I was intrigued when I heard the report of this paper in view of the
widely held belief that copper jewellery is also beneficial in the
treatment of arthritis.
In the case of the gold rings it has to be remembered that gold rings
are seldom pure gold. Even 22 carat gold rings are 22/24 parts gold, the
rest being copper.
In view of this what evidence is there that the gold and not the...
I was intrigued when I heard the report of this paper in view of the
widely held belief that copper jewellery is also beneficial in the
treatment of arthritis.
In the case of the gold rings it has to be remembered that gold rings
are seldom pure gold. Even 22 carat gold rings are 22/24 parts gold, the
rest being copper.
In view of this what evidence is there that the gold and not the
copper was responsible for the observed effect? Where the team able to
observe anyone with a platinum, copper or silver ring; and what effects if
any, where noted on the arthritis in such cases? Taking it further was
there anyone who had a pure (24ct) gold ring and what had been the effect
on their case?
We read with great interest the study by Tsifetaki et al. on the
efficacy and side effects of the use of oral pilocarpine for the treatment
of ocular symptoms in Sjõgren’s syndrome.[1] In terms of patient
selection, we noted the authors excluded patients with significant medical
conditions, but we are not sure about the status of their concomitant
medications. For women in their late 50s, suc...
We read with great interest the study by Tsifetaki et al. on the
efficacy and side effects of the use of oral pilocarpine for the treatment
of ocular symptoms in Sjõgren’s syndrome.[1] In terms of patient
selection, we noted the authors excluded patients with significant medical
conditions, but we are not sure about the status of their concomitant
medications. For women in their late 50s, such as in the study population,
drugs like beta blockers and hormone replacement therapy are commonly
used, and it is well known that they may exacerbate dry eye symptoms.[2]
The authors also did not specify the type and frequency of artificial
tears used and whether the lubricants contained any preservatives, which
could exacerbate the symptoms of keratoconjunctivitis sicca.[3] A
standardization of the artificial tears across the groups seems necessary
in testing the efficacy of oral pilocarpine on ocular symptoms.
We are interested to know the timing of the Schirmer’s-I tests, with
respect to the administration of the oral pilocarpine. In a study of
salivary flow rates, the pilocarpine effect occurred within 30 minutes
after the oral intake of the drug and it lasted for about 3 to 5 hours.[4]
This might be the reason for the negative outcome of the Schirmer’s-I test
in this study, especially when oral pilocarpine was taken twice a day
rather than four times daily. The latter regime was established in a
similar study on salivary secretion to be the optimal therapeutic
regimen.[4]
Another area of concern is about the safety of long-term systemic
medication to treat a chronic local symptomatic problem. In this series, 4
out of 29 patients presented with headaches, sweating, nausea and
vomiting, despite the fact that they were mild and tolerable. The
parasympathomimetic effects of pilocarpine may cause potential problems in
patients with history of asthma, chronic obstructive pulmonary disease,
cardiac arrhythmia and uveitis.[4,5] These patients should be alerted
for the possible complications from the drug.
The lack of information about the use of oral pilocarpine in
preventing serious ocular complications from sicca also undermines its
clinical value. For symptomatic relief alone, we advocate local treatment
for local symptoms with a balance of the efficacy and adverse effects of
the drugs. Apart from maximum lubrication using artificial tears or
ointments, topical cyclosporine or topical steroids have also been shown
to be effective for dry eye symptoms in Sjõgren’s syndrome.[6] Other
treatment strategies include partial or total occlusion of the upper
puncta, in addition to the lower ones, may also be considered.[7]
Systemic treatment may be reserved for patients who are resistant to local
therapy or those with co-existent xerostomia symptoms.
References
(1) Tsifetaki N, Kitsos G, Paschides CA, Alamanos Y, Eftaxias V,
Voulgari PV et al. Oral pilocarpine for the treatment of ocular symptoms
in patients with Sjogren's syndrome: a randomised 12 week controlled
study. Ann Rheum Dis 2003;62:1204-7.
