3+ 4/2002 - Společnost pro pojivové tkáně

ilarly appeared later on but lasted up to two
months after the end of treatment. Contrariwise
DCF caused prompt and plain
reduction of clinical symptoms,which reappeared
after its withdrawn.
According to the Lequesne Index all
three kinds of treatment applied suppressed
troubles in BOA patients. Bone
injury in this disease is characterized similarly
like in RA by formation of collagen
type III (Adam et al., 1980, Adam, Deyl
1983). In such a newly formed tissue activity
of metaloproteinases is upregulated,
what is reflected by an increased urinary
excretion of pyridinolines – crosslinks of
bone and cartilage collagen. Evaluating
UPD, UDPD, and BAP as well as chondrex
values it should be kept in mind of what
processes they are markers. Both the urinary
pyridinolines reflect bone and cartilage
breakdown as they are hardly present
in other tissues. The evident downregulation
of serum chondrex levels in treatment
with PCH suggest its inhibitory action upon
breakdown components of joint compartment
(Harvey et al., 1998), as pyridinoline
excretion was unchanged by treatment, it
means that mainly metabolic pathways of
soft joint tissues were inhibited by PCH, On
the other hand BAP,which has tendency for
an increase in some patients during treatment,
is supposed to be a marker of bone
formation (Van Straalen et al., 1991).
Treatment of OA with PCH is effective
and moreover it is harmless for chondrocytes.
Bečvář et al. (1988) showed an
inhibitory effect of phenylbutazone and
naproxen on chondrocytes and fibroblasts
proliferation, which was blocked by addition
of glycosaminoglycan-peptides complexes
to the culture medium. Similarly
according to our results collagen peptides
also posses such a counteraction to DCF on
cell proliferation and turnover, therefore
combination of DCF with PCH in the therapy
of OA may have some advantage.
Conclusions: According to the presented
results PCH may be classified as
SYSADOA (symptomatic slow-acting drugs
for the treatment of OA) (Lequesne et al.,
1994). Nowaday good evidence is available
that SYSADOA are valuable for OA treatment.
No substantial adverse event PCH was
assessed as related to the study medication.
The presented results showed that treatment
of OA with PCH is effective and safe.
REFERENCES
– Adam M., (1991) Welche Wirkung haben die
Gelatinäpräparate?,Therapiewoche 41:2461
– Adam M., Deyl Z.,(1983) Altered expression of
collagen phenotype in osteoarthrosis, Clin chim
Acta, 133:25-198?.
– Adam M.,Krabcová M.,Miterová L. et al. (1980)
Presence of collagen type III in pathologically
altered cartilage and bone (in Czech), Čas Lék čes
119:1043
– Adam M., Špaček P., Hulejová H. et al (1998)
May collagen hydrolysate rich diet (CHRD) extend
the effect of calcitonin in postmenopausal osteoporosis?
Conn.Tiss. Dis. (Italia) 17:25-36.
– Bečvář R., Baráčková M., Macek J. et al.(1988),
Competitive effect of nonsteroidal drugs and glycosaminoglycan
peptide complexes on the cell cultures,
Conn.Tiss. Dis. 7:13-17.
– Copper C., Dieppe P., Snow S., et al., (1997)
Determinants of the incidence and progression of radiographic
knee osteoarthritis,Arthritis Rheum 40: 331.
– Harvey S., Weisman M., O'Dell J. et al, (1998)
Chondrex: new marker of joint disease Clin Chem
44:509–516
– Kellgren J. H., Lawrence J. S. (1957) Radiological
assessment of osteoarthritis, Ann Rheum Dis
16:494-501
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