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Nailfold capillary abnormalities and organ involvement in scleroderma.

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and a significant deterioration in renal function (BUN 112
mg/dl, creatinine 4.1 mg/dl). Peritoneal dialysis was started
and effectively lowered BUN and serum creatinine levels
(63.0 mg’dl and 2.8 mg/dl, respectively). Serum and dialysate
gold levels were assayed using a modification of previously
described methods, improving sensitivity to as low as 1.0
pg% (5). In 2 separate clearance trials performed 20 days
apart, dialysate gold levels were 1 . 1 pg% and 1 .O pg%, while
serum gold levels were 60 pg% and 28 pg%, respectively.
Using Boen’s formula (6), peritoneal clearance of gold was
calculated to be 0.46 mlhinute and 0.57 mlhinute in
respective trials.
Although conventional gold therapy involves weekly
administration of gold, higher dosage schedules are reported
in the literature describing adult patients and are known to
be associated with more frequent adverse reactions (7,8).
Similar dosage schedules are not described in the pediatric
rheumatology literature. We cannot justify the biweekly
injections our patient received since they were prescribed by
another physician. We acknowledge that he received an
extraordinary amount of gold over a 3-week period and that
the medication should have been discontinued when liver
dysfunction was observed.
Combs and colleagues observed the peritoneal
clearance of gold to be 14.6 mlhinute in a patient with gold
toxicity and renal failure (4). In our patient, peritoneal
clearance of gold was between 0.46 and 0.57 ml/minute. The
reason for the discrepancy between patients is unclear. Both
patients had renal failure and received a similar amount and
type of gold injection (285 mg and 325 mg of sodium
thiomalate). Since our patient’s serum gold level was almost
2.5 times that of Combs’ patient a greater clearance rate
would be expected.
Combs et al attributed the high peritoneal clearance
of gold to protein loss from dialysis (4). The exact protein
lo!js in dialysate of their patient is not reported, and we did
not measure the protein lost in our patient. We suspect, as
thley did (4), that both patients lost amounts similar to those
previously reported in the literature (6). Thus, a difference in
protein lost in the dialysates is also an unlikely explanation
for the discrepancy between peritoneal gold clearances.
In our patient, the peritoneal clearance of gold was
approximately 0.5 ml/minute, compared with 14.6 mlhinute
relported by Combs et a1 (4). Our findings suggest that
peritoneal dialysis alone is not as efficacious as previously
relported for removal of gold from patients with gold toxicity
and renal failure.
Jeffery S. Garland, MD
K. J. Sheth, MD
Dorothy W. Wortmann, MD
Medical College of Wisconsin
Milwaukee, WI
Cassidy JT: Textbook of Pediatric Rheumatology. New York,
John Wiley & Sons, 1982, pp 113-1 IS
Levinson ML, Lynch JP, Bower JS: Reversal of progressive,
life-threatening gold hypersensitivity pneumonitis by corticosteroids. Am J Med 71:908-912, 1981
Lorber A, Baumgartner WA, Bovy RA, Chang CC, Hollcraft R:
45 1
Clinical application for heavy metal cornplexing potential of
N-acetylcysteine. J Clin Pharmacol 13:332-336, 1973
Combs RJ, Dentino MN, Lehrman L, Szwed JJ: Gold toxicity
and peritoneal dialysis. Arthritis Rheum 19:936-938, 1976
Harth M, Itaines DS, Bondy DC: A simple method for the
determination of gold in serum, blood, and urine by atomicabsorption spectroscopy. Am J Clin Pathol S9:423428, 1973
Boen ST: Peritoneal Dialysis in Clinical Medicine. Springfield,
MA, Bannerstone House, 1969, pp 16-73
Furst DE, Levine S, Srinivasan R, Metzger AL, Bangert R,
Paulus HE: A double-blind trial of high versus conventional
dosages of gold salts for rheumatoid arthritis. Arthritis Rheum
20: 1473-1480, 1977
Gottlieb NL: Gold compounds ifl the rheumatic diseases, Textbook of Rheumatology. Edited by WN Kelly, ED Harris Jr, S
Ruddy, CB Sledge. Philadelphia, WB Saunders, 1981, pp 808-81 1
Nailfold capillary abnormalities and organ
involvement in scleroderma
To the Editor:
Nailfold capillary patterns in scleroderma have been
studied by many investigators. In general, a subjective,
qualitative rating scale has been used for the evaluation of
capillary patterns (I); some reports have dealt with quantitative evaluation as well (2,3). Nailfold microscopy has been
used primarily for diagnostic reasons. However, the possible
relationship between nailfold capillary abnormalities and
organ involvement in scleroderma also is interesting as it
relates to the concept of a microvascular pathogenesis of this
connective tissue disease.
Lovy et al recently published their findings on this
subject in Arthritis and Rheumatism (4). Contrary to the
findings of Maricq et al (l), they did not find a significant
correlation between organ involvement and nailfold capillary
loss or capillary enlargement, using a qualitative method of
scoring. The authors could not explain the discrepancy
between their results and those of Maricq et al.
Although results of qualitative scoring may be reproducible within an institution (3), quantitative scoring seems
preferable for comparing data from different centers and,
more importantly, for correlation with clinical data. We have
recently documented an inverse relationship between the
number of capillary loops (scored quantitatively in 5 mm of
the distal row of capillaries) and the number of organs
involved, in patients with secondary Raynaud’s phenomenon ( scleroderma, CREST syndrome [calcinosis, Raynaud’s
phenomenon, esophageal dysmotility, sclerodactyly,
telangiectasias], and mixed connective tissue disease) (5).