(2) Schaumberg DA, Buring JE, Sullivan DA, Dana MR. Hormone
replacement therapy and dry eye syndrome. JAMA 2001;286:2114-9.
(3) Albietz JM, Bruce AS. The conjunctival epithelium in dry eye
subtypes: effect of preserved and non-preserved topical treatments.
Curr.Eye Res 2001;22:8-18.
(4) Vivino FB, Al-Hashimi I, Khan Z, LeVeque FG, Salisbury PL 3rd, Tran-
Johnson TK, et al. Pilocarpine tablets for the treatment of dry mouth and
dry eye symptoms in patients with Sjogren syndrome: a randomized, placebo
-controlled, fixed-dose, multicenter trial. Arch Intern Med 1999;159:174-
81.
(5) Greco JJ, Kelman CD. Systemic pilocarpine toxicity in the
treatment of angle closure glaucoma. Ann Ophthalmol 1973;5:57-9.
(6) Avunduk AM, Avunduk MC, Varnell ED, Kaufman HE. The comparison of
efficacies of topical corticosteroids and nonsteroidal anti-inflammatory
drops on dry eye patients: a clinical and immunocytochemical study. Am J
Ophthalmol 2003;136:593-602.
(7) Balaram M, Schaumberg DA, Dana MR. Efficacy and tolerability
outcomes after punctal occlusion with silicone plugs in dry eye syndrome.
Am.J Ophthalmol 2001;131:30-6.
The recent leader was well balanced and comprehensive.[1]
However, there was no mention of why they are used and by whom. Thus, the mortality
data from ARAMIS and other dara-bases showing an increased mortality in
rheumatoid patients taking prednisone is acceptable if it's reserved for
the more severe patient. The published evidence suggests to me that use is
more physician determined than pa...
The recent leader was well balanced and comprehensive.[1]
However, there was no mention of why they are used and by whom. Thus, the mortality
data from ARAMIS and other dara-bases showing an increased mortality in
rheumatoid patients taking prednisone is acceptable if it's reserved for
the more severe patient. The published evidence suggests to me that use is
more physician determined than patient. Thus, some prescribe them frequently
or even routinely and some rarely, if ever. If this is true, then the longer-term mortality data does warrant serious concern. The clinical description
of the efficacy of "biologics" often includes a successful decrease -or
discontinuation-of steroids. This appears to be widely accepted as a
beneficial outcome,and suggests that,despite the "controversy" most of us
know the right answer!
Reference
(1) J W J Bijlsma, M Boers, K G Saag, and D E Furst.
Glucocorticoids in the treatment of early and late RA
Ann Rheum Dis 2003; 62: 1033-1037.
In this letter we would like to respond to the comments made by Frank
Conijn to our leader.[1]
Firstly, we are aware of the differences in the
content of physiotherapy in the three trials at issue, and briefly
mentioned this in our leader. The fact that passive mobilisations were not
allowed in the trial by Winters et al.[2] may, indeed, partly explain the
differences in effectiveness of...
In this letter we would like to respond to the comments made by Frank
Conijn to our leader.[1]
Firstly, we are aware of the differences in the
content of physiotherapy in the three trials at issue, and briefly
mentioned this in our leader. The fact that passive mobilisations were not
allowed in the trial by Winters et al.[2] may, indeed, partly explain the
differences in effectiveness of physiotherapy across the three trials.
These differences in the content of physiotherapy were already addressed
by Hay et al. [3] in the same issue of the ARD. Therefore, we decided to
focus our leader on the potential influence of heterogeneity in outcome
measures. Clinimetric issues receive little attention in the medical
literature, but may have considerable impact on the outcome of trials, as
was demonstrated in our leader.
We agree with Conijn that it is potentially confusing that the term
physiotherapy may refer to a wide range of interventions. It is perfectly
valid to evaluate the effectiveness of massage, exercises and physical
applications for shoulder pain (as was done by Winters et al.), but it
seems, indeed, inadequate to refer to such an intervention as
"physiotherapy". For many physiotherapists passive mobilisation is an
important component of the treatment of shoulder pain. In future studies
terms should be used that adequately describe the content of treatment,
and not simply refer to the profession of the care providers involved in
the trial.
