I would like to offer some comments on the paper: Evaluation
of clinically relevant changes in patient-reported outcomes in
knee and hip osteoarthritis: the minimal clinically important
improvement by Florence Tubach, et al.
The authors did a good job of collecting a mass of data and
deriving a delta for the Minimal Clinically Important Improvement for the three core efficacy variables in osteo...
I would like to offer some comments on the paper: Evaluation
of clinically relevant changes in patient-reported outcomes in
knee and hip osteoarthritis: the minimal clinically important
improvement by Florence Tubach, et al.
The authors did a good job of collecting a mass of data and
deriving a delta for the Minimal Clinically Important Improvement for the three core efficacy variables in osteoarthritis.
The result is, however, not quite convenient because three
deltas are derived depending on the value of the baseline
variable. This is awkward - as e.g. also the definition of
three relevant difference delts for proportion of
responders as given in the 80's by the FDA. I wonder
whether one could derive a smooth, constant delta on
another scale. The floor effect of the scale (0 - no pain)
and the decrease of pain which often follows the shape of a
proportional decrease suggest that a percentage scale of
decrease or difference in logarithms might be easier to
handle and also more appropriate for the data.
(Andiometrists are very happy with their dB scale for
andiometry perception.)
I would appreciate the authors doing some additional work to
obtain a constant delta. A pre-post scattergram of BAS
values would be a good starting point. (See, for example,
Chambers, Cleveland, Kleiner, Tukev, Graphical Methods for
Data Analysis, Duxbury Press, Boston).
Sieper et al. propose a set of early referral criteria for ankylosing
spondylitis (AS) using HLAB27 as an central test.[1] The supporting data
were presented in a previous paper.[2] The HLAB27 data were taken from
six study populations. In two groups the control population were either
symptom free blood donors or no clinical data was known.[3, 4] There are
three published trials using back pain contro...
Sieper et al. propose a set of early referral criteria for ankylosing
spondylitis (AS) using HLAB27 as an central test.[1] The supporting data
were presented in a previous paper.[2] The HLAB27 data were taken from
six study populations. In two groups the control population were either
symptom free blood donors or no clinical data was known.[3, 4] There are
three published trials using back pain controls with ankylosing
spondylitis (AS) patients.[5-7] When reviewed these produce lower figures
for sensitivity and specificity than are quoted in the paper by Rudwaleit
et al. A further trial with back pain controls has been seen only in
abstract form and the patient numbers quoted do not match those from the
abstract.[8] If using only the data from studies with back pain controls
the recalculated post test probability is 19% so that the utility of
HLAB27 as a screening and diagnostic tool is greatly reduced .
The authors have used a history of inflammatory back pain[9] as the
entry point for both their diagnostic and referral algorithms. However in
the most recent paper the initial questions are reduced from five to two.
The full set are suggested only if the HLAB27 is difficult to perform.
This recommendation of HLAB27 as the primary test in determining referral
is of concern. While it may ensure most patients are seen early by a
rheumatologist it will certainly overwhelm many of the assessing clinics.
Even in moderately well funded health systems the level of service
provision is already far below recommendation.[10]
Some years ago HLAB27 positive mechanical back pain was a regular
cause for referral to rheumatology clinics [11] and we would not wish to
return to this situation. Further, HLAB27 testing may not be routinely
available in primary care in many areas. Given this we believe that a well
taught clinical history is still the best (albeit poor) indicator of
inflammatory spinal disease in primary care.
References
1. Sieper, J. and M. Rudwaleit, Early referral recommendations for
ankylosing spondylitis (including pre-radiographic and radiographic forms)
in primary care. Ann Rheum Dis, 2005. 64(5): p. 659-63.
2. Rudwaleit, M., et al., How to diagnose axial spondyloarthritis early.
Ann Rheum Dis, 2004. 63(5): p. 535-43.
