[Adrenal hemorrhage simulating a nonhyperfunctional adenoma].
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Biomedical subjects
Publications and source records attributed to J Anglada.
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The aetiology of autoimmune diseases remains unknown. The relationship between virus, and more recently retrovirus, has been suggested with this group of diseases. Immunoblotting is a useful method for determining the presence of proteins coded by different retrovirus genes. Since the prevalence of these types of proteins in patients with primary Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and autoimmune thyroid diseases has not been fully established, the aim of this work was to determine the prevalence of antibodies to immunodeficiency human virus type 1 (HIV-1) proteins in these diseases and their possible relationship with the presence of anti-nuclear, anti-DNA, anti-SSA (Ro) and anti-SSB (La) autoantibodies. Antibodies to human immunodeficiency virus (HIV-1) were studied in a group of 341 patients with autoimmune diseases (77 SS, 98 SLE, 75 RA, 91 autoimmune thyroid diseases) and 126 blood donors as a control group. A Western blot was used to detect antibodies to HIV-1, and a double polymerase chain reaction (PCR) using nested primers in the gag and pol gene of HIV-1. Antinuclear antibodies, anti-DNA, anti-SSA (Ro) and anti-SSB (La) were determined by enzyme-linked immunosorbent assays. At least one band was shown on immunoblotting in 26% of patients with autoimmune diseases and 35% of controls. The presence of antibodies to p55 or p68 proteins in patients with SS or SLE proved to be the only statistically significant difference between the other autoimmune diseases studied and the control group. These antibodies were not associated with autoantibodies ANA, DNA, SSA (Ro) or SSB (La).(ABSTRACT TRUNCATED AT 250 WORDS)
We report the results of short-term tamoxifen treatment (20 mg two times a day orally) in 2 patients with metastatic medullary thyroid carcinoma. Patient A had a rapid tumor progression with development of Cushing's syndrome before initiation of tamoxifen treatment. Patient B had a slowly progressive course. In both cases, neither clinical nor biochemical improvement were observed, after 1 and 3 months of tamoxifen therapy, respectively.
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The efficacy and tolerability of lovastatin and gemfibrozil were compared in a randomized double-blind 12-week study including 182 patients with primary hypercholesterolemia, from 7 hospitals in Spain. Inclusion criteria were total-cholesterol of at least 250 mg/dl and triglycerides less than 350 mg/dl. Patients were stratified in two groups: group 1, cholesterol less than 300 mg/dl, and group II, cholesterol equal to or more than 300 mg/dl. Patients were randomized to gemfibrozil (600 mg b.i.d.) or lovastatin (20 mg q.p.m., group I and 40 mg q.p.m., group II). If after 6 weeks of treatment cholesterol remained above 200 mg/dl, lovastatin does were doubled. In group I, lovastatin decreased cholesterol by 20%, LDL-C by 28%, and triglycerides by 17%, and increased HDL-C by 8%. In group II the results were: -26%, -33%, -19% and +6% respectively. The corresponding results with gemfibrozil were: -8%, -9%, -28% and +14% (group I); and -13%, -14%, -33% and +9% (group II). In both groups, lovastatin was more effective in reducing cholesterol and LDL-C (P less than 0.001) and gemfibrozil in reducing triglycerides (P less than 0.05 group I and P less than 0.01 group II). Both drugs were well tolerated. Thus, lovastatin and gemfibrozil are effective lipid-lowering agents; lovastatin has more pronounced effects in patients with hypercholesterolemia.
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