Joint fluid

The quantification of kinins in human tissues or body fluids has been limited due to the inherent difficulties in accurately measuring the concentration of ephemeral peptides. Today HPLC-based and RIA/capture-ELA measurements are established to determine kinins in human plasma, liquor or mine. Serine protease inhibitors need to be added to prevent rapid degradation of the kinins in vitro during sample preparation. Kinins and their degradation products have been studied in various biological milieus such as plasma/ serum, urine, joint fluids, kidney, lung and skeletal muscle [2]. Under normal conditions, the concentration of kinins in these compartments is extremely low for... 

Aspiration of affected joint fluid is essential for a definitive diagnosis. Joint fluid containing negatively birefrin-gent monosodium urate crystals confirms the diagnosis. Joint fluid has an elevated WBC count with neutrophils predominating. 

I low incidence of side effects. Joint fluid obtained by arthro-centesis should be examined for evidence of joint-space infection and crystal identification. If no infection is present, intraarticular injection can proceed. 

The pain of OA arises from activation of nociceptive nerve endings within joints by mechanical and chemical irritants. OA pain may result from distension of the synovial capsule by increased joint fluid microfracture periosteal irritation or damage to ligaments, synovium, or the meniscus. 

Blood cultures should be performed in the acutely ill, febrile patient. Less accessible fluids or tissues are obtained when needed to assess localized signs or symptoms (e.g., spinal fluid in meningitis, joint fluid in arthritis). Abscesses and cellulitic areas should also be aspirated. 

Caution must be used in the evaluation of positive culture results from normally sterile sites (e.g., blood, cerebrospinal fluid, joint fluid). The recovery of bacteria normally found on the skin in large quantities (e.g., coagulase-negative staphylococci, diphtheroids) from one of these sites may be a result of contamination of the specimen rather than a true infection. 

Fox, R. O. and P. K. Yeung (1999). Forward and backward spectral transfer in the modeling of scalar mixing in homogeneous turbulence. In Proceedings of the 3rd ASME/JSME Joint Fluids Engineering Conference, San Francisco, CA. 

Therapy should always be streamlined if and when a microbiological report becomes available. Erysipelas caused by streptococci can be treated by penicillin. In arthritis and osteomyelitis, culture of the joint fluid or of deep tissue is recommended before the start of treatment. 

A 65-year-old man with bilateral osteoarthritis of the knees developed an effusion in the left knee. The swollen joint was treated with an intra-articular injection of triamcinolone hexacetonide 40 mg. The next day, he developed acute arthritis in the injected knee the joint was swollen and tender and he was unable to walk. Examination of the joint fluid showed 35 ml of a thick, turbid, yellowish synovial fluid with a leukocyte count of 13 x 106/1 (95% neutrophils). Gram and acridine orange stains were negative. Wet preparations of... 

Hyaluronan, despite the simplicity of its structure, has a surprisingly wide range of functions. In high concentrations, as found in the ECM of the dermis, it regulates water balance, osmotic pressure, functions as an ion exchange resin, and regulates ion flow. It functions as a sieve, to exclude certain molecules, to enhance the extracellular domain of cell surfaces, particularly the luminal surface of endothelial cells.28 It can also function as a lubricant and as a shock absorber. Hyaluronan can also act as a structural molecule, as in the vitreous of the eye, in joint fluid, and in Wharton s jelly. 

Rheumatoid factors of the IgM and IgG classes have been shown to form immune complexes in serum or joint fluid either by self-association (K17, M4, M26, P13, Sll, W21) or by reaction with native IgG (C4, K17, M4, N5, Sll, W21, W22), and these appear to be the predominant immune complex material in rheumatoid arthritis (C4, Gl, K17, M4, M26, N5, Sll, W21, W22). The primary cause of rheumatoid factor production in rheumatoid arthritis is unknown. However, rheumatoid factors are known to be present in other diseases associated with chronic antigenic stimulation (C14, M14) and can be induced in vitro by stimulation with antigens, autologous aggregated IgG, anti-idiotype reagents, and polyclonal B cell activators such as lipopolysaccharide and Epstein-Barr virus (C4, Dll, F6, F7, Gil, 16, P10, S24). Rheumatoid factors, including IgG rheumatoid factors which form selfassociating intermediate-sized (11-19 S) complexes, play a major role in... 

W23. Winchester, R. M., Kunkel, H. G., and Agnello, V., Occurrence of 7-globulin complexes in serum and joint fluid of rheumatoid arthritis patients Use of monoclonal rheumatoid factors as reagents for their demonstration. J. Exp. Med. 134, 286s-295s (1971). 

HA is an unsulfated glycosaminoglycane composed of repeating disaccharide units of D-glucuronic acid and A-acetylglucosaminc linked a-( 1 —4) and p-( 1—3), respectively. HA has special importance because it is a component of the ECM [53] in the soft tissues of mammals, where it mainly ensures water retention [54], This enables the transport of nutrients to, and removal of waste from, cells that do not have a direct blood supply, such a cartilage cells. Moreover, HA is present in the synovial joint fluid, the vitreous humor of the eye, cartilage, blood vessels, and the unbilical cord. More detailed information about the biological functions and physicochemical properties of HA can be found elsewhere [55, 56],... 

