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Neovascularization around the optic nerve in giant cell arteritis.

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Arthritis & Rheumatism (Arthritis Care & Research)
Vol. 49, No. 5, October 15, 2003, pp 735–740
© 2003, American College of Rheumatology
LETTERS
DOI 10.1002/art.11376
New standards for uric acid excretion and
evidence for an inducible transporter
To the Editor:
In a recent article, Perez-Ruiz et al summarize their
studies of uric acid excretion in 100 men with gouty arthritis and in 72 age- and sex-matched controls (1). Two
aspects of this important work seem particularly noteworthy.
The 24-hour excretion in gouty subjects (628 ⫾ 154
mg/day/1.73 m2) covers essentially the same range as that
of the matched controls (594 ⫾ 143 mg/day/1.73 m2).
Despite these apparently comparable findings, 35 of the
gouty individuals were considered to be overexcreters, i.e.,
their excretion rate was considered to be abnormally high.
My concern is that the cut-off point of 700 mg/day/1.73 m2
that was chosen here (and is widely used elsewhere) lies
well within 1 standard deviation of the normal mean and
therefore lacks both statistical and physiologic validity. It
would be helpful to see the individual values from normal
and gouty subjects plotted in parallel vertical arrays to
permit a visual comparison of the frequency distributions.
I suspect that it then would become clear that a more
appropriate cut-off of 880 mg/day/1.73 m2 (2 standard
deviations above the normal mean) would avoid categorizing as overexcretors most of the individuals so classified in
this report. The control group reported by Perez-Ruiz et al
is large, current, normalized to a constant body size, and
well studied. It seems appropriate to use this population to
reset the normal upper limit of daily uric acid excretion at
880 mg/1.73 m2 (while bearing in mind that the precision
of this test is poor and no overexcretor should be so labeled on the basis of any single high value) (2).
The clearance of uric acid (Cu; in milliliter minute/1.73
meter2) (as well as its corollary the fractional excretion
[FEu; in percent]) remained remarkably constant in 58
gouty patients studied before and after their hyperuricemia was controlled by allopurinol. This finding stands in
marked contrast to those of previous studies of uric acid
excretion in individuals studied at baseline, after allopurinol administration, or after hyperuricemia was induced by
an oral bolus of yeast RNA (metaanalyzed in reference 3).
Those studies consistently found the urinary excretion of
uric acid to vary as an exponential function of the serum
level, i.e., the efficiency of excretion increased when the
serum level rose and fell when the serum did too. Is it
possible to reconcile these disparate findings? I think
maybe so.
A plausible hypothesis suggests that the transporter responsible for tubular reabsorption may be inducible by its
substrate. Thus, more filtered urate leads to more carrier,
whereas a lower burden results in less carrier. This idea is
teleologically attractive (why should the tubule be bur-
dened with more carriers than it needs?), it has abundant
exemplars in the realm of enzymology, and it has been
demonstrated in other transcellular transport systems (including some in the renal tubules). If this feedback system
involves a significant response time, an acute urate load
may overwhelm the tubular reabsorptive capacity, while
an acute fall may lead to supereffective reabsorption as an
excess of transporters competes for both filtered and secreted urate (it is thought that absorption and secretion
may be coextensive systems within the proximal tubule)
(4).
Additional support for the hypothesis may lie in the
remarkably high clearance of infused uric acid (5), the
marked overexcretion seen in acute leukemia and the tumor lysis syndrome (which may occur with only moderate
hyperurcemia) (6), and (on the other end of the scale) the
sometimes sluggish response of the serum urate level after
institution of allopurinol therapy. Now that the apparent
transporter has been identified and sequenced, the hypothesis of inducibility should be testable on a molecular level
(7).
