I read with interest the article by Katz et al on the prevalence and
predictors of disability in valued life activities among individuals with
rheumatoid arthritis (1).
It is encouraging that patient based assessments are being explored
among rheumatic diseases. Rheumatoid arthritis (RA) and osteoarthritis
(OA) have received the most attention in this regard. It is thus
reassuring that...
I read with interest the article by Katz et al on the prevalence and
predictors of disability in valued life activities among individuals with
rheumatoid arthritis (1).
It is encouraging that patient based assessments are being explored
among rheumatic diseases. Rheumatoid arthritis (RA) and osteoarthritis
(OA) have received the most attention in this regard. It is thus
reassuring that in this study, the Health Assessment Questionnaire (HAQ)
was predictive (B 2.44 for "unable" , 6.4 for "affected" and 0.56 for
"difficulty) of the overall valued activity disability.
I have some comments and queries. The study population is comprised
of individuals receiving treatment from rheumatologists, and had expressed
their interest in RA research. This may be a surrogate for people with
positive health behaviors, compliance and better educational status.
Patients that visit a rheumatologist may not reflect the general RA
patient population, as they may have better access to medical care,
especially for those 65 years or older (Medicare). In such recruitment, we
not only compromise generalizability of the results, but also the
variation in the disease spectrum. It would have been helpful to include
educational status and ethnicity data, since lower educational level is
known to be associated with work disability (2). Furthermore, lower socio
economic status is related with disease severity, more co morbidity and
higher mortality in RA (3).
The mean age of the study participants was 60 years and mainly
comprised of women, the subgroups that also have a higher prevalence of
osteoarthritis (OA). Can patients differentiate between limitations due to
RA or their coexistent OA or other co-morbidities (obesity, cardiac or
pulmonary disease, vision etc)? More than 50% of the subjects had one or
more co-morbidities, as mentioned in Table 2; however the multiple
regression models did not include co-morbidities as an independent
variable in the models for VLA.
Knowledge about the distribution of the data and range for age,
duration of disease and HAQ scores would have been helpful. Standard
deviations that are larger than the mean scores, on the difficulty ratings
(Table 3), may suggest the presence of outliers or lack of data. Table 3,
indicates the problem with fewer observations in the difficulty ratings in
the last two columns for "a lot" and "unable".
Lastly, it is not evident from the methods section about the recall
period used for VLA assessments. The methods section notes a six months
recall period for development of the VLA scale. However, it has since been
revised as mentioned by the authors. If six month recall period was also
used for this study, it may be too long a period for 60 years old patients
to recall. Similarly, detail about the method used for (physician/patient)
assessment of the number of swollen/painful joints would add to our
knowledge, to ascertain if this is was a completely patient based
assessment or included additional physician assessment.
It would be nice to see a similar study in early RA patients, so that
modifiable factors (including clinical information such as lag period
between disease onset to its diagnosis, time taken to start the treatment
with disease modifiers, and period between onset of disease and
therapeutic remission, presence of erosions, nodules, ESR/CRP, access to
health care, satisfaction with treatment, compliance, education,
ethnicity)which can predict potential disability in VLA, can be
determined, so that we can devise ways to prevent potential disability.
Sincerely
Meenakshi Jolly, MD, MS
References
1) Katz PP, Morris A, Yelin EH. Prevalence and predictors of disability in
valued life activities among individuals with rheumatoid arthritis. Ann
Rheum Dis 2006;65:763-769
2) Morales-Romero J, Gonzalez-Lopez L, Celis B et al. Factors associated
with permanent work disability in Mexican Patients with Rheumatoid
Arthritis. A case control study. J Rheumatol 2006;33:1247-9
3) Harrison MJ, Tricker KJ, Davies L et al. The relationship between social
deprivation, disease outcome measures, and response to treatment in
patients with stable, long standing rheumatoid arthritis. J Rheumatol
2005;32:2330-6.
