Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperthyroidism developed in three patients during the administration of potassium iodide given for the purpose of blocking the thyroid uptake of radioactive iodine liberated in the course of the 125I-fibrinogen test. In a consecutive series of 31 geriatric patients, who received potassium iodide for the same reason, biochemical hyperthyroidism developed in three instances and significant depression of thyroid function was observed in 10. The performance and the interpretation of the 125I-fibrinogen test are unaffected if iodide is not administered to the patient. The possible hazards to some patients of either induced hyperthyroidism or faulty assessment of thyroid function may be greater than the risk of thyroid irradiation. It is suggested that for the performance of the 125I-fibrinogen test potassium iodide need not be given to the elderly and should be given in a dose of 30 mg daily for two weeks to younger patients. Under certain circumstances potassium perchlorate may be a preferable drug for preventing the accumulation of radioactive iodine by the thyroid.
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PMID:Hyperthyroidism induced by potassium iodide given in the course of 125I-fibrinogen test. 445 24

In a study of 55 persons with dengue haemorrhagic fever-36 of whom showed the dengue shock syndrome-clinical, haematological, virological, and serological changes were correlated with serial measurements of complement components and immunopathological studies. Viruses dengue-1 or dengue-2 were isolated from the sera of 9 patients. Serological responses indicative of secondary dengue virus infections were observed in 53 patients; 2 (infants) had primary infections. During the acute phase of the disease, dengue antibody titres rose logarithmically. Marked depression of complement components, especially C3, was observed. Activation of both the classical and alternative complement pathways was demonstrated, with depression of both C4 and C3 proactivator levels in most instances, although in some cases it appeared that one mechanism was involved to a greater extent than the other. The level of depression of C3 was correlated with the severity of the disease. Relatively stable transferrin levels indicated that depletion of complement proteins was not primarily due to extravasation. Fibrinogen levels were depressed and fibrinogen split products were found in the plasma. The accumulated data provide further evidence of the central role that activated complement components play in the pathogenesis of dengue haemorrhagic fever.
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PMID:Pathogenetic mechanisms in dengue haemorrhagic fever: report of an international collaborative study. 457 23

Studies of serum proteins, platelets, and fibrinolysis in patients after renal allografting show that a fall in plasma fibrinogen in the postoperative period can be associated with early rejection and that a rise in serum fibrin degradation products when accompanied by a fall in platelets is associated with rejection. Fibrinolysis is depressed in these patients until two months after transplantation and marked depression of fibrinolysis may precede rejection. The late coincidence of fibrinolytic depression with a rise in fibrin degradation products suggests chronic insidious rejection.
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PMID:Proteins and fibrinolysis in recipients of renal allografts. 492 37

In order to study the possible relation between blood viscosity and exercise ST segment depressions in hyperlipidemia the former was lowered by infusion of dextran and by treatment with clofibrate 1 g twice daily. Acute decrease of blood viscosity with dextran infusion in two cases increased the ST segment depressions during work. Nine subjects with asymptomatic hyperlipidemia, hyperfibrinogenemia and exercise ST segment depressions were treated with clofibrate in order to lower plasma fibrinogen and serum lipids. This did not influence the area of ST segment depression with either Frank leads or CH leads as determined by computer estimation. As the plasma fibrinogen level is of major importance for the blood viscosity it is concluded that the ischaemic ST segment depression seen in hyperlipidemia is not due to increased blood viscosity but more likely to a premature subclinical coronary atherosclerosis.
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PMID:Effect of blood viscosity decrease on exercise ST segment depressions in hyperlipidemia. 616 35

Disseminated intravascular coagulation was induced in kittens by intraperitoneal inoculation of feline infectious peritonitis virus (FIPV). Kittens seronegative to FIPV survived significantly (P less than 0.05) longer than those seropositive to FIPV. Pyrexia, anemia, icterus, hyperbilirubinemia, and elevated concentrations of liver-specific enzymes were detected in the inoculated cats. Lesions induced included disseminated fibrinonecrotic and pyogranulomatous inflammation, hepatic necrosis, and widespread phlebitis and thrombosis. Localization of FIP viral antigen and immunoglobulin G was demonstrated in foci of heptic necrosis by immunofluorescence miroscopy. Lymphopenia, thrombocytopenia, hyperfibrinogenemia, and increased quantities of fibrin-fibrinogen degradation products were present in cats after the onset of clinical illness. Depression of factor VII, VIII, IX, X, XI, and XII plasma activities and prolongation of prothrombin and partial thromboplastin times also developed in infected cats. The accelerated onset of clinical disease and mortality in seropositive kittens vs seronegative kittens and the association of virus and antibody in multiple foci of hepatic necrosis suggest an immune-mediated component is involved in the pathogenesis of this disease.
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PMID:Disseminated intravascular coagulation in experimentally induced feline infectious peritonitis. 625 Apr 26