The relevance of this hypothesis to the earlier exponential evidence lies in the fact that past studies tended to be
short term, whereas I suspect that a longer time may have
elapsed between the pre- and posttherapy observations of
Perez-Ruiz et al. Up- or downregulation of the reabsorptive
capacity may require a substantial period after a change in
the filtered load (days or weeks) before balance is restored
at the previous clearance rate. Clearly, the hypothesis also
implies that inefficient excretion (with resultant hyperuricemia) may be caused not by defective carriers, but by a
lower setting of the undiscovered feedback system that
regulates their number.
Do these new data mean that we should change the way
we evaluate the renal component of our patients’ hyperuricemia? I think that the best answer is yes, but not by
much. It remains desirable to identify the unusual patient
who significantly overexcretes urinary uric acid, and I
believe the best way to do so is to screen with the Eu/GF
that is easily measured in midmorning spot urine samples
by taking the product of the urinary uric acid and serum
creatinine and dividing by the urinary creatinine. The
result is the milligrams of urinary uric acid per deciliter of
glomerular filtrate or, alternatively, it may be considered
the excretion rate of uric acid, in milligrams/minute, after
the glomerular filtration rate (GFR) has been normalized to
100 ml/minute. The test is simple, it is uncomplicated by
24-hour collection problems, and it includes (in the GFR)
a meaningful correction for differences in body size. If 2 or
more such determinations are significantly elevated (greater than 0.6 mg/dl), then more extensive evaluations may be
made starting with 3 24-hour collections on a low purine
diet (2).
The quantitative information obtained by the Eu/GF may
be extended to the qualitative realm by simply dividing it
735
736
by the serum urate concentration. This yields the FEu that
Perez-Ruiz et al found to be unchanged when it was examined before and after allopurinol therapy. This value is
the decimal fraction of uric acid in the glomerular filtrate
that is ultimately excreted in the urine. Although the bidirectional tubular transport of uric acid means that virtually all filtered urate is reabsorbed and most of the excreted
molecules enter the nephron by tubular secretion, the FEu
remains a useful measure of overall excretion efficiency.
Again using approximately 2 standard deviations from the
mean of the new Spanish data, inefficient excretion begins
when the FEu falls below 4%. It must be noted here that
the utility of clearance (or FEu) has long been emphasized
by other observers, most notably Brian Emmerson (8).
As a final thought, may I suggest that we try to do away
with the term underexcretion? Generations of medical students have been confused by the idea that overexcretion of
uric acid is associated with hyperuricemia and gout, and,
by the way, so is underexcretion. The fact that the first
term is quantitative but the second is qualitative often
escapes the naı̈ve reader. To me, it makes sense to retain
overexcretion for those unusual patients who overproduce
urate with a resultant abnormally high excretion rate of
uric acid. For those who cope badly with a normal urate
burden, “inefficient excretion” seems a more clear and
useful descriptor. Doesn’t it make sense to say simply that
hyperuricemia results from making too much uric acid
(which we can evaluate by studying the excretion rate)
and/or from clearing it inefficiently (which we evaluate by
measuring the fractional excretion)?
Peter A. Simkin, MD
University of Washington, Seattle
1. Perez-Ruiz F, Calabozo M, Garcı́a Erauskin G, Ruibal A, Herrero-Beites AM. Renal underexcretion of uric acid is present in
patients with apparent high urinary uric acid output. Arthritis
Rheum (Arthritis Care Res) 2002;47:610 –3.
2. Simkin PA. When, why, and how should we quantify the
excretion rate of urinary uric acid? J Rheumatol 2001;28:1306 –
10.
3. Simkin PA. Uric acid excretion in patients with gout. Arthritis
Rheum 1979;22:98 –9.
4. Steele TH. Hyperuricemic nephropathies. Nephron 1999;81:
45–9.
5. Berliner RW, Hilton JG, Yü TF, Kennedy TJ. The renal mechanism for urate excretion in man. J Clin Invest 1950;29:396 –
401.
6. Rieselbach RE, Bentzel CJ, Cotlove E, Frei E, Freireich EJ. Uric
acid excretion and renal function in the acute hyperuricemia of
leukemia. Am J Med 1964;37:872– 84.