3. Schlosstein, L., et al., High association of an HL-A antigen, W27, with
ankylosing spondylitis. N Engl J Med, 1973. 288(14): p. 704-6.
4. Brewerton, D.A., et al., Ankylosing spondylitis and HL-A 27. Lancet,
1973. 1(7809): p. 904-7.
5. Sadowska-Wroblewska, M., et al., Clinical symptoms and signs useful in
the early diagnosis of ankylosing spondylitis. Clin Rheumatol, 1983. 2(1):
p. 37-43.
6. Mau, W., et al., Clinical features and prognosis of patients with
possible ankylosing spondylitis. Results of a 10-year followup. J
Rheumatol, 1988. 15(7): p. 1109-14.
7. Braun, J., et al., Prevalence of spondylarthropathies in HLA-B27
positive and negative blood donors. Arthritis Rheum, 1998. 41(1): p. 58-
67.
8. Rudwaleit, M., et al., Clinical parameters in the differentiation of
inflammatory back pain from non-inflammatory back pain. Ann Rheum Dis,
2002. 61 ((suppl 1)): p. 57.
9. Calin, A., et al., Clinical history as a screening test for ankylosing
spondylitis. Jama, 1977. 237(24): p. 2613-4.
10. Harrison, A., Provision of rheumatology services in New Zealand. N Z
Med J, 2004. 117(1192): p. U846.
11. Helliwell, P.a.W., V., Seronegative spondyloarthropathies, in Clinical
Rheumatology International Practice and Research: Epidemiological,
Sociological and Environmental Aspects of Rheumatology, J.A.D. Anderson,
Editor. 1987, Balliere Tindall: London. p. 491-524.
The article, "Circadian Rhythms in RA" postulates a dynamic
equilibrium between melatonin and cortisol as at least part of the
etiology of rheumatoid arthritis. The authors note that the clinical
symptoms of pain and stiffness seem to peak around 5:00 o'clock in the
morning and that this coincides with the diurnal rhythms of melatonin and
cortisol. Because melatonin enhances inflammatory cytokine and...
The article, "Circadian Rhythms in RA" postulates a dynamic
equilibrium between melatonin and cortisol as at least part of the
etiology of rheumatoid arthritis. The authors note that the clinical
symptoms of pain and stiffness seem to peak around 5:00 o'clock in the
morning and that this coincides with the diurnal rhythms of melatonin and
cortisol. Because melatonin enhances inflammatory cytokine and nitric
oxide production, they suggest that inhibitors of melatonin or melatonin
antagonists should be considered as possible therapeutic tools.[1]
Another variable that changes throughout the sleep cycle is regional
cerebral blood flow. The lowest absolute cerebral blood flow values occur
during REM sleep towards the end of the sleep cycle.[2] Nitric oxide release
causes the depressed cerebral blood flow. It can persist for several
hours.[3] Nitric oxide synthase inhibition abolishes sleep-wake differences
in cerebral circulation.[4]
Nitric oxide release correlates with disease activity in patients
with rheumatoid arthritis.[5] Additionally, nitric oxide synthase inhibitors
are currently under consideration for the treatment of the pain associated
with rheumatoid arthritis.[6]
On the other hand, melatonin and its precursors scavenge nitric
oxide.[7] Thus, it would seem that any therapeutic benefit achieved by
suppressing melatonin would be reduced, if not eliminated, by the loss of
the nitric oxygen scavenging ability of endogenous melatonin production on
the nitric oxide released during the sleep cycle.
References
1. Cutolo M, Seriolo B, Craviotto C, Pizzorni C, Sulli A. Circadian
Rhythms in RA. Ann. Rheum. Dis 2003; 63:593-596.
2. Braun A, Balkin T, Wesenten N, et al. Regional cerebral blood flow
throughout the sleep-wake cycle. An H2 (15) O PET study. Brain, 120:1173-
97.
3. Lauritzen M. Cerebral blood flow in migraine and cortical
spreading depression. Acta Neurol Scand Suppl.1987; 113:1-40.
