEFT sided appendix to rupture (talk about being thrown a curve?!).
Most significantly, he had been troubled with recurrent non-sustained
ventricular tachycardia, atrial fibrillation and episodic CHF all of which
increasingly escaped therapeutic control with the usual measures. This
resulted in frequent hospitalizations, He had a small myocardial
infarction of the diagonal branch in the past. A MUGA scan revealed an
ejection fraction (a measure of cardiac output and pump function) of only
21% which is quite low. His exercise intolerance due to shortness of
breath fluctuated but interfered substantially with his quality of life.
During a 1993 hospitalization for acute CHF compounded by ventricular
arrythmias, we found that these problems were resisting attempts to
completely regulate pharmacologically. In the past, I had noted that when
his LD was flaring up, his cardiac status would deteriorate. As the
patient had incurred Pulmonary Fibrosis (ultimately reversible) as a side
effect of an antiarrythmic drug, he was not deemed a suitable candidate for
cardiac biopsy.
Intravenous Claforan was begun empitically and to our astonishment, he
recuperated from his CHF in short order. A repeat MUGA scan on day 5 of IV
Claforan showed a NORMAL ejection fraction of 51%! This welcome and
salutory change in status was maintained by prolonged IV therapy. On a
program of continued oral antibiotics, CHF was controlled to such good
effect that he was able to walk 5 miles in the dead of winter to my office
without any shortness of breath or chest pain.
To my mind, one of the more remarkable aspects of this case was the
disproportionate way in which cardiac complications dominated the clinical
course relative to the other LD symptoms and yet all responded fortuitously
to IV antibiotics. Thus treatment may not eradicate symptoms
synchronously. The other salient lesson here is that he probably has
CHRONIC LD, a diagnosis made purely on clinical grounds as serologies were
always negative.
Again, differentiating Lyme cardiomyopathy from a mere exacerbation of
cardiomyopathy (due to other causes) by LD remains an unresolved issue.
Intuitively, we might suppose that the other component etiologies which
contributed to his cardiomyopathy would not respond so briskly to
antibiotics, unless there was an as yet undefined relationship with the LD.
His cardiac and BP medications are now providing the customary benefits in
a predictable fashion. On oral therapy alone, mild shortness of breath to
stairs is once again emerging over time. Further evaluation is forthcoming.
Mitral valve prolapse is not uncommonly found in LD. MVP can be
associated with confounding chest pain and ventricular arrythmias. It is
often accompanied by Mg++ deficiency and LD can cause Mg++ levels to be
low. In a few of my patients, MVP developed only after the onset of LD and
resolved with LD treatment. Chest pain due to LD may arise from numerous
causes: myocarditis, pericarditis, angina, asthma, bronchitis, periostitis
of the ribs, pectoral myositis and tendonitis, sternoclavicular and
costochondral arthritis, esophagitis and esophageal spasm, stomach acid
reflux, and gastritis.
Elevated ACE (angiotensin converting enzyme) levels have been detected
in LD (Leigner, 1990). The relationship between high ACE levels and heart
disease may provide a mechanism to explain LD's anecdotally suspected
tendency to accelerate Coronary Heart Disease and incite hypertension.
Possibly, Syndrome X (angina with normal coronary arteries at
catheterization) is due to LD induced arterial spasm, an event that might
be enhanced by direct perivasculitis and/or Mg++ deficiency (see Grisold, M
abstract No. 55F, V Intnat'l Lyme Symposium).
Potassium deficiency without an obvious origin irregularly evolves in
LD. Rarely, the K+ losses are profound. This could be due to Mg++
deficiency. New onset or difficult to control hypertension is more likely
to be seen. LD should be part of the evaluation of hypertension. LD
treatment has permitted easy BP control in several patients, some of whom
were able to forego using their traditional hypertension medications.
Increasingly, I am encountering thyroid disease in LD. A local
endocrinologist has remarked to me privately that the incidence of thyroid
involvement in LD may be greater than expected from the normal population.
