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Poe's fingerThe tell-tale digit.

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concurrent with a defective response to IL-1 by their T
lymphocytes, partictllarly by those of patients whose monocytes spontaneously produced IL-I .
It would therefore seem that scleroderma patients,
who JSO
have been shown to have increased function of T
helper cells (4-6), a T cell subpopulation particularly responsive it0 IL-1 (7), and an early proliferative response in
autologous mixed lymphocyte reactions (8), have, as an
important pathogenetic factor, increased in vivo production
of mcinokines, including IL-1. This could cause fibroblast
proliferation and increased synthesis of both collagen (9) and
glycosaminoglycan (1).
Donato Alarc6n-Segovia, MD
Jorge Alcocer-Varela, MD
Instituto Nacional de la Nutricibn
Salvador Zubirtin
Mexico City, Mexico
With the rationale that patients with chronic primary
uveitis have a relative protease excess due to low levels of
alphal-antitrypsin (3), we have tried to stop the inflammatory process by using eaminocaproic acid.
We describe 1 of our patients, a 52-year-old white
woman who, for 2 years, had chronic primary uveitis that
was resistant to local and systemic treatment with steroids.
She was HLA-B27 negative and her level of alpha,-antitrypsin was 160 mg/ml (normal 240-370).
After 30 days of treatment with .s-aminocaproic acid,
the patient had complete clinical remission of her symptoms.
After discontinuation of the treatment for 7 days, she
developed a flare of the disease, which was controlled after a
second trial with the same drug.
These findings have prompted us to develop a controlled trial to demonstrate the effectiveness of s-aminocaproic acid in the treatment of chronic primary uveitis.
1. Whiteside TL, Worrall JG, Prince RK, Buckingham RB, Rodnan
G. P. Astorga, MD, FACP
M. T. Cuchacovich, MD
University of Chile School of Medicine
Santiago, Chile
GP: Soluble mediators from mononuclear cells increase the
synthesis of glycosaminoglycan by dermal fibroblast cultures
derived from normal subjects and progressive systemic sclerosis
patients. Arthritis Rheum 28: 188-197, 1985
2. Schmidt JA, Mizel SB, Cohen D, Green I: Interleukin 1, a
potential regulator of fibroblast proliferation. J Immunol
128:2 177-2 182, 1982
3. Alcocer-Varela 3, Martinez-Corder0 E, Alarc6n-Segovia D:
Spontaneous production of, and defective response to, interleukin- I by peripheral blood mononuclear cells from patients with
scleroderma. Clin Exp Immunol 59:666-672, 1985
4. Alarc6n-Segovia D, Palacios R, Ibafiez de Kasep G: Human
post-thymicprecursor cells in health and disease. VIII. Immunoregulatory circuits of the peripheral blood mononuclear cells
fromi patients with progressive systemic sclerosis. J Clin Lab
Immunol5:143-148, 1981
5 . Inoshita T, Whiteside TL, Rodnah GP, Taylor FH: Abnormalities of T lymphocyte subsets in patients with progressive systemic sclerosi; (PSS, scleroderma).J Lab Clin Med 97:264-277, 1981
6. Krakauer RS, Sundeen J, Sauder DN, Scherbel A: Abdormalities
of inimunoregulation in progressive systemic sclerosis: evidence
for excess helper cell function and altered B cell function. Arch
Demnatol 117:80-82, 1981
7. Fishlbein E, Alcocer-Varela J, Alarc6n-Segovia D: Cellular bases
of the production of and response to interleukin-2 in man: role of
autollogous rosette-forming T-cell subsets defined with monoclonal antibodies. Immunology 50:223-227, 1983
8. Alcocer-Varela J, Laffon A, Alarcbn-Segovia D, Ibafiez de
Kasep G: Early proliferative response in the human autologous
mixed lymphocyte reaction in scleroderma. J Rheumatol 11:4852, 1984
9. GonzAlez-Amaro R, Alarc6n-Segovia D, Alcocer-Varela J, DiazDe-L.e6n L: Mononuclear cell-fibroblast interactions in scleroderma. Submitted for publication
Is primary chronic uveitis responsive to treatment with
nonsteiroidal antiinflammatory drugs?
To the Editor:
We have read with great interest the article by
Wakefield et al (1) on HLA-B27 and alphal-antitrypsin in
patients with chronic primary uveitis. The relationship between this disease and alpha,-antitrypsin level has been
explored by others as well (2).
1. Wakefield D, Breit SN, Clark P, Penny R: Immunogenetic
factors in inflammatory eye disease: influence of HLA-B27 and
alpha,-antitrypsin phenotypes on disease expression. Arthritis
Rheum 25:1431-1434, 1982
2. Brown WT, Mamelok AE, Beam AG: Anterior uveitis and alpha
1 antitrypsin (letter). Lancet 1:646, 1979
3. Morse JO: Alpha 1-antitrypsin deficiency. N Engl J Med 299:
1045-1048, 1978
Poe’s finger: the tell-tale digit
To the Editor:
It is widely known that cold can precipitate episodes
of Raynaud’s phenomenon, blanching of a digit succeeded
by cyanosis and sometimes hyperemia. That psychological
stress may be another cause of this phenomenon has also
been observed. This is illustrated by the clinical pattern of a
patient recently seen by us.