7. Enomoto A, Kimura H, Chairoungdua A, Shigeta Y, Jutabha P,
Cha SH, et al. Molecular identification of a renal urate anion
exchanger that regulates blood urate levels. Nature 2002;417:
447–52.
8. Emmerson BT. The management of gout. N Engl J Med 1996;
334:445–51.
DOI 10.1002/art.11373
Reply
To the Editor:
We thank Dr. Peter Simkin’s for his comments. Nevertheless, some points should be emphasized.
Letters
Figure 1. Correlation between 24-hour urinary uric acid (Uur)
and Simkin’s Index stratified by creatinine clearance (Ccr). GF ⫽
glomerular filtration.
First, we used 700 mg/day/1.73 m2 as the cut-off value
for 24-hour urinary uric acid because it is widely used in
clinical practice and only to ascertain if it was an appropriate cut-off point for classifying patients with gout. I
agree with Dr. Simkin that 880 mg/day/1.73 m2 may be a
more appropriate value. Indeed, we designed the study
because we thought that 700 mg/day/1.73 m2 was not the
proper cut-off point.
Second, the fact that the clearance of uric acid did not
change significantly in patients taking allopurinol may be
interpreted as follows. Our patients did not have exogenously induced hyperuricemia or hypouricemia after
high doses of allopurinol, and data were strictly paired,
contrary to other studies (1). Thus, the levels of serum uric
acid during therapy were within those observed in clinical
practice during urate-lowering therapy. Indeed, we have
recently published a retrospective study on the long-term
efficacy of urate-lowering therapy in a large cohort of renal
transplant patients. Again, clearance of urate was unchanged in patients on allopurinol therapy (2). Dr.
Simkin’s hypothesis suggesting that the tubular transporter for reabsorption may be an inducible one is attractive and surely warrants further investigation to ascertain
if this is true in any range of serum urate level.
Third, I also agree with Dr. Simkin about the usefulness
of the excretion of uric acid per volume of glomerular
filtration (EuGF) test in everyday clinical practice— easy to
do, cheap, and showing a good correlation with other
parameters— but related to renal function (3–5). In fact,
since the serum creatinine to urinary creatinine ratio (Pcr/
Ucr) quotient may rise in patients with significant renal
function impairment, this increase may result in a high
EuGF result. Thus, patients showing moderate to severe
renal function impairment may show EuGF ⬎ 0.6 mg/dl
and may be misclassified as overproducers. They are not
actually overproducers, but relative good excretors when
considering the low glomerular filtration rate, as it occurs
with fractional excretion of urate in patients with significant renal function impairment. Figure 1 shows the good
correlation between 24-hour urinary uric acid and EuGF
Letters
when patients are stratified according to clearance of creatinine in our cohort of 404 gouty patients (unpublished
data). Nearly 50% of the patients with apparent overproduction according to EuGF due to renal insufficiency will
not show serum creatinine values ⬎1.5 mg/dl (most of
them older patients with low body mass index). Thus,
patients showing EuGF ⬎ 0.6 mg/dl, even with “normal”
serum creatinine, should be tested with 24-hour urinary
samples, and clearance of urate and creatinine should be
calculated.
Finally, the suggestion of eliminating the term “underexcretion” is certainly plausible, but “overexcretion”
should also be eliminated. Indeed, patients with overproduction and normal renal function will show apparent
overexcretion if compared at hyperuricemia with normal
controls at normal serum urate levels (6), but similar uric
acid excretion when both groups show similar glomerular
filtered load of urate (6). Thus, we suggest that “inefficient
excretion” and “efficient excretion” may be more proper
physiopathologic terms than “underexcretion” or “overexcretion,” respectively, when we are talking about renal
handling of uric acid.
In addition, we suggest that EuGF should be changed to
Simkin’s Index as a tribute to Dr. Simkin’s work in this,
most of the times undervalued, field of gout.