Dear Editor, I read with interest this work. Indeed ultrasonography has
increasing role in this field so the interpretation of its images is so
important for the rheumatologist. From a radiological and pathological
point of view we can divide the changes of the bone in this disease
into two types. Type one, which is the pre-erosive stage appears as
many hyperechoic bone islands in the ostoid tissue of the cortical and
en...
Dear Editor, I read with interest this work. Indeed ultrasonography has
increasing role in this field so the interpretation of its images is so
important for the rheumatologist. From a radiological and pathological
point of view we can divide the changes of the bone in this disease
into two types. Type one, which is the pre-erosive stage appears as
many hyperechoic bone islands in the ostoid tissue of the cortical and
endocortical parts associated with multiple black areas which lost its
normal mineralization. This can be seen in most of the figures, like
figure 2{C and D ], figure 3 … The second type with punched out
cortical areas that denote severe changes and real ostoid loss like
figure 4d. Figure 8 show both of the two types. Figure 8 shows
also that the hypodense areas detected by plain X-ray may correspond
either to type one or type two at ultrasound examination. The
presence of this speckled bone islands in type one is a good indicator of
the ostoid presence. This could be used as a predictor of the future
healing on the course of treatment. Neither the plain X-ray nor the MRI
can differentiate type one from type two. So ultrasound can detect two
stages - first = the stage of bone deminieralization with scattered hyperechoic bone islands {type one or pre-erosive stage} denoting presense of ostoid bone - second the stage of the real bone erosion with no or minimally present ostoid tissue {type two ore the erosive stage }.
This will help certainly in prediction of out come of treatment ...
Dear Editor, plain X-ray films will demonstrate the bony defect and its margin whether it is sclerotic or not. In that lesions due to excessive bone marrow infiltration and soft tissue formation , the soft tissue formed is
directly proportional to the bone marrow infiltration and disease activitynot to the size of the bone defect. The accurate parameter to follow up the bone marrow infiltration or recovery is to follow up t...
Dear Editor, plain X-ray films will demonstrate the bony defect and its margin whether it is sclerotic or not. In that lesions due to excessive bone marrow infiltration and soft tissue formation , the soft tissue formed is
directly proportional to the bone marrow infiltration and disease activitynot to the size of the bone defect. The accurate parameter to follow up the bone marrow infiltration or recovery is to follow up the soft tissue
mass. The soft tissue formation in long bones and flat bones has a similar mechanism. In skull with its outer and inner tables and diplopic space inbetween the follow up and characterization of any abnormality is available by ultrasonography. For example a case with ongoing improvement, a 7-month infant with histiocytosis x follow up on spirulina extract {Polysaccharideas} as antionchogenic activity agent [1],the bone defect and soft tissue formation was examined by high resolution
ultrasonography every third day to do serial films. The base line study show multiple bony destructive lesion with soft tissue formation and periosteal elevation ... in large lesion the inner table was also affected and even the brain tissue was easily visualized in a manner closely similar to trans-fontanellar ultrasonography. In small lesion the inner table was not affected to the same degree. First of all the periosteal elevation was reduced as a direct sign to soft tissue mass reduction. The second sign was inner table new bone formation and echogenic dots of mineralization. The next sign was libing of the outer table from the margin of the bone defect together decreased ability to better characterization of the small bone defects in comparison to the base line study. ...the latest sign is outer table healing with still minimal periosteal elevation. In that exacerbation of the disease due to the mother misunderstanding of the treatment method the soft tissue reformation did not cope with the small size of the defect which seen at late stages ... so the ultrasonography is an ideal modality to follow up the soft tissue changes and new bone formation.
Reference
1. El-Ayouty, Y. M., Salah, S. H. Basha, O. M. and El-Tohamy, A. M. Polysaccharide extracted from spirulina sp as hepatoprotective agent against Oncogen cells. 2007 in Press.
