Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total hydroxyproline excretion in 24-hour urine was determined in 20 cases of systemic lupus erythematosus (SLE) before and during treatment. Additionally the excretion of hydroxyproline was determined in 14 patients receiving steroids for various other diseases (endocarditis, thrombocytopenia, acute leukemia, apofocal polyarthritis, ischialgia, spastic bronchitis, pleuritis and Dressler's post-infarction syndrome). The normal hydroxyproline value was established in 40 healthy persons. The normalization of pathologically increased hydroxyproline excretion in patients with SLE during treatment with prednisone in doses from 1.0 to 1.35 mg/kg/daily was associated with remission of clinical symptoms. Large doses of prednisone in pathological processes not primarily affecting connective tissue increased the 24-hour excretion of hydroxyproline and small doses of prednisone had no effect on hydroxyprolinuria.
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PMID:Effect of antiphlogistic steroids on urinary hydroxyproline excretion in systemic lupus erythematosus. 95 50

The complications arising out of the installation of pacemakers are listed and classified and it is suggested that a syndrome characterized by recurrent pleural effusion recalcitrant to the usual medico-depletive therapies, observed in four patients with pacemakers, should be included among such complications. The clinical pictures of the syndrome is described in detail and particular attention is paid to its date of onset in relation to installation of the pacemaker, early symptomatology, the most typical symptoms, clinico-humoral development, prognosis and therapy. Some theoretical and practical remarks are also offered, specifically three pathogenetic suggestions are formulated on the basis of clinical and developmental features but mainly in relation to humoral and immunological findings. These suggestions stress alternative interpretations of the syndrome: A) as an autoimmune disease arising secondary to surgical denaturation of myocardial and/or endocardial autoantigens; B) as a systemic autoimmune disease due to congenital or acquired insufficiency of immunological homeostasis; C) as a monosymptomatic pleural form of systemic lupus erythematodes with late clinical outbreak. The fascinating pathogenetic, clinical, biological and therapeutic resemblances between the present syndrome and the post-infarctual syndrome of Dressler and Johnson's post-pericardiotomic syndrome are pointed out and it is suggested that complications of medical nature already described as being secondary to the installation of pacemakers, such as endocarditis and pericarditis, should be looked at from an autoimmune type of pathogenetic viewpoint. Finally, in the light of personal observations, the need for immunological study of high risk patients, namely relations of patients with autoimmune diseases, is stressed. All candidates for pacemaker installation should also be included. Routine screening of this type would take on enormous practical importance as it would enable preventive or curative treatment to be undertaken to modify the immunitary balance of those subjects in whom pacemaker installation is liable to trigger off critical, irreversible breakdown in immunitary homoeostasis of which the syndrome in question would seem to be the most dramatic, but perhaps no the only, clinical manifestation.
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PMID:[On a syndrome of immunopathic type with pleural and systemic localization observed in patients with intracavitary electrostimulators. Considerations on 4 cases]. 96 39

In 50 patients treated from January 1998 through March 2002 for pericardial effusion and tamponade, we retrospectively investigated the efficacy of percutaneous placement of an indwelling pericardial catheter guided by 2-dimensional echocardiography and fluoroscopy. We also investigated causation. In 80% of the patients, we were able to determine specific causes through clinical, serologic, and cytologic investigation: cancer in 15 patients, chronic renal failure in 11, systemic lupus erythematosus in 2 rheumatoid arthritis in 2, Dressler syndrome in 2, tuberculosis in 1, blunt chest trauma in 1, purulent pericarditis in 1, and probably viral pericarditis in 5. No specific cause could be determined in 10 patients (20%). We did not observe any complication due to the procedure. Two patients died during hospitalization. After hospitalization, 9 patients with metastatic cancer died within 3 months. A 2nd percutaneous drainage procedure was required in 2 cancer patients. Recurrence of pericardial effusion and tamponade and the requirement of pericardiectomy occurred in 2 patients with perfusion of unknown cause and in 1 patient with perfusion due to rheumatoid arthritis. Histologic examination of pericardial tissue in patients with idiopathic disease showed fibrinous pericarditis but no causal factor. In the group with idiopathic pericardial effusion, 2 patients with multiple mediastinal lymphadenopathy underwent mediastinal exploration; biopsy revealed nonspecific lymphadenitis and fibrinous pericarditis. In patients with large pericardial effusions and tamponade, the specific cause was in most cases already known or obtained by initial clinical and laboratory investigation. Sufficient cardiac decompression was achieved by percutaneous pigtail catheter drainage.
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PMID:Pericardial tamponade and large pericardial effusions: causal factors and efficacy of percutaneous catheter drainage in 50 patients. 1574 92