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Biomedical subjects

N W McGill

Publications and source records attributed to N W McGill.

18 recordsLinked to original sources
PubMed2000

Gout and other crystal-associated arthropathies.

Intra-articular crystals (monosodium urate monohydrate, calcium pyrophosphate dihydrate, basic calcium phosphates) can cause acute and chronic inflammation and joint damage. Identification of the crystals by polarized microscopy is the key step in diagnosis but improved reliability of synovial examination is required. Treatment of disorders associated with gout or calcium pyrophosphate deposition may reduce non-joint morbidity and assist treatment of the arthritis. Various forms of anti-inflammatory therapy work for acute crystal-induced arthritis; prompt commencement is usually more important than which option is used. In gout, recurrent attacks are usual, but hypouricaemic therapy is almost never urgent, is life-long, and is too often negated by poor compliance. In most patients, allopurinol or any of the potent uricosuric drugs will allow maintenance of normouricaemia but renal failure, renal calculi, transplantation, and allopurinol allergy narrow the options and complicate management.

Calcium↗
PubMed2000

Crystal unclear.

Explore the source record for details and available documents.

Aged↗
PubMed1997

Quality assurance for synovial fluid examination for crystals: an improved method.

OBJECTIVE: To determine the best method of preparing synovial fluid specimens for use in quality assurance (QA) surveys designed to assess accuracy of crystal identification. METHODS: A previously published method (A) was compared with a new method (B) in the setting of a QA survey. Ten Australian, one New Zealand, and one Hong Kong hospital laboratories took part in the survey. Each laboratory examined six different synovial fluid specimens prepared using method A (first round) and a separate six specimens using method B (second round). In method A, a drop of synovial fluid on a glass slide was surrounded by a rim of Ultramount, sealed with a coverslip, and distributed. The participating laboratory did not need to perform any processing of the specimen before examination. In method B, a capillary tip was filled with synovial fluid, heat sealed, and distributed. The fluid was expelled onto a glass slide in preparation for examination after arrival in the participating laboratory. RESULTS: Using method A 36 of 71 (51%) of the specimens were rated as satisfactory, compared with 53 of 61 (87%) of the specimens using method B (Fisher's exact test, p < 0.001). CONCLUSIONS: An improved method of preparation of synovial fluid specimens for QA surveys is described. Using the new method it is feasible to perform a synovial fluid QA survey covering a large area (Australasia).

Chondrocalcinosis↗
PubMed1992

Morphological evidence for biological control of urate crystal formation in vivo and in vitro.

Urate crystal formation, and subsequent gout, occurs in only a minority of hyperuricaemic subjects indicating that factors other than hyperuricaemia are involved. Biological substances (especially proteins) alter crystal growth in vitro independently of uric acid concentration. Physiological crystal formation, known to be under biological control, is characterised morphologically by uniformity of size and constraint of crystal shape. To determine whether pathological urate crystal formation is influenced by the surrounding biological milieu we examined, using scanning electron microscopy, the morphology of urate crystals formed either in vivo or in vitro. We found morphological evidence of biological control of in vivo urate crystal formation and demonstrated that those characteristics could be induced in vitro by the addition of serum, synovial fluid and certain serum proteins to the growth medium during crystal formation. Urate crystal formation is dependent, not only on the degree of hyperuricaemia, but also on the surrounding biological milieu.

Blood Proteins↗
PubMed1992

The effect of age on the inflammatory response to arthritis-associated crystals.

The effect of age on the inflammatory response to urate and hydroxyapatite crystals was examined using both in vivo (intradermal skin testing) and in vitro (neutrophil death following incubation with urate crystals) methods. No significant difference in crystal-induced inflammation was found between young (< 25 years) and elderly (> 75 years) subjects and there was no correlation between the in vivo and in vitro tests. There was good correlation (0.63, p < 0.001) between the intradermal responses to urate and hydroxyapatite, suggesting that subjects, regardless of their age, are consistent in their response to these two types of arthritis-associated crystal. Advanced age does not lead to a major alteration in the inflammatory response to arthritis-associated crystals.

