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Biomedical subjects

P Hasselbacher

Publications and source records attributed to P Hasselbacher.

33 records · Page 2Linked to original sources
PubMed1978

Synovial fluid eosinophilia following arthrography.

A patient recovering from an acute gouty attack developed inflammation and eosinophilia of the synovial fluid following arthrography of the gouty joint. There was no evidence of systemic allergy to the contrast agent used. It is postulated that non-immune mechanisms were involved in the accumulation of eosinophils. An additional one of six synovial fluids obtained after arthrography contained 24% eosinophils. A review of the literature emphasizes the infrequency with which eosinophils are observed in synovial fluid.

Diatrizoate↗
PubMed1977

Bilateral protusio acetabuli following pelvic irradiation.

A 77 year old man developed bilateral protrusio acetabuli three years following pelvic irradiation for transitional cell carcinoma of the prostatic urethra. There was no evidence of metastasis or coexistent systemic arthritis. Aseptic necrosis of acetabular bone is the postulated etiology. Gross and pathologic evidence of aseptic necrosis of both femoral heads was observed. Vascular fibrosis was a prominent pathologic finding, as was eosinophilia of the synovial fluid and joint tissue. Protrusio appears to be an infrequently described complication of pelvic irradiation.

Acetabulum↗
PubMed1976

Scurvy and hemarthrosis.

Scurvy developed in a 56-year-old man with poor dietary intake and was associated with knee hemarthroses and synovial thickening. The synovial membrane showed interstitial hemorrhage and many large fibroblasts but little collagen and some disarray of vascular basement membrane. Hemarthroses and all knee symptoms completely resolved on a normal diet. To our knowledge, these are the first electron-microscopic studies of synovial membrane in human scurvy, and our findings support a defect in collagen synthesis as a factor in etiology.

Ascorbic Acid↗
PubMedDate not supplied

Measuring synovial fluid viscosity with a white blood cell diluting pipette. A simple, rapid,and reproducible method.

A convenient and accurate way to measure the relative viscosity of synovial fluid is to use a white blood cell diluting pipette as a simple viscometer. The technique is reproducible with 2% accuracy and adds little to the time required for routine synovial fluid analysis. The magnitude of the variation of synovial fluid viscosity with temperature is demonstrated, and it is suggested that routine clinical measurements be made at room temperature. Clinical data confirm that a single viscosity measurement has little or no diagnostic value.

Hematology↗
PubMedDate not supplied

Inhibition of complement by gold sodium thiomalate.

The effect of gold sodium thiomalate on C3 and factor B activation by monosodium urate monohydrate (MSUM) and zymosan was studied using a quantitative immunoelectrophoretic assay for complement activation. C3 and factor B conversion by the classical pathway activator MSUM, was inhibited 50% and 100% by 3.2 x 10(-4)M and 10(-3)M gold sodium thiomalate, respectively. C3 and factor B conversion by the alternative pathway activator, zymosan, was much less susceptible to inhibition by gold. Gold at 10(-3)M, inhibited alternative pathway activation by only 30%. A 50% inhibition would have required 10(-2)M gold. There was no significant inhibition of complement activation through either pathway by less than 10(-4)M gold. Sodium thiomalate alone showed no inhibition. Studies using other crystals and immune complexes were confirmatory. Thus, there was no appreciable inhibition of the complement system at concentrations of gold attainable in the serum of patients receiving chrysotherapy. The in vivo significance of these findings is unknown.

Complement C3↗
PubMedDate not supplied

Interactions of murine macrophages with monosodium urate crystals: stimulation of lysosomal enzyme release and prostaglandin synthesis.

Exposure of murine peritoneal macrophages to crystals of monosodium urate monohydrate (MSUM) stimulated release of inflammatory mediators from the cells. There was an early, rapid burst of prostaglandin E2 (PGE2) synthesis which was complete by 2 h. Release of N-acetyl glucosaminidase (NAG), a lysosomal enzyme, was evident within 1 h and was maximal by 8 h. Early release of lysosomal enzymes (1-2 h) was not accompanied by leakage of cytoplasmic enzymes; however, treatment with high concentrations of MSUM, or prolonged exposure to crystals, provoked release of the cytoplasmic enzyme lactate dehydrogenase, presumably as a result os cell lysis. Responses of macrophages to MSUM occurred in the absence of serum but were modified by serum proteins. Prior exposure of crystals to IgG potentiated release of NAG and PGE2. Exposure to albumin slightly enhanced release of PGE2 induced by MSUM but did not affect NAG release. However, albumin prevented enhancement of NAG release by IgG. The interaction of MSUM with macrophages, and subsequent release of inflammatory mediators, may contribute to the inflammation association with both acute and chronic gouty arthritis.

Acetylglucosaminidase↗
PubMedDate not supplied

Antigen-induced arthritis: an immunohistologic study of articular tissue and synovial fluid using the horseradish peroxidase technique.

Articular tissue and synovial fluid from rabbits with antigen-induced arthritis were stained for localization of immunoglobulin (Ig) and egg albumin (EA) using the immunoperoxidase technique. Discrete granules containing Ig and EA were initially observed within vascular synovial tissue with later occurrence in synovial fluid and dense connective tissue. Homogeneous staining for Ig was not always associated with the presence of antigen and, therefore, cannot be used alone as evidence of the presence of immune complexes. Discrete granules of Ig and EA are formed in dense connective tissue during the period of maximal inflammation and persist for at least 30 days. These granules presumably represent precipitated immune complexes of Ig and EA but can be stained for Ig alone longer than for EA. Insoluble, particulate immune complexes of Ig and EA appeared in synovial fluid within 2 h after injection and remained at least 24 h. These were identical in appearance to the Ig precipitates occurring in synovial fluids from human rheumatoid arthritis.

Animals↗
PubMedDate not supplied

Extracellular aggregates of immunoglobulin in synovial fluid from rheumatoid arthritis.

Particulate extracellular aggregates of immunoglobulin can be demonstrated in many whole synovial fluids from patients with rheumatoid arthritis but not in other diseases. These occur only in seropositive patients and correlate with more active inflammation and lowered synovial fluid C3. Aggregates were associated with intracellular inclusions but were more abundant and always contained both IgG and IgM. No aggregates were seen in 50 control fluids. These aggregates are compatible with immune complexes and should be included in studies of immunologic events in rheumatoid fluids.

Animals↗