4. Zoccoli G, Grant D, Wild J. et al. Nitric oxide inhibition
abolishes sleep-wake differences in cerebral circulation 2001. Am J
Physiol Heart Circ Physiol, 280 Issue 6, H2598-2606.
5. St Clair EW, Wilkinson WE, Lang T. et al. Increased expression of
blood mononuclear cell nitric oxide synthase type 2 in rheumatoid
arthritis patients. J Exp Med. 1996 Sep 1; 184(3):1173-8.
6. Nakamura H, Ueki Y, Sakito S, Matsumoto K. et al. Clinical effects
of actarit in rheumatoid arthritis: improvement of early disease activity
mediated by reduction of serum concentrations of nitric oxide. Clin Exp
Rheumatol. 2000; 18(4):445-50.
7. Noda Y, Mori A, Liburdy R. et al. Melatonin and its precursors
scavenge nitric oxide. J Pineal Res. 1999; 27(3):159-63.
Brandt has given an excellent comprehensive review on the non
surgical management of Osteoarthritis. For the sake of completeness, it
would be useful to include the place of long acting intrarticular steroids
in OA.
We read with great interest the recent paper by Pappas et al. [1] and
we would like to add some considerations about brucellosis as a cause of
carpal tunnel syndrome (CTS).
Brucellosis has been an endemic disease in Castilla y León (Spain)
until the 1990’s. In 1992 we reported a series of 44 cases of brucellosis
with musculoskeletal manifestations diagnosed in the division of
rheumatology of...
We read with great interest the recent paper by Pappas et al. [1] and
we would like to add some considerations about brucellosis as a cause of
carpal tunnel syndrome (CTS).
Brucellosis has been an endemic disease in Castilla y León (Spain)
until the 1990’s. In 1992 we reported a series of 44 cases of brucellosis
with musculoskeletal manifestations diagnosed in the division of
rheumatology of the Hospital General Yagüe of Burgos between 1988 and 1991 [2]. Seven of them (15.9%) had CTS, confirmed by nerve conduction studies,
concurrently with the clinical picture of brucellosis. They were five
males and two women. Four of the patients were stockbreeders, one was a
butcher, another was slaughterhouse worker, and a last one used to drink
not-pasteurized milk. The time from the beginning of the symptoms to the
diagnosis of brucellosis was less than three months in five of the
patients and more than a year in the other two. Four patients had
bilateral CTS. In one case, CTS was the only manifestation of brucellosis.
Three patients had flexor tenosynovitis and/or wrist arthritis
considered as the cause of the CTS; in the other four, with not evident
local inflammation, the suggested cause of compression of the median nerve
could be a subclinic joint or tendinous affectation or a peripheral
neuropathy due to brucellosis. Two patients were submitted to carpal
surgical decompression of the median nerve. In both cases there was a
significant infiltrate of lymphocytes and plasma cells, with
microgranulomas in one. Antibiotic treatment for brucellosis was effective
in all of the patients except the one with the more chronic evolution, who
sustained a nervous residual damage in spite of antibiotic and surgical
treatment.
Our belief is that CTS associated with brucellosis could be more
frequent than one would found reported in the literature, and sometimes
can be the only clinical manifestation of brucellosis. As Pappas et al., we
emphasize that brucellosis should be included in differential diagnosis of
CST in countries where the disease is endemic. Furthermore, this disease
has to be considered in those cases in which the pathological study shows
a dense infiltrate of lymphocytes and plasma cells and/or microgranulomas.
B Alvarez Lario, JL Alonso, J Macarrón*
Division of Rheumatology and Neurology*
Hospital General Yagüe. Burgos. Spain.
References
1. Pappas G, Markoula S, Sitaridis S, Akritidis N, Tsianos E. Brucellosis
as a cause of carpal tunnel syndrome. Ann Rheum Dis 2005; 64: 792-793.
