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Effects of Triiodothyronine-Induced Hypermetabolism on Factor VIII and Fibrinogen in Man

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Effects of Triiodothyronine-Induced Hypermetabolism on Factor VIII and Fibrinogen in Man Effects of triiodothyronine-induced hypermetabolism on factor VIII and fibrinogen in man John C. Hoak, … , Glenna L. Fry, Fred L. Benoit J Clin Invest. 1969;48(4):768-774. https://doi.org/10.1172/JCI106034. Research Article Triiodothyronine (liothyronine sodium) (400-500 μg/day for 14 days) was given to six normal subjects. Factor VIII (antihemophilic globulin) activity increased from 109 to 167% (P < 0.05); fibrinogen increased from 344 to 581 mg/100 ml (P < 0.01). To test whether the increases in factor VIII activity and fibrinogen were mediated by beta adrenergic receptors, propranolol (20 mg every 6 hr) was given orally to four other normal subjects in addition to triiodothyronine for 14 days. Factor VIII increased from 100 to 161%; fibrinogen increased from 374 to 564% (P < 0.01). Factor VIII activity did not change in a severe classical hemophiliac made hypermetabolic with triiodothyronine, but it increased from 39 to 82% in a patient with von Willebrand's disease. Triiodothyronine-induced hypermetabolism increased the incorporation of selenomethionine-75Se into plasma fibrinogen. These results suggest that the increases in clotting factor activity during triiodothyronine-induced hypermetabolism reflect an effect of increased protein synthesis rather than enhanced stimulation of beta adrenergic receptors. Find the latest version: https://jci.me/106034/pdf Effects of Triiodothyronine-Induced Hypennetabolism on Factor VIII and Fibrinogen in Man JOHN C. HoAK, WILLIAM R. WILSON, EMORY D. WARNER, ERNEST O. THEILEN, GLENNA L. FRY, and FRED L. BENOIT From the Blood Coagulation Research Laboratory and the Departments of Internal Medicine and Pathology, University of Iowa, College of Medicine, Iowa City, Iowa 52240 ABSTRACT Triiodothyronine (liothyronine sodium) roid or triiodothyronine, and the increased factor VIII (400-500 pAg/day for 14 days) was given to six normal activity in the hyperthyroid patients also returned to subjects. Factor VIII (antihemophilic globulin) ac- normal after antithyroid therapy (2). tivity increased from 109 to 167% (P < 0.05); fibrino- Simone, Abildgaard, and Schulman suggested that the gen increased from 344 to 581 mg/100 ml (P < 0.01). elevated levels of factor VIII in hyperthyroidism re- To test whether the increases in factor VIII activity and sulted from increased sensitivity to catecholamines (2). fibrinogen were mediated by beta adrenergic receptors, There is evidence in the older literature which suggests propranolol (20 mg every 6 hr) was given orally to that the cardiovascular and metabolic changes in thyro- four other normal subjects in addition to triiodothyronine toxicosis may be a manifestation of increased sensitivity for 14 days. Factor VIII increased from 100 to 161%; to catecholamines (3-5). More recent studies in ani- fibrinogen increased from 374 to 564% (P <0.01). mals and man, however, indicateothat there is no in- Factor VIII activity did not change in a severe classi- creased sensitivity to catecholamines in the hyperthyroid cal hemophiliac made hypermetabolic with triiodothyro- state, and that the cardiovascular and metabolic abnor- nine, but it increased from 39 to 82% in a patient with malities result from a direct effect of thyroid hormones von Willebrand's disease. Triiodothyronine-induced hy- (6-10). In preliminary reports, triiodothyronine-induced permetabolism increased the incorporation of seleno- hypermetabolism in normal subjects was associated with methionine-75Se into plasma fibrinogen. These results significant increases in both factor VIII and fibrinogen suggest that the increases in clotting factor activity dur- (11, 12). Since the mechanism responsible for these ing triiodothyronine-induced hypermetabolism reflect an coagulation changes was unknown,, the present studies effect of increased protein synthesis rather than enhanced were designed to test the hypothesis that triiodothyro- stimulation of beta adrenergic receptors. nine-induced hypermetabolism causes increases in these coagulation factors by enhanced stimulation of beta adrenergic receptors. The present report also involves a INTRODUCTION study of the effects of triiodothyronine upon factor VIII Elevated factor VIII activity has been reported in pa- activity in patients with congenital deficiencies of factor tients with thyrotoxicosis (1, 2). In contrast, a signifi- VIII. cant decrease in factor VIII activity and episodes of clin- ical bleeding were found in patients with hypothyroidism METHODS (2). The coagulation changes seen in hypothyroidism returned to normal after treatment with desiccated thy- Subjects. The subjects in this study were 16 men from the Iowa State Penitentiary, Fort Madison, Iowa. In addi- This work was presented in part at the annual meeting of tion, four patients at University Hospitals were studied. the Federation of American Societies for Experimental We obtained informed consent from each individual. All Biology, April 1968. subjects and patients were hospitalized in the Clinical Re- Received for publication 15 October 1968 and in revised search Center, University Hospitals, Iowa City. None had form 26 December 1968. clinical or laboratory evidence of thyroid or cardiac disease. 