Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
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Protein C deficiency can lead to cerebrovascular occlusive disease. We describe a patient in whom heterozygous protein C deficiency (type 1) is suspected on the grounds of reduced protein C activity and who suffered from multiple thrombo-embolic events involving the brain and peripheral organs. The patient developed hypothalamic failure with hypernatraemia, hypodipsia, hypersomnolence and hyperkapnia, obesity, hyperprolactinaemia, hypogonadotropic hypogonadism and growth hormone deficiency. We hypothesize that protein C deficiency caused cerebrovascular occlusions which eventually led to hypothalamic insufficiency in this patient. Disorders of the anticoagulant system should be looked for in patients with unexplained hypothalamic disease.
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PMID:Hypothalamic failure as a sequela of heterozygous protein C deficiency? 162 70

It is well known that in thrombotic disease the alteration of biological factors such as antithrombin III, protein C, and protein S deficiency, and congenital disfibrinogenimias and displasminogenemias are determining factors being the acquired alterations not so well known. With this in mind was studied 85 patients with arterial thrombosis and 196 with venous thrombosis, who were again divided into three groups: unique or of repetition, less or more than 35 years and with or without immediate apparent cause. The general clinical-biological profile in patients with thrombosis in whom a congenital deficit is not detected, can help establish prognosis and treatment in these patients. In our patients, together with the importance of factors such as obesity, hyperlipemia, and tabaquism, an increase in fibrinogen (Fg), antigenic Factor VII (vWF:Ag), total protein S is observed as well as a decrease in total fibrinolytic activity related to an increase in the inhibitor of the plasminogen tissue activator (PTA).
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PMID:[Hemostasis profiles in thrombotic disease]. 178 55

Postoperative deep-vein thrombosis can lead to fatal pulmonary embolism on one side, and the development of a disabling postthrombotic syndrome, which can occur after some time. General thrombo-embolic prophylaxis can reduce the risk of postoperative thrombo-embolic complications. Predisposing factors include age, obesity, immobilization and recumbency. Cardiovascular diseases, malignant neoplasms, venous disorders, diseases associated with increased viscosity of blood, past deep-vein thrombosis and pulmonary embolisms, some infectious diseases with raised fibrinogen levels, and inherited or acquired clotting factor deficiency syndromes (antithrombin III, protein C, protein S) have an elevated risk of thrombosis. The surgery itself, when taking more than 20 minutes and performed under general anesthesia, is a major risk factor, as proven initiation of thrombosis is often on the operation table. Patients receiving regional or local anesthesia have a clearly reduced risk of thrombosis. After general surgery without thrombosis prophylaxis, a deep-vein thrombosis can be demonstrated by the fibrinogen uptake test in about 30% of all patients over the age of 40. After abdominal surgery an incidence of thrombosis of 14-33%, and after hip surgery an incidence of nearly 50%, have been established by means of the fibrinogen uptake test. However only 10% of these thromboses are expressed clinically. We therefore recommend Liquid Crystal Contact Thermography, which has a sensitivity of 94% and a specificity of over 80%, as a non-invasive, easily performed screening method in the diagnosis of deep-vein thrombosis. Apart from the physical methods, the use of heparin is also indicated in thrombo-embolic prophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The thrombo-embolic risk in surgery. 193 69

The pre-surgery identification of patients at risk for the development of post-operative venous thromboembolism has not yet been achieved. It is a well recognized fact that major surgery without prophylaxis encompasses a high risk for thrombosis, in particular orthopaedic operations (hip/knee surgery approximately 50%) and abdominal surgery (approximately 20%). Other well-defined risk factors, though rarely occurring, are deficiencies of the major inhibitors of blood coagulation (i.e. protein C, protein S and antithrombin III). Less well-defined risk factors are a history of previous thrombosis, obesity, varicosis, cancer etc. In an attempt to identify patients at risk for thrombosis prior to surgery, several investigators have developed complicated risk predictors, i.e. formulae comprising combinations of coagulation test results and physical characteristics such as body weight. However, the clinical usefulness has only been demonstrated in two small studies evaluating gynaecological surgery patients. These prognostic indices have not, however, found general acceptance and are not used routinely. The importance of all these risk factors for patient management with regard to thrombosis prevention is relatively small. Irrespective of the absence or presence of identified risk factors, currently the majority of patients will receive some formal thrombosis prophylaxis. The major problem at present is the development of proximal vein thrombosis despite the best possible thrombosis prophylaxis (approximately 10% after hip surgery). Identification of these patients pre-operatively or in an early stage in the post-operative phase by single screening tests should be a major research issue. Furthermore, the development of a prophylactic regimen which eliminates proximal deep vein thrombosis is still desperately needed.
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PMID:Pre-surgical identification of the patient at risk for developing venous thromboembolism post-operatively. 228 76

We studied 30 control women and 131 pill users to evaluate effects of birth control pills and clinical factors on hemostasis. When control patients were matched with an equal number of pill users, none of the direct markers of activated hemostasis (fibrinopeptide A, platelet factor 4, and beta thromboglobulin) were increased. Plasminogen, prekallikrein, and protein C (protective against clotting) were significantly higher in pill users. Fibrinogen, antithrombin, alpha-2 antiplasmin, and fibronectin were comparable. Among the 131 pill users, antithrombin levels decreased with a family history of thromboembolism. Fibrinogen and fibronectin were increased with obesity, but there was no evidence of activated hemostasis. Overall, pill use did not appear to result in hypercoagulability. Considering family history of thromboembolism might further improve the safety of oral contraceptive use.
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PMID:Oral contraceptives and the hemostatic system. 335 50

