Wilson v. Blue Cross: a case synopsis.
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Biomedical subjects
Publications and source records attributed to S Roman.
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The case of a 55-year-old woman with a duodenal ulcer developing since 6 months is reported, in whom the surgical indication was early established on the basis of increasing of suffering and inefficacy of the medical treatment. Intraoperatively an exophytic pancreatic tumour sited on the upper border of the isthmus, sized 5/6/4 cm, was found. In view of the suspicion of gastrinoma and considering that total gastrectomy or splenopancreatectomy would be excessive taking into account the patient's state, option was made for exeresis of the tumour. The ulcerous suffering disappeared and the histological examination of the specimen (weighting 70 g) confirmed a benign gastrinoma. The peculiarities of the case and data from the literature dealing with gastrinomas are discussed.
The paper reports on an observation of hepatic nonparasitic solitary cyst, size 10/12 cm, noncomplicated, in a 77-year-old woman. The lesion was treated by digital enucleation and suture of the hepatic wound, with a good result. The paper presents literature data on the hepatic nonparasitic solitary cyst.
Medical education in New York is unique in the country in its scope and its diversity. It is important, as we go forward, that these strengths be neither eroded nor compromised. The AMS member institutions are making a collective commitment to work together to promote changes that will improve medical education for all students by providing them with enriched experience in primary care. Our major resource is faculty. To whatever degree medical schools can influence career choice, it is essential to this aim that the best possible people are placed in the settings in which primary care is taught. The schools will intensify their efforts to recruit and retain such faculty and, in whatever way is appropriate to each institution, provide them with the stature needed to emphasize the value which the school places on primary care. The schools will also work to provide exposure to primary care early in a student's academic career given anecdotal evidence, at least, that such early experience can influence subsequent specialty choice. Finally, the medical schools will assume greater responsibility for graduate medical education. If, with state support, ambulatory teaching sites are developed, the schools will make every effort to assure that they are staffed with high-quality faculty. Residents and students must see primary care practiced with total commitment to quality. It is hoped that, with state-initiated improvements in the practice environment, the ultimate outcome will be an increase in the number of our graduates selecting primary care disciplines for their practices and locating in areas in need of physicians.2+ Corporation, and the Greater New York Hospital Association. We are ready to work with others toward our common objectives, and we call on all of those who share these concerns to participate with us.
One hundred patients admitted to a centre of interventional cardiology with acute myocardial infarction of less than 6 hours, underwent coronary angioplasty of first intention because of contra-indications to thrombolytic therapy (n = 20) or after thrombolytic therapy with streptokinase (n = 54), acylenzymes (n = 12) or tissue type plasminogen activator (n = 14). The indication of angioplasty were those of the TIMI (Thrombolysis in Myocardial Infarction) classification (occluded artery, TIMI grade 0) (n = 60) (suboccluded artery, TIMI grade 1) (n = 40). The criterion of success of angioplasty was an increase greater than 1 of TIMI grade. Reperfusion of the coronary artery was obtained by angioplasty in 95% of failures of thrombolysis and in 90% of patients with contra-indications to thrombolytic therapy. The early reocclusion rate at D1 was 2%. Repeat angioplasty at D1 was successful in both these cases and the arteries were still patent at D21. The reocclusion rate at the third week in 75 patients who underwent control coronary angiography was 5.3%. In patients with arterial occlusion, immediate angioplasty attained two objectives in the same procedure: a high rate of emergency myocardial reperfusion and a low rate of reocclusion. The average left ventricular ejection fraction (all arteries) significantly improved (+9.2% in absolute values) when the artery remained patent (p less than 0.001), especially when the initial ejection fraction was low. In the patients who had occluded arteries at control angiography at 3 weeks, the ejection fraction decreased (-4% in absolute values) (NS). The following complications were observed: 4 coronary artery dissections and haematomas at the site of femoral puncture in patients who had received thrombolytic therapy (10 drained surgically). The hospital mortality was 3% and global mortality after an average follow-up period of 19.6 months was 5%. Coronary angioplasty in acute myocardial infarction carries a low risk and seems to be beneficial in patients with contra-indications to or failure of thrombolysis.
The production of antibodies that react with the Fc fragment of IgG, i.e., rheumatoid factors (RF), is now regarded as a normal host immune response. It is not clear, however, if such putative physiologic RF are different from their counterparts which characterize pathologic states like rheumatoid arthritis (RA). Using Staphylococcus aureus Cowan I as an in vitro stimulant of RF production, we now report that the IgM-RF secreted by blood mononuclear cells obtained from healthy newborn infants and healthy adults can be distinguished not only from classic monoclonal RF and polyclonal RA serum RF, but also from the RF secreted by blood mononuclear cells obtained from RA patients. Whereas the Fc-binding activity of all RF secreted in vitro was easily inhibited by aggregated human IgG, only the RF produced by the normal umbilical cord cells and the normal adult cells were inhibited by monomeric Fc(IgG). The normal RF were also selectively inhibited by monomeric rabbit and guinea pig (Fc(IgG). The RF secreted by umbilical cord blood cells utilized lambda and kappa light chains, with a disproportionate use of lambda light chains relative to the total IgM secreted. Together, these data provide evidence for distinct subsets of RF in health and in disease.
