Effect of Corticosteroids upon Fibrinogen Metabolism in Rabbits

Seligsohn, Uri; Rapaport, Samuel I.; Shen, Stephen; Kuefler, Paul R.

doi:10.1055/s-0038-1649131

Cited by 5 publications

(2 citation statements)

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“…In the rabbits, both ACTH preparations induced similar elevations in plasma fibrinogen and fibronectin, despite a difference in the extent and duration of the induced increase in plasma corticosterone values. The administration of pharmacological doses of corticosteroids to rabbits can increase the incorporation of [ 5Se]-methionine into fibrinogen and elevate plasma fibrinogen values (Seligsohn et al, 1973b). However, the effect of corticosteroids on fibrinogen metabolism in the rabbit is partly influenced by the presence or absence of a coexistent inflammatory stimulus (Seligsohn et al, 1973b), suggesting that, in this species also, other factors are also involved in the regulation of fibrinogen.…”

Section: Discussionmentioning

confidence: 99%

“…The administration of pharmacological doses of corticosteroids to rabbits can increase the incorporation of [ 5Se]-methionine into fibrinogen and elevate plasma fibrinogen values (Seligsohn et al, 1973b). However, the effect of corticosteroids on fibrinogen metabolism in the rabbit is partly influenced by the presence or absence of a coexistent inflammatory stimulus (Seligsohn et al, 1973b), suggesting that, in this species also, other factors are also involved in the regulation of fibrinogen. It has also been shown that, while the administration of dexamethasone to rabbits can induce a similar increase in fibrinogen and fibronectin, it is less effective than ACTH (Lichen, 1988;Licheng and Gentry, 1991).…”

Section: Discussionmentioning

confidence: 99%

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Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits

et al. 1992

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The intramuscular administration of adrenocorticotrophic hormone (ACTH) to calves, in either a short-acting form (cosyntrophin) or a longer-acting form (ACTHAR Gel), failed to induce any alteration in circulating fibrinogen or fibronectin values, despite marked elevations in plasma cortisol concentrations. With the longer-acting ACTH, plasma cortisol was elevated for at least 12 h following treatment and induced the expected physiological response of an elevation in blood glucose. In contrast, both forms of ACTH induced marked increases (p < 0.01) in plasma fibrinogen and fibronectin when administered to rabbits. The elevation in the circulating levels of these proteins was first observed 24 h after ACTH administration, by which time plasma corticosteroid values had returned to pre-treatment values. With both ACTH preparations the increases in the circulating levels of these proteins were sustained for at least 96 h. The results suggest that, in cattle, the well-recognized increases in plasma fibrinogen values following stress are not associated with the concomitant increase in plasma cortisol. Further, the results clearly illustrate the marked species differences in the response of acute-phase reactant proteins to elevated glucocorticoids.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits

et al. 1992

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Fibrinogen catabolism in systemic lupus erythematosus

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Sherman

Al‐Mondhiry

1976

Arthritis & Rheumatism

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Because there is mounting evidence that localized intravascular coagulation maycontribute to tissue injury following a variety of immunologic events, including immune complex diseases, fibrinogen catabolism was studied in patients with systemic lupus erythematosus to determine factors correlating with accelerated coagulation. 125I‐fibrinogen half‐life in controls was 80.1 ± 11 hours and the mean SLE half‐life was 60.5 ± 12. SLE patients in complete clinical remission had normal half‐lives, but patients with symptomatic clinical disease, including renal disease, had significantly reduced fibrinogen survival. Accelerated fibrinogen consumption also correlated with positive tests for anti‐DNA antibodies, but not with hypocomplementemia. These observations support the hypothesis that the coagulation system is activated in patients with immune complex diseases. Further studies are required to define the role, if any, that coagulation may play in causing tissue injury.

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Fibrinogen Turnover in Progressive Systemic Sclerosis

Gratwick

Klein

Sergent

et al. 1978

Arthritis & Rheumatism

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Large amounts of fibrin are seen in the intima of the renal arterioles in progressive systemic sclerosis (scleroderma). The half-life or half disappearance time of plasma fibrinogen in 15 patients with scleroderma was studied using '''1 fibrinogen to find whether there is an increased turnover of plasma fibrinogen paralleling this morphologic abnormality. Patients had a more rapid fibrinogen turnover than normal controls (60.7 versus 90.6 hours); the subgroup of patients with "progressive" scleroderma had a more rapid fibrinogen half-life than those with "stable" scleroderma (56.5 versus 73.2 hours).The mean fibrinogen half-life of 8 patients given intravenous heparin increased to within one standard deviation of normal, a finding that suggested that the fibrinogen molecule in these patients was capable of normal survival. There was a considerable variation of fibrinogen half-lives in individual scleroderma patients over time (not seen in the normal controls) which may be the result of intermittently increased fibrinogen consumption. Increased amounts of fibrin are seen in renal afferent arterioles, pulmonary arterioles, and in the perivascular areas of tendon sheaths and joints in progressive systemic sclerosis (scleroderma). This fibrin can be demonstrated both morphologically as small, fibrous strands and by specific immunofluorescent anti-fibrin staining (1). The presence of fibrin is in itself not surprising; deposition of fibrin is a frequent response to inflammatory stimuli and may be found in many inflammatory states. What is distinctive about scleroderma is the large amount of fibrin present. It is considerably more than that seen in vasculitic syndromes such as lupus erythematosus, and equalled only by that seen in malignant hypertension and some of the microangiopathic hemolytic anemias (2).In this study the authors have looked at the plasma fibrinogen level and the fibrinogen half-lifewhich together permit an estimation of the fibrinogen turnover-in an attempt to find a plasma abnormality potentially corresponding to the morphologic abnormalities seen in scleroderma. Because of the large amount of fibrin seen in perivascular areas we postulated an increased fibrinogen turnover which could in turn be the result of three abnormalities: 1 ) increased excretion of fibrinogen, 2) rapid utilization of fibrinogen by an activated coagulation system, or 3) altered catabolism of fibrinogen. We have previously found that increased amounts of fibrinogen are not excreted in systemic lupus erythematosus and other vasculitic syndromes (3). Standard hematologic parameters were used to investigate the possibility of increased intra-

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Effect of Corticosteroids upon Fibrinogen Metabolism in Rabbits

Cited by 5 publications

References 0 publications

Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits

Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits

Fibrinogen catabolism in systemic lupus erythematosus

Fibrinogen Turnover in Progressive Systemic Sclerosis

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