A 61-year-old man noted the initial manifestation of
his illness 40 years ago. The first evidence was that he
consistently lost money in poker games. Later, a friend
called attention to the fact that his fingers would blanche
when he was dealt a winning hand. Consequently, the other
players had quickly learned not to bet when his fingers were
Twenty years later he developed the other features of
the CREST syndrome (calcinosis, Raynaud’s phenomenon,
esophageal dysmotility, sclerodactyly, and telangiectasias),
as well as discharge of gritty material from the skin, dysphagia, thickening and tightness of the digital skin, arthralgias,
moderately severe restrictive lung disease, impotence, and
Clearly, the digital blanching was due to Raynaud’s
phenomenon induced by the psychological stress of being
dealt winning cards. This interesting and unusual circumstance deserves a memorable name. Among those considered were “poker player’s handicap,” “tattling digit
syndrome,” and “Raynaud’s revenge.” Since there is a
similarity to the murderer who became pale and developed
severe palpitations under psychological stress in Edgar Allen
Poe’s short story, “The Tell-Tale Heart” (Poe EA: Tales of
Mystery and Imagination. New York, Weathervane Books,
1935), we prefer to call this condition “Poe’s finger: the telltale digit.” The name is particularly appropriate since the
patient who manifested the condition was seen in Richmond,
the childhood home of Poe.
Elam Toone, MD
George F. Moxley, MD
David M. Hudgins, MD
Medical College of Virginia
McGuire Veterans Administration
Medical Center
Richmond, VA
synovial environment are better able to proliferate in response to IL-2-containing synovial fluids than are IL-2dependent lines generated similarly from peripheral blood
Richard J. Warrington, MB, BS, PhD
Rachel McKenna, PhD
William Ofosu-Appiah, MSc
John A. Wilkins, PhD
University of Manitoba
Winnipeg, Manitoba, Canada
1. Husby G, Williams RC Jr: Immunohistochemical studies of
interleukin-2 and yinterferon in rheumatoid arthritis. Arthritis
Rheum 28:174-181, 1985
2. Wilkins JA, Warrington RJ: The generation of interleukin-2
dependent continuous T cell lines from synovial fluid mononuclear cells in rheumatoid arthritis (abstract). Clin Res 30:810A,
3. Fontaine A, Hengartner H, Weber E, Fehr K, Grob PJ, Cohen G:
Interleukin 1 activity in the synovial fluid of patients with
rheumatoid arthritis. Rheumatol Int 2:49-53, 1982
demonstration of an interleukin-2 like activity in the synovial
fluids of rheumatoid arthritis patients. J Rheumatol 10: 109-1 13,
4. Wilkins JA, Warrington RJ, Sigurdson SL,Rutherford
5 . Wilkins JA, Olivier SL, Warrington RJ: Generation of interleukin-2-dependent T cell lines from synovial fluids in rheumatoid
arthritis. Clin Exp Immunol 58: 1-6, 1984
Comment on article by Husby and Williams
To the Editor:
We read with interest the article by Husby and
Williams (1) on the immunohistochemical studies of interleukin-2 (IL-2) and y-interferon in rheumatoid arthritis (RA)
synovial tissue. The authors refer to our finding that IL-2dependent T cells are detectable in the synovial fluids of RA
patients (2) and mention that interleukin-1, which has also
been demonstrated in such fluids (3), acts as a stimulus for
IL-2 production. We would like to point out that we have
also found IL-2-like activity in synovial fluids of 12 of 14 RA
patients studied (4), but not in degenerative or traumatic
joint disease fluids, as detected by the IL-2-dependent
murine T cell line, CT-6.
One of the problems of demonstrating this IL-2
activity was the presence of a high molecular weight inhibitor, which had to be inactivated or diluted out before IL-2
was detectable. These findings would certainly suggest that
IL-2-producing cells are present in the synovial environment. We were similarly able to demonstrate interferon
(IFN) activity in RA synovial fluids, using a functional viralinhibition test system, in 22 of 31 samples tested.
In contrast, when the lymphokine-producing capabilities of IL-2-dependent T cell clones derived from synovial
fluids and tissues were examined, a dissociation between IL2 and IFN was noted; all T cell clones tested, no matter what
their phenotype, released IFN in response to mitogen stimulation, whereas none of these clones produced IL-2. Of
course, this dissociation may simply reflect an in vitro
selection process for IL-2 dependency, rather than a specific
defect in IL-2 production or in vivo selection. However, we
have some evidence that T cell lines generated from the
Regulation of susceptibility to bacterial cell
wall-induced arthritis in rats
To the Editor:
Chronic proliferative and erosive synovitis can be
induced in rats by systemic injection of an aqueous suspension of cell wall fragments from selected bacteria such as
Streptococcus pyogenes, group A or Lactobacillus casei
(1,2). This experimental model exhibits many of the clinical,
pathologic, and immunologic features of rheumatoid arthritis
and various other inflammatory arthritides, and thus provides an experimental system to explore mechanistic questions relevant to human disease. We have been particularly
interested in defining mechanisms that regulate susceptibility and resistance to chronic disease in this experimental
We have previously demonstrated that following an
intraperitoneal injection of an aqueous suspension of cell
wall fragments from group A streptococci into LEW/N
female rats, the cell wall fragments disseminate to and
persist in synovial tissues of peripheral joints (3). The
localization of cell wall antigens to synovial tissues in this
strain of rats is associated with the development of severe,
chronic, proliferative and erosive synovitis. In the same
study, we were able to obtain only equivocal evidence, by
immunofluorescence techniques, of cell wall antigens in the
synovium of chronic arthritis-resistant F344/N female rats.
Prompted by our observations that l4C-radio1abeled
cell wall fragments from L casei disseminate to and persist in
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