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Biomedical subjects

D L Robbins

Publications and source records attributed to D L Robbins.

At least 55 records · Page 3Linked to original sources
PubMed1985

Serum IgG and IgM rheumatoid factors and complement activation in extraarticular rheumatoid disease.

Rheumatoid factors (RF) may participate in both synovial and extraarticular (EA) inflammation in rheumatoid disease (RD). The relative roles of serum IgG RF and IgM RF in extraarticular rheumatoid disease (EARD) are unclear, as is the importance of complement (C) activation by these proteins. To investigate the relation of C activating properties of IgM RF (RF CAP) and total IgG RF and IgM RF to EARD we compared 18 patients with only articular disease to 27 patients with various EA manifestations (nodules, cutaneous vasculitis, neuropathy, Felty's syndrome) using radioimmunoassays for IgG and IgM RF and an established hemolytic assay for C activation by IgM RF. We calculated RF CAP by determining the mean hemolysis of sensitized SRBC/ml of RF serum (MH/ml). Normal volunteers and patients with other inflammatory arthritides served as controls. Controls had negligible amounts of IgG RF, IgM RF, and RF CAP. Mean IgG and IgM RF levels and RF CAP values were significantly higher in patients with EARD than those in the arthritis-only (AO) group. Mean IgM RF concentrations and IgM RF CAP correlated with each other and EARD. IgG RF also correlated with IgM RF and EARD, but did not contribute to RF CAP or EARD when adjusted for IgM RF. Further, some patients had high RF CAP values despite modest IgM RF levels. These data suggest that quantitative differences in IgM RF CAP and total IgM RF may be more important than IgG RF as determinants of EARD.

Arthritis, Rheumatoid↗
PubMed1985

Comparative specificities of serum and synovial cell 19S IgM rheumatoid factors in rheumatoid arthritis.

Rheumatoid factor (RF) may play a role in sustaining the inflammatory events and tissue damage in rheumatoid arthritis (RA). However, many serum RF have greater specificity for rabbit IgG than for human IgG, thus raising questions about RF pathogenicity in RA. Serum RF also has specificity for human IgG subclasses 1, 2 and 4, but not for IgG3. The synovium is central to the pathology of RA; thus, RF made there may have greater pathogenicity than serum RF. We examined the specificity of 19S IgM RF in an RF plaque forming cell assay (RF-PFC) using RA synovial cells (RSC). We found that: (1) RSC produced greater numbers of RF-PFC/10(6) cells than did RA peripheral blood mononuclear cells (PBM); (2) RSC RF-PFC had greater specificity for human than for rabbit IgG compared to autologous serum RF; (3) RSC RF had significantly greater specificity for human IgG3 relative to autologous serum RF. In contrast, RSC RF and autologous serum RF had the same relative specificities for polyclonal human IgG, IgG1, IgG2, and IgG4. Thus, the specificity of much of the RF synthesized by RSC differed from serum RF. The potential pathogenic significance of these observations is discussed.

Animals↗
PubMed1983

Septic arthritis due to Fusarium solani.

A case of Fusarium arthritis is reported. Fusarium, a mold ubiquitous in soil and on plants commonly causes keratomycosis and infects burns. Recent reports demonstrate that Fusarium may produce serious visceral infection in compromised hosts. Disseminated infection has been universally fatal. In contrast, our case and several others with localized visceral infection were cured by intravenous amphotericin B and drainage. Although Fusarium grows readily on mycologic media, blood and other cultures have usually been negative in disseminated infection. Physicians should be aware of this uncommon but potentially lethal pathogen because deep fungal infections may first appear as arthritis.

Adult↗
PubMed1980

Quantitative determination of circulating immune complexes by inhibition of the hemolytic activity of polyclonal IgM rheumatoid factor.

A practical and sensitive method for detection and quantification of soluble complement-fixing immune complexes in sera of patients with various disease states has been developed. The assay is based on inhibition of complement-dependent sheep red cell hemolysis mediated by polyclonal IgM rheumatoid factor. Aggregated human IgG was used as an in vitro model of C-fixing human immune complexes and was quantified by its ability to inhibit hemolysis of sensitized sheep red cells by isolated IgM rheumatoid factor. The limit of sensitivity of this assay was 1--3 micrograms/ml. Fixation of complement in competition with isolated IgM rheumatoid factor, resulting in inhibition of hemolysis of sensitized sheep red cells, was used for detection and quantification of immune complexes in human sera. IgM rheumatoid factor was incubated with sensitised sheep red cells followed by addition of test sera; guinea pig complement was added; and the amount of IgM rheumatoid factor mediated hemolysis was determined spectrophotometrically and referred to a standard curve of inhibition of hemolysis by increasing amounts of aggregated human gamma-globulin. Good discrimination between sero-positive rheumatoid arthritis and systemic lupus erythematosus patients compared with normal and hospitalized subjects was found.

Antigen-Antibody Complex↗
PubMed1980

Lack of hidden complement fixing IgM rheumatoid factor in adult seronegative rheumatoid arthritis.