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One case of T-cell lymphoma with atypical malignant cells is reported. Some of the clinical features, morphological characteristics and functional activity (erythrophagocytosis) of malignant cells suggested malignant histiocytosis. The malignant disease started with splenomegaly and developed with hepatomegaly, bone marrow infiltration, discrete lymphadenopathy and leukaemic picture. Proliferated cells were characterized by ambiguity. In addition to phagocytic capability, presence of complement receptors and ultrastructural features proper to the macrophagic lineage, the cells expressed T-cell determinants (E receptors, T3, T4 and T11 antigens) and were peroxidase and esterase-negative. Erythrocytes were partially or completely dehaemoglobinized and presented the phenomenon of autolysis in different stages of development. Because this lymphoma is difficult to diagnose and apparently resistant to therapy, its recognition and further study are warranted.
When compared to normal weight normolipidemic control subjects, dilute blood clot lysis time was found to be obviously (p less than 0.001) prolonged in hypertriglyceridemic patients without proteinuria and slightly (p less than 0.05) accelerated in hyperlipidemic nephrotic patients in spite of their very high levels of plasma fibrinogen. As a result the ratio plasma fibrinogen (mg/dl) per clot lysis time (minutes) was 1.241 +/- 0.08 (X +/- SEM) in control subjects, 0.574 +/- 0.07 in hypertriglyceridemic patients and 2.69 +/- 0.172 in nephrotic patients. This finding suggesting that a larger amount of fibrin is rather readily dispersed from dilute blood clots of nephrotic patients was associated with higher levels of plasma t-PA:Ag (9.45 ng/ml +/- 1.18 in nephrotic patients versus 5.8 ng/ml +/- 1.23 in controls before venous occlusion and respectively 33.1 ng/ml +/- 3.83 versus 20.3 +/- 3.40 in controls after venous occlusion). Plasminogen activator activity of the euglobulins as assessed by the bovine fibrin-agarose plate was significantly higher in nephrotic patients only after venous occlusion. Plasma samples of nephrotic patients exerted a more potent inhibition of fibrinolysis in a urokinase activated system. This effect was, however, mainly due to the high levels of alpha 2 macroglobulin in nephrotic plasma which apparently have little influence on dilute blood clot lysis time.
A patient with non-cutaneous lymphocytic lymphoma with leukaemic spread is reported. The large majority of the peripheral blood mononuclear cells formed rosettes with sheep erythrocytes (E), had receptors for the Fc portion of IgG (Fc gamma R) and displayed an unusual enzymatic profile. Part of these cells had also labile bound surface membrane IgG. The leukaemic cells were morphologically characterized as large granular lymphocytes (LGL) and consisted of two different types of cells: lymphoid cells and monocytoid cells. The histopathological diagnosis was T-cell lymphoma, pleomorphic type, diffuse. Despite their morphological heterogeneity, all the proliferative cells had the same immunological phenotype, showed normal ADCC activity but no NK activity. After three months, without specific treatment, the surface pattern changed: the cells resembled mature LGL and the NK activity increased. The cytochemical study of the leukaemic cells revealed an enzymatical peculiarity: besides an enzymatic profile characteristic for relatively mature LGL, the cells also displayed peroxidase activity. This unusual aspect--the expression by an individual malignant cell of markers believed to be restricted to a single cellular lineage--might be interpreted as a lineage infidelity or lineage promiscuity. The observation that this lymphoma developed in a patient with a long history of hypogammaglobulinaemia is of particular interest.