A final judgement awaits formal statistical analysis. In many of these
patients, the thyroid dysfunction was seen to originate in the pituitary or
hypothalmus. Remaining alert to the possibility of thyroid disease is
essential because there can be considerable clinical overlap with LD.
Subacute thyroiditis is the most prevalent thyroid phenomenon I see in LD.
Hypoadrenalism can uncommonly develop. Uncorrected hormonal aberrations
can vitiate otherwise effective LD therapy. Like any infection, LD can
provoke the onset of hyperglycemia and alter the facility with which
diabetes is managed.
Impaired fertility and a loss of libido is not infrequent in LD. A
reversible cause of infertility should be sought and ought to include LD.
Reduced sexual interest without an ostensible justification is usually
misinterpreted by the partner with predictable social and psychological
turmoil. LD infection in the CNS or in the sex glands may be causal. In a
few female LD patients, disturbed estrogen and progesterone levels were
found. Early "menpause", skipped menses, and heavy menstrual flow
represent a few of the perturbations in LD.
Women with symptomatic LD can experience new onset or heightened PMS
(ballistic mood swings and irritability), or perimenstrual headache or
cramps. The last of these theoretically could also be due to Pelvic LD
infection (ooperitis or salpingitis) and/or elevated PGE-2 (prostaglandin
E-2) levels, the latter having been reported in LD. A surfeit of PGE-2,
free radicals, altered fat metabolism and general immunosuppression by LD
may contribute to a predilection (stimulate or predispose) for oncogennesis
(forming cancer). Carcinomas are not unknown in LD: melanoma, thyroid
cancer, and lymphoma have been published. Free radicals, by engendering
connective tissue cross-linking, could be responsible for intraabdominal
adhesions to form, and for some LD patients to appear older than their
stated age, or have a haggard facial appearance.
Breast pain due to mastitis and testicular pain from orchitis have
been described by some of my patients. So far, there are 3 men in our
files whose chief complaint with LD was pelvic pain due to chronic
prostatitis. The therapeutic strategems for LD provided superior relief
whereas using Cipro or Doxycycline alone gave partial or temporary
improvement
Flawed studies have created the impression that pregnancy outcomes are
not influenced by LD. There is substantial documentation to suggest a
causal relationship between LD and stillbirths, congenital abnormalities,
spontaneous abortion, low birth weight babies, prematurity and intrauterine
fetal infection acquired from the mother. An outcome of untreated LD
arising from Mg++ deficiency could be pre-eclampsia (hypertension) or
eclampsia (hypertension with seizures). Magnesium is often relied on to
treat these problems. Women with LD in pregnancy can experience severe
morning sickness, gestational diabetes mellitus and prominent flares of
Lyme related symptoms. As both LD and Sudden Infant Death Syndromeare
attended by sleep apnea, this should impel further research to determine if
some babies with SIDS are actually suffering from LD. Bb can appear in the
breast milk.
Lyme patients very often complain of heel pain. This may be due to
an underlying plantar fasciitis, with or without a heel spur, or
periostitis of the heel. Epicondylitis (tennis elbow) is another
complication. Carpal Tunnel Syndrome can also develop in untreated LD.
Lyme patients tend to heal slowly and are prone to musculoskeletal
injuries, sometimes without the usual antecedents. One patient sustained a
vertebral facet dislocation while shaving ( the usual context is athletic).
Even in the well conditioned athlete, there can be an unexpected spate of
muscle cramps, sprains, tendonitis and bone or joint pains at the sites of
load bearing.
Muscle weakness occurs in some LD patients, More commonly, exertional
performance is limited by shortness of breath, poor coordination,
musculoskeletal discomfort, or fatgue. Exercise without or early in
treatment can precipitate a flare of fatigue, especially the following day.
Low back ache can arise from sacroilitis, paravertebral lumbosacral
muscle strain/spasm, and herniated vertebral discs. In a few patients,
spinal stenosis is encountered.
