Elevated plasma levels of hyaluronate in patients with osteoarthritis and rheumatoid arthritis

Goldberg, Ronald; Huff, J P; Lenz, Mary Ellen; Glickman, Paul B.; Katz, Robert S.; Thonar, Eugene J.‐M.A.

doi:10.1002/art.1780340704

Cited by 127 publications

(57 citation statements)

References 35 publications

(16 reference statements)

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“…54,55) It also has been reported that serum HA level was associated with the presence of radiographic knee OA. [56][57][58][59] It has been reported normal human the HA level in the ranged from 53.9 to 55.2 ng/mL. 60) In the present study, we used serum COMP and HA levels to evaluate these effects during CS therapy.…”

Section: )mentioning

confidence: 95%

Efficacy of Chondroitin Sulfate for Painful Knee Osteoarthritis: A One-Year, Randomized, Double-Blind, Multicenter Clinical Study in Japan

Morita

Yamada

Date

et al. 2018

Biological & Pharmaceutical Bulletin

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We explored the effects of chondroitin sulfate on knee osteoarthritis in a one-year, randomized, doubleblind, dose-comparison study. Patients with painful, Kellgren-Lawrence grade 2-3, osteoarthritis of the knee were treated with oral chondroitin sulfate at a dose of either 260 mg/d (low-dose group, control group) or 1560 mg/d (high-dose group). Symptoms were evaluated by the Lequesne's index and visual analog scale for pain. We made subgroup analyses according to background symptom severity (Lequesne's index ≥8 or <8) in 73 patients. Serum level of cartilage oligomeric matrix protein and hyaluronic acid were also determined. In the subgroup with severe symptoms (Lequesne's index ≥8), the chondroitin sulfate dose of 1560 mg/d improved pain faster after 6 and 9 months' therapy. However, no dose-related effects were found on cartilage oligomeric matrix protein or hyaluronic acid levels. Chondroitin sulfate also had good tolerability. We conclude that chondroitin sulfate is useful for pain control in knee osteoarthritis.Key words chondroitin sulfate; pain-management; clinical trial; randomized controlled trial Osteoarthritis (OA) is the most common form of arthritis and is a major cause of morbidity, activity limitation, physical disability, excess health care utilization, and reduced healthrelated QOL, especially in people aged 65 years and older.

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Section: )mentioning

confidence: 95%

Efficacy of Chondroitin Sulfate for Painful Knee Osteoarthritis: A One-Year, Randomized, Double-Blind, Multicenter Clinical Study in Japan

Morita

Yamada

Date

et al. 2018

Biological & Pharmaceutical Bulletin

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“…Disease duration and presence or absence of knee effusion were recorded. Additionally, the presence of OAaffected joints was evaluated using an articular index, the numerical value of which is the sum of the total cartilage surface area (in cm 2 ) of each symptomatic joint as previously reported (34).…”

Section: Methodsmentioning

confidence: 99%

Uncoupling of type II collagen synthesis and degradation predicts progression of joint damage in patients with knee osteoarthritis

Garnero¹,

Ayral²,

Rousseau³

et al. 2002

Arthritis & Rheumatism

264

200

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Objective. The hallmark of osteoarthritis (OA) is the loss of articular cartilage. This loss arises from an imbalance between cartilage synthesis and cartilage degradation over a variable period of time. The aims of this study were to investigate the rates of these processes in patients with knee OA using two new molecular markers and to investigate whether the combined use of these markers could predict the progression of joint damage evaluated by both radiography and arthroscopy of the joints during a period of 1 year.Methods. Seventy-five patients with medial knee OA (51 women, 24 men; mean ؎ SD age 63 ؎ 8 years, mean ؎ SD disease duration 4.8 ؎ 5.2 years) were studied prospectively. At baseline, we measured serum levels of N-propeptide of type IIA procollagen (PIIANP) and urinary excretion of C-terminal crosslinking telopeptide of type II collagen (CTX-II) as markers of type II collagen synthesis and degradation, respectively. Joint space width (JSW) on radiography and medial chondropathy at arthroscopy (assessed using a 100-mm visual analog scale [VAS]) were measured in all patients at baseline and in 52 patients at 1 year. Progression of joint destruction was defined as a decrease of >0.5 mm in JSW on radiography and as increased chondropathy (an increase in the VAS score of >8.0 units) between the baseline and 1-year evaluations.Results. At baseline, compared with 58 healthy age-and sex-matched controls, patients with knee OA had decreased serum levels of PIIANP (20 ng/ml versus 29 ng/ml; P < 0.001) and increased urinary excretion of CTX-II (618 ng/mmole creatinine [Cr] versus 367 ng/ mmole Cr; P < 0.001). The highest discrimination between OA patients and controls was obtained by combining PIIANP and CTX-II in an uncoupling index (Z score CTX-II ؊ Z score PIIANP), which yielded a mean Z score of 2.9 (P < 0.0001). Increased baseline values in the uncoupling index were associated with greater progression of joint damage evaluated either by changes in JSW (r ‫؍‬ ؊0.46, P ‫؍‬ 0.0016) or by VAS score (r ‫؍‬ 0.36, P ‫؍‬ 0.014). Patients with both low levels of PIIANP (less than or equal to the mean ؊ 1 SD in controls) and high levels of CTX-II (greater than or equal to the mean ؉ 1 SD in controls) had an 8-fold more rapid progression of joint damage than other patients (P ‫؍‬ 0.012 and P < 0.0001 as assessed by radiography and arthroscopy, respectively) and had relative risks of progression of 2.9 (95% confidence interval [95% CI] 0.80-11.1) and 9.3 (95% CI 2.2-39) by radiography and arthroscopy, respectively.Conclusion. Patients with knee OA are characterized by an uncoupling of type II collagen synthesis and degradation which can be detected by assays for serum PIIANP and urinary CTX-II. The combination of these two new markers could be useful for identifying knee OA patients at high risk for rapid progression of joint damage.