Adolescent↗
PubMed1991

The effect of biological crystals and human serum on the rate of formation of crystals of monosodium urate monohydrate in vitro.

A simple, reproducible method of measuring monosodium urate monohydrate (urate) crystal formation in the presence of biological materials in vitro is described. The method allows both seeded and unseeded crystal formation to be examined. Urate seed crystals markedly promoted urate crystal growth whereas the presence of hydroxyapatite or calcium pyrophosphate dihydrate crystals had a minimal effect on crystal formation. Serum promoted urate crystal formation in a concentration-dependent fashion, the effect probably being due to enhancement of nucleation.

Adult↗
PubMed1991

Reproducibility of synovial fluid examination for crystals.

A quality assurance survey of synovial fluid examination for crystals was performed at six teaching hospitals. Aliquots of 12 different fluids (three with no crystals, one with betamethasone crystals, four with calcium pyrophosphate dihydrate (CPPD) crystals and four with monosodium urate monohydrate [urate] crystals) were examined by all six laboratories. Four laboratories performed well (10 or more correct out of 12) but two did poorly (50% or less correct). False positive crystal identification occurred in eight of 72 samples, but all false positive reports were from two laboratories. CPPD and urate crystals were missed in seven of 24 (29%) and five of 24 (21%) samples respectively. The standard of synovial fluid examination for crystals in Sydney teaching hospitals is not uniform and in some cases appears unsatisfactory.

Betamethasone↗
PubMed1991

Survival of calcium pyrophosphate crystals in stored synovial fluids.

Eleven synovial fluids containing calcium pyrophosphate dihydrate (CPPD) were examined repeatedly over an eight week period to assess whether storage conditions and duration influenced the number of crystals present. Aliquots of each fluid were stored at room temperature, 4 degrees C, and -70 degrees C. At -70 degrees C there was no change in crystal count after eight weeks' storage. At room temperature and 4 degrees C crystal counts declined slowly over the eight week period, though CPPD crystals were still readily apparent after eight weeks in 10/11 (4 degrees C) and 8/11 (room temperature) fluids. No change in crystal morphology was detected and, apart from one fluid kept at room temperature in which fungal hyphae were noted at six weeks, no new crystals were seen. Calcium pyrophosphate dihydrate crystals in synovial fluid can be maintained for prolonged periods by freezing.

Calcium Pyrophosphate↗
PubMed1991

Evidence for a promoter of urate crystal formation in gouty synovial fluid.

The effect of serum and synovial fluid obtained from six healthy subjects and from 12 patients with gout, six with rheumatoid arthritis and 18 with calcium pyrophosphate dihydrate arthropathy (CPPD) on the rate of in vitro urate crystal formation was measured. Gouty and normal serum produced similar results. Gouty synovial fluids promoted urate crystal formation significantly more than did rheumatoid or CPPD fluids. The promotion of urate crystal formation by gouty synovial fluid was not due to native urate crystals nor to an effect on the level of urate supersaturation. The development of gout in some, but not other, hyperuricaemic subjects may relate to the presence of promoters (or relative lack of inhibitors) of urate crystal formation in the group who develop gout.

Adult↗
PubMed1991

The role of serum and synovial fluid components in the promotion of urate crystal formation.

The effect of various components of serum and synovial fluid (SF) on in vitro urate crystal formation was measured. Serum and SF has been shown to promote urate crystal formation. The component(s) responsible for this promotion was found to be a macromolecule, sensitive to heat denaturation. Albumin, alpha and beta globulins and chondroitin sulphate had little effect, whereas gamma globulin markedly promoted crystal formation and insoluble collagen also promoted crystal formation in a dose dependent fashion.

Blood Physiological Phenomena↗
PubMed1990

Brown's syndrome: an unusual ocular complication of rheumatoid arthritis.