2. Alvarez Lario B, Alonso JL, Alegre J, Vidal J. Síndrome del túnel
carpiano asociado a brucelosis. Rev Esp Reumatol 1992; 17: 185-186.
We read with interest the recent article
by Ripley et al. describing a
linear (negative coefficient) correlation
between levels of IL-6 and
hemoglobin in patients with systemic lupus
erythematosus (SLE).[1] What
needs mention is that the correlation is
due to a recently described
peptide, hepcidin.[2]
Hepcidin is a small
peptide with dual roles as an effector of the innate
immune system an...
We read with interest the recent article
by Ripley et al. describing a
linear (negative coefficient) correlation
between levels of IL-6 and
hemoglobin in patients with systemic lupus
erythematosus (SLE).[1] What
needs mention is that the correlation is
due to a recently described
peptide, hepcidin.[2]
Hepcidin is a small
peptide with dual roles as an effector of the innate
immune system and
a negative regulator of iron transport.[3] It regulates
total body
iron content through the inhibition of iron absorption by the
small
intestine and by the sequestration of iron within the macrophages.[4] Hepcidin synthesis is induced by IL-6 released during infection and it
decreases circulating iron, essential for pathogen survival.[3] IL-6
also
released during inflammation, acts directly on hepatocytes to
stimulate
hepcidin production, thus giving basis to the long known but
poorly
understood anemia of chronic disease.[4,5] As this anemia is
an integral
part of many chronic inflammatory diseases such as
rheumatoid arthritis
and SLE it has become known as the anemia of
chronic inflammation.[6] The correlation between IL-6 and anemia noted
by Ripley in his SLE cohort
is real and a manifestation of
inflammation but due not to IL-6 itself but
to its product, hepcidin.
References
1. Ripley BJM, Goncalves B, Isenberg DA, Latchman DS,
Rahman A. Raised
levels of interleukin 6 in systemic lupus
erythematosus correlate with
anaemia. Ann Rheum Dis 2005;64: 849-853.
2. Nemeth E, Rivera S, Gabayan V, Keller C, Taudorf S, Pedersen BK,
Ganz
T. IL-6 mediates hypoferremia of inflammation by inducing the
synthesis of
the iron regulatory hormone hepcidin. J Clin Invest 2004;
113:1271-6.
3. Park CH, Valore EV, Waring AJ, Ganz T. Hepcidin, a
urinary
antimicrobial peptide synthesized in the liver. J Biol Chem.
2001;276:
7806-10.
4. Ganz T. Hepcidin – a regulator of intestinal
iron absorption and iron
recycling by macrophages. Best Pract Res Clin
Haematol 2005;18: 171-82.
5. Andrews NC. Anemia of inflammation: the
cytokine-hepcidin link. J Clin
Invest 2004;113:1251-53.
In a recent study, Heiberg et al. [1] reported that in 2001 37% of
their rheumatoid arthritis (RA) patients were using nonsteroidal
antirheumatic drugs (NSAIDs); 15%, coxibs; 43%, corticosteroids; 48%,
disease-modifying anti-rheumatic drugs (DMARDs); and 3%, biologicals. In
2003 we performed a follow-up study on drug use and quality of life (QoL)
in a cohort of RA patients who had been hospitalised in...
In a recent study, Heiberg et al. [1] reported that in 2001 37% of
their rheumatoid arthritis (RA) patients were using nonsteroidal
antirheumatic drugs (NSAIDs); 15%, coxibs; 43%, corticosteroids; 48%,
disease-modifying anti-rheumatic drugs (DMARDs); and 3%, biologicals. In
2003 we performed a follow-up study on drug use and quality of life (QoL)
in a cohort of RA patients who had been hospitalised in 1998 in the
department of rheumatology of Tartu University Hospital. Tartu University
Hospital is responsible for rheumatological care for all of South Estonia,
a catchment area of 600,000 inhabitants.