Regarding the results in Lovy’s study, some comments may be made on the scoring of capillary patterns and
the composition of the patient groups. First, the qualitative
description of capillary patterns and the division of the
patients into only 2 groups according to organ system
involvement may be the reasons for the lack of any statistically significant relationships. Second, in our experience (6),
nailfold capillary patterns in scleroderma patients are largely
determined by the rate of progression of the disease, and not
by the duration of the disease. Patients with rapidly progressive disease have more extensive capillary loss than those
with slowly progressive disease. This implies that a time
factor has to be taken into consideration in studies on
correlation between capillary findings and clinical data.
When a group of patients with slowly progressive
disease is studied, a relationship between microscopic findings and clinical findings is less likely to be found. From a
pathogenetic point of view, we hypothesized (6) that in
patients with slowly progressive disease, repair mechanisms
of microvascular damage may be active, resulting in a lesser
extent of microthrombosis and capillary loss.
Nella M. Houtman, MD
Cees G. M. Kallenberg, MD
Aaktje A. Wouda, MD
University Hospital
Groningen, The Netherlands
1. Maricq HR, Spencer-Green G , LeRoy EC: Skin capillary abnor-
malities as indicators of organ involvement in scleroderma,
Raynaud’s syndrome and dermatomyositis. Am J Med 61:
862-870, 1976
Roeun LR, Terry EN, Doft BH: Classification and measurement
of surface microvessels in man. Microvasc Res 4:285-292, 1972
Lee P, Leung FYK, Alderdice C, Armstrong SK: Nailfold
capillary microscopy in the connective tissue diseases: a
semiquantitative assessment. J Rheumatol 10:930-938, 1983
Lovy M, MacCarter D, Steigenvald JC: Relationship between
nailfold capillary abnormalities and organ involvement in systemic sclerosis. Arthritis Rheum 28:49&501, /985
Houtman PM, Kallenberg CGM, Wouda AA: Decreased nailfold
capillary density in Raynaud’s phenomenon: a reflection of
immunologically mediated local and systemic vascular disease?
Ann Rheum Dis 44:603-609, 1985
Houtman NM: Microvascular and immunological studies in
Raynaud’s phenomenon (thesis). State University, Groningen,
The Netherlands, 1985
To the Editor:
I agree with Houtman et a1 that the rate of progression of the disease is an important aspect to consider in
studies of scleroderma. Capillary loss is, indeed, more
extensive in patients with early, rapidly progressive disease
than in patients presenting with a slow and gradual development of this disorder (1,2).
It is, however, difficult to properly evaluate the rate
of progression, because the evolution of the disease is
neither continuous nor uniform. As a consequence, an
attempt to quantitate the disease progression by the extent of
skin andlor organ involvement does not yield truly comparable data among different groups of patients. It is even more
difficult to evaluate the “activity” of the disease which,
however, may be more important in understanding the
pathogenesis than is the stage of the disease.
I also agree with the authors that it is advisable to use
quantitative scoring for better communication between investigators from different centers. This quantitation should
include not only the diameters of nailfold capillaries and
counts of capillaries per millimeter, but additional morphometnc analysis, especially since the distribution of capillary loss and presence of enlarged capillaries is not uniform
within the nailfold and also varies from finger to finger. The
comparison of results from nailfold capillary observations
can also be improved if semiquantitative scales are described
in quantitative terms (3).
Hildegard R. Maricq, MD
Medical University of South Carolina
Charleston, SC
I . Maricq HR: The microcirculation in scleroderma and allied
diseases. Adv Microcirc 10:17-52, 1982
2. Maricq HR, Harper FE, Khan MM, Tan EM, LeRoy EC:
Microvascular abnormalities as possible predictors of disease
subsets in Raynaud phenomenon and early connective tissue
disease. Clin Exp Rheumatol 1: 195-205, 1983
3. Maricq HR: Quantitative analysis of nailfold capillary abnormalities in patients with scleroderma (abstract). Int J Microcirc Clin
Exp 3561, 1984
Juvenile primary fibromyalgia syndrome
To the Editor:
We wish to congratulate Drs. Yunus and Masi on
their excellent account of juvenile fibromyalgia (1). This is
the first report in the entire world literature of a large series
of patients with childhood fibromyalgia and a group of
matched normal controls.
In their report, Yunus and Masi comment on “growing pains” in the differential diagnosis of juvenile
fibromyalgia. We agree entirely with their view that tender
(trigger) points do not occur in the syndrome called “growing pains” ( 2 ) . Consequently, the labeling of patient 2 in our
report on 4 patients with “growing pains” (3) is incorrect.
The 13-year-old girl in question clearly had juvenile
fibromyalgia, documented by a typical history (including
vague abdominal discomfort) and symmetric tender points,
as well as anterior chest wall tenderness.
On the issue of growing pains, we agree with
Peterson that in the investigation of children with leg aches,
it is essential to identify those with demonstrable underlying
organic disease (4).Moreover, “growing pains” is a poorly
named, nebulous entity that can be diagnosed only by
exclusion (4).
John J. Calabro, MD
Robert F. Perry, MD
Saint Vincent Hospital
Worcester, MA
1. Yunus MB, Masi AT: Juvenile primary fibrornyalgia syndrome: a
clinical study of thirty-three patients and matched normal controls. Arthritis Rheum 28: 138-145, 1985
2. Calabro JJ: Soft tissue rheumatism, Musculoskeletal Diseases of
Children. Edited by ME Gershwin, DL Robbins. New York,
Grune & Stratton, 1983, pp 57-71
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involvement, nailfold, abnormalities, scleroderma, organy, capillary
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