In their recent report, Armstrong and colleagues highlight the high
prevalence of falls in patients with rheumatoid arthritis (RA)[1], show
that falls increase with functional disability and antidepressant use, and
comment that fracture prevention extends beyond the pharmacological
treatment of osteoporosis. This concurs with current guidelines for the
management of steroid induced osteoporosis[2], whi...
In their recent report, Armstrong and colleagues highlight the high
prevalence of falls in patients with rheumatoid arthritis (RA)[1], show
that falls increase with functional disability and antidepressant use, and
comment that fracture prevention extends beyond the pharmacological
treatment of osteoporosis. This concurs with current guidelines for the
management of steroid induced osteoporosis[2], which also recommend falls
risk assessment. However, they did not address another important risk
factor for falls i.e. visual impairment.
Older people with visual impairment are seven times more likely to
fall and sustain an injury[3] and the risk of hip fracture is doubled by
poor or moderately impaired vision.[4] Visual impairment (classified as
binocular visual acuity (VA) of <6/18[5]) affects 12.4% of the
population aged 75 years or more[6], while 30% of the over 65s have
reduced binocular VA to <6/12.[7] The latter study assessed people
wearing their spectacles, thus measuring day-to-day vision. In three
quarters of these cases vision was potentially remediable.
Visual impairment may have implications beyond fall risk, including
potentially reduced safety of medication-taking, social isolation,
depression, reduced functional status and quality of life[8], features
also well recognised in RA patients.[9] The cumulative effects of both
could be devastating.
We investigated the prevalence of impaired VA in patients with RA
attending routine outpatient clinics. 75 RA patients were examined (78.7%
female). The mean age was 58.9 years (SD 11.73), disease duration 14.8
years (range 1-48 years), HAQ 1.62 (SD 0.8). 39.7% had a VA of <6/18 in
either eye, which was corrected with the patients’ spectacles in all
except 2 patients who did not use them (1 of which had amblyopia, the 2nd
patients vision corrected with pin-hole which signifies potential for good
eyesight). 84% of patients had had an eye test within 18 months. Patients
with normal vision were less likely to have had a recent test (c2=6.15;
p<0.05).
Although uncorrected visual impairment is rare in RA and most
patients had had an eye test within the previous 18 months, we have
included in our multidisciplinary annual reviews[10] a systematic enquiry
of the latest refraction test date as part of routine falls assessment in
RA patients.
In response to the hypothesis article ‘Is progressive osteoarthritis
an atheromatous vascular disease?’ [Conaghan, Hvanharanta, PA Dieppe Ann
Rheum Dis V64 No11 Nov 2005 1539-1541].
The hypothesis paper Atheroma and the Progression of Osteoarthritis
of Conaghan et al.[1] confuses four questions. Is progressive OA related
to local atheroma? Is it related to systemic atheroma? Do statins have
an...
In response to the hypothesis article ‘Is progressive osteoarthritis
an atheromatous vascular disease?’ [Conaghan, Hvanharanta, PA Dieppe Ann
Rheum Dis V64 No11 Nov 2005 1539-1541].
The hypothesis paper Atheroma and the Progression of Osteoarthritis
of Conaghan et al.[1] confuses four questions. Is progressive OA related
to local atheroma? Is it related to systemic atheroma? Do statins have
an effect of OA progression? Would using statins improve mortality in
osteoarthritis? For good measure a fifth consideration might be added...does osteoartrhitis cause progression of atheroma?
Each question needs different evidence and experiment. However
present knowledge about OA provides remarkably little evidence to support
the first two hypotheses. The evidence presented in the article could
easily support the counter thesis that there is no relationship between
the two conditions.
If local atheroma caused progression the mechanism is presumably
ischaemia. If this is a major or necessary condition for progression then
there should be a stronger association with conditions associated with
severe atheroma. No marked association with hyperlipidaemia, diabetes, or
those with established peripheral vascular disease has been reported. A
clear association should also be apparent in patients with premature OA or
ischaemic disease.
