acid-phosphatase and Arthritis--Gouty

To explore the potential roles of serum Dickkopf-1 (DKK-1) and tartrate-resistant acid phosphatase 5b (TRAP5b) in gouty arthritis.. Blood serum DKK-1 and TRAP5b were assessed by ELISA method. The serum samples were collected from 150 patients with gouty arthritis, 100 with hyperuricemia and 100 healthy controls. Of the 150 gouty arthritis patients, 40 were diagnosed as acute gout (joint rash and pain), and the other 110 as chronic gout. At the time of serum sampling, various clinical and laboratory parameters were assessed. The correlations of DKK-1 or TRAP5b and clinical/laboratory parameters were analyzed.. (1) The serum levels of DKK-1 were elevated in the patients with gouty arthritis [(2 574.8± 997.9) ng/L] and with hyperuricemia [(2 009.4±756.9) ng/L] compared with the healthy controls [(981.8±770.7) ng/L],F=49.59, P<0.001. (2) The serum levels of TRAP5b in the three groups were (3.2±1.4)U/L, (2.5±1.4)U/L and (0.2±0.2)U/L, respectively. F=103.039, P<0.001. (3) A significant difference of DKK-1 was observed between the patients with gouty arthritis and with hyperuricemia (t=3.998, P<0.001). Similarly, a significant difference of TRAP5b was observed between the patients with gouty arthritis and with hyperuricemia(t=3.391, P=0.004). (4) In the patients with gouty arthritis, there was a positive correlation between DKK-1 and TRAP5b(r=0.47, P<0.001), while the levels of DKK-1 were not related with age, disease duration, body mass index or serum uric acid(r=-0.153, -0.123, 0.158, 0.00,P=0.126, 0.509, 0.381, 0.926). (5) In the patients with gouty arthritis, the serum levels of TRAP5b were elevated in the patients with tophi compared with the patients without tophi[(8.4±6.4)U/L vs. (4.0±1.6)U/L,t=-2.938,P=0.007]. The level of TRAP5b was associated with the disease duration(r=0.455,P=0.01), while there was no correlation between TRAP5b and age, body mass index or serum uric acid (r=0.135, 0.278, 0.144,P=0.595, 0.117,0.132).. In the patients with gouty arthritis, the levels of DKK-1 were remarkably elevated, and there was a positive correlation between DKK-1 and TRAP5b. Our results demonstrate that DKK-1 is involved in bone destruction in gouty arthritis.

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Aged, 80 and over; Arthritis, Gouty; Female; Humans; Hyperuricemia; Intercellular Signaling Peptides and Proteins; Isoenzymes; Male; Middle Aged; Osteolysis; Tartrate-Resistant Acid Phosphatase; Young Adult

In the present study, we have investigated the efficacy of Indian ayurvedic herbal formulation Triphala on monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis and compared it with that of the non-steroidal anti-inflammatory drug, Indomethacin. The anti-arthritic effect of Triphala was evaluated by measuring changes in the paw volume, lysosomal enzyme activities, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-alpha in control and monosodium urate crystal-induced mice. The levels of beta-glucuronidase and lactate dehydrogenase were also measured in monosodium urate crystal-incubated polymorphonuclear leucocytes (PMNL). Triphala treatment (1 gm/kg/b.w. orally) significantly inhibited the paw volume and the levels of lysosomal enzymes, lipid peroxidation and inflammatory mediator tumour necrosis factor-alpha; however the anti-oxidant status was found to be increased in plasma, liver and spleen of monosodium urate crystal-induced mice when compared to control mice. In addition, beta-glucuronidase and lactate dehydrogenase level were reduced in Triphala (100 microg/ml) treated monosodium urate crystal-incubated polymorphonuclear leucocytes. In conclusion, the results obtained clearly indicated that Triphala exerted a strong anti-inflammatory effect against gouty arthritis.

Topics: Acetylglucosaminidase; Acid Phosphatase; Administration, Oral; Animals; Ankle Injuries; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Arthritis, Experimental; Arthritis, Gouty; beta-Galactosidase; Dose-Response Relationship, Drug; Glucuronidase; Indomethacin; Injections, Intradermal; L-Lactate Dehydrogenase; Lipid Peroxides; Liver; Lysosomes; Mice; Neutrophils; Plant Extracts; Powders; Spleen; Tumor Necrosis Factor-alpha; Uric Acid