August 21, 2010 posted by Denise Nichols
Hypercoagulation’s relationship to nonalcoholic fatty liver disease, metabolic syndrome, increase risk in Cardiovascular disease, diabetes, cadium toxicity, osteomalacia, anemia, increase risk of thrombosis, cellular thrombosis are discussed in these 6 studies.
Gulf War Veterans have you been diagnosed with Liver problems? You must realize that the liver is important in order to detoxify the body and is damaged by chemicals, heavy metals , and viruses. Gulf War veterans need to not be using alcohol, need to be aware to follow and watch liver function values that the doctors should be monitoring, and also the pharmacist and the gulf war veteran patient should closely monitor other drugs that are prescription that might have adverse effects or side effects related to the liver.
Symptoms of Liver problems include:
1. See if the patient has discoloration of skin. The skin and eyes acquire a yellowish tinge and the urine turns dark yellow. It is called jaundice and this is considered to be the primary sign of liver disease.
2. Track the patient’s diet. Loss of appetite leading to weight loss is indicative of liver dysfunction. The patient may become anemic and have a nauseating feeling.
3. Check for light colored stools as it indicates the beginning of liver disorder. A liver patient may also complain of irritable bowels or irregular bowel movements.
4. Find out if there is distended abdomen. Swelling under the right lower ribs is a common complaint of liver patients. It can put severe pressure on the diaphragm that results in painful breathing.
5. Examine the shape and appearance of the nails. Curved and whitish look of nails also suggests a liver problem.
6. Notice nose bleeding and easy bruises as it shows liver abnormality and deficiency of proteins.
7. Test for polydipsia and polyuria-excessive thirst and frequent urination can occur in case of a liver disease.
8. Frequent headaches, dizziness, spasms, irritability, depression and so on are also indicative of liver problem.
9. Other items to watch for:
--Itchy skin that doesn’t seem to go away
--Dark urine color
--Bloody or tar-colored stool
--Chronic fatigue
Here are the 6 research studies:
1. Clin Liver Dis. 2009 Feb;13(1):109-16.
Hypercoagulation in liver disease.
Northup PG. Division of Gastroenterology and Hepatology, University of Virginia Health System, JPA and Lee Streets, MSB 2142, Charlottesville VA 22908-0708, USA. pgn5qs@virginia.edu
Abstract
The coagulopathy of liver disease is complex and often unpredictable. Despite clear evidence of an increased tendency for bleeding in patients who have cirrhosis, many circumstances also promote local and systemic hypercoagulable states. The consequences of hypercoagulability include the obvious morbidity and mortality of portal vein thrombosis, deep vein thrombosis, and pulmonary embolism, but possibly also include other end-organ syndromes, such as portopulmonary hypertension, hepatorenal syndrome, and spontaneous bacterial peritonitis. A more subtle contribution also could be responsible for progression of early fibrosis to decompensated cirrhosis. Future research is needed to elucidate specific mechanistic pathways that might lead to local hypercoagulation and the clinical interventions that might prevent morbidity and mortality related to hypercoagulation in patients who have cirrhosis.
PMID: 19150315 [PubMed - indexed for MEDLINE]
2. Semin Thromb Hemost. 2009 Apr;35(3):277-87. Epub 2009 May 18.
Nonalcoholic fatty liver disease as a contributor to hypercoagulation and thrombophilia in the metabolic syndrome.
Targher G, Chonchol M, Miele L, Zoppini G, Pichiri I, Muggeo M. Department of Biomedical and Surgical Sciences, University of Verona, Italy. giovanni.targher@univr.it
Comment in:
Semin Thromb Hemost. 2009 Apr;35(3):257-9.
Abstract
Nonalcoholic fatty liver disease (NAFLD), comprising its whole spectrum of conditions ranging from simple steatosis to steatohepatitis (nonalcoholic steatohepatitis; NASH) and cirrhosis, is the most frequent liver disease in developed countries and is now regarded as the liver manifestation of the metabolic syndrome. Several studies indicate that NAFLD, especially in its necro-inflammatory form (NASH), is associated with a systemic proinflammatory/prothrombotic state, independently of shared metabolic risk factors. This suggests that NAFLD/NASH is not simply a marker of the proinflammatory/prothrombotic state in the metabolic syndrome but is actively involved in its pathogenesis, possibly through the systemic release of proinflammatory and procoagulant factors from the steatotic liver (C-reactive protein, plasminogen activator inhibitor-1, interleukin-6, fibrinogen, and other proinflammatory cytokines). The clinical impact of NAFLD on the proinflammatory/prothrombotic risk profile deserves particular attention in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD.
PMID: 19452403 [PubMed - indexed for MEDLINE]
3. Diabetologia. 2008 Nov;51(11):1947-53. Epub 2008 Sep 2.
Increased risk of cardiovascular disease in non-alcoholic fatty liver disease: causal effect or epiphenomenon?
Targher G, Marra F, Marchesini G.
Department of Biomedical and Surgical Sciences, University of Verona, Ospedale Civile Maggiore, Verona, Italy. giovanni.targher@univr.it
Abstract
Non-alcoholic fatty liver disease (NAFLD), comprising a spectrum of conditions ranging from pure steatosis to steatohepatitis and cirrhosis, has reached epidemic proportions and represents the most common cause of chronic liver disease in the community. The prevalence of NAFLD has been estimated to be between 20% and 30% in the general population, but this value is much higher ( approximately 70-80%) in type 2 diabetic patients, who are also at higher risk of developing advanced fibrosis and cirrhosis. Increasing recognition of the importance of NAFLD and its strong relationship with the metabolic syndrome has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Several epidemiological studies indicate that NAFLD, especially in its more severe forms, is linked to an increased risk of CVD, independently of underlying cardiometabolic risk factors. This suggests that NAFLD is not merely a marker of CVD, but may also be actively involved in its pathogenesis. The possible molecular mediators linking NAFLD and CVD include the release of pro-atherogenic factors from the liver (C-reactive protein, fibrinogen, plasminogen activator inhibitor-1 and other inflammatory cytokines) as well as the contribution of NAFLD per se to whole-body insulin resistance and atherogenic dyslipidemia, in turn favouring CVD progression. The clinical impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD.