Joints have a remarkably good blood supply with good collateral
networks. Perfusion phase bone scan changes in OA have not been
highlighted as being abnormal and much of the change seen in MRI is non-
specific. The demonstration of focal necrosis by Bullough is the only
definite evidence there might be a problem due to ischaemia. However it
is not zonal , not associated with arterial changes and could be due to
local effects on blood perfusion in bone. The lack of more extensive
ischaemic change would suggest the opposite hypothesis…ischaemia is rarely
the cause of progression.
If systemic atheroma is somehow driving progression some suggestion
of the likely process is needed. This would not be ischaemia and indicate
a shared causative factor. The high frequency of atheroma in the aging
population will make analysis difficult, and the hypothesis improbable. It
can not be a sufficient condition to have atheroma and get progression.
Atheroma is so common it will have to relate to severity or extent of
atheroma. There would a have to be a dose related phenomena or everyone
should get progressive osteoarthritis. Equally people with non progressive
OA should have little artheroma ...but slow or no progression in OA is
common and many will have atheroma. Both processes are likely to be
linked by common factors such as age but this does not make
interdependence of cause between atheroma and oa likely. OA reducing
exercise and needing nonsterooidal treatment might indirectly increase
atheroma progression.
The third and fourth questions are very different. Statins have
multiple effects including effects on bone. They may very well influence
the development of OA. However their present widespread use makes it
unlikely any effect is large and of real life significance. Use of statins
is however likely to improve mortality in OA patients given the increased
mortality in both non and presumably ‘progressive’ OA s from
cardiovascular causes. With risks associated with use of non steroidals
and lack of exercise, a drug to reduce risk that is relatively safe and
cheap is attractive. Any study of statins should be powered to assess
this effect.
It is optimistic to hope to explain one poorly understood condition
with a second. The task is not made easier when both conditions are
difficult to measure. A hypothesis needs to generate a question that can
be answered by observation and experiment. Study of the value of statins
on OA survival does not need justification form speculation on how
atheroma may affect OA progression.
Dr Charles Hutton Derriford Hospital Plymouth UK
I have no competing interest.
References:
1. Is progressive osteoarthritis an atheromatous vascular disease?
PG Conaghan, Hvanharanta, PA Dieppe
Anals of Rheumatic Disease V64 No11 Nov 2005 1539-1541.
We read with interest the recent article of Jonsdottir and
colleagues,[1] in which the authors describe an increase in the rate of
ACLA in RA patients who received any anti-TNF therapy; a potentially very
interesting finding. However, this article commits multiple errors in
scientific methodology and we are concerned that the presumed apparent
correlations of ACLA are actually the result of inherent b...
We read with interest the recent article of Jonsdottir and
colleagues,[1] in which the authors describe an increase in the rate of
ACLA in RA patients who received any anti-TNF therapy; a potentially very
interesting finding. However, this article commits multiple errors in
scientific methodology and we are concerned that the presumed apparent
correlations of ACLA are actually the result of inherent bias in study
design, flawed analyses and an overinterpretation of a limited registry
database.
Of particular concern, without specification of the selection criteria, a
subgroup of patients on TNF-á antagonists in STURE was analyzed. A small
group of 121 patients has been extracted from a much larger registry
experience - not to suggest a hypothesis generating observation – but to
support a very far reaching headline and conclusion. The increase in the
rate of ACLA in the reported patients who received any anti-TNF therapy
appears to be real and quite interesting. However, following that
observation, this article commits a variety of serious errors in
scientific methodology and reporting. As of March 2004, the Swedish
Rheumatology Registry had entered 2334 patients treated with biologics,
including 1715 treated with infliximab.– it is not explained how the
subgroup of 121 patients was selected. Only a subgroup of this
subgroup, i.e. 44 of the 64 infliximab-treated patients, is then utilized
to begin exploring the relationship of ACLA formation to other clinical
outcomes, such as ACR response and infusion reactions. No explanation is
provided as to why 20 of the 64 patients were not utilized in the
analysis. No information is given regarding other known predictors of
these outcomes, nor whether a proper analysis was done to determine if
this was a major independent risk factor. What was done to adjust for
baseline variables? Why wasn’t a proper regression analysis done? Why is
there no disclaimer stating that the presence of ACLA cannot be assumed to
have a causal relation to these outcomes based on these exploratory
analyses?