IgM rheumatoid factors capable of complement fixation and activation are commonly present in the sera of adults with rheumatoid arthritis. Hidden complement fixing IgM rheumatoid factor has been demonstrated in the majority of patients with juvenile RA and hidden agglutinating IgM rheumatoid factors have been demonstrated in the serum of adults with seronegative rheumatoid arthritis. We studied 27 adults with seronegative rheumatoid arthritis and were unable to demonstrate hidden complement fixing IgM rheumatoid factor in their sera.

Adult↗
PubMed1976

Rheumatoid factor-producing cells detected by direct hemolytic plaque assay.

Lymphocytes secreting anti-IgC antibodies, rheumatoid factors (RF), can be detected in the peripheral bloods, synovial fluids, and bone marrows of patients with seropositive rheumatoid arthritis by using a direct plaque-forming cell (PFC) assay with sheep erythrocytes sensitized with reduced and alkylated rabbit IgG hemolysin. The autospecific nature of the RF produced by RF-PFC was indicated by inhibition studies in which the order of patency was human IgG greater than rabbit IgG greater than bovine IgG. In metabolic studies puromycin, cycloheximide, and venblastine suppressed RF-PFC. Cyclic AMP and cyclic GMP were without effect. A need was recognized for using full tissue culture media during the cell separation and plaquing procedures to optimize detection of the RF-PFC. RF-PFC may appear in the blood of patients intermittently despite their continuing presence in the bone marrow. They have been found in the peripheral blood, especially during acutely exacerbating polyarticular synovitis, generalized vasculities, or generally active, aggressive disease. RF-PFC were found in synovial effusions of new or recrduescent acute synovitis. RF-PFC were observed to disappear from the peripheral circulation and the bone marrow during therapy with cytotoxic drugs. The data are consistent with the hypothesis that the appearance of RF-PFC in the peripheral blood represents an anamnestic response to transiently appearing antigen. The nature of the antigen is not specified. The bone marrow may be a site of origin of RF-PFC.

Antibody Specificity↗
PubMedDate not supplied

Drugs affecting the release of rheumatoid factor in a plaque-forming cell assay.

Addition of propranolol to the agarose phase of a plaque-forming cell (PFC) assay for rheumatoid factor (RF) caused reduction in the number of plaques seen. This reduction in rheumatoid factor plaque-forming cell (RF PFC) did not depend upon an effect at the beta-adrenergic receptor, since d- and 1-propranolol reduced equally well. Furthermore, in a series of polycyclic compounds with varying beta-receptor blocking capabilities there was no agreement between plaque reduction and blocking. When propranolol was tested in the agarose in an anti-sheep erythrocyte (SRC) plaque assay (anti-SRC PFC), it had no inhibitory effect, but it was capable of inhibiting the generation of new anti-SRC PFC in an in vitro culture. Propranolol is thought to exert these effects through its membrane stabilizing (anesthetic) properties.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Relative reactivities of rheumatoid factors in serum and cells. Evidence for a selective deficiency in serum rheumatoid factor.

Investigations of rheumatoid factors by a hemolytic plaque forming cell assay of blood lymphocytes with sensitized sheep cells have suggested that the rheumatoid factors released from the cells have higher affinities for human IgG than do the rheumatoid factors measured in the patient's serum. This study reaffirms this observation and provides evidence that the reported differences are not artifacts of technique. The findings imply that rheumatoid factors of higher affinity for IgG than those of the serum are being released into the tissue fluids by lymphocytes and locally precipitated. Such rheumatoid factors may never reach the peripheral blood serum in detectable quantity or may do so only infrequently.

Animals↗
PubMedDate not supplied

Eosinophilic fasciitis: a distinct clinical entity?

Eosinophilic Fasciitis is a syndrome characterized by exertion related scleroderma-like skin changes, peripheral eosinophilia, hypergammaglobulinemia and diffuse faciitis. Controversy exists as to the precise classification of the syndrome, i.e., whether it is a distinct entity or a variant of scleroderma. We describe a patient with eosinophilic faciitis but with several unique features: 1) progressive skin changes unresponsive to corticosteroid therapy; 2) elevated anti-DNA antibodies; 3) hypocomplementemia; and 4) a followup biopsy showing sclerodermatoid skin changes. These features and others relating to the controversial aspects of classification of eosinophilic fasciitis are discussed.

Diagnosis, Differential↗
PubMedDate not supplied

Infectious arthritis due to Hemophilus influenzae.

A healthy 51-year-old male developed multiarticular infectious arthritis due to Hemophilus influenzae, a rare cause of infectious arthritis in adults. Previous case reports are reviewed. Predisposing factors include chronic illness, underlying joint disease, joint trauma, and respiratory infection. H. influenzae is frequently misidentified on Gram stain, being mistaken for gonococci or pneumococci. Infections due to H. influenzae may occur in normal adults. Aspects of immunity are discussed.

Adult↗
PubMedDate not supplied

Pyogenic sacroiliitis.

Two cases of pyogenic sacroiliitis are reported and the literature reviewed. Gluteal pain, tenderness in the sacroiliac area, and pain elicited by maneuvers which stress the joint are characteristic. Delay in diagnosis may result from failure to suspect the sacroiliac joint. Onset is acute in 86% with fever, severe pain, and inability to walk. A bone scan is useful for localization. Blood cultures are positive in one-third. Definitive diagnosis can be established by needle aspiration of the joint, a technically difficult procedure. Therapy is discussed.

Adult↗