In 1998, all patients were
prescribed DMARD therapy; the mean age of the 77 patients followed in this
study was 54 years (range 25-74) and the mean duration of the disease was
12.4 years. Study participants answered the Short Form-36 Health Survey
(SF-36) questionnaire and filled in a checklist of the most often used
antirheumatic drugs in Estonia to ascertain current use of medication.
The 2003 follow-up revealed that NSAIDs and/or corticosteroids were being
used by 33% of the patients; DMARDs were being used by 51%. Thus, within
five years, only about half of the RA patients were continuing their DMARD
therapy. While this percentage is comparable with the result of Heiberg
et al. [1] in Norway, we observed two major differences as well.
1) There were no patients receiving biologicals in our study, as they are
not available in Estonia due to their high cost (only 2 individuals in all
of Estonia receive them). Expanding use of biologicals represents one
possible approach to improving RA patients’ QoL.[1-3] In a country
where biologicals are not available due to their high costs, the
alternative approach can be improving compliance with the prescribed
course of treatment with the conventional DMARDs.
2) In the Norwegian sample, there were no patients reported without drug
treatment. In our study, 16% of the patients were not receiving any drug
treatment at the time of the follow-up investigation. Interestingly, the
QoL of this subgroup was better than that of the subgroup continuing to
receive drug treatment and did not differ significantly from that of the
general Estonian population. There were no differences between these two
subgroups either in the patients’ age or in the duration of disease
reported in 1998. It will be important to investigate to see if the high
QoL of the patients no longer receiving drug treatment reflects a cyclic
pattern of disease progression or the remission of RA [4], but our data
support the suggestion that, in a long perspective, the course of RA for
some patients is not as ominous as has been suggested.[5-6]
Looking at our group of RA patients as a whole, we have not noticed any
improvement in QoL as measured on any of the SF36 subscales; indeed, there
has been a significant deterioration on the subscales measuring “emotional
role” and “pain” despite drug therapy. Our results thus do not support
the proposition that over time the QoL of RA patients as a cohort is
improving.
References
1. Heiberg T, Finset A, Uhlig T, Kvien TK. Seven-year changes in
health status and priorities for improvement of health in patients with
rheumatoid arthritis. Ann Rheum Dis 2005; 64:191-195.
2. Pincus T, Sokka T, Kavanaugh A. Relative versus absolute goals of
therapies for RA: ACR 20 or ACR 50 responses versus target values for
"near remission" of DAS or single measures. Clin Exp Rheumatol. 2004; 22:
50-56.
3. Roberts L, McColl GJ. Tumour necrosis factor inhibitors: risks and
benefits in patients with rheumatoid arthritis. Intern Med J. 2004; 34:
687-93.
4. Masi AT. Articular patterns in the early course of rheumatoid
arthritis. Am J Med. 1983; 75: 16-26.
5. Suarez-Almazor ME, Soskolne CL, Saunders LD, Russell AS. Outcome in
rheumatoid arthritis. A 1985 inception cohort study. J Rheumatol. 1994;
21:1438-1446.
6. Sokka T, Mottonen T, Hannonen P. Disease-modifying anti-rheumatic drug
use according to the 'sawtooth' treatment strategy improves the functional
outcome in rheumatoid arthritis: results of a long-term follow-up study
with review of the literature. Rheumatology (Oxford). 2000; 39:34-42.
There are issues that deserve more thought and discussion as they
relate to the Geborak et al. paper [1] on the tumour and lymphoma incidence
associated with TNF alpha inhibitor use.
The title says a) these drugs do not raise the overall incidence of tumours
and b) they may be associated with an increased risk of lymphoma. Given
that lymphomas are also counted under tumours, I cannot see how "a" and...
There are issues that deserve more thought and discussion as they
relate to the Geborak et al. paper [1] on the tumour and lymphoma incidence
associated with TNF alpha inhibitor use.
