Platelets were isolated by gel filtration from paired samples of peripheral blood and synovial fluid (SF) aspirated from inflamed knee joints from 20 adult patients with rheumatoid arthritis (RA) as well as from peripheral blood obtained from 20 healthy subjects. The platelets from the three different sources were investigated for quantitative differences in the number of two distinct types of intracellular storage organelles using immunofluorescence staining for platelet factor 4 (PF4) and labelling with the fluorescent substance mepacrine (MC). The number of PF4-stained organelles per cell was the same in the peripheral normal and RA platelets. This number was distinctly lower in the SF platelets. The peripheral and SF platelets from the RA patients had the same number of MC-labelled organelles. This number was distinctly lower than in the normal cells. The results suggest that the peripheral RA platelets had been activated to liberate serotonin and other substances from one type of organelles, and that the SF platelets had been activated to an additional liberation of PF4 from another such type. Liberated PF4, serotonin, and other substances from SF platelets may, in several ways, contribute to the inflammatory responses of RA.

Chronic fatigue syndrome (CFS) and fibromyalgia syndrome (FMS) are characterised by a lack of consistent laboratory and clinical abnormalities. Although they are distinguishable as separate syndromes based on established criteria, a great number of patients are diagnosed with both. In studies using polymerase chain reaction methods, mycoplasma blood infection has been detected in about 50% of patients with CFS and/or FMS, including patients with Gulf War illnesses and symptoms that overlap with one or both syndromes. Such infection is detected in only about 10% of healthy individuals, significantly less than in patients. Most patients with CFS/FMS who have mycoplasma infection appear to recover and reach their pre-illness state after long-term antibiotic therapy with doxycycline, and the infection can not be detected after recovery. By means of causation and therapy, mycoplasma blood infection may permit a further subclassification of CFS and FMS. It is not clear whether mycoplasmas are associated with CFS/FMS as causal agents, cofactors, or opportunistic infections in patients with immune disturbances. Whether mycoplasma infection can be detected in about 50% of all patient populations with CFS and/or FMS is yet to be determined.

Synovial fluid (SF) aspirated from inflamed knee joints from each of 13 patients with adult rheumatoid arthritis (RA) was mixed with ACD in the ratio SF/ACD=9:1 with subsequent addition of an equivalent amount of an edta-tris buffer. The mixture was centrifuged to obtain a platelet-rich supernatant. The platelets were washed three times and counted. The same procedure was performed with SF from non-inflamed knee-joints from 3 patients with osteoarthrosis (OA). Direct immunofluorescence (IF) studies were performed with aliquots of platelet suspensions from each SF. In most RA specimens observed under the microscope before separation of platelets, a few small platelet aggregates were observed and platelets were seen in contact with lymphocytes. In all instances, the platelet count appeared to be positively correlated to the total number of white blood cells. In the OA specimens, relatively few platelets were detected, a few lymphocytes were seen in contact with platelets, but no platelet aggregates or correlation between platelets and white blood cell counts were found. Results of the IF studies of RA specimens provide evidence that IgG, IgM and C3 are located on the platelet surface. On the surface of OA platelets, however, only IgG and C3 were detected. Identical staining results were found with washed peripheral platelets from 3 of the RA and 1 of the OA patients. Neither medical treatment nor Waaler serology influenced the staining results. In inflamed SF from RA patients, both IgG aggregates, immune complexes, collagen, and prostaglandins can induce a platelet release reaction with liberation of vasoactive compounds, chemotactic substances and enzymes which can destroy connective tissue, cartilage and bone structures. Interpretations and the significance of the different results are discussed.

Suspensions of human platelets were incubated with various immunoglobulin preparations and subsequently stained with FITC-conjugated antisera. Incubation with monomeric IgG, but not with monomeric IgM, IgA, IgD nor with IgE, gave a positive staining of the platelets. Incubation of platelets with monomeric IgG1 and IgG3 as well as with Fc and pFc′ fragments from IgG3 also gave a positive staining while incubation with monomeric IgG2 and IgG4 did not. Thus, IgG binds to Fc receptors on the surface of human platelets with the CH3 domain of the Fc region. Heat aggregation also caused binding of IgG2 but not with IgG4 proteins to human platelet Fc receptors. The majority of platelet preparations both from ITP and SLE patients gave a positive staining using direct immunofluorescence technique. Incubation of normal human platelets with sera from ITP and SLE patients gave a strong surface staining of normal platelets. Strong staining was also obtained with pepsin-digested sera from most patients with ITP while pepsin-digested sera from patients with SLE did not give a positive staining. It is therefore concluded that the majority of sera from patients with ITP contain antibodies with specificities for platelet surface antigens while sera from patients with SLE contain immune complexes that react with platelet Fc receptors through the Fc parts of the IgG antibodies.