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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The condition of generalized periarthritis calcarea (hydroxyapatite deposition disease) is characterised by multiple periarticular calcification which can be localised around practically any joint and also in proximity to the spine. This calcification consists of hydroxyapatite crystals which are responsible for the episodes of acute, subacute or chronic periarticular or articular inflammation so typical of the condition. Because of this one can classify periarthritis calcarea along with gout and chondrocalcinosis in the group of crystal deposition diseases. The actual cause of the calcification remains unknown but it is probable that, along with hereditary factors, disturbances in metabolism play an important role. The diagnosis of generalised periarthritis is made from the characteristic X-ray picture in conjunction with the clinical findings and, on occasion, the demonstration of hydroxyapatite crystals in the affected tissues. In the differential diagnosis gout, chondrocalcinosis, various inflammatory rheumatic conditions and septic arthritis must be excluded and various calcification processes, particularly interstitial calcinosis and lipocal cinogranulomatosis, must also be considered. Since the etiology of the calcification remains unknown to specific treatment is available. Symptomatic treatment with colchicine is mostly inadequate which is why one often has recourse to the use of non-steroid anti-inflammatory drugs and corticosteroids.
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PMID:[Generalized periarthritis calcarea (generalized hydroxyapatite disease)]. 39 90

Although microscopic studies have shown similarities between bursal and joint membranes, little is known about bursae and their response to disease states. Eighty-six cases of superficial bursitis due to trauma, bacterial infection, or gout were reviewed and compared with cases of joint inflammation due to the same etiologies. In traumatic bursitis the bursal fluid mucin test was more abnormal and the viscosity lower than that of joint fluid in traumatic arthritis. The bursal fluid total leukocyte count of septic bursitis was less than 20,000/mm3 in 8 of 13 cases but in only 1 of 21 synovial fluids from cases of septic arthritis (P = 0.005). In gouty bursitis the mean total leukocyte count of bursal fluid was 2800/mm3, compared with a mean synovial fluid total leukocyte count of 28,700 in gouty arthritis (P less than 0.02). These findings indicate that superficial bursae react less intensely than diarthrodial joints to specific disease stimuli and that a relatively low bursal fluid leukocyte count is often present in cases of septic and gouty bursitis.
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PMID:Reaction of superficial bursae in response to specific disease stimuli. 51 17

The systematic examination of synovial fluid confirms the noninflammatory nature of degenerative joint disease, is diagnostic of gout, pseudogout, and septic arthritis, and will usually allow the identification of rheumatoid arthritis, systemic lupus erythematosus and Reiter's syndrome.
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PMID:Current concepts in synovial fluid analysis. 72 54

Lysozyme and lactoferrin levels were measured in 71 synovial fluids (SF) of patients with traumatic effusions, osteoarthritis, rheumatoid arthritis, pseudogout, septic arthritis, and gout, as well as in 91 synovial fluids graded according to their neutrophil count. Elevated lysozyme levels were found in all the inflammatory arthritides and also in osteoarthritis. Lactoferrin levels were not increased in osteoarthritis but displayed a close correlation to the extent of the inflammatory response as judged by SF neutrophilia. The ratio of lysozyme to lactoferrin decreased progressively with increasing SF neutrophilia. In vitro experiments showed that lactoferrin is released from neutrophils isochronously with lysozyme and beta-glucuronidase. Lactoferrin was not found in hyaline cartilage, a tissue known to contain lysozyme. These results are consistent with belief that SF lysozyme has a major derivation from both cartilage and neutrophils, and that lactoferrin arises only from neutrophils. These findings indicate that the simultaneous measurement of lysozyme and lactoferrin provides a potentially useful index of both joint inflammation and cartilage degradation.
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PMID:Lactoferrin and lysozyme levels in synovial fluid: differential indices of articular inflammation and degradation. 83 40

The American Rheumatism Association sub-committe on classification criteria for gout analyzed data from more than 700 patients with gout, pseudogout, rheumatoid arthritis, or septic arthritis. Criteria for classifying a patient as having gout were a) the presence of characteristic urate crystals in the joint fluid, and/or b) a topus proved to contain urate crystals by chemical or polarized light microscopic means, and/or c) the presence of six of the twelve clinical, laboratory, and X-ray phenomena listed in Table 5.
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PMID:Preliminary criteria for the classification of the acute arthritis of primary gout. 85 19