Secondly, we are familiar with the trial by Bang et al,[4] in which
the added value of passive mobilisations was studied in patients with
shoulder impingement syndrome, and also referred to this trial in our
leader. We strongly believe that the promising results of this study need
further confirmation in larger and different patient groups.
Thirdly, Conijn feels that our leader is one that shows little real-
life insight, because we limited our discussion to the effectiveness of
corticosteroid injection versus physiotherapy. As our leader was written
in connection with the publicaton by Hay et al, we decided to focus our
paper on the research question addressed in this trial. There are, indeed,
many more questions in the treatment of shoulder pain that need to be
resolved. Conijn may be quite right that a stepwise approach (advice,
NSAIDs, physiotherapy, corticosteroid injection) with combined
interventions for those with persistent shoulder problems is the best
strategy for treating shoulder pain in primary care. In fact, most current
guidelines are based on this principle. Further research is needed to
provide evidence for the effectiveness of this management strategy.
Finally, the author seems to have misread Table 3 of the paper by
Winters et al.[2] We were not involved in this trial, but like to correct
this misunderstanding. This table does not present the proportion of
patients cured, but the mean pain scores after 11 weeks of follow-up,
separately for patients who felt cured and for those who did not feel
cured. Conijn highlights the results in the injection group, but pain
scores were very similar in patients treated with physiotherapy (mean
score 8.3 versus 8.2 points). Relapse rates after 11 weeks of follow-up
were also presented in this paper: recurrences were reported by 13% in the
physiotherapy group, and 18% in the injection group (and not by more than
90% as Conijn seems to imply).
We were surprised to be accused of being insufficiently objective in
this opinionated letter, but leave it to others to judge the quality of
our work.
References
(1) Van der Windt DAWM, Bouter LM. Physiotherapy or corticosteroid
injection for shoulder pain. Ann Rheum Dis 2003;62:385-7.
(2) Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de Jong, B.
Comparison of physiotherapy, manipulation, and corticosteroid injection
for treating shoulder complaints in general practice: randomised, single
blind study. BMJ 1997;314:1320-5.
(3) Hay EM, Thomas E, Paterson SM, Dzieczic K, Croft PR. A pragmatic
randomised controlled trial of local corticosteroid injection and
physiotherapy for the treatment of new episodes of unilateral shoulder
pain in primary care. Ann Rheum Dis 2003;62:394-9.
(4) Bang MD, Deyle GD. Comparison of supervised exercise with and without
manual physical therapy for patients with shoulder impingement syndrome. J
Orthop Sports Phys Ther 2000;30:126-37.
We thank dr Barta for his comments on our manuscript ‘anti-
Saccharomyces cerevisiae IgA antibodies are raised in ankylosing
spondylitis and undifferentiated spondyloarthropathy’.[1]
We are fully aware of the importance of gut inflammation in
spondyloarthropathies (SpA).[2] In our view, the finding of ASCA in SpA
provides further evidence for the concept that inflammatory bowel disease
and SpA...
We thank dr Barta for his comments on our manuscript ‘anti-
Saccharomyces cerevisiae IgA antibodies are raised in ankylosing
spondylitis and undifferentiated spondyloarthropathy’.[1]
We are fully aware of the importance of gut inflammation in
spondyloarthropathies (SpA).[2] In our view, the finding of ASCA in SpA
provides further evidence for the concept that inflammatory bowel disease
and SpA are related. However, we were not able to demonstrate an
association between gut inflammation and ASCA levels in our cohort. We are
currently analyzing in a larger cohort of SpA patients the relationship
between ASCA levels and the presence of clinical and histological bowel
inflammation.
We are aware of the fact that ASCA levels are raised in patients with
celiac disease. However, it seems highly unlikely that this would explain
our results. None of the patients in whom ileal biopsies were available
did fulfill histopathologic criteria of celiac disease (increased number
of intra-epithelial lymphocytes, flattening of villi and crypt
hyperplasia). These findings might be expected in ileal biopsies if celiac
disease was present.