The title says a) these drugs do not raise the overall incidence of tumours
and b) they may be associated with an increased risk of lymphoma. Given
that lymphomas are also counted under tumours, I cannot see how "a" and "b"
can be biologically true at the same time other than for TNF alpha
inhibitors having a diminishing effect on the incidence of tumours other
than lymphomas. Every other explanation, I am afraid, will have its basis
on one or more problems in data collection and interpretation.
The authors correctly, but without giving due emphasis, say that active
exclusion of malignant tumours from the TNF alpha group might be
contributory to the lower incidence of malignant tumours in this group.
This, in fact, is an important bias true when interpreting data from all
such registries. We do not, as a rule, start TNF alpha inhibitors in
patients with cancer and as a TNF alpha registry gets "older" the
frequency of malignant tumours in that registry will certainly be less and
less when compared to what will be seen in the general population or, for
that matter, among patients with RA not put on TNF alpha inhibitors. In
this scheme it will be perfectly and very deceivingly possible to have,
let’s say, identical malignant tumour incidences in a TNF alpha inhibitor
registry and in the general population, the ones in the registry coming
from drug effects (if such association proves to be true) and those in the
population from random occurrence.
Another issue, at least to me, that needs clarification is how the authors
correct for the widely known sex predilection of rheumatoid arthritis for
females and that of lymphoma for males in one standardized incidence ratio
(SIR)? Why not give two SIR’s, one for each sex separately?
Hasan Yazici
Reference
1. Geborek P, Bladström A, Turesson C et al. Tumor necrosis factor
blockers do not increase overall tumour risk in patients with rheumatoid
arthritis, but may be associated with an increased risk of lymphomas. Ann
Rheum Dis 2005; 64: 699-703.
I was intrigued by the observations of Drs. Marasini, De Monti and
Ghilardi on the risk factors for accelerated atherosclerosis in patients
with systemic lupus erythematosus. Most interesting was the high
percentage of ANA negative lupus patients they evaluated. Given the
sensitivity of the Hep2 substrate, I would expect no more than one such
patient in a total population of 48.
I was intrigued by the observations of Drs. Marasini, De Monti and
Ghilardi on the risk factors for accelerated atherosclerosis in patients
with systemic lupus erythematosus. Most interesting was the high
percentage of ANA negative lupus patients they evaluated. Given the
sensitivity of the Hep2 substrate, I would expect no more than one such
patient in a total population of 48.
The fact that these patients were older and more likely to have
comorbidities (hypertension), I suspect other less specific measures were
used to make the diagnosis of SLE (proteiuria, cytopenias, arthritis,
rash...). In my institution a negative ANA (using Hep2 substrate and
Immunoflorecence Microscopy) is considered to make the diagnosis of SLE
highly unlikely.
Possibly this study makes the case that the ARA criteria should be
updated to require a positive ANA for the diagnosis of SLE.
We read with great interest the report of Graninger et al. about a
small randomized study on local radiotherapy of painful joints in
rheumatoid arthritis [1]: They treated series of six patients on one
painful site with a total dose of 20 Gy in 10 daily fractions. A single
inflamed joint on the contralateral side of the body was used as internal
control and received sham irradiation. Swelling and t...
We read with great interest the report of Graninger et al. about a
small randomized study on local radiotherapy of painful joints in
rheumatoid arthritis [1]: They treated series of six patients on one
painful site with a total dose of 20 Gy in 10 daily fractions. A single
inflamed joint on the contralateral side of the body was used as internal
control and received sham irradiation. Swelling and tenderness, general
disease activity and pain scales was assessed by blinded investigators
before and until 3 months after the irradiation. The authors could not
detect any difference between the irradiated and the unirradiated joint,
so the trial was stopped after the inclusion of six patients.
On behalf of the German Cooperative Group on Radiotherapy for Benign
Diseases (GCG-BD) we welcome any effort of carrying out a prospective-controlled, randomized studies in non-malignant diseases, to broaden the
base of evidence in these disorders.
