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Treatment of asymptomatic retrospectively diagnosed Lyme diseasecomment on the report by Christian.

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1637
LETTERS
4. Scott JP, Gerber P, Maryjowski MC, Pachman LM: Evidence for
intravascular coagulation in systemic onset, but not polyarticular, juvenile rheumatoid arthritis. Arthritis Rheum 28:256-261,
1985
5 . Schwartz D, Averbruch M, Pines A, Kornovsky R, Lev0 Y:
Disseminated intravascular coagulation with renal and liver damage as the predominant manifestations of recurrent relapses in
systemic juvenile rheumatoid arthritis. Ann Rheum Dis 5 1:347349, 1992
6. Brewer EJ Jr, Giannini EH, Barkley E: Gold therapy in the
management of juvenile rheumatoid arthritis. Arthritis Rheum
23:404411, 1980
7. Furst DE: Proposition: methotrexate should not be the first
second-line agent used in NSAID failures. Semin Arthritis
Rheum 2369-75, 1990
8. Furst DE: Toxicity of antirheumatic medications in children with
juvenile arthritis. J Rheumatol 19 (suppl 33):ll-15, 1992
Rheumatoid arthritis, fecundity, and coital rates:
comment on the article by Nelson et a1
To the Editor:
In their analysis of rates of conception in rheumatoid
arthritis (RA) patients, Nelson et a1 (1) reported that prior to
disease onset, women with RA have significantly lower
fecundity than control subjects. The authors give grounds
for supposing that the probability of pregnancy was merely
lowered in most patients rather than reduced to zero in
some: the proportions without children were almost equal in
the patient and control groups.
A number of possible physiologic causes of the
diminished fecundity were suggested. I should like to suggest a behavioral cause: low coital rates. Sexual difficulties
and dysfunction are common in patients with arthritis (2,3),
but they may pre-date the disease. I have reviewed the data
on androgen levels in RA patients and found that low levels
of androgens seem t o be (at least partially) genetically
programmed precursors of the disease rather than (or as well
as) effects of it (4).
The relationship between androgen levels and coital
rate is undoubtedly complex in both men and women (5).
However, both total testosterone and free testosterone levels at mid-cycle have been reported to correlate significantly
with coital rate in married women (6).
The relationship between coital rate and fecundability (the probability of conceiving in a month at risk) is strong
(7). I therefore suggest that the low fecundity of women who
later develop RA is due to low coital rates, which in turn, are
caused by the low androgen levels characteristic of people
who later develop RA. If this argument is correct, it would
presumably also apply to men who develop the disease.
William James, PhD
University College London
London, U K
1. Nelson JL, Koepsell TD, Dugowson CE, Voigt LF, Daling JR,
Hansen JA: Fecundity before disease onset in women with
rheumatoid arthritis. Arthritis Rheum 36:7-14, 1993
2. Blake DJ, Maisiak R, Koplan A: Sexual dysfunction among
subjects with arthritis. Clin Rheumatol 7:50-60, 1988
3. Currey HLF: Osteoarthritis of the hip joint and sexual activity.
Ann Rheum Dis 29:488-493, 1970
4. James WH: Rheumatoid arthritis, the contraceptive pill and
androgens. Ann Rheum Dis 52:470-474, 1993
5 . Kemper TD: Social Structure and Testosterone. London, Rutgers University Press, 1990
6. Moms NM, Udry JR, Khan-Dawood F, Dawood MY: Marital
sex frequency and midcycle female testosterone. Arch Sex
Behav 16:27-37, 1987
7. Potter RG, Millman SR: Fecundability and the frequency of
marital intercourse: new models incorporating the aging of gametes. Popul Stud 40:159-170, 1986
Reply
To the Editor:
We thank Dr. James for his suggestion regarding
another possible explanation for our study finding of decreased fecundity in women with RA prior to disease onset.
Studies to date appear to lack consensus regarding androgen
levels in women with established RA (1,2). We look forward
to his forthcoming article about androgens in RA (3).
J. Lee Nelson, MD
Fred Hutchinson Cancer Research Center
Thomas D. Koepsell, MD, MPH
Carin E. Dugowson, MD, MPH
University of Washington
Lynda F. Voigt, PhD
Fred Hutchinson Cancer Research Center
Seattle, W A
1. Bird HA: The epidemiology of rheumatic diseases in relation to
hormonal factors, Pregnancy, Autoimmunity, and Connective
Tissue Disorders. Edited by JS Scott, HA Bird. New York,
Oxford University Press, 1990
2. Spector TD, Perry LA, Tubb G, Huskisson EC: Androgen status
of females with rheumatoid arthritis. Br J Rheumatol26:316-318,
1987
3. James WH: Rheumatoid arthritis, the contraceptive pill and
androgens. Ann Rheum Dis 52:470-474, 1993
Treatment of asymptomatic, retrospectively diagnosed,
Lyme disease: comment on the report by Christian
To the Editor:
Dr. Charles Christian (1) has welcomed advice about
a patient he presented who developed a classic picture of
Lyme arthritis a quarter-century ago, who never received
therapy for it, and who has been asymptomatic for 23 years.
This is one of the earliest cases documented in retrospect, its
onset a decade before we offered Lyme disease as a distinct
clinical entity (2). In January 1992 this individual was found
to have high-titer antibodies against Borrelia burgdorferi by
enzyme-linked immunosorbent assay (ELISA), and 15 bands
on Western blot analysis. (Note that this clinical situation is
diametrically opposed to the one seen most frequently at our
referral center and others [3], where patients arrive with
histories of often repetitive treatment, and it is a reasonable
basis for diagnosis that is lacking.)