Fernando Perez-Ruiz, MD
Ana Herrero-Beites, MD
Hospital de Cruces, Baracaldo, Vizcaya, Spain
1. Puig JG, Mateos F, Lopez M, Conthe P. Renal handling of uric
acid in gout: impaired tubular transport of urate not dependent
on serum urate levels. Metabolism 1986;35:1147–53.
2. Perez-Ruiz F, Gomez-Ullate P, Amenabar JJ, Zarraga S, Calabozo M, Herrero-Beites A. Long-term efficacy of urate-lowering drugs in renal transplant patients. Nephrol Dial Trasplant
2003;18:603– 6.
3. Perez-Ruiz F, Calabozo M, Alonso-Ruiz A, Ruiz-Lucea E, Herrero-Beites A. Analysis of the methods for the classification of
renal handling of urate in gout. Arthritis Rheum 1997;40(9
suppl):S48.
4. Perez Ruiz F, Calabozo Raluy M, Herrero Beites A, Ruiz Lucea
E, Alonso Ruiz A. Analysis of the methods for classifying gout
according to renal excretion of uric acid. Rev Esp Reumatol
1998;25:335–9.
5. Perez-Ruiz F, Calabozo M, Herrero-Beites AM, Ruibal A,
Alonso-Ruiz A. Influence of serum uric acid levels and glomerular filtration rate on the tests used to classify patients with
gout. Arthritis Rheum 2001;44(9 suppl):S128.
6. Perez-Ruiz F, Calabozo M, Garcia-Erauskin G, Ruibal A, Herrero-Beites AM. Renal underexcretion of uric acid is present in
patients with apparent high urinary uric acid output. Arthritis
Rheum 2002;47:610 –3.
DOI 10.1002/art.11371
Hodgkin’s lymphoma presenting as Tietze’s
syndrome
To the Editor:
We read with great interest the report of Fioravanti et al
about malignant lymphoma presenting as Tietze’s syndrome (Fioravanti A, Tofi C, Volterrani L, Marcolongo R.
Malignant lymphoma presenting as Tietze’s syndrome. Ar-
737
thritis Rheum [Arthritis Care Res] 2002;47:229 –30). We
would like to add to the 4 reported cases a patient seen
recently at our medical center.
A 26-year-old woman was seen at the American University of Beirut Medical Center with pain over the upper
parasternal area of several months duration. The pain was
worse at night and associated with morning stiffness in the
chest for 30 minutes. No other associated symptoms were
reported. Initial blood studies, including a complete blood
count, erythrocyte sedimentation rate, rheumatoid factor,
antinuclear antibodies, and chemistry profile, yielded results within normal guidelines. Her pain responded very
well to nonsteroidal antiinflammatory drugs; however,
each time these drugs were discontinued, her pain would
recur. Six months after her initial presentation, a radiograph of the chest and costochondral joints did not reveal
any abnormalities. The patient presented a few months
later with a bulging mass over the upper chest wall. A
chest computed tomography scan showed an anterior mediastinal mass measuring 11 cm ⫻ 9.5 cm. Osteolytic involvement of the whole sternum and proximal adjacent
aspect of the ribs was also noted. The lung parenchyma
was clear. An excisional biopsy revealed a Hodgkin’s lymphoma of the nodular sclerosis type.
Our case adds additional support to the view that malignancy should always be suspected in the differential
diagnosis of Tietze’s syndrome, and that the use of the
appropriate radiographic studies will help in the early
detection of these tumors.
Imad Uthman, MD
Ihab El-Hajj, MD
Rana Traboulsi, MD
Ali Taher, MD
American University of Beirut, Beirut, Lebanon
DOI 10.1002/art.11372
Neovascularization around the optic nerve
in giant cell arteritis
To the Editor:
Neovascularization in giant cell arteritis (GCA) has been
described (1). The response of the artery to the injury
includes mobilization and proliferation of smooth muscle
cells in conjunction with matrix production and angiogenesis (2). Increased tissue and serum angiogenic activity has
been associated with low prevalence of ischemic complications in patients with GCA (3). We report a GCA patient
with several episodes of amaurosis fugax. Magnetic resonance imaging (MRI) disclosed collateral circulation
around the left optic nerve.