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“…Serum HA levels have been reported to be elevated in patients with liver cirrhosis, cancers, rheumatoid arthritis, scleroderma, psoriasis and osteoarthritis [5][6][7][8]. Increased urine HA levels have been found in rheumatoid arthritis [1], cancers [9] and premature aging syndromes, including Werner's syndrome (WS) [10,11] and the Hutchinson-Gilford syndrome [12].…”

Section: Introductionmentioning

confidence: 99%

Elevation of Serum Hyaluronan Level in Werner’s Syndrome

Tanabe¹,

Goto²

2001

Gerontology

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Background: There is a well-established association between Werner’s syndrome (WS) and hyperhyaluronic aciduria; however, to date hyaluronan (HA) in the serum has not been statistically linked with WS. Recently, the gene that causes WS has been defined as a DNA helicase on chromosome 8, and 19 different mutations in WS patients have been identified. It is not known whether the mutation type of the Werner helicase gene affects the levels of serum and urine HA in WS patients. Objective: To evaluate the association of serum HA with WS, and the relationship of the serum and urine HA levels to the mutation type. Methods: HA both in the serum and the urine was measured in 40 patients with WS and 114 normal controls. The serum and urine HA were quantified by sandwich binding protein assay and competitive ELISA-like method, respectively. The muation on WS helicase gene was analyzed by mutant-allele-specific amplification and oligomer ligation assay. Results: WS patients showed significantly higher levels of HA in the serum (mean ± SD: 115.7 ± 119.8 ng/ml, p < 0.001) and urine (1,040.8 ± 777.3 ng/mg creatinine, Cre, p < 0.001) than age-matched controls (serum HA: 15.8 ± 14.2 ng/ml, urine HA: 379.7 ± 124.2 ng/mg Cre). The serum and urine HA levels of WS patients are almost equal to those of normal controls over 80 years (serum HA: 118.5 ± 108.4 ng/ml, urine HA: 914.5 ± 712.1 ng/mg Cre). There was a significant correlation between serum and urine HA levels in WS patients (r = 0.42, p = 0.007). Analysis of the mutation on the helicase gene in 22 WS patients showed that among 44 chromosomes, 3 (6.8%) chromosomes had type 1 mutation, 22 (50.0%) had type 4 mutation, 14 (31.8%) had type 6 mutation, and the rest had other mutations. The serum and urine levels of HA did not show any significant association with the mutation type. Conclusion: The hyperhyaluronic aciduria in WS reflects the high level of serum HA. The serum and urine HA levels are useful biochemical markers for WS irrespective of the muation type of the Werner helicase gene.

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Elevated plasma levels of hyaluronate in patients with osteoarthritis and rheumatoid arthritis

Cited by 127 publications

References 35 publications

Efficacy of Chondroitin Sulfate for Painful Knee Osteoarthritis: A One-Year, Randomized, Double-Blind, Multicenter Clinical Study in Japan

Efficacy of Chondroitin Sulfate for Painful Knee Osteoarthritis: A One-Year, Randomized, Double-Blind, Multicenter Clinical Study in Japan

Uncoupling of type II collagen synthesis and degradation predicts progression of joint damage in patients with knee osteoarthritis

Elevation of Serum Hyaluronan Level in Werner’s Syndrome

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