Previous reports by a number of laboratories have shown that Ig-binding factors may play a role in the regulation of Ig production by B cells. Although numerous studies have addressed the specificity and biologic function of Ig-binding factors at the cellular level, little information is available regarding the mechanism whereby Ig-binding factor modulates Ig production by B cells at the molecular level. Herein we have examined the specificity and molecular mechanism of the suppression of IgA production mediated by IgA-binding factor. Using the IgA-secreting plasmacytoma, MOPC-315, as a target cell, we have demonstrated that: 1) IgA-binding factor binds to IgA, but not to IgG, IgM, or BSA; 2) IgA-binding factor can suppress proliferation as well as IgA production by MOPC-315; 3) soluble IgA, but not IgG or IgM can inhibit the action of IgA-binding factor; 4) suppression of Ig production by IgA-binding factor is maximal within 8 to 12 h after exposure to the factor and is reversible; 5) IgA-binding factor suppresses IgA production by selectively down-regulating synthesis of IgA H and L chain proteins; 6) IgA-binding factor selectively suppresses transcription of alpha-H chain and lambda-2-L chain genes; 7) IgA-binding factor suppresses accumulation of c-myc mRNA. These findings suggest that IgA-binding factor binds selectively to surface IgA on MOPC-315 and suppresses IgA production by down-regulating transcription of H and L chain genes. Suppression of MOPC-315 proliferation by IgA-binding factor may be related to the concomitant down-regulation of the expression of the c-myc gene. c-myc is deregulated in MOPC-315 by virtue of the reciprocal 15:12 chromosomal translocation present in MOPC-315 where the c-myc gene is translocated and rearranged into the alpha-H chain gene complex. Simultaneous suppression of the expression of c-myc and alpha-H chain genes suggests that these two genes may be coordinately modulated, in plasmacytomas, by IgA-binding factor.
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27 patients with primary myocardial infarction are treated, in the first 6 hours, with intravenous thrombolysis with immediate coronary angiographic control showing a patent artery in 76 p. cent of the cases. The treatment is completed with intracoronary thrombolysis (5 times) and transluminal angioplasty (6 times), enabling to obtain a patency rate of 88 p. cent. The overall left ventricular function is evaluated at D21 and in the 6th month (M6). Among anterior infarctions, those treated during the first three hours have a better ejection fraction (EF) at D21 than those treated later (40.3 p. cent +/- 6 versus 33.2 p. cent +/- -NS); this functional benefit is confirmed at M6 (42.8 p. cent +/- 12 versus 30.6 p. cent +/- 8; p less than 0.06). On the contrary, among inferior infarctions, the EF is comparable at D21 and M6 regardless of the early nature of the treatment. One patient died prematurely from a cerebral vascular accident which occurred during the thrombolysis. These results are in favor of a significant myocardial salvation in anterior infarctions revascularised at an early stage and of an active approach in order to obtain the most complete possible revascularisation.
We studied in vivo and in vitro the possible influence of the indwelling line on the measurement of cyclosporin A (CSA) levels. CSA levels measured in samples taken from the catheter lumen used for CSA administration were significantly higher than those taken either from a second lumen or from a peripheral vein. Reversible fixation of the drug to the catheter walls might explain this alteration. The degree of fixation varies for different types of plastic material.
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When compared to age-matched normal weight normolipidemic control subjects, plasma factor XIII, plasma fibronectin and serum cholinesterase levels were found to be markedly decreased in patients with decompensated cirrhosis of the liver, not significantly changed in hyperlipoproteinemia type IIa (heterozygous subjects) and increased in hypertriglyceridemic subjects (type IIb and IV) as well as in hyperlipidemic nephrotic patients. A possible accelerated hepatic synthesis of certain plasma proteins including factor XIII and fibronectin in patients with the nephrotic syndrome as well as in endogenous hypertriglyceridemia is envisaged. It is also considered that mural thrombi, richer in factor XIII and fibronectin, would be more resistant to fibrinolysis and more readily attached to subendothelial structures.
The results obtained by using the protein A-rosette assay for human peripheral blood lymphocytes treated with a series of monoclonal antibodies were very close to the estimates obtained by indirect fluorescence. The percentages of T3-, T4-, T8- and DR-positive cells (T3 = T lymphocytes, T4 = helper T lymphocytes, T8 = suppressor T lymphocytes, DR = B, L and null cells) in normal and pathological peripheral blood were found to vary within the limits reported by many other authors using different techniques for the identification of cells binding the specific monoclonal antibody.
We previously reported that an extract of uremic plasma reduces binding of phenytoin and tryptophan by normal plasma and plasma albumin. This effect appears to reproduce the impaired binding of many drugs and several endogenous metabolites by uremic plasma. In the present study we further characterized the properties of extracts from uremic sera and body fluids using binding of salicylate as a model. Salicylate was chosen because it binds to both of the main albumin binding loci for aromatic, acidic drugs. Using a computer-assisted, least-squares, curve-fitting program, LIGAND, we found that the most satisfactory model for salicylate binding to 1:10 diluted normal plasma was a binding number (n) of 2 mol of salicylate per mole of albumin with an association constant (k) of 2.85 X 10(4) L/mol, an additional binding of 0.5 mol to other sites on albumin or to other proteins, and nonspecific binding of 21%. Addition of uremic pleural fluid extract to diluted normal plasma produced a monotonic decline in k to 0.17 X 10(4) L/mol with no change in n except possibly at the highest dose of uremic inhibitor. This pattern of competitive inhibition indicates presence of unknown ligands in the uremic extract that compete at both binding loci. More efficient extraction methods might also yield additional ligand(s) that inhibit through a noncompetitive mechanism.