Inflammation of the abdominal wall muscles, in particular the rectus
abdominus is not an infrequent problem. Usually the tender sites are
focal, involving more often than not, the lateral borders of the rectus
abdominus muscle. Nausea is often present as well. The sites are best
located when the patient is performing a Valsalva maneuver or doing a
partial sit up. Failure to appreciate the abdominal myositis may lead to
avoidable extensive GI workup.
A very helpful diagnostic maneuver is palpatory tenderness of the
medial tibia shaft due to periostitis (inflammation of the tissue around
the bone if not the bone itself). Periostitis is also common in another
spirochetal disease, syphilis (Textbook of Medicine, Ed: Kelley, 1989, p.
1587) and is responsible for the bone pain that both syphlitic and Lyme
patients experience. Tenderness is easily elicited in 95% or more of LD
patients simply by pressing the bony aspect of the thumb joint against the
medial aspect of the tibia about 3-6 inches above the ankle. The intensity
of the pain experienced by the patient can vary, but is often exquisite and
will cause the leg to recoil abruptly. The pain often lingers after this
procedure. In a minority of LD cases, periostitis is generalized and I
have appreciated skull involvement in a few instances. A small proportion
of LD patients have periostitis.
As a result of fibrositis, myositis, periostitis, is it any wonder tha
the ill LD patient view hugs as potential torment? The chagrin of
mystified family members is understandable. Self-examination for
periostitis can be unreliable. Periostitis pubis (of the pubic bone) can
mimic bladder pain or be the origin of lower midline abdominal pain,
especially in children.
Lyme (and Brucella) should be included in the differential diagnosis
of Desert Storm Syndrome, with which LD shares many features.
The abundant research opportunites should be clear to all. It is
unnecessary to give Lyme Disease the "Galileo" treatment. Thank you for
your interest. comments and criticisms are welcome.
* * * * * * * * * * * * * * * * * * * **
John Bleiweiss, MD. committed suicide Aug 13, 1995.
May we never forget.
Rita Stanley
JoeGriz <joe...@aol.com> wrote in article
<19970816151...@ladder01.news.aol.com>...
> Thanks Rita for the post. It is similar to the one on Donna's wb site.
> The essay at her site is dated November, 1992. It will be interesting to
> read and compare the 11/92 with this aticle dated 4/94. Do you have a
> reference on this article? Was it ever published?
No, never published.
Has his personal story
> been written or published?
No, not to my knowledge. I think his story along with the other doctors'
stories who have lost their licenses or had their practices limited because
they chose to treat and diagnose in nonconservative (Big Al's Cookbook
style) ways should be told far and wide to the public. Let the public see
what tactics are used by the well-heeled and connected "researchers" and
"doctors" to keep their theories foremost and how they engender fear in
physicians who would dare practice any other way.
He sounds like a true hero that needs to be
> remembered.
I agree.
Rita
JWissmille
I had heard about Dr. Bleiweiss,also, but never knew any of the story.
I found his info about Lyme disease when I first started using the
computer. That wasn't very long ago. When I read the article, "When to
Suspect Lyme Disease", I couldn't believe it. I have spent many hours
at the medical library in the past few years reading medical journal
articles, not because I wanted to. I wanted the facts to help people
close to me and I could see not too many people had them. Dr.
Bleiweiss's article is closer than any other at putting "the big picture"
together. He must have been a very special person. When we get ready to
David Bartholomew
>John D. Bleiweiss, M.D. committed suicide on Aug 13th 1995.
>May we never forget.
How could I possibly forget?
My ICD-9's keep reminding me constantly;
1 Ld
2 Encephalopathy
3 Myositis
4 Periostitis
5 Ataxia
6 Proximal Myopathy
7 Tendinitis
8 Sacroiliitis
9 Neuritis
10 Costochondritis
11 Fatigue
12 Imbalance
13 Rash
14 Motor Neuropathy
He only missed a few! Notably the arthropathies and
and the osteoporosis onset age 36. And a blip in my brain<G>.