Of greater concern, comparative statements are made throughout the
article regarding the comparable effects in etanercept-treated patients –
but the data to support these statements are not shown! This is
remarkable and it is hard to understand how an article could be published
without such information being provided. How many of the 57 etanercept-
treated patients had this information available? Why is their data not
presented? How was the subset of 57 etanercept-treated patients selected
from the much larger number in the registry? Importantly, there is no
mention made that this registry does not randomize patients to infliximab
vs. etanercept and no attempt is made to discuss their comparability. The
presumed, not displayed, differences between infliximab and etanercept
could have been caused by imbalances in baseline, and confounding
variables between the infliximab-treated and etanercept-treated group. As
just one observation, there is a great imbalance in the use of
methotrexate at baseline in infliximab and etanercept groups (90% vs. 50%,
respectively), possibly indicating differences in the disease severity of
the two groups. Therefore, it is of particular concern that definitive
statements are made throughout the article regarding the comparable
effects in etanercept-treated patients – but the data to support these
statements are not shown, nor do the baseline data shown support their
comparability.
A registry database can potentially provide certain data very well,
e.g. large real world safety outcomes. It can also be a good source for
hypothesis generating exploratory observations. However, registry data is
rarely able to answer questions in the way a well designed randomized
trial can. This report appears to represent the worst type of data
dredging- a concern that makes people wary of the use of registry data
for mischief making. In this case that concern is warranted.
Referenc
1. Jonsdottir T, Forslid J, Van Vollenhoven AM, Harju A, Brannemark
SA, Klareskog L, et al. Treatment with TNF-{alpha} antagonists in patients
with rheumatoid arthritis induces anticardiolipin antibodies (ACLA): ACLA
predict worse clinical outcome with infliximab and more frequent treatment
limiting infusion reactions. Ann Rheum Dis 2004.
We read with interest the article by Shanahan et al [1] on
suprascapular nerve blocks and the accompanying editorial by Hall and
Buchbinder [2]. It is gratifying to know that in this context the indirect
method of needle placement produces a similar outcome to the
radiologically-guided method. However, we would like to point out an
important methodological flaw in the study.
We read with interest the article by Shanahan et al [1] on
suprascapular nerve blocks and the accompanying editorial by Hall and
Buchbinder [2]. It is gratifying to know that in this context the indirect
method of needle placement produces a similar outcome to the
radiologically-guided method. However, we would like to point out an
important methodological flaw in the study.
The patients who received injections via the landmark approach were
injected with 40mg of methylprednisolone and 10 mls of 0.5% bupivacaine,
whereas those who underwent CT-guided injection received 40mg of
methylprednisolone and 3 mls of 0.5% bupivacaine. Previous studies have
shown that suprascapular nerve blocks produce effective analgesia for a
variety of painful shoulder conditions, including frozen shoulder [3],
rotator cuff lesions [4], and rheumatoid arthritis [5]. Fundamentally,
however, in a double-blind study of 58 rheumatoid shoulders, suprascapular
nerve block with bupivacaine alone has been shown to be as effective as
bupivacaine plus methylprednisolone at improving pain, stiffness, and
range of movement [6]. The authors of this study concluded that the
addition of methylprednisolone conferred no additional benefit.
Thus, if one concludes from this that the local anaesthetic is the
active ingredient, Shanahan’s two patient groups were given different
doses of the same drug (10 mls compared with 3 mls). Consequently the
study may have underestimated the effect of the CT-guided approach.