A 55 year old man with rheumatoid vasculitis and an apparent left inferior oblique palsy is described. This unusual extraocular complication of rheumatoid arthritis probably resulted from a tenosynovitis of the superior oblique tendon sheath, and resolved with steroid treatment.

Arthritis, Rheumatoid↗
PubMed1988

Autoantibodies to type II collagen: occurrence in rheumatoid arthritis, other arthritides, autoimmune connective tissue diseases, and chronic inflammatory syndromes.

Serum IgG antibodies to native and denatured human type II collagen (Col II) were measured using an enzyme linked immunosorbent assay (ELISA). One hundred and thirty one patients with various forms of arthritis such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PSA). Reiter's Syndrome (RS), osteoarthritis (OA), and gout, 60 with autoimmune connective tissue disease, and 37 with the chronic inflammatory conditions--graft versus host disease and leprosy--were studied. With the exception of RS, PSA, OA, and gout, significant levels of Col II antibodies were detected in each disease group. Blocking studies with types I and II collagen on selected serum samples confirmed the specificity to native Col II, though some cross reactivity was apparent with denatured collagen. The patients with RA who were Col II antibody positive tended to fall into stage III of disease progression. There was, however, no correlation with rheumatoid factor, erythrocyte sedimentation rate, or disease duration and this, together with the finding that Col II antibodies are present in a wide array of diseases, makes their role in the pathogenesis of RA questionable. They may arise as a secondary disease perpetuating mechanism in some patients, or in turn may be an epiphenomenon secondary to generalised disturbed immunoregulation or B cell hyperreactivity, or both, that characterises these clinical conditions.

Adult↗
PubMed1987

Juvenile rheumatoid arthritis in Auckland: a long term follow-up study with particular reference to uveitis.

Although features of juvenile rheumatoid arthritis (JRA) have been well described in British, American, and to a lesser extent Australian communities we can find no previous study of the clinical characteristics of this disease in a New Zealand population or indeed in any population containing Polynesians. In a follow-up study of 55 Auckland residents with juvenile rheumatoid arthritis, current information was obtained for 78% of the study group with a mean interval from disease onset to follow up of 9.3 years. The outcome for the group as a whole was excellent although patients with a polyarticular course, regardless of onset subtype, had a poorer outcome with respect to both ongoing disease activity and functional disability. Polynesian patients were represented in all onset subtypes in proportion to their frequency in the general community and there was no recognisable influence of race on the course of the disease. Despite careful ophthalmological examination only one case of mild uveitis was detected, a much lower incidence than in British and American reports.

Adolescent↗
PubMed1986

Severe autonomic neuropathy in amyloidosis secondary to rheumatoid arthritis.

Autonomic neuropathy, although reported to occur in 15% of patients with AL primary) amyloidosis, is extremely rare in AA (secondary) amyloidosis. We report a patient with amyloidosis secondary to rheumatoid arthritis in whom autonomic neuropathy resulted in severe and disabling orthostatic hypotension. Extensive amyloid deposits were found throughout the autonomic nervous system.

Amyloid↗
PubMed1986

Nailfold capillaroscopy: a blinded study of its discriminatory value in scleroderma, systemic lupus erythematosus, and rheumatoid arthritis.

The appearances of the nailfold capillaries can be used to distinguish between various connective tissue diseases. In a study of 30 patients (10 with scleroderma, nine with systemic lupus erythematosus, and 11 with rheumatoid arthritis), photographs were taken of the eight nailfolds of each patient (thumbs excluded) and then coded. Each of the photographs was later analysed by a rheumatology registrar and an attempt was made to predict the patient's diagnosis using only the appearance of the nailfold. The diagnostic specificity and sensitivity were 89% and 80%, respectively. The results indicate that nailfold capillaroscopy, performed by a relatively inexperienced observer, can accurately distinguish between patients with scleroderma and those with systemic lupus erythematosus or rheumatoid arthritis.

Adult↗