A simple method was developed to identify large mononuclear (LMN) cells in human synovial fluid based on morphology and staining with Sudan black B. All cells were classified as monocyte-derived macrophages (MDM), lymphoblasts (LB), or synovial lining cells (SLC). Lymphoblasts were seen in 58 of 60 rheumatoid fluids (mean: 69 * 18% LB per LMN cells). However lymphoblasts were rarely seen in synovial fluids from patients with crystal-induced synovitis or bacterial infections. Little is known about large mononuclear (LMN) cells in synovial fluids from patients with inflammatory synovitis (1). The recent availability of techniques for identifying mononuclear cells by surface markers-erythrocyte-E rosettes (2), erythrocyte antibody complement -EAC rosettes (3), and histochemistry (4)-prompted a reevaluation of mononuclear cells in human synovial fluid. These techniques were used to develop a simple procedure for identifying L M N cells in synovial effu-sions based on cell morphology and avidity for Sudan black B. The distribution of L M N cells in synovial fluids from patients with inflammatory synovitis was studied in order to determine if a particular cell or distribution of cells was unique to any type of arthritis. The occurrence and diagnostic value of lymphoblasts in synovial fluids are discussed. MATERIALS AND METHODS Synovial Membrane Synovial membrane from 2 patients with torn menisci, 3 patients with rheumatoid arthritis. and 2 patients with os-teoarthrosis provided the source for synovial lining cells. Touch imprints of the lining cell layer were stained with Wright's stain and with Sudan black B. Minced synovial membrane was suspended in 50 ml of medium 199 (Microbiological Associates) containing 50 mg of clostridial collagenase (Worthington) and was incubated at 37°C for 3 hours in 5%' CO,. Mononuclear cells isolated from the digested membrane were washed, resuspended in medium 199, then separated into aliquots containing 2 X 10s mononuclear cells. Smears and cytocentrifuge preparations of one aliquot were stained with Sudan black B (5). A second aliquot was incubated with 2-1 latex particles for 2 hours at 37°C. Viability was determined by trypan blue dye exclusion. One-half of these cells was in-cubated with sheep red blood cells and permitted to form E rosettes (2). The remaining cells were incubated with sheep red
We have previously reported the existence of a subfraction of serum calcium that is tightly bound to normal human serum proteins. This tightly bound calcium fraction (TBC) is thought to be a calcium-albumin-fatty acid complex (ACP) because similar complexes can be prepared by the sequential addition of albumin to calcium in the presence of palmitic acid. These studies deal primarily with TBC from rat serum and the uptake of calcium by bone cells in palmitate-treated serum. It is reported that TBC does not exchange with ionized calcium and that calcium binds strongly to albumin in the presence of palmitate. The uptake of calcium in palmitate-treated serum is three times greater than the uptake of calcium in control serum in both in vitro and in vivo systems. These findings demonstrate that 1) a tightly bound albumin-calcium fraction is present in both human and rat sera; 2) calcium in TBC may be complexed to albumin via fatty acids; 3) TBC does not participate in the maintenance of the level of ionized calcium in serum and 4) circulating TBC or ACP complexes may be taken up by living cells.
Sacrococcygeal pain can arise from the sacrococcygeal joint, from contiguous structures sharing the same innervation, or from distant sites. True coccygodynia consists of pain arising from the sacrococcygeal joint, whereas pseudococcygodynia consists of pain referred to but not arising from the coccyx. Coccygodynia can usually be distinguished from pseudococcygodynia by physical examination with the diagnosis being confirmed by injection of local anesthetic into the sacrococcygeal joint. The etiology of pain not relieved by intraarticular injection can be further defined by selective neuroblockade. A method for defining the anatomic basis for sacrococcygeal pain is presented as well as a discussion of the relevant anatomy and differential diagnosis of sacrococcygeal pain.
Polyethylene glycol precipitation assays (PEG-A) have been promoted as technically simple, inexpensive methods for detecting and quantitating circulating immune complexes; however, their specificity and sensitivity have not been clearly defined. Data are presented showing that the percent recovery of IgG in 3.5% PEG increases as the concentration of IgG increases such that hypergammaglobulinemia alone can cause a positive test result. When sera from 25 patients with rheumatoid arthritis were studied, no correlations were found between results obtained by either Raji cell assay, or cryoprecipitation and those obtained by PEG-A. We conclude that 3.5% PEG-A, although appealing because of simplicity, can not be used as a substitute for established, but technically more demanding assays for circulating immune complexes.
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