References
(1). Shanahan EM, Smith MD, Wetherall M et al. Suprascapular nerve
block in chronic shoulder pain: are the radiologists better? Ann Rheum Dis
2004;63:1035-1040
(2). Hall S, Buchbinder R. Do imaging methods that guide needle
placement improve outcome? Ann Rheum Dis 2004;63:1007-1008
(3). Dahan TH, Fortin L, et al. Double blind randomized clinical trial
examining the efficacy of bupivacaine suprascapular nerve blocks in frozen
shoulder. J Rheumatol. 2000 Jun;27(6):1464-9.
We read with great interest the article by Allanore et al, and
commend on their efforts in studying this important issue[1]. We would be
most grateful if the authors can help to clarify a few points.
Mean Deviation (MD) is the average of the numbers on the total
deviation plot with each value weighted according to the magnitude of the
normal range at that point. It signifies the over...
We read with great interest the article by Allanore et al, and
commend on their efforts in studying this important issue[1]. We would be
most grateful if the authors can help to clarify a few points.
Mean Deviation (MD) is the average of the numbers on the total
deviation plot with each value weighted according to the magnitude of the
normal range at that point. It signifies the overall severity of the field
loss. Thus, a MD of -2 dB depression may indicate a 2 dB depression
everywhere in the field (not necessarily a glaucomatous field loss) or a
depression of 4 dB over half of the field (more specific for a
glaucomatous process). According to one of the commonly employed criteria
from Anderson [2] glaucomatous visual field defects may be defined by (1)
three or more adjacent points in an expected location of the central 24o
field, on the same side of the horizontal meridian, that have p <_5 on="on" the="the" pattern="pattern" deviation="deviation" pd="pd" plot="plot" one="one" of="of" which="which" must="must" have="have" p1.="p1." _2="_2" glaucoma="glaucoma" hemifield="hemifield" test="test" ght="ght" being="being" outside="outside" normal="normal" limits.="limits." _3="_3" corrected="corrected" standard="standard" cpsd="cpsd" with="with" p="p" _5.="_5." as="as" and="and" are="are" routine="routine" printout="printout" statistics="statistics" humphrey="humphrey" sita="sita" _24="_24" visual="visual" it="it" would="would" be="be" interest="interest" if="if" authors="authors" can="can" provide="provide" these="these" indices="indices" for="for" their="their" subjects="subjects" will="will" helpful="helpful" in="in" confirming="confirming" that="that" field="field" defect="defect" was="was" indeed="indeed" glaucomatous.="glaucomatous."/> In the absence of progression of glaucomatous visual field
loss, a patient having such field loss at a normal intraocular pressure
(IOP) is at the most a normal tension glaucoma suspect. The authors may
like to report any progression of glaucomatous visual field loss in the
future, which will truly define normal tension glaucoma.
We concur with the author that cup-disc ratio (CDR), if
measured vertically and > 0.7 in the absence of an extremely large or
tilted cup, usually suggest glaucomatous optic neuropathy. A CDR of >
0.3, however, will have much less bearing in indicating a glaucomatous
process. Studies have shown that vertical CDR must be interpreted with the
vertical disc diameter (VDD) [3]. For example, in normal population (glaucoma
eyes excluded) with VDD of 1.9 mm, the 50th percentile of vertical CDR is
0.55, with a 95th percentile at 0.74.
In addition, nowadays, the neuroretinal rim is regarded as more
important than the cup or CDR. The cardinal feature of glaucomatous optic
neuropathy is a loss of tissue from inner edge of the rim [4]. Other features
include rim notching, hemorrhage crossing the rim, undercutting of rim,
and asymmetry of rim between eyes, etc [4]. The authors may like to provide
these data in support of a glaucomatous optic nerve damage.
Finally, both eyes of each subject were used in analysis. Any effect
may be double-represented in the study population. This may be overcome by
including only one eye of each patient, or if both eyes are to be
included, using statistical means such as a generalized estimating
equation [5].