A 65-year-old man was sent to our hospital because of
episodes of amaurosis fugax of 6 months duration. One
year prior, he had been diagnosed with biopsy-proven
GCA in another center. After diagnosis, he was started on
treatment with prednisone. However, within the 6 months
prior to admission he complained of left supraorbitary
headache and suffered several episodes of left amaurosis
738
Letters
Carlos Garcia-Porrua, MD, PhD
Robustiano Pego-Reigosa, MD, PhD
Victor Armesto, MD
Miguel A. Gonzalez-Gay, MD, PhD
Hospital Xeral-Calde, Lugo, Spain
1. Kaiser M, Younge B, Bjornsson J, Goronzy JJ, Weyand CM.
Formation of new vasa vasorum in vasculitis: production of
angiogenic cytokines by multinucleated giant cells. Am J
Pathol 1999;155:765–74.
2. Weyand CM, Goronzy JJ. Pathogenic principles in giant cell
arteritis. Int J Cardiol 2000; 31;75 Suppl 1:S9 –15; discussion
S17–9.
3. Cid MC, Hernandez-Rodriguez J, Esteban MJ, Cebrian M, Gho
YS, Font C, et al. Tissue and serum angiogenic activity is
associated with low prevalence of ischemic complications in
patients with giant-cell arteritis. Circulation 2002;24:1664 –71.
4. Cid MC, Font C, Oristrell J, de la Sierra A, Coll-Vinent B,
Lopez-Soto A, et al. Association between strong inflammatory
response and low risk of developing visual loss and other
cranial ischemic complications in giant cell (temporal) arteritis. Arthritis Rheum 1998;41:26 –32.
Figure 1. Orbital magnetic resonance image showing collateral
circulation around the left optic nerve.
DOI 10.1002/art.11374
Education for patients with rheumatoid
arthritis: is it worth it?
fugax. No adequate information was obtained about the
initial dosage of prednisone and the way in which prednisone dosage was tapered. Despite having episodes of
amaurosis fugax, he was receiving only 10 mg of prednisone per day at the time of admission. Physical examination including funduscopy did not disclose abnormalities. Laboratory data, including coagulation test
results, anticardiolipin antibodies, full blood cell count,
and hepatic and renal function parameters, were negative
or normal. Erythrocyte sedimentation rate was 41 mm/
hour (normal ⬍20 mm/hour) and C-reactive protein was
12 mg/liter (normal ⬍5 mg/liter). Plain chest radiograph
and carotid angio-MRI did not show abnormalities. Orbital
and cerebral MRI showed collateral circulation around the
left optic nerve (Figure 1).
Treatment with acetylsalicylic acid (300 mg/day) was
started and prednisone dosage was increased to 40 mg/
day. Following this procedure, a dramatic improvement of
headache was achieved. Also, no new visual complications have occurred over the following 6 months.
Inflammation of the artery wall in GCA induces a series
of structural changes, including the formation of new vasa
vasorum. Angiogenesis has been proven more prominent
in patients with a strong acute phase response (4).
In our patient, an inappropriately low dose of prednisone might have been responsible for the persistent inflammatory response, manifested by headache and elevation of the inflammatory laboratory markers. It is possible
that the persistence of chronic inflammatory response
might have played a role in the striking neovascularization
phenomena around the optic nerve. Based on that, we are
tempted to speculate that neovascularization may be a
compensatory mechanism to maintain an adequate blood
supply to the optic nerve in GCA.