Dr. Christian’s four specific questions are 1) Should
LETTERS
1638
the patient have a lumbar puncture and other, more detailed
neurologic studies? 2) Should he be treated, and, if so, 3)
with oral or intravenous antibiotics? 4) If he is treated,
should there be concern about a Jarisch-Herxheimer reaction? We venture the following opinions. We would treat the
patient with a 30-day regimen of oral antibiotics. We would
choose doxycycline, 100 mg twice daily, because it penetrates the central nervous system better than amoxicillin (the
other major choice), and because it is at least as efficacious
as the latter, has fewer side effects (especially given protection against sunlight), and is easier to comply with than a
3-times-a-day drug (4). A Jarisch-Herxheimer reaction,
should one occur, is not likely to cause more than transient
discomfort.
Why treat? Because, like Dr. Christian, we are
concerned about the possibility, however small, of late
Lyme disease. Like the individual described here, patients
with untreated Lyme arthritis tend to stop having attacks of
joint disease, at a rate of 10-20% per year (3,
but that does
not guarantee that they are home free. Among 39 untreated
children who recovered from Lyme arthritis and were
watched instead of treated (6), 12 had occasional episodes of
joint pain and 1 had marked fatigue. Two of the 39 patients,
neither of whom had neurologic complaints early in the
disease, had a subtle encephalopathy, with memory impairment, headache, and fatigue 11 and 12 years after disease
onset. Among 27 patients with chronic neurologic syndromes due to Lyme disease (7), 44% of whom had not been
treated with antibiotics, the most common chronic central
nervous system involvement was subacute encephalopathy,
affecting memory, mood, sleep, and language ability. Polyneuropathy and, rarely, leukoencephalopathy were seen.
The time from onset of disease to onset of symptoms was
often years.
Why oral antibiotics? Because the man is well. There
is no evidence to support either route of administration in
this situation. The inconvenience, risk, and expense of
parenteral therapy seem unwarranted.
Additional evaluation before treatment-e.g., lumbar puncture, neuropsychological testing, nerve conduction
studies, IgM ELISA, IgM Western blot? Not necessary,
because they would not change the projected program of
therapy. Of course these things are of considerable interest,
and might well be done with an informed study patient. In
the current situation, they can always be carried out later,
should the patient cease to be well, or should the level of
anxiety become higher than it seems to have been here.
Incidentally, why was that Lyme titer obtained in
January 1992, during a general health assessment-i.e.,
which came first, the history or the titer?
Jane D. Cooper, MD
Robert T. Schoen, MD
Stephen E. Malawista, MD
Yale University School of Medicine
New Haven, CT
1 . Christian CL: Management of asymptomatic Borrelia burgdorferi
infection. Arthritis Rheum 35: 1395, 1992
2. Steere AC, Malawista SE, Snydman DR, Shope RE, Andiman
WA, Ross MR, Steele FM: Lyme arthritis: an epidemic of
oligoarticulararthritis in children and adults in three Connecticut
communities. Arthritis Rheum 20:7-17, 1977
3. Sigal LH: Summary of the first 100 patients seen at a Lyme
disease referral center. Am J Med 88577481, 1990
4. Rahn D, Malawista S: Lyme disease: recommendations for
diagnosis and treatment. Ann Intern Med 114:472-481, 1991
5. Steere AC, Schoen RT, Taylor E: The clinical evolution of Lyme
arthritis. Ann Intern Med 107:725-731, 1987
6. Szer IS, Taylor E, Steere AC: The long-term course of Lyme
arthritis in children. N Engl J Med 322159-163, 1991
7. Logigian EL, Kaplan RF, Steere AC: Chronic neurologic manifestations of Lyme disease. N Engl J Med 323:1438-1444, 1990
Reply
To the Editor:
The invitation for advice regarding the management
of asymptomatic Lyme disease generated recommendations
that varied from “do nothing” to “treat with intravenous
ceftriaxone”; a few respondents thought more detailed neurologic evaluations, including serologic study of cerebrospinal fluid, should be performed. I am indebted to Drs.
Cooper, Schoen, and Malawista for their rational recommendation (oral doxycycline), implementation of which would be
convenient and inexpensive.
One respondent gave me a lesson in geography:
Cuttyhunk is in Buzzard’s Bay, near its confluence with
Vineyard Sound, not Long Island Sound. The lesson was
reinforced when the New York Times, at about the same
time, published a map showing where Queen Elizabeth I1
(the boat) scraped her bottom, near Cuttyhunk.
Regarding the last sentence in the letter from Cooper
et al, the history came first. When the patient and I met in
1968 I concluded that he had “atypical rheumatoid arthritis”
although the migratory, pauciarticular pattern of disease
(particularly with the medical history) now would be easily
recognized as “typical” Lyme disease. I knew from indirect
information that the patient’s illness remitted and that he had
remained well, but once the Yale group described and
characterized Lyme disease, both he and I concluded that he
almost certainly had had it. The followup evaluation early
this year was requested by me (for intellectual purposes), but
maybe the communications stimulated by the report in
Arthritis and Rheumatism will result in treatment-the patient and I will discuss it.
Charles L. Christian, MD
The Hospital for Special Surgery
New York, NY
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