As for the suggestion of attempting a yeast-free diet in patients
with Crohn’s disease, to our knowledge, one study has been published using
such an approach.[3] In this study, exclusion of yeast-intake did not
result in a lower Crohn’s disease activity index (CDAI) during the
exclusion period, compared to baseline, although the CDAI was
significantly lower during the exclusion compared to the inclusion period.
Furthermore, such a diet is demanding for the patients and resulted in a
significant weight loss. This limits the practical feasibility of this
possible therapy.
References
(1) Hoffman IE, Demetter P, Peeters M, De Vos M, Mielants H, Veys EM et al.
Anti-Saccharomyces cerevisiae IgA antibodies are raised in ankylosing
spondylitis and undifferentiated spondyloarthropathy. Ann Rheum Dis 2003;62:455-459.
(2) De Keyser F, Elewaut D, De Vos M, De Vlam K, Cuvelier C, Mielants H.
Bowel inflammation and the spondyloarthropathies. Rheum Dis Clin North Am 1998;24(4):785-813.
(3) Barclay GR, McKenzie H, Pennington J, Parratt D, Pennington CR. The
effect of dietary yeast on the activity of stable chronic Crohn’s disease.
Scand J Gastroenterol 1992;27:196-200
Anti-Saccharomyces cerevisiae antibodies (ASCA) are known as specific
markers in Crohn's disease albeit the clinical relevance of these
antibodies to some oligomannose epitope of the Saccharomyces cerevisiae is
not clear. Neither the origin and nor the clinicopathological role are
clarified.
Hoffman et al, investigated whether ASCAs are present in
spondyloarthropathies (SpA) in comparison w...
Anti-Saccharomyces cerevisiae antibodies (ASCA) are known as specific
markers in Crohn's disease albeit the clinical relevance of these
antibodies to some oligomannose epitope of the Saccharomyces cerevisiae is
not clear. Neither the origin and nor the clinicopathological role are
clarified.
Hoffman et al, investigated whether ASCAs are present in
spondyloarthropathies (SpA) in comparison with healthy and inflammatory
controls. ASCA IgA levels were raised in ankylosing spondylitis (AS) and
undifferentiated SpA (uSpA) and no correlation between the presence of
subclinical bowel inflammation and ASCA IgA levels was noted. They
conclude that ASCA IgA levels are significantly higher in SpA, and more
specifically in AS, than in healthy controls and patients with RA, so ASCA
is a possible associated serum marker of SpA.[1] But what about other
possible ASCA associated diseases of their patients gut?
Over recent
years, there has been a special interest in the relation between
spondylitis/synovitis and gut inflammation in patients with SpA. Two
thirds of patients with undifferentiated SpA show histologic signs of gut
inflammation, and a fraction of these patients go on to develop clinically
overt Crohn's disease.[2] Clinical studies indicate an important role for
bowel inflammation in ankylosing spondylitis and other
spondyloarthropathies as bowel and peripheral joint inflammation are
clinically, histologically and pathogenetically linked.[3] It is also
known that ASCA positivity correlates principally with small intestines'
Crohn's disease and in these cases both the IgG and IgA type antibodies
are present.[4] The sporadic information about ASCA positivity in
patients suffering in gluten sensitive enteropathy (GSE) in the literature
suggests another occurrence.[5-6]
In a pilot study, we also examined
whether there was ASCA positivity in our patients with biopsy-confirmed
celiac disease. We found a relatively high incidence of ASCA in GSE and
think that ASCA positivity correlates with the (auto-) immune inflammation
of small intestines and it is not only a specific marker of Crohn’s
disease.
The antibodies in the sera of the ASCA positive cases prove a systemic
immune response against Saccharomyces cerevisiae and suggest the end of
the oral tolerance against the yeast's antigens so a yeast-free diet as a
part of the therapy for the ASCA positive patients can be reasonable both
in Crohn’s disease, celiac disease and maybe in spondyloarthropathies.[7]
References
(1) Hoffman IE, DemetterP, Peeters M, De Vos M, Mielants H, Veys EM et al. Anti-Saccharomyces cerevisiae IgA antibodies are
raised in ankylosing spondylitis and undifferentiated spondyloarthropathy. Ann Rheum Dis 2003;62:455-9.