To the Editor:
Rheumatoid arthritis (RA) is the most frequent chronic
inflammatory disease affecting approximately 1% of the
white population, particularly females (3 times more often
than males) (1). Because of its articular and extraarticular
manifestations and complications, such as infections and
osteoporosis, RA has a considerable impact on a patient’s
quality of life, with mayor physical, psychological, and
social consequences. Treatment of RA includes not only
medications but also education and cognitive-behavioral
interventions (2). Recently, Riemsma et al described the
impact of the use of education as a therapeutic tool in
patients with RA (3). These authors proposed a categorization of educational practices into information only,
counseling, and behavioral therapy. This approach is important because it emphasizes the various types of educational systems and allows analysis of data more objectively
to avoid comparisons of unrelated interventions. Surprisingly, Riemsma’s results indicated only a modest and
short-term effect of education on RA patients, including
global assessment, psychological status, and general well
being (3). However, education may not only be important
for the psychological well being of the patients but also for
improving their adherence to therapy and for guiding patient’s participation on therapeutic decisions. Indeed, adherence tends to be higher in patients who have participated in educational programs (4,5). Moreover, the trend
toward a favorable effect of education on depression may
warrant its use as a therapeutic tool in patients with RA
due to its known association with adherence (6).
The clinical expression of RA varies among populations
and is influenced by several factors, including race, genetics, environmental factors, and access to medical care (7).
Letters
739
Table 1. Level of knowledge about rheumatoid arthritis (RA) in patients compared with the general population (no RA)
Characteristic
Sex, male:female
Age, years, mean ⫾ SD
Education, %
None
Primary school
High school
Technical
University
Postgraduate
Socioeconomic status, %*
2
3
4
Correct answers to true or false questions, %
1. There is only a single therapy for all RA patients
(Existe un tratamiento único para los pacientes con artritis reumatoidea)
2. All RA patients have a bad prognosis
(Todos los pacientes con artritis reumatoidea tienen un mal pronóstico)
3. The neck is the most commonly affected area of the spine in patients with RA
(El cuello es la parte de la columna que se afecta mas comúnmente en los pacientes
con artritis reumatoidea)
4. RA is caused by cold weather, inadequate nourishment and humidity
(La artritis reumatoidea es causada por la mala alimentación, el frı́o y el clima
húmedo)
5. Patients with RA should not play a role in the management of their disease because
the physician is the one in charge
(Los pacientes con artritis reumatoidea no deben asumir un papel muy activo en su
proceso de recuperación porque el médico es el encargado principal)
6. RA and osteoporosis are the same disease
(Artritis y osteoporosis son la misma enfermedad)
7. RA can produce dryness in the eyes and mouth
(La artritis reumatoidea puede causar resequedad en los ojos y en la boca)
8. Patients with RA should include all kinds of food in their meals but must avoid meat
(Los pacientes con artritis reumatoidea deben incluir en su dieta alimentos variados
pero no deben comer carnes rojas)
9. RA never compromises the lungs
(La artritis reumatoidea nunca afecta los pulmones)
10. To confirm the diagnosis of RA, it is necessary to perform some blood tests
(Para confirmar el diagnóstico de artritis reumatoidea es necesario hacer algunos
exámenes de sangre)
More than 6 correct answers, %
Number of correct answers, mean ⫾ SD
RA
(n ⴝ 448)
No RA
(n ⴝ 269)
44:402
54 ⫾ 13
40:227
49.3 ⫾ 16
2
38
35
13
10
2
1
26
32
14
22
5
29
44
14
25
44
16
58
68†
43
58†
38
27
56
59
59
64
80
85
52
33†
33
30
26
31
87
75†
47
4.97 ⫾ 2.31
48
5 ⫾ 2.36
* According to the Colombian socioeconomic classification.
† P ⬍ 0.01 after adjusting for age and education level.
Disability is one of the most important consequences of RA
and is not free from the influence of sociocultural factors,
such as attitudes towards health, illness, the patient’s sociocultural level (8). Physicians should be aware of these
factors before extrapolating findings on RA populations
different from their own. In addition, RA treatment and
outcome are better managed by rheumatologists than by
other physicians (9).
