[Gingival hyperplasia as an adverse reaction to nifedipine].
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Biomedical subjects
Publications and source records attributed to A Collado.
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We report the case of a female aged 67 years suffering a Waldenström's macroglobulinemia which began with arthritis at the knee and pleural effusion. In both locations the anatomopathological examination showed infiltration by typical lympho-plasmatic cells. Other possible etiologies such as amyloid, infection or arthritis produced by microcrystals were ruled out. The relevant finding in this case was the presence of infiltrative reaction at the synovial tissue which has been rarely reported in the literature. We review the incidence of articular manifestations in cases of Waldenström's macroglobulinemia and the possible pathogenetic mechanisms involved.
We used the U937 cell line to analyze CD14, CD11/CD18, HLA class-I and DR antigen expression during PMA-induced differentiation. Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression. Protein kinase C may play a major role in regulating the expression of these antigens. The protein kinase inhibitor H7 abrogated the inductive effect of PMA. Calcium ionophore, when added alone or in the presence of PMA, had no effect. The inhibitory effect of the calcium antagonist verapamil, EGTA, and of chlorpromazine, an antagonist of calcium-binding proteins, supports a role for calcium-dependent protein kinase C in the up-regulation of CD14 and CD11/CD18 surface expression. The specific calmodulin inhibitors R24571 and W7 had no effect on antigen expression. Our findings suggest that protein kinase C activation is an important step in the PMA-induced differentiation of U937 cells.
Fourty four patients suffering non traumatic rhabdomyolysis (RM) are studied. The most frequently encountered etiologies were neurologic abnormalities in 26 patients, followed by infections in 7 patients and metabolic abnormalities in four cases. Eleven patients (25%) presented several associated factors. The clinical manifestations of RM were not very significant, with only 18% of patients presenting muscle pain, 38.6% proteinuria and 36.4% hematuria. A significant increase in K, CPK, LDH, and ASAT values was observed after the RM episode (p less than 0.05). Those patients with an infectious RM were older (p less than 0.05) and presented higher urea (p less than 0.01) and creatinine (p less than 0.05) values. Only two patients presented renal failure. One patient with septic shock died. RM is a relatively common condition, often secondary to multiple systemic processes, which can go unnoticed due to the underlying disease.
We describe the clinical and anatomopathological findings in an 85-year-old male presenting with a lateral medullary syndrome and ipsilateral hemiplegia (Opalski's syndrome) due to giant-cell arteritis of the vertebral artery. Other common associated symptoms of the disease were absent, and the erythrocyte sedimentation rate was only of 30 mm/h. This case emphasizes that limited intracranial giant-cell arteritis may present rarely as a stroke.
Cutaneous immunofluorescence studies were carried out in 21 patients with ankylosing spondylitis (AS) and the results compared with those for 18 healthy subjects. The most prominent finding was the presence of IgA in dermal vessels of patients with AS (71% compared with 17% of the control group). IgG and IgM cutaneous deposits were also observed in patients with AS, but these results did not differ from those of the control group. A renal biopsy was performed in three of the patients presenting with unexplained microscopic haematuria. One of them had an IgA nephropathy, but no correlation was found between kidney and skin deposits of IgA. These findings suggest that IgA cutaneous deposits in AS are not a marker of IgA nephropathy but stress the role of immunoglobulin A in the pathogenesis of this disease.
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Fifty one patients with ankylosing spondylitis (AS) were typed for HLA-A, B, C, DR, and DQ antigens. The antigen frequencies were compared with those of a normal population and with a B27 positive control group. All but one of the patients with AS were HLA-B27 positive. A positive linkage disequilibrium between Cw1, Cw2, DR1, and the B27 antigen was observed. Patients with AS showed a significant increase in DQw2 antigen compared with the B27 positive control group. No differences in antigenic frequencies were observed in patients having peripheral arthritis and patients with only axial involvement. Seven out of nine patients (78%) with an erosive peripheral arthritis were DR7 positive, suggesting that DR7 or genes closely linked could be related with a more aggressive peripheral joint involvement in patients with AS.
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A monoclonal antibody IgG1K against a P24 antigen has been obtained. This antigen is present on a subgroup of non-T-ALL and platelets. GR2110 monoclonal antibody was produced by immunizing with a CALL (CALLA+, Ia+, IgS-, E-, T3-) This P24 antigen is absent in normal T-lymphocytes, monocytes, mitogen-activated T-cells; weakly expressed on B-cells and granulocytes and negative with several cell lines, except with KM3. GR2110 monoclonal antibody was tested with chronic and acute human leukemias. It was positive only with some CALL, NULL ALL, B-ALL and negative with B-CLL, T-CLL, T-cell lymphoma, Hairy cell leukemia, AML, T-ALL. The immunoprecipitation of 125I-labeled cell membrane with the monoclonal antibody and SDS-PAGE analysis revealed a 24 kD molecular weight polypeptide. The comparison of GR2110 and FMC 8 in capping experiments and cellular reaction patterns, showed that both antibodies react with the same molecule but probably with different epitopes.
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The identification of different mechanisms by which tumours escape from the immune system has helped to evaluate the clinical relevance of a variety of phenotypic changes that occur during tumour development. Among them, changes in HLA class I expression play a leading role in the tumour-host environment since HLA class I molecules interact with T lymphocytes for antigen presentation and with NK cells for inhibition/activation of these immune effector cells. Our laboratory has proposed a classification of the altered HLA class I phenotypes frequently found in human tumours, into five major groups. This review focuses on the tumour phenotypes found in primary and metastatic lesions, the molecular mechanisms that give rise to each phenotype and the clinical implications of these findings.