Dave
Mark & Maureen Conrad
Rita,
It seems the first and third parts to the writings of Dr. Bleiweiss
which you posted are no longer online - message says that perhaps they
have expired.
Would you kindly repost these parts of his most interesting writing?
-- Thank you, Mark & Maureen
Rita Stanley
Mark & Maureen Conrad <mcs...@rmi.net> wrote in article
<33F746...@rmi.net>...
Will repost all 3 sections incase others did not get one section or
another.
Rita
Rita Stanley
MHHirsch <mhhi...@aol.com> wrote in article
<19970816234...@ladder02.news.aol.com>...
Dear ann,
Thank you for recognizing Dr. Paul Lavoie. Although he was not my docotr,
I have many Lyme friends who went to him on the West coast. Truly a
wonderful, caring and years ahead thinker.
As you note, I often speak of "losing my doctor". Well, he was lost not to
cancer, but to the powers that be. He was investigated by the Medical
Board, and had his practice limited (he was given the choice of losing his
license or his Lyme practice) because he treated long-term antibiotics and
over diagnosed Lyme. And I must report we are talking oral medication, not
IV. That was three years ago.
Going through the experience of losing the doc who saved your life and that
of a hundred others, seeing it up close and personal, inheriting the
situation as a support person, and then seeing how docs become unwilling to
touch Lyme as a result is one of the primary reasons why I am outspoken
about what is going on. I deal on a daily basis with people who cannot get
help even though they test positive (seronegatives - guess?), fall down in
front of doctors, or are suicidal. Experience has opened my eyes real
wide.
And my ex-doc was only one of many who went "quietly into the night" to
survive as doctors. There are quite a few unsung heroes out there, and my
ex-doc is right up there with them. He was truly brillant and years ahead
in his approaches, too, as his former patients so well know.
And I will never forget what happened to him. Never.
Rita
CRESCH1
In article <19970816234...@ladder02.news.aol.com>,
mhhi...@aol.com (MHHirsch) writes:
>think people do need to know that your doctor, who died so much too
>early from cancer, was Dr. Paul LaVoie, a true scientist and physician. I
>am sorry I never got to meet him. I still admire his writing and have the
>Conn's Current Therapy article he wrote - 1992, wasn't it? I know he was
>much respected by his peers and his patients.
> Thought I would mention the above, to show that we have lost two
>dedicated docs.
Make that three. Although Dr. Natole of Saginaw, Michigan, is still alive,
Lyme patients have also lost this dedicated doctor through the
persecutation he has had to endure by the state health department, and the
Michigan Board of Medicine. At this time, while his appeal of the MBM's
decision is being considered, he is not allowed to treat Lyme patients.
Even if his appeal is successful, and the state and MBM don't pursue this
further, he may never return to treating Lyme patients because of what he
has had to endure over the past several years.
If you would like this hero of ours to know how much the Lyme community
supports him, why don't you drop him a line: Dr. Joseph Natole, 4701 Towne
Center, Saginaw, MI 48604. I'm sure it would mean alot to him to realize
how many people still are behind him.
Sharon
DenimN
Dear Sharon,
Does Dr. Natole still need legal funds? If so, let me know = I can still
donate a little every month if he needs it. Please give him my warm
wishes and good thoughts, OK? My heart is with him tho I don't know him.
Denim
DenimN
Denim, I know you have already sent a donation to support this study - you
are always in the first ranks. Thank you.><>>
Dear Sharon,
You are very welcome for the donations. What I like is that you put an
envelope in with your newsletter so I won't forget to send another monthly
donation...only I didn't get one the last time! I'll try to remember to
send a check. I'll try to send $25.00 to $50.00 every month. Thanks for
the address on this NG. I hope the rest of the people here will send
donations, too.
HBOT research is very important - even tho it did not help me, I still
support it all I can. There may be something that someone can figure out
that will help us. We're all in such bad shape and I know that all of us
are waiting for a cure.
Denim