Reference
(1). Allanore Y, Parc C, Monnet D, Brezin AP, Kahan A. Increased
prevalence of ocular glaucomatous abnormalities in systemic sclerosis. Ann
Rheum Dis. 2004 Oct; 63(10):1276-8.
(3). Crowston JG, Hopley CR, Healey PR, Lee A, Mitchell P; Blue
Mountains Eye Study. The effect of optic disc diameter on vertical cup to
disc ratio percentiles in a population based cohort: the Blue Mountains
Eye Study. Br J Ophthalmol. 2004 Jun;88(6):766-70.
(4). South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific
Glaucoma Guidelines. 2004. p 21
(5). Katz J, Zeger S, Liang KY. Appropriate statistical methods to
account for similarities in binary outcomes between fellow eyes. Invest
Ophthalmol Vis Sci. 1994 Apr;35(5):2461-5.
We wish to comment on the conclusions of a study recently published
in Annals: A randomized controlled trial of intra-articular injection of
the carpometacarpal joint of the thumb in osteoarthritis (Ann Rheum Dis
2004: 63:1260-1263).
This study was designed as a randomized control
trial, which was powered to detect a difference "between the placebo and
steroid injection which was likely t...
We wish to comment on the conclusions of a study recently published
in Annals: A randomized controlled trial of intra-articular injection of
the carpometacarpal joint of the thumb in osteoarthritis (Ann Rheum Dis
2004: 63:1260-1263).
This study was designed as a randomized control
trial, which was powered to detect a difference "between the placebo and
steroid injection which was likely to be clinically significant was 20%"
(pg. 1261). Non parametric prospective power calculations established
that 45 patients were required in each group in order to detect a
difference with an alpha level of 5% and power of 80%. The authors are to
be commended for planning their study with this in mind. However, the
authors reported difficulty in recruitment which, rightly so, resulted in
the early termination of the project.
While the authors report the difficulty in recruitment to achieve
appropriate power, it appears that they have not considered the impact of
the under-recruitment on their results and therefore the conclusions that
they can draw from this study. The purpose of appropriate a-priori
powering of a study is to ensure that the chance of incorrectly accepting
a null hypothesis (i.e. a type II error) is sufficiently small. It is a
way of ensuring that a non-significant result is probabilistically likely
to be due to no difference between two groups.
Failure to reach the intended recruitment leads to difficulty in
interpreting studies with non-significant results. Two possible
explanations may be drawn from such non significant results:
1) There
may be no actual difference between the group or
2) There may indeed be a
difference, however the sample size was insufficiently large to detect
this.
Either way, this conundrum must be reflected in the discussion and
conclusions of the study.
As such, the authors of this article cannot claim, as they do in
their conclusions that "no clinical benefit was gained from inta-articular
steroids into the CMCJ...". At best, they can claim that there study, due
to the unfortunate, but very real problems associated with recruitment for
hand osteoarthritis trials, was unable to provide conclusive evidence to
evaluate whether steroids were effective.
Reference
(1). Baskin L. Statistical interpretation can also bias research evidence.
BMJ 2003; Jun 28;326(7404):1453-5.
Over quarter of a century of experience with injecting steroids has
led me to believe in the value of steroid injections for OA of small and
large joints. I have used Depot-Medrone with lidocaine for the CMC
Joint, especially in the elderly who have disabling CMC joint OA, leading
to inability to lift a pot of Tea, an extremely important activity of
daily living for the elderly at least in UK!
Many...
Over quarter of a century of experience with injecting steroids has
led me to believe in the value of steroid injections for OA of small and
large joints. I have used Depot-Medrone with lidocaine for the CMC
Joint, especially in the elderly who have disabling CMC joint OA, leading
to inability to lift a pot of Tea, an extremely important activity of
daily living for the elderly at least in UK!