A retrospective study in 20 seronegative and 61 seropositive (complement fixation) first cadaver donor graft recipients brought evidence that in cytomegaly, not the infection alone, but curtailment of azathioprine shortly after transplantation (or summation of both) may result in rejection and impaired graft survival. Preliminary data (accumulation of 125I-labelled fibrinogen in two and morphology of the graft in two other patients) showed that depression of graft function in cytomegaly is not necessarily due to rejection.
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PMID:Renal allograft function and cytomegaly. 626 21

Of 20 patients who presented to our hospital with the histologically confirmed diagnosis of SLE, nine met the criteria of presence of both a rapidly progressive disease state and contraindications for conventional therapy required for admission to our plasma exchange programme. Five patients improved; two patients progressed to end-stage renal failure; two patients died as a result of complications of advanced SLE. Severe lupus erythematosus (SLE) is usually treated with a combination of steroids and cytotoxic drugs. Even when treated with high dose therapy some patients develop life-threatening complications, such as renal failure, heart failure and respiratory insufficiency. Moreover, both treatment with high dose of corticosteroids and long lasting cytotoxic therapy may produce troublesome side-effects, including severe infections, gastroduodenal ulcers, bone marrow depressions and lymphomas (1, 2). One of the manifestation of SLE is the presence of antibodies against ds-DNA and ss-DNA. These antibodies can either react with DNA bound to te basement membrane and induce an inflammatory reaction (3), or can form circulating immune complexes which deposit in tissues and may impair the function of lymphocytes or macrophages in the RES (4, 5). The presence of anti-DNA-antibodies appears to be secondary to enhanced B-cell activity along with a depression of suppressor T-cells function proteins mediating the inflammatory process, such as fibrinogen, may deposit in membranes already compromised by the disease. Even though the pathogenic mechanisms operating in SLE are not completely understood, it can be expected, from a theoretical point of view, that the extracorporeal removal of any immunopathogens could improve the disease state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma exchange in systemic lupus erythematosus. 664 35

Previous studies have demonstrated that intravenous administration of erythrocyte stroma is followed by a depression of RES phagocytic function. The present study evaluated the possibility that depression of hepatic blood flow, activation of the coagulation system, or depletion of opsonic factors mediates the RES depression induced by erythrocyte stroma. Stroma was prepared from washed rat erythrocytes and injected into rats at doses of 0.3, 0.5, 0.75, and 1.0 ml/100 gm. RES depression increased progressively after stroma doses greater than 0.3 ml/100 gm. Hepatic blood flow was decreased only after the 1.0 ml/100 gm dose. Fibrinogen levels were decreased with the 1.0 ml/100 gm dose but were unchanged with the 0.5 ml/100 gm dose of stroma, and the RES depression induced by the 0.5 ml/100 gm dose was not modified by the administration of heparin. Circulating fibronectin levels were not consistently depressed after stroma injection, and in vitro incubation of stroma with serum did not affect fibronectin levels. Erythrocyte stroma decreased hemolytic complement levels but depletion of complement with purified cobra venom factor did not depress RES phagocytic function. Preopsonization of the RES test particle did not modify the stroma-induced RES depression. These results indicate that decreased hepatic blood flow, activation of the coagulation system, or depletion of opsonins did not contribute to the RES depression induced by the 0.5 ml/100 gm dose of stroma. These results suggest that impairment of phagocytic cell function may mediate the effect of erythrocyte debris on RES phagocytic function.
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PMID:Effect of erythrocyte stroma on reticuloendothelial system phagocytic function. 686 72

Eleven patients with leukemia and lymphoma were treated with 14 courses of E. coli L-asparaginase. Abnormalities of the coagulation screening tests and decreased fibrinogen levels were observed in all patients during treatment. Significant depressions of functional (mean 32%) and antigenic (mean 48%) antithrombin III were observed by day 14 of therapy. There was no laboratory evidence of intravascular coagulation during 11/14 courses of L-asparaginase. Crossed immunoelectrophoresis of plasma obtained at the antithrombin nadir did not demonstrate an abnormal pattern which can be associated with an abnormal antithrombin III or an increase in antithrombin III-coagulation factor complexes. The major underlying mechanism of this depression is believed to be decreased hepatic synthesis, and the low levels of antithrombin III may be associated with an increased risk of thrombosis.
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PMID:Depression of functional and antigenic plasma antithrombin III (AT-III) due to therapy with L-asparaginase. 704 2

Three-week-old turkey poults receiving 250 micrograms/kg of dietary aflatoxin displayed prolonged prothrombin times due to decreased fibrinogen levels and depressed activity of factor II. Decreased body weights and increased mortality were also evident. Poults experiencing an Eimeria adenoeides infection had slightly increased prothrombin times that were not corrected by the addition of specific clotting factors. These birds exhibited significant reductions in total plasma protein levels. The combination of E. adenoeides and aflatoxicosis resulted in a significant depression in body weight, altered prothrombin time, and decreased levels of plasma calcium, protein, and fibrinogen. Increased mortality was also observed. E. adenoeides did not affect the hemostatic system of the turkey as severely as does aflatoxin. Turkeys were shown to be highly susceptible to aflatoxin when compared to chickens.
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PMID:Relationship between Eimeria adenoeides infection and aflatoxicosis in turkey poults. 713 9


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