768 The Journal of Clinical Investigation Volume 48 1969 Each subject received a high caloric diet ranging from 2500 per cent of normal = units administered/body wt in kg X 0.4.) to 5000 calories throughout the study. One factor VIII unit is defined as the activity present in 1 Duplicate coagulation studies were done in each subject ml of fresh normal pooled human plasma with 100% factor at three separate times. The first studies were performed be- VIII activity. In addition, an incubation experiment with an fore treatment with triiodothyronine; the second set of stud- inhibitor against factor VIII was performed to compare ies was done after 14 days of treatment with triiodothyronine, the neutralizing effect of plasma from hypermetabolic sub- 400-500 ug/day; the third set of studies represented a post- jects with that of plasma taken when the subjects were treatment control and was performed 21 days after triiodo- euthyroid. thyronine had been discontinued. Body weight and radial The effect of epinephrine (4.2 Log/kg of body weight over pulse rates during sleep were measured daily. The average a 30 min period i.v.) on plasma factor VIII and fibrinogen weight and the average sleeping pulse pulse rate for the last concentrations was studied in one subject during the eu- 3 days of each period, oxygen consumption, serum cholesterol, thyroid and hypermetabolic periods and in the splenectomized and clinical evaluation were used as indexes of the subject's patient. Plasma free fatty acid concentrations were deter- metabolic state. mined by the method of Trout, Estes, and Friedberg (16). Six of the subjects received only triiodothyronine while Selenomethionine-'5Se incorporation into fibrinogen. The four subjects received the beta adrenergic blocking agent, incorporation of selenomethionine-'7Se' into plasma fibrino- propranolol, 20 mg every 6 hr orally, in addition to triiodo- gen was studied in four additional subjects. The first study thyronine. was performed when the subjects were hypermetabolic. The The effects of D-thyroxine, 3-8 mg/day orally, and L-thy- second study was done when the subjects returned to their roxine, 3 mg/day orally, upon factor VIII and fibrinogen usual metabolic state 3 wk after triiodothyronine had been concentrations were studied in two other subjects. stopped. Fasting subjects received 25 uc of selenomethionine- The effects of triiodothyronine-induced hypermetabolism 75Se intravenously at the time each study was performed. upon factor VIII activity were also studied in one patient Citrated blood samples were obtained before, 1/2, 1, 2, 3, 4, with classical hemophilia, another with von Willebrand's 6, and 24 hr after the injection of labeled methionine. disease, and in one patient who had undergone splenectomy Fibrinogen was separated by a modification of the pro- for idiopathic thrombocytopenic purpura 2 yr earlier. cedure described by McFarlane (17). Fibrinogen was first Blood samples. Blood was obtained from subjects and precipitated by addition of 11.5%o sodium sulfate solution. patients in the fasting state by venipuncture with disposable The precipitate was dissolved in saline-citrate phosphate buf- needles and plastic syringes. Blood was added immediately fer, pH 6.0, and reprecipitated with 11.5%o sodium sulfate. to citric acid-sodium citrate anticoagulant (9.6 g of citric The precipitate was then dissolved in 0.5 ml of the saline- acid, 14.7 g of sodium citrate in 100 ml of aqueous solution citrate buffer. To 0.5 ml of the resulting solution, 10 U of titrated to pH 4.7) in a siliconized glass centrifuge tube in thrombin, 0.2 ml of 0.25 M calcium chloride, and 125 mg of a ratio of 9.9 parts blood to 0.1 part anticoagulant. The epsilon aminocaproic acid were added. The fibrin clot which blood was then centrifuged for 20 min at 4000 rpm at 40C in formed was washed three times with 0.9% saline and then an International refrigerated centrifuge. The plasma was was dissolved in 1 ml of 10%o sodium hydroxide and was separated immediately and transferred to siliconized glass heated in a water bath at 100'C for 10 min. After cooling, tubes. The plasma was frozen and stored at - 200C. The pH the sample's radioactivity was determined by use of a of the stored plasma was 7.4. Samples were tested within 48 Picker well-counter. The fibrinogen content of the counted hr. sample
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