Many of these patients cannot tolerate many analgesics and anti
inflammatory drugs, compounded by co-morbidities. In my experience the
pain relief has been as long as 3 years, but could be as short as 4 weeks
for very few. The pain and functional improvement has been longest with
injections for OA in CMC Joints and first Metartarsophalageal joints
without large osteophytes. A community based study on a larger number of
patients will be illuminating! CMC Joint OA is very common in primary
care.
Dear Editor,
I read with interest the article by Katz et al on the prevalence and predictors of disability in valued life activities among individuals with rheumatoid arthritis (1).
It is encouraging that patient based assessments are being explored among rheumatic diseases. Rheumatoid arthritis (RA) and osteoarthritis (OA) have received the most attention in this regard. It is thus reassuring that...
Dear Editor, I read with interest this work. Indeed ultrasonography has increasing role in this field so the interpretation of its images is so important for the rheumatologist. From a radiological and pathological point of view we can divide the changes of the bone in this disease into two types. Type one, which is the pre-erosive stage appears as many hyperechoic bone islands in the ostoid tissue of the cortical and en...
Dear Editor, plain X-ray films will demonstrate the bony defect and its margin whether it is sclerotic or not. In that lesions due to excessive bone marrow infiltration and soft tissue formation , the soft tissue formed is directly proportional to the bone marrow infiltration and disease activitynot to the size of the bone defect. The accurate parameter to follow up the bone marrow infiltration or recovery is to follow up t...
Dear Editor,
In their recent report, Armstrong and colleagues highlight the high prevalence of falls in patients with rheumatoid arthritis (RA)[1], show that falls increase with functional disability and antidepressant use, and comment that fracture prevention extends beyond the pharmacological treatment of osteoporosis. This concurs with current guidelines for the management of steroid induced osteoporosis[2], whi...
Dear Editor,
In response to the hypothesis article ‘Is progressive osteoarthritis an atheromatous vascular disease?’ [Conaghan, Hvanharanta, PA Dieppe Ann Rheum Dis V64 No11 Nov 2005 1539-1541].
The hypothesis paper Atheroma and the Progression of Osteoarthritis of Conaghan et al.[1] confuses four questions. Is progressive OA related to local atheroma? Is it related to systemic atheroma? Do statins have an...
Dear Editor
We read with interest the recent article of Jonsdottir and colleagues,[1] in which the authors describe an increase in the rate of ACLA in RA patients who received any anti-TNF therapy; a potentially very interesting finding. However, this article commits multiple errors in scientific methodology and we are concerned that the presumed apparent correlations of ACLA are actually the result of inherent b...
Dear Editor,
We read with interest the article by Shanahan et al [1] on suprascapular nerve blocks and the accompanying editorial by Hall and Buchbinder [2]. It is gratifying to know that in this context the indirect method of needle placement produces a similar outcome to the radiologically-guided method. However, we would like to point out an important methodological flaw in the study.
The pat...
Dear Editor,
We read with great interest the article by Allanore et al, and commend on their efforts in studying this important issue[1]. We would be most grateful if the authors can help to clarify a few points.
Mean Deviation (MD) is the average of the numbers on the total deviation plot with each value weighted according to the magnitude of the normal range at that point. It signifies the over...
Dear Editor,
We wish to comment on the conclusions of a study recently published in Annals: A randomized controlled trial of intra-articular injection of the carpometacarpal joint of the thumb in osteoarthritis (Ann Rheum Dis 2004: 63:1260-1263).
This study was designed as a randomized control trial, which was powered to detect a difference "between the placebo and steroid injection which was likely t...
Dear Editor,
Over quarter of a century of experience with injecting steroids has led me to believe in the value of steroid injections for OA of small and large joints. I have used Depot-Medrone with lidocaine for the CMC Joint, especially in the elderly who have disabling CMC joint OA, leading to inability to lift a pot of Tea, an extremely important activity of daily living for the elderly at least in UK! Many...
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