(2) De Keyser F, Baeten D, Van den Bosch F, De Vos M, Cuvelier
C, Mielants H et al. Gut inflammation and spondyloarthropathies. Curr Rheumatol Rep 2002;4:525-32.
(3) Baeten D, De Keyser F, Mielants H, Veys, EM. Ankylosing
spondylitis and bowel disease. Best Pract Res Clin Rheumatol 2002;16:537-49.
(4) Quinton JF, Sendid B, Reumaux D, Duthilleul P, Cortot A,
Grandbastien B et al. Anti-Saccharomyces cerevisiae mannan antibodies
combined with antineutrophil cytoplasmic autoantibodies in inflammatory
bowel disease: prevalence and diagnostic role. Gut 1998;42:788-91.
(5) Damoiseaux JG, Bouten B, Linders AM, Austen J, Roozendaal
C, Russel MG et al. Diagnostic value of anti-Saccharomyces cerevisiae
and antineutrophil cytoplasmic antibodies for inflammatory bowel disease:
high prevalence in patients with celiac disease. J Clin Immunol
2002;22:281-8.
(6) Barta Z, Csipo I, Antal-Szalmas P, Sipka S, Szabo G,
Szegedi G. [Anti-Saccharomyces cerevisiae antibodies in patients with
Crohn's disease]. Orv Hetil 2001;142:2303-7.
The Leader [1] is an insufficiently objective reaction, and
one that demonstrates rather little real-life insight from the authors.
Insufficiently objective, because it strongly highlights the matter
of the outcome measures, while it only slightly touches on the question:
is the study by Winters et al,[2] one of the two other (Dutch)
randomised studies they use for their substantiation, a valid...
The Leader [1] is an insufficiently objective reaction, and
one that demonstrates rather little real-life insight from the authors.
Insufficiently objective, because it strongly highlights the matter
of the outcome measures, while it only slightly touches on the question:
is the study by Winters et al,[2] one of the two other (Dutch)
randomised studies they use for their substantiation, a valid study? The
answer is: No. As the full text [2] shows, the physiotherapists in the
study were not allowed to use manual mobilization or manipulation. This
is an aberration from the average daily practice in physiotherapy practices.
Not only internationally speaking, but concerning the Netherlands as well.
In the Netherlands, in June 2001 there were 12,600 physiotherapists working
in primary care practices. The Dutch Association for Manual Therapy ("Nederlandse
Vereniging voor Manuele Therapie", NVMT) approached 2000 members then.
Important, then, is to note that that association only represents those
manual therapists that have passed their exam, after having gone
through
their course. There are many more (post-academic)
manual therapy schools in the Netherlands, but they are not recognized
by the NVMT (for some scientifically unproved, and in my opinion largely
invalid reason). I cannot, at this time, get the figures from the other
manual therapy schools, but I'd expect at least half of the Dutch
physiotherapists to be sufficiently trained post-academically to apply
manual techniques in a professional manner. Besides that, physiotherapy
schools themselves since decades teach basic manual techniques. As early
as 1979, when I started, they were already taught.
The question "Does manual therapy offer an additional effect, even in
what is referred to as synovial complaints?" can be answered with yes,
even though the evidence consisted of just one randomised controlled trial:
Bang & Deyle [3] found that additional manual therapy gave a pain decrease
from ~575 to ~175, and physiotherapy without from ~560 to ~360. With
6 treatments.
The Leader is one that shows rather little real-life insight, because
it skips the most important question: How are we doing? We = primary care
in general. How have we come up with a cure for the majority of the patients?