The authors confirm the great rarity of joint complications in patients with Kahler's disease. Among the records of 1953 cases the following complications were the only one found: 2 cases of proved articular amylosis, 2 cases of probable articular amylosis, 3 cases of possible articular amylosis, 20 cases of arthropathy that were impossible to classify, 27 cases of compression of the median nerve in the carpan canal, 6 cases of gouty arthritis, and 3 cases of septic arthritis. The data on symptoms obtained in the course of this enquiry are in conformity with the data in the literature. Articular amylosis often takes on the appearance of a polyarthritic syndrome of progressive installation and extension, involving in particular the hands and the wrists, but sometimes involving in a symmetrical bilateral manner the elbows, the shoulders, and the knees. The affected joints are swollen, stiff, and painful. Local signs of inflammation are, however, often absent. The deformations characteristic of rheumatoid arthritis do not develop. The joints do not show radiological signs for most of the time. In addition, it is not possible to detect the rheumatoid factor in the serum. The arthropathies can also assume an oligo-articular topography. Articular discharges are very frequent: they are usually of a mechanical nature. Whatever the clinical appearance, an exact diagnosis can be established only by means of anatomo-pathological examination of the synovial membrane or of certain para-articular amyloid nodules. Myelomas complicated by amyloid articular deposits are often light chain, with only little increase in the erythrocyte sedimentation rate, discrete hyperproteinaemia, moderate medullary plasmocytosis, and rare or limited radiological lesions. The carpal canal syndrome is either isolated or included within the framework of a polyarthropathy. Compression of the median nerve is due to amyloid infiltration into the synovial sheath of the tendons of the finger flexors, proof of which is not always easy. Gout is rare despite the frequency of hyperuricacidaemia caused by renal insufficiency. Septic arthritis is often caused by renal insufficiency. Septic arthritis is often caused by pneumococci to which those with a myeloma appear particularly suceptible.
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PMID:[Articular complications of Kahler's disease. Results of a survey of 1953 cases of plasmocytic myelomas]. 112 74

Synovial effusions from various kinds of arthritis have been examined both morphologically and histochemically. These two methods give complementary evidence, and show (i) that there are two fundamentally different types of cell present in rheumatoid arthritis (ii) that the synovial fluid from septic arthritis can clearly be separated from that of all other forms of arthritis and (iii) that intracellular crystals can be demonstrated in gout. Laboratory methods also give information on the polysaccharide and fat content of synovial fluid, in particular on the lipid material in the cell free supernatant. Large mononuclears in the fluid are probably generated in the local tissue and reflect minimal differentiation from a basic cell type.
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PMID:[Cytology and histochemistry of synovial cells in various forms of arthritis]. 122 5

Rheumatic manifestations are common and varied in infective endocarditis. We performed a retrospective case analysis on 87 patients with 93 episodes of infective endocarditis admitted to Flinders Medical Centre over an 11 year period (1980-1990). Disabling musculoskeletal symptoms and signs were documented in 22 (25%) of the patients. Thirteen patients developed severe or moderately severe low back pain during their illness, two with radiological evidence of a septic discitis or vertebral osteomyelitis. Two patients developed polyarthralgia/arthritis, four had septic arthritis (all with acute Staphylococcus aureus endocarditis), three developed severe loin pain, two acute gout, two had severe buttock pain and sacroiliac joint tenderness and two each developed disabling jaw/facial pain, neck/scapular pain and flank pain respectively. Five patients presented initially to the orthopaedic or rheumatological unit for management of their musculoskeletal symptoms. Four of seven patients with Streptococcus bovis endocarditis demonstrated prominent low back pain supporting a previously noted association between this organism and back symptoms. Furthermore, in one patient who had three separate episodes of endocarditis involving three different organisms, florid back symptoms were only seen in the infective episode involving Streptococcus bovis.
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PMID:Rheumatic manifestations of infective endocarditis. 141 Oct 84

The diagnostic clarification of joint effusions of unknown origin is a challenge to every primary-care physician. Important diagnostic procedures are arthrocentesis and analysis of the aspirated synovial fluid. Synovial fluid analysis frequently allows differentiation between harmless effusions due to osteoarthritis and crystal induced inflammation, or the more devastating septic arthritis. 4475 synovial fluids were evaluated retrospectively to calculate the identification rate of crystals compatible with calcium pyrophosphate dihydrate (CPPD) and monosodium urate monohydrate (MSUM). 40.8% (1827) of synovial fluids were taken from females and 59.2% (2648) from males. The frequency of crystal identification varied considerably: 13.2% CPPD crystal identification in females, 10.9% in males; MSUM was identified in 1.5% of females, and in 10.9% of males. The spectrum of joint involvement was nearly identical in CPPD and MSUM positive synovial fluids. Exceptions were the higher frequency of CPPD identification in shoulder joints (CCPD:MSUM = 15.6:1), the higher frequency of MSUM identification in the ankle (MSUM:CPPD = 15.6:1) and the first metatarsophalangeal joints (MSUM:CPPD = 8:1). Clinical suspicion correlated well with crystal identification in MSUM positive samples (60%), but was poor in CPPD positive samples (36%). The poor correlation between clinical suspicion and crystal identification in CPPD positive synovial fluids is explicable by the less characteristic clinical presentation of pyrophosphate arthropathy in contrast to classical gout. A high percentage of crystal identification was found in joints or periarticular swellings in which aspiration is difficult and therefore rare (e.g. tendon sheaths, first metatarsophalangeal and first metacarpophalangeal joints), underlining the importance of synovial fluid aspiration despite the difficulty of arthrocentesis.
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PMID:[Identification of crystals in synovial fluid: joint-specific identification rate and correlation with clinical preliminary diagnosis]. 162 Oct 79

This paper reports the case of a 48 year old patient with chronic tophaceous gout who was admitted to the hospital with a pneumococcal polyarthritis affecting the same joints previously involved by gout attacks. The authors emphasize that the possibility of a septic arthritis should always be considered in the gouty patient, and not only in the elderly, as stressed in the literature, but also in younger patients.
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PMID:Septic polyarthritis in chronic tophaceous gout. 175 37


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