However, several caveats of the study warrant emphasis:
(1) Even though radiation treatment in rheumatic diseases has a very long
tradition in central Europe [8], rheumatoid arthritis seems not be the
best suitable paradigm for a controlled clinical trial. Local irradiation
in a systemic, autoimmunogenic disorder like rheumatoid arthritis is of
limited value causing only temporary pain relief at the inflamed joints
and is not generally recommended [2].
(2) The number of treated objects is with 12 units very small and to our
opinion not adequate to exclude a beneficial effect of radiotherapy. The
authors did particularly not mention the primary statistical design and
the initially aimed number of patients to include.
Therefore, we think it is not clear, whether it is justified to stop the
trial at this point and to state that the observations from that pilot
trial did not support the use of teleradiotherapy in rheumatoid arthritis.
(3) Finally, our major concern against this study is the chosen total
radiation dose of 20 Gy in ten daily fractions of 2 Gy. This total dose is
far from any recommendation for radiation treatment in painful joint
disorders, ranging from 3 to 12 Gy for tendonitis or activated
osteoarthritis, with two to three weekly fractions of 0.5 to 1 Gy [2].
There are many clinical [3,6] and experimental data [5] supporting these
recommendations. In particular, in acute inflammatory condition it is
recommended to use smaller total doses like 3 Gy and smaller fraction
sizes like 0.5 Gy [9,10]. Several experimental data showed, that in the
low dose range a quasi “paradox” phenomenon can be observed, that lower
dose have an anti-inflammatory effect whereas higher doses promote
inflammation [4,5,9].
In addition, we think that it is radiobiologically incorrect to derive the
dose concept from the prophylactic treatment of heterotopic ossifications,
because the biology of the diseases is completely different: Heterotopic
ossifications are a hyperproliferative disorders needing higher
antiproliferative doses of 1 x 7 Gy or 5 x 3.5 Gy for example [7].
In conclusion, we feel that these preliminary results are not
suitable to discredit the use of radiotherapy in inflammatory, painful
joint disorders, because of the inappropriate patient collective,
statistical study design and applied total radiation doses.
References
1. Graninger M, Handl-Zeller L, Hohenberg G, Staudenherz A,
Kainberger F, Graninger W. Teleradiotherapy of joints in rheumatoid
arthritis: lack of efficacy. Ann Rheum Dis 2005;64:138-140.
2. Micke O, Seegenschmiedt MH. Consensus guidelines for radiation
therapy of benign diseases: a multicenter approach in Germany. Int J
Radiat Oncol Biol Phys 2002;52:496-513.
3. Micke O, Seegenschmiedt MH. Radiotherapy in painful heel spurs
(plantar fasciitis) - results of a national patterns of care study. Int J
Radiat Oncol Biol Phys 2004;58:828-843.
4. Micke P, Blaukat A, Micke O. Effect of Cobalt-60 irradiation on
bradykinin B2 receptor expression on human HF-15 cells. EXCLI Journal
2003;2:52-57.
5. Rödel F, Kamprad F, Sauer R, Hildebrandt G. [Functional and
molecular aspects of anti-inflammatory effects of low- dose radiotherapy].
Strahlenther Onkol 2002;178:1-9.
6. Seegenschmiedt MH, Keilholz L, Katalinic A, Stecken A, Sauer R.
Heel spur: Radiation therapy for refractory pain - Results with three
treatment concepts. Radiology 1996;200:271-276.
7. Seegenschmiedt MH, Makoski HB, Micke O. Radiation prophylaxis for
heterotopic ossification about the hip joint - a multicenter study. Int J
Radiat Oncol Biol Phys 2001;51:756-765.
8. Sokoloff N. Röntgenstrahlen gegen Gelenkrheumatismus. Fortschr
Röntgenstr 1898;1:209-213.
