26th July 21:21
3 WHEN TO SUSPECT LYME DISEASE (diabetes gastritis fibrositis syphilis apnea)
WHEN TO SUSPECT LYME DISEASE
John D. Bleiweiss, MD
Trenton, NJ 4/94
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 ****ysis (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rescinded an earlier prohibition for intravenous antibiotics.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 do***ented.
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 ****s. A relationship to LD can't be
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\0
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 do***ented 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 the****utic 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
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
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
ontributed 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 ****ysis. 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
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 ***ual 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 *** 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 the****utic 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 do***entation 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
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
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
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.