The state of Antioquia (capital, Medellı́n) is geographically located in northwestern Colombia between the central and western branches of the Andean Mountains and
has a population of 4,500,000. A large number of patients
in this area do not know which physician should manage
their illness, and access to specialized rheumatology care
is limited by the restriction of social security laws, as well
as by the low number (only 11) of rheumatologists in
practice. A sizeable number of patients are treated with
alternative medicine while others have no treatment at all.
We wanted to explore the general knowledge about RA
of patients attending our rheumatology unit, as well as that
of the general population. To that purpose, we surveyed
448 RA patients and 269 healthy individuals, using a
10-point questionnaire on RA knowledge (10) (Table 1).
The questionnaire had been validated with a pilot study
and through construct validity analyses (11). Patients with
RA knew more about the disease’s symptoms than healthy
persons but the latter had more knowledge concerning
prognosis and therapy than the patients. There were no
740
Letters
significant differences in knowledge about the etiology of
disease in these 2 groups.
The poor knowledge about RA in both patients and the
general population, and the finding that patients had the
same level of knowledge as the general population, suggest
that educational programs are sorely needed to provide
adequate and rational information on RA. This opens the
discussion concerning the need to balance the importance
of education as a therapeutic tool, and the ethical and
social implications of providing education in an environment where managed care and cost-benefit issues are the
prevailing forces.
Jose Cadena, MD
Juan-Manuel Anaya, MD
Universidad Pontificia Bolivariana, Medellı́n, Colombia
4.
5.
6.
7.
8.
9.
1. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT,
Giannini EH, et al. Estimates of the prevalence of arthritis and
selected musculoskeletal disorders in the United States. Arthritis Rheum 1998;41:778 –99.
2. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management
of rheumatoid arthritis, 2002 update. Arthritis Rheum 2002;
46:328 – 46.
3. Riemsma RP, Kirwan JR, Taal E, Rasker JJ. Patient education
10.
11.
for adults with rheumatoid arthitis. Cochrane Database Syst
Rev 2002;3:CD003688.
Hill J, Bird H, Johnson S. Effect of patient education on adherence to drug treatment for rheumatoid arthritis: a randomised controlled trial. Ann Rheum Dis 2001;60:869 –75.
Viller F, Guillemin F, Briancon S, Moum T, Suurmeijer T, van
den Heuvel W. Compliance to drug treatment of patients with
rheumatoid arthritis: a 3 year longitudinal study. J Rheumatol
1999;26:2114 –22.
DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk
factor for noncompliance with medical treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern Med 2000;160:2101–7.
Anaya JM, Correa PA, Mantilla RD, Jimenez F, Kuffner T,
McNicholl JM. Rheumatoid artritis in African Colombians
from Quibdo. Semin Arthritis Rheum 2001;31:191– 8.
Escalante A, del Rincón I. The disablement process in rheumatoid arthritis. Arthritis Rheum 2002;47:333– 42.
Emery P, Breedveld FC, Dougados M, Kalden JR, Schiff MH,
Smolen JS. Early referral recommendation for newly diagnosed rheumatoid arthritis: evidence based development of a
clinical guide. Ann Rheum Dis 2002;61:290 –7.
Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF,
Cooper NS, et al. The American Rheumatism Association
1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988;31:315–24.
Cadena J, Alvarez A, Correa M, Bonilla LM, Gómez MP, Montoya MA, et al. Encuesta de conocimiento sobre artritis
reumatoidea: ¿vale la pena educar? Rev Colomb Reumatol
2002;9:262–9.
DOI 10.1002/art.11395
Erratum
In the article by McQuillan et al published in the June 2003 issue of Arthritis Care & Research (pp 368 –76),
the headings False Positive and True Positive on Figure 2 were transposed, and the last column heading on
Table 4 should read 1⫺Specificity. Also, in the first paragraph of the Results section it should read “current
affective disorder” instead of “current major depressive episode,” and the last sentence in the Results should
read “. . . we found that the sensitivity (0.89) is much better than 1⫺ the specificity (0.24) at the standard cut
off score of 16.
We regret the errors.
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