In 24 women using oral contraceptives, protein C antigen was higher than in 24 women of the same age and of the same degree of obesity who were not using OC. In the pooled data for all 48 women, there was an increase in protein C of about 1% (of standard) for each 1.0 mm increase in skinfold thickness. Protein C tends to be high rather than low in circumstances predisposing to thrombosis.
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PMID:Effects of oral contraceptives and obesity on protein C antigen. 383 5

The authors define pro-thrombotic states as conditions associated with a high frequency of thrombosis; this association is based on pathogenetic or simply clinical and epidemiological relationships. Thrombophilic states have well-defined, specific causes: antithrombin III, protein C and S and similar deficiencies for inherited thrombophilias, and lupus anticoagulant, antiphospholipid antibodies for the acquired forms. Another identifiable group is made up of several conditions predisposing to thrombosis (CPT) characterized by less specific and multiple mechanisms (e.g. malignancy, inflammatory bowel disease, nephrotic syndrome, diabetes, obesity, etc.). These conditions may induce thrombosis by themselves or contribute to its clinical onset in patients with true thrombophilic states. This is especially the case for patients who are taking contraceptive drugs, are pregnant, have undergone surgery or trauma. The term hypercoagulability states is by no means equivalent to either thrombophilia or CPT. In fact, hypercoagulability may be defined as "activation of blood coagulation" in the presence of specific markers such as fibrinopeptide A and prothrombin fragment F1 + 2. Hypercoagulability is therefore a laboratory rather than a clinical condition and can be a transient feature appearing during certain phases of thrombophilia or CPT. Lastly, conditions involving the presence of hemostatic risk factors for atherothrombosis are simply terms used to describe a statistical-epidemiological relationship between certain hemostatic variables (fibrinogen, factor VII, PAI, etc.) involving the risk of cardiovascular morbidity and mortality but not necessarily indicating a hypercoagulability state.
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PMID:Pro-thrombotic states and their diagnosis. 800 87

There are a number of predisposing factors to thrombosis. Blood stasis and hypercoagulability are two important factors for the development of venous thrombosis. Several clinical situations are associated with these two factors. Congenital deficiencies in antithrombin III, protein C or protein S, the antiphospholipid antibodies represent well established risk factors. Arterial hypertension, dyslipidemia, tobacco, diabetes and obesity represent risk factors for arterial thrombosis. Hypofibrinolysis high levels fibrinogen and factor VII increases the risk of arterial thrombosis.
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PMID:[Predisposing factors for thrombosis]. 833 21

Little is known about the pattern of Deep Vein Thrombosis in Saudi Arabia. Over 4 year period, 62 cases with strong evidence of venous thrombosis were studied in King Abdulaziz University and King Fahad Hospitals to learn the pattern of deep vein thrombosis in Jeddah, Western Saudi Arabia. There were 32 females and 30 males. The mean age of the group was 36.0 years (range 6-90 years). One or more risk factors was/were detected in 40 patients. Among these 14 factors, age more than 50 years, obesity, vasculitis, malignancy and postpartum were the common factors encountered. In other 22 patients, no risk factor was found. However, extensive laboratory search diagnosed 9 rare disorders out of these 22 cases. Antithrombin III, protein C, protein S deficiencies in 5, 2, 1 patients, consecutively. The last patient had significantly shortened PTT. The other 13 (21.0%) patients were considered real idiopathic DVT. Extremities were involved in 54 patients compared to only 8 cases with inferior vena cava or visceral thrombosis. The upper limb was affected in only 10 patients unlike the lower limb which was more commonly affected n = 37.
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PMID:Pattern of deep venous thrombosis in Jeddah area, western Saudi Arabia. 837 13

Based on previous cross-sectional findings, we hypothesized that weight loss could improve several hemostatic factors associated with cardiovascular disease. In a randomized controlled trial, moderately overweight men and women were assigned to one of four weight loss treatment groups or to a control group. Measurements of plasminogen activator inhibitor-1 (PAI-1) antigen, tissue-type plasminogen activator (t-PA) antigen, D-dimer antigen, factor VII activity, fibrinogen, and protein C antigens were made at baseline and after 6 months in 90 men and 88 women. Net treatment weight loss was 9.4 kg in men and 7.4 kg in women. There was no net change (p > 0.05) in D-dimer, fibrinogen, or protein C with weight loss. Significant (p < 0.05) decreases were observed in the combined treatment groups compared with the control group for mean PAI-1 (31% decline), t-PA antigen (24% decline), and factor VII (11% decline). Decreases in these hemostatic variables were correlated with the amount of weight lost and the degree that plasma triglycerides declined; these correlations were stronger in men than women. These findings suggest that weight loss can improve abnormalities in hemostatic factors associated with obesity.
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PMID:Impact of weight loss on plasminogen activator inhibitor (PAI-1), factor VII, and other hemostatic factors in moderately overweight adults. 842 53


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