The logical sequence would be: first find a basic cure, even if that would
consist of multiple methods combined, and then seek out what the most economic
method or therapeutical sequence is, for which patient. It is disappointing
that the authors of the Leader ask the question: "Physiotherapy or
corticosteroid injection for shoulder pain?" From what I have been
reading, and in my experience, there is every reason to believe that a
combination of the two, with the inclusion of a wait-and-see period and
NSAIDs, in select patients, would be the most (cost-)effective treatment.
As figure 1 of the Leader shows, the separate methods cannot even cure
20% each. (The results of Winters et al [74% of the injection group
feeling cured at 5 weeks] should be seen in the light of the follow-up
at 11 weeks [table 3 of their text]: at that time only 8.3% of the injection
group felt cured, indicating an extremely high relapse percentage.) Nor
has science come up with a clear and valid answer as to why it would be
impossible to cure more of them. Patients and policy makers reading the
Leader may therefore well think: "What on earth are they doing? Fighting
each other over economic details while the vast majority of us/them is
not cured, nor an acceptable answer is found as to why that would be impossible??"
To maximize the chance of a cure, I would therefore think there is no
reason to divert from a pragmatic one. Consisting, in most non-traumatic
shoulder complaints, roughly of physiotherapy (which should include manual
therapy; if in doubt the general practitioner should contact the therapist)
for scapular pain (a frequently presented shoulder complaint, but
in fact usually referred pain from the cervico-thoracic spine), corticosteroids
and/or anaesthetics and/or distension with saline for serious glenohumeral,
subacromial or acromioclavicular complaints, and again physiotherapy for
the rest. Depending on the course of the complaints, a wait-and-see period
with NSAIDs may be appropriate and should be discussed with the patient
as well, just as that all treatment options should (I'd think that should
be standard practice). For an example of such a pragmatic guideline, further
differentiation, and the substantiation of a number of items mentioned
above, see www.ptlitup.com | Archive
& Search | Shoulder Complaints: Diagnosis & Treatment.
References
(1) Van der Windt DAWM, Bouter LM, Physiotherapy or corticosteroid
injection for shoulder pain? Ann Rheum Dis 2003; 62: 385-387. [Full
text]
(2) Winters JC, Sobel JS, Groenier KH, Arendzen HJ, Meyboom-de
Jong B. Comparison of physiotherapy, manipulation, and corticosteroid injection
for treating shoulder complaints in general practice: randomised, single
blind study. BMJ 1997;314:1320–5. [Abstract/Free
Full Text]
(3) Bang MD, Deyle GD. Comparison of supervised exercise with
and without manual physical therapy for patients with shoulder impingement
syndrome. J Orthop Sports Phys Ther 2000;30:126–37. [Medline]
This critique will be brief and applicable to much of our research
today, por desgracia:
Fifty six experimental research candidates seems anecdotal at best
and misleading at worst.
Who are these people? Are they from Greece or Norway, or both?
The placebo effect seems less than sanguine in 2003. More folks
seem capable of monitoring themselves and using bio feedback, an
apparently legitimate form of self healing. This capacity seems to
diminish or nullify the so-called palcebo effect.
More folks seem aware that science may be pseudo-sciense and seems
to be traveling back to protect its hallowed ground.Witness the re-turn by
ordinary folk to Nature and her remedies. Why is this growing by leaps and
bounds in direct confrontation with anecdotal experiments plastered all
over the Web. Do we see this? I am not sure.
We all want to see "scientia" succeed. This RH experiment is not a
step forward. Please consider this.
We are grateful for the thoughtful comments by Grindulis et al.[1]
concerning osteoarthritis (OA) as a predictor of cardiovascular
mortality.[2] We agree that our results could have been presented in more
detail. A priori, however, we had focused our comprehensive study on the
prevalence of finger OA, on its risk determinants and on its association
with total mortality. Interestingly, we ob...
We are grateful for the thoughtful comments by Grindulis et al.[1]
concerning osteoarthritis (OA) as a predictor of cardiovascular
mortality.[2] We agree that our results could have been presented in more
detail. A priori, however, we had focused our comprehensive study on the
prevalence of finger OA, on its risk determinants and on its association
with total mortality. Interestingly, we observed that finger OA in men, in
particular, predicts cardiovascular deaths.[2] As a respose to Grindulis
et al.[1], we wish to present an ad hoc analysis. To emphasise the
etiological approach, we entered more potential confounders into the
survival analysis and excluded the subjects who were diagnosed as having a
cardiovascular disease at the baseline survey (Table 1).