PMID: 18762907 [PubMed - indexed for MEDLINE]
4. J Thromb Haemost. 2008 Jan;6(1):2-9. Epub 2007 Sep 24.
Hypercoagulation and thrombophilia in liver disease.
Northup PG, Sundaram V, Fallon MB, Reddy KR, Balogun RA, Sanyal AJ, Anstee QM, Hoffman MR, Ikura Y, Caldwell SH; Coagulation in Liver Disease Group. Division of Gastroenterology and Hepatology, University of Virginia Health System, Charlottesville, VA 22908-0708, USA. pgn5qs@virginia.edu
Abstract
A complex balance exists between endogenous procoagulants and the anticoagulant system in liver disease patients. Hypercoagulable events occur in cirrhosis patients despite the well-known bleeding diathesis of liver disease. These events may be clinically evident, such as in portal vein thrombosis or pulmonary embolism, but these conditions may also be a silent contributor to certain disease states, such as portopulmonary hypertension or parenchymal extinction with liver atrophy as well as thrombosis of extracorporeal circuits in dialysis or liver assist devices. Moreover, liver disease-related hypercoagulability may contribute to vascular disease in the increasingly common condition of non-alcoholic fatty liver disease. Despite the incidence of these problems, there are few widely accessible and practical laboratory tests to evaluate the risk of a hypercoagulable event in cirrhosis patients. Furthermore, there is little research on the use of commonly accepted anticoagulants in patients with liver disease. This article is a result of an international symposium on coagulation disorders in liver disease and addresses several areas of specific interest in hypercoagulation in liver disease. Critical areas lacking clinical information are highlighted and future areas of research interest are defined with an aim to foster clinical research in this field.
PMID: 17892532 [PubMed - indexed for MEDLINE]
5. Pathophysiol Haemost Thromb. 2006;35(6):411-6.
The effects of chronic cadmium toxicity on the hemostatic system.
Koçak M, Akçil E. Department of Pathophysiology, Faculty of Medicine, Ankara University, Ankara, Turkey. mkocak@epdk.org.tr
Abstract
Cadmium, a highly toxic heavy metal, is distributed widely in the general environment. The characteristic clinical manifestations of chronic cadmium intoxication include renal proximal tubular dysfunction, osteomalacia and anemia. Accumulating evidence suggests that cadmium toxicity may also affect various organs such as the liver, lung, testis and hematopoietic system. The aim of this study was to determine the effect of chronic cadmium exposure on the anticoagulant system in rats. Fourty-five adult Wistar albino rats were randomly allocated into 2 groups. While the control group was given tap water, the animals in the cadmium group were treated with 15 ppm CdCl(2) for 4 weeks. Blood cadmium concentration, prothrombin time, activated partial thromboplastin time, plasma protein C and antithrombin activity, and platelet count were determined in the rats. Blood cadmium concentrations increased in the experiment group compared to the control group (p < 0.001). Results also show that cadmium exposure shortened prothrombin time (p < 0.05) and activated partial thromboplastin time (p < 0.01) in rats. Protein C (p < 0.001) and antithrombin (p 0.05). In conclusion, when the parameters of the hemolytic system are considered, the decrease in protein C and antithrombin activities and the shortening of prothrombin time and activated partial thromboplastin time suggests the presence of a hypercoagulable state during chronic cadmium intoxication. Therefore, it may be stated that chronic cadmium toxicity sets the stage for hypercoagulation and hence increases the risk of thrombosis.
PMID: 17565233 [PubMed - indexed for MEDLINE]
6. Cell Biochem Funct. 2006 Mar-Apr;24(2):173-92.
Tissue factor upregulation drives a thrombosis-inflammation circuit in relation to cardiovascular complications.
Chu AJ. Surgery Department, Wayne State University, Detroit, MI 48201, USA. ajchu91@hotmail.com
Abstract
The extrinsic coagulation is recognized as an ‘inducible’ signalling cascade resulting from tissue factor (TF) upregulation by exposure to clotting zymogen FVII upon inflammation or tissue injury. Following the substantial initiation, an array of proteolytic activation generates mediating signals (active serine proteases: FVIIa, FXa and FIIa) that lead to hypercoagulation with fibrin overproduction manifesting thrombosis. In addition, TF upregulation plays a central role in driving a thrombosis-inflammation circuit. Coagulant mediators (FVIIa, FXa and FIIa) and endproduct (fibrin) are proinflammatory, eliciting tissue necrosis factor, interleukins, adhesion molecules and many other intracellular signals in different cell types. Such resulting inflammation could ensure ‘fibrin’ thrombosis via feedback upregulation of TF. Alternatively, the resulting inflammation triggers platelet/leukocyte/polymononuclear cell activation thus contributing to ‘cellular’ thrombosis. TF is very vulnerable to upregulation resulting in hypercoagulability and subsequent thrombosis and inflammation, either of which presents cardiovascular risks. The prevention and intervention of TF hypercoagulability are of importance in cardioprotection. Blockade of inflammation reception and its intracellular signalling prevents TF expression from upregulation. Natural (activated protein C, tissue factor pathway inhibitor, or antithrombin III) or pharmacological anticoagulants readily offset