9. Trott KR, Kamprad F. Radiobiological mechanisms of anti-
inflammatory radiotherapy. Radiother Oncol 1999;51:197-203.
10. von Pannewitz G. Degenerative Erkrankungen. In: Zuppinger A,
Ruckensteiner E, eds. Handbuch der medizinischen Radiologie. Berlin-
Heidelberg-New York: Springer, 1970:96-98.
Dear Editor,
I would like to offer some comments on the paper: Evaluation of clinically relevant changes in patient-reported outcomes in knee and hip osteoarthritis: the minimal clinically important improvement by Florence Tubach, et al.
The authors did a good job of collecting a mass of data and deriving a delta for the Minimal Clinically Important Improvement for the three core efficacy variables in osteo...
Dear Editor,
Sieper et al. propose a set of early referral criteria for ankylosing spondylitis (AS) using HLAB27 as an central test.[1] The supporting data were presented in a previous paper.[2] The HLAB27 data were taken from six study populations. In two groups the control population were either symptom free blood donors or no clinical data was known.[3, 4] There are three published trials using back pain contro...
Dear Editor,
The article, "Circadian Rhythms in RA" postulates a dynamic equilibrium between melatonin and cortisol as at least part of the etiology of rheumatoid arthritis. The authors note that the clinical symptoms of pain and stiffness seem to peak around 5:00 o'clock in the morning and that this coincides with the diurnal rhythms of melatonin and cortisol. Because melatonin enhances inflammatory cytokine and...
Dear Editor,
Brandt has given an excellent comprehensive review on the non surgical management of Osteoarthritis. For the sake of completeness, it would be useful to include the place of long acting intrarticular steroids in OA.
Dear Editor,
We read with great interest the recent paper by Pappas et al. [1] and we would like to add some considerations about brucellosis as a cause of carpal tunnel syndrome (CTS).
Brucellosis has been an endemic disease in Castilla y León (Spain) until the 1990’s. In 1992 we reported a series of 44 cases of brucellosis with musculoskeletal manifestations diagnosed in the division of rheumatology of...
Dear Editor,
We read with interest the recent article by Ripley et al. describing a linear (negative coefficient) correlation between levels of IL-6 and hemoglobin in patients with systemic lupus erythematosus (SLE).[1] What needs mention is that the correlation is due to a recently described peptide, hepcidin.[2]
Hepcidin is a small peptide with dual roles as an effector of the innate immune system an...
Dear Editor,
In a recent study, Heiberg et al. [1] reported that in 2001 37% of their rheumatoid arthritis (RA) patients were using nonsteroidal antirheumatic drugs (NSAIDs); 15%, coxibs; 43%, corticosteroids; 48%, disease-modifying anti-rheumatic drugs (DMARDs); and 3%, biologicals. In 2003 we performed a follow-up study on drug use and quality of life (QoL) in a cohort of RA patients who had been hospitalised in...
Dear Editor,
There are issues that deserve more thought and discussion as they relate to the Geborak et al. paper [1] on the tumour and lymphoma incidence associated with TNF alpha inhibitor use. The title says a) these drugs do not raise the overall incidence of tumours and b) they may be associated with an increased risk of lymphoma. Given that lymphomas are also counted under tumours, I cannot see how "a" and...
Dear Editor,
I was intrigued by the observations of Drs. Marasini, De Monti and Ghilardi on the risk factors for accelerated atherosclerosis in patients with systemic lupus erythematosus. Most interesting was the high percentage of ANA negative lupus patients they evaluated. Given the sensitivity of the Hep2 substrate, I would expect no more than one such patient in a total population of 48.
The fact...
Dear Editor,
We read with great interest the report of Graninger et al. about a small randomized study on local radiotherapy of painful joints in rheumatoid arthritis [1]: They treated series of six patients on one painful site with a total dose of 20 Gy in 10 daily fractions. A single inflamed joint on the contralateral side of the body was used as internal control and received sham irradiation. Swelling and t...
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