After my return to Boston, I extended my work on hyaluronan from the vitreus and the rooster comb to the synovial fluid. The physical properties, such as viscosity and elasticity, of synovial fluid were poorly understood, especially in human joints. I started to investigate the physical properties of cattle synovial fluid. As I had done 20 years earlier in Budapest, I went to the slaughterhouses of the Boston area and collected joint fluids. This time I was interested in how aging affects the physical properties and hyaluronan content of the joint fluid. The physical properties or, in more scientific terms, the rheology of the fluid is important because its role is to protect and lubricate the tissues of the joint. I traveled to Iowa to collect synovial fluids from cattle herds fed various diets that contained hormones. I hoped to discover a hormonal control of hyaluronan synthesis, similar to the one Szirmai and I had found that controlled hyaluronan synthesis in the rooster comb. 

A number of laboratories have been successfiil in obtaining semipurified/purified PLAj preparations fi om a number of sources, including platelets (47-70). These studies have been helpful to understand the molecular size as well as the nature of active sites of these enzymes. Several reports have demonstrated the presence of two substrate specific and distinct etjzymes, including secretory PLA (sPLA,) and cytosolic PL (cPLAj) in platelets. cPL appears to have a molecular mass of 85 kDa that is structurally distinct fi-om that of the mammalian Type II, a 14 kDa non-pancreatic PLAj, which exists in an extracellular form in many tissues, including platelets, inflammatory joint fluid, spleen and placenta (47-70). The human non-pancreatic PLA enzyme purified is also present in platelets and is enriched in rheumatoid synovial fluid. 

The lower degree of polymerization of hyaluronic acid present in rheumatoid fluids (B3, BIO, B13, B18) undoubtedly impairs the effectiveness of the fluid as a lubricant between joints. Another factor contributing to this may be the lower concentration of hyaluronic acid found in certain rheumatoid effusions. Special viscosity and elastic properties are exhibited by hyaluronic acid in synovial fluid in concentrations in excess of 0.2 g/lOO ml (Bll) the concentration of hyaluronic acid in inflamed joint fluids of rheumatoid arthritis is generally less than this value. In a recent investigation, Hamerman and Sandson (H4) found that, apart from a reduced anomalous viscosity, the hyaluronate-protein complexes of synovial fluid differed from normal and showed increases in both protein content and amounts of basic amino acids. 

Local treatment of rheumatoid arthritis with hydrocortisone usually results in restoration to normal of the qualitative hyaluronic acid changes occurring in joint fluids (J9, S23). The increase in viscosity and hyaluro-nate concentration of synovial fluid after treatment with hydrocortisone is believed to result either from the influence of the hormone on synthesis of hyaluronic acid, or, indirectly from its anti-inflammatory action (J9, S23). The molecular sizes of hyaluronate in rheumatoid fluids usually show a continuous but skewed distribution treatment with hydrocortisone was found to reduce the less polymerized fractions, which were marked in severe cases (Nl). 

Sundblad, L., EgeUus, N., and Jonsson, E., Action of hydrocortisone on the hyaluronic acid of joint fluids in rheumatoid arthritis. Scand. J. Clin. Lab. Incest. 6, 295-302 (1954). 

Case Conclusion In addition to having urate crystals present in the joint fluid aspirate, KM has met several criteria to support the diagnosis of gout. This acute gout attack is treated with high-dose ibuprofen, which is tapered over 7 days. Once the attack is resolved, maintenance therapy with allopurinol is initiated to lower uric acid levels and prevent future acute gout attacks. 

A 65-year-old woman has had several acute gout attacks and now needs to be placed on prophylactic therapy. She has a CrCI rate of 45 mL/min and a uric acid level of 12 mg/dL. The patient refuses to undergo a joint fluid aspiration procedure, but she has 6 of the 11 criteria for epidemiologic diagnosis for gout. Which agent is the best choice for this patient ... 

The adsorption of macromolecules at interfaces may be the reason why molecules such as those of hyaluronic acid can act as biological lubricants in joint fluids. In healthy joints only 0.5 cm of synovial fluid is required to provide almost perfect lubrication in diseased joints there are sometimes faults in this system and some research has been aimed at producing synthetic substitutes for synovial fluid. 

A major difference may exist between HA in vivo and HA chains that are extricated from the in situ situation. Very little is known about the properties of the HA within the narrow confines of the ECM or the restricted volume of the intercellular space. However, when HA undergoes aqueous extraction from major sources, such as from the mucoid layer of the rooster comb, from joint fluid, the perivascular space of the umbilical cord (Wharton s jelly), or from bacterial capsules, the extraction fluid has very high viscoelasticity. Such HA is in a random coil conformation. However, HA is unlikely to be in such a conformation in vivo, and little is known about the state of the HA within tight tissue spaces. It is probably much more structured, and probably has many additional functions that are unknown and lost when examined in vitro [15]. 

HA is a major molecule in joint fluid, and plays a major role in that tissue in joint motion and maintenance of normal joint homeostasis. In inflammatory diseases of the joint such as rheumatoid arthritis (RA), and in degenerative joint disease such as osteoarthritis (OA), the levels and average molecular size of HA chains are much reduced. Expressions of both HASl and 2 are decreased, while the hyaluronidases are increased in the various forms of arthritis, compared to control, with a concomitant decrease in average molecular sizes [112]. 

IgM, being 19 S, when it finds its way directly from the marrow or lymph into the bloodstream is only slowly distributed to tissue or joint fluids (B17, 04), some 75% being retained in the circulation. This shows an FCR of 36% with an estimated daily turnover of 0.4 g. The same remarks upon increased catabolism apply as for IgA (Section 2.2), so that a subnormal serum level of IgM is almost always due to impaired synthesis. 

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