Immune reactions in infective endocarditis. II. Relevance of circulating immune complexes, serum inhibition factors, lymphocytotoxic reactions, and antibody-dependent cellular cytotoxicity against cardiac target cells

Circulating immune complexes (IC) were detected in 35 out of 41 patients (85%) with infective endocarditis of known bacterial origin in contrast to only 9 out of 20 patients (45%) with endocarditis but negative blood cultures (p less than 0.05). Peak IC levels of 33.25 +/- 24.33 micrograms/ml in the early period fell significantly to 8.38 +/- 13.37 micrograms/ml after antibiotic treatment (p less than 0.001). High levels of IC coincided with relative hypocomplementemia. Erythrocyturia was observed in 51 of 58 IC-positive patients demonstrating peripheral sequelae of circulating IC. Incidence and concentrations of IC correlated neither with the mere presence of the rheumatoid factor nor with the titers of antimyolemmal antibodies, nor with antibody mediated cytolysis in the presence of complement. Serum inhibition factors (SIF) and E-rosette inhibitory factors (RIF) were not demonstrated, indicating that IC in endocarditis do not suppress phytohemagglutinin-induced lymphocyte proliferation or the E-rosetting of T cells. Significant lymphocytotoxicity against heterologous cardiac target cells without serum (LC) could be demonstrated in 11 out of 23 patients (48%) with endocarditis as compared to its absence in controls (n = 33, p less than 0.01). In assays of antibody-dependent cellular cytotoxicity (ADCC), either enhancement or blocking of lymphocytotoxicity by autologous serum or both was observed. The modulation of lymphocytotoxicity was most likely due to antimyolemmal antibodies, to IC, or to both, although effects of other serum factors cannot be ruled out completely.     

Macroglobulinemia-myeloma double gammopathy. A study of four cases and a review of the literature

The coexistence of macroglobulinemia and myeloma type M components in the same serum is very rare. The following features were observed in four patients with this condition: (1) Hyperviscosity syndrome with widespread amyloidosis and foci of calcification; the serum contained an IgG4(κ), 7S and 17S IgM(κ) M components. (2) Polyarthritis, high fever, lymphadenopathy, hepatosplenomegaly and skin rash; IgA(λ) cryoglobulin and IgM(λ) pyroglobulin were found in the serum. (3) Plasmacytoma of the liver; IgG(λ) and IgM(λ) were detected. (4) Malignant lymphoma of a diffuse histiocytic type; IgG(κ) and IgM(κ) were present in the serum. A review of the literature disclosed 26 other examples of macroglobulinemia-myeloma type double gammopathy. The clinical picture, well described in 17 of these, was heterogeneous and not necessarily typical of either condition. Whereas some investigators stated that each M component was produced by a distinct population of malignant cells, others presumed that the same clone was capable of synthesizing more than one immunoglobulin.     

Variable susceptibility to dynamic coronary obstruction: An elusive link between coronary atherosclerosis and angina pectoris

Growing evidence suggests that dynamic coronary obstructions play an important but elusive role in the genesis of ischemic events. Dynamic coronary obstructions can develop during certain phases of coronary disease as a result of a variable combination of vasoconstriction, arterial wall lesions, and increased thrombotic tendency. In a certain phase of their disease some patients develop dynamic coronary obstruction, while others with a similar degree of fixed atherosclerotic obstruction do not.     

Pulmonary varix: report of a case with additional anomalies of the vascular pulmonary tree

A 65-year-old woman developed a bloody pleural effusion $\text{2-}\text{1}\text{2}\text{years}$ after the onset of Dressler's syndrome. Since an extensive evaluation failed to reveal a specific etiology, the effusion was presumed to be a manifestation of Dressler's syndrome. Because of the therapeutic implications involved, we are reporting this case to emphasize that pleural effusions may occur as a manifestation of Dressler's Syndrome in the distant post-infarction period.     

Plasma beta-thromboglobulin as a measure of platelet activity: Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 ± 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 ± 1.2 ng/ml, n = 56), those who smoked (31.8 ± 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 ± 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 ± 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 ± 1.4 ng/ml, p < 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 ± 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 ± 1.8 ng/ml, n = 44), patients with 2 or more risk factors had a significantly elevated plasma BTG level (45.2 ± 2.2 ng/ml, n = 47, p < 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.     

Neutropenia as a Complication of Tumefactive Demyelinating Disease: A Case Report

Tumefactive demyelination is an aggressive, localized, generally solitary area of demyelination that often mimics a neoplasm. We present a case of a 13-year-old female patient who presented with sudden-onset progressive hemiplegia and hemianopsia. Magnetic resonance imaging of the brain showed tumefactive demyelination with partial rim of enhancement. During inpatient rehabilitation, she developed myalgias, rash, and abdominal and mouth pain with evidence for severe neutropenia. The neutropenia was determined to be a secondary complication of the tumefactive disease process. This scenario may be concerning in an inpatient rehabilitation setting, as patients share common areas, increasing the risk of acquired infection while neutropenic.