Grindulis et al. claimed that the association between finger OA and
cardiovascular death can be mediated by an effect of social class.[1] It
is true that manual workers whose jobs demand higher physical input tend
to be poorly paid compared to professionals. But we found that further
adjustment for household income, in addition to educational level and
history of workload, did not alter the results. The three indicators of
socio-economical status rather suppressed the association between finger
OA and cardiovascular mortality (Table 1).
Grindulis et al. also suggested that disability caused by OA may
increase the risk of cardiovascular disease.[1] This comment was well
founded, because we had not adjusted the association between finger OA and
cardiovascular mortality for physical activity at leisure. However,
entering this potential factor into the Cox model did not alter our
results. Further adjustment for well established risk factors, such as
systolic and diastolic pressures, serum HDL and total cholesterol, body
mass index, diabetes and smoking history did not weaken the association
between finger OA and cardiovascular mortality (Table 1). Again, the
modelling rather suggested suppression than confounding.
We conclude that physical activity, social class or the conventional
risk factors for coronary heart disease are unlikely to explain the
increased cardiovascular mortality in the presence of finger OA. We
therefore suggest a metabolic or genetic factor or their interaction as
the mechanism of the association between OA and cardiovascular death. A
circulating endogenous factor leading to OA may exist.[3] Previous studies
suggest that hypertension, hypercholesterolemia and raised blood glucose
are associated with both unilateral and bilateral knee OA independently of
obesity [4] and that patients with non-insulin dependent diabetes mellitus
have more often bilateral knee or hip OA.[5] Insulin-like growth factor I
(IGF-I) may also play a role in such mechanism.[6]
References
(1) Grindulis KA, Bhatia G, Davis R, Sosin M, Connolly D, Khattak F.
Osteoarthritis and cardiovascular death [electronic response to Haara MM et al. Osteoarthritis of finger joints in Finns aged 30 or over: prevalence, determinants, and association with mortality] annrheumdis.com 2003http://ard.bmjjournals.com/cgi/eletters/62/2/151#24
(2) Haara MM, Manninen P, Kröger H, Arokoski JPA, Kärkkäinen A, Knect P,
et al. Osteoarthritis of finger joints in finns aged 30 years or over: prevalence, determinants and associations with mortality. Ann Rheum Dis 2003;62:151-158.
(3) Felson DT, Chaisson CE. Understanding the relationship between body
weight and osteoarthritis. Bailliére’s Clinical Rheumatology 1997;11:671-681.
(4) Hart DJ, Doyle DV, Spector TD. Association between metabolic factors
and knee osteoarthritis in women: the Chingford Study. J Rheumatol
1995;22:1118-1123.
(5) Sturmer T, Brenner H, Brenner RE, Gunther KP. Non-insulin dependent
diabetes mellitus (NIDDM) and patterns of osteoarthritis. The Ulm
osteoarthritis study. Scand J Rheumatol 2001;30:169-171.
(6) Denko CW, Malemud CJ. Metabolic disturbances and synovial joint
responses in osteoarthritis. Front Biosci 1999;4:D686-693.
Table 1 Relative risk (RR) and 95% confidence interval (CI) of cardiovascular death by finger joint osteoarthritis in 945 men (72 deaths during 11,972 person-years) and 1,242 women (48 deaths during 16,343
person-years) who had been free from cardiovascular diseases at entry.
Model
Men
Women
Both
sexes*
RR
CI
95%
RR
CI
95%
RR
CI
95%
Adjusted for age
2.01
1.09-3.68
1.98
0.76-5.11
1.98
1.19-3.29
Further
adjusted foreducational level, history of workload,
and householdincome
2.06
1.12-3.79
1.92
0.75-4.93
2.02
1.22-3.36
Further
adjusted forphysical activityat
leisure
2.10
1.14-3.89
1.92
0.75-4.95
2.07
1.24-3.45
Further
adjusted forsystolic and diastolicpressures,
serum HDL andtotal cholesterol, bodymass
index, diabetes,and smoking history
We read with interest the letter by Bernhard et al.[1] Pulmonary
embolism caused by polymethylmethacrylate (PMMA) is not an exceptional
complication of percutaneous vertebroplasty for the treatment of
osteoporotic vertebral fractures. It occured in one patient (2.9%) in our
study [2] (34 vertebroplasties), in two patients (4.3%) in the study by
Jensen [3] et al. (47 vertebroplasties) and i...
We read with interest the letter by Bernhard et al.[1] Pulmonary
embolism caused by polymethylmethacrylate (PMMA) is not an exceptional
complication of percutaneous vertebroplasty for the treatment of
osteoporotic vertebral fractures. It occured in one patient (2.9%) in our
study [2] (34 vertebroplasties), in two patients (4.3%) in the study by
Jensen [3] et al. (47 vertebroplasties) and in one patient (4.8%) in the
study by Legroux-Gérot [4,5] et al. (21 vertebroplasties). Fortunately, there
were no symptoms : small emboli were discovered fortuisly on routine chest
films. To our knowledge, eleven cases of pulmonary embolism caused by PMMA
after percutaneous vertebroplasty have been reported, six [1-6] in the
treatment of osteoporotic vertebral fractures, three [7] in the treatment of
spinal metastasis, one in the treatment of histiocytosis [8] and osteogenesis
imperfecta.[9] Five cases were symptomatic, one case was lethal.[6]
Like Bernhard et al,[1] our experience suggests that a venography before
vertebroplasty is not required in the treatment of osteoporotic vertebral
fractures. We believe that this complication can be prevented by ensuring
that the viscosity of the cement is not too thin and by injecting the
cement into the vertebral body under continuous meticulous lateral
fluoroscopic control. We recommend in futures studies systematic chest
radiograph after vertebroplasty or kyphoplasty to precisely evaluate the
risk of this potentially serious complication.
References
(1) Bernhard J, Heini PF, Villiger PM. Asymptomatic diffuse pulmonary
embolism caused by acrylic cement : an unusual complication of
percutaneous vertebroplasty. Ann Rheum Dis2003;62:85-6.
(2) Grados F, Depriester C, Cayrolle G et al. Long-term observations of
vertebral osteoporotic fractures treated by percutaneous vertebroplasty.
Rheumatology 2000;39:1410-4.
(3) Jensen ME, Evans AJ, Mathis JM et al. Percutaneous
polymethylmethacrylate vertebroplasty in the treatment of osteoporotic
vertebral body compression fractures : technical aspects. AJNR Am J
Neuroradiol 1997;18:1897-904.
(4) Legroux-Gérot I, Lormeau C, Boutry N et al. Suivi à long terme de
fractures vertébrales ostéoporotiques traitées par vertébroplastie
percutanée. Rev Rhum 2002;69:1039.
(5) Lormeau C. Suivi à long-terme de fractures vertébrales ostéoporotiques
traitées par vertébroplastie percutanée. [Mémoire de rhumatologie] Lille,
France, 2001.
(6) Chen HL, Wong CS, Ho ST et al. A lethal pulmonary embolism during
percutaneous vertebroplasty. Anesth Analg 2002;95:1060-2.
(7) Jang JS, Lee SH, Jung SK. Pulmonary embolism of polymethylmethacrylate
after percutaneous vertebroplasty : a report of three cases. Spine 2002;27:E416-8.
(8) Padovani B, Kasriel O, Brunner Ph, Peretti-Viton P. Pulmonary embolism
caused by acrylic cement : a rare complication of percutaneous
vertebroplasty. >AJNR Am J Neuroradiol 1999;20:375-7.
(9) Tozzi P, Abdelmoumene Y, Corno AF et al. Management of pulmonary
embolism during acrylic vertebroplasty. Ann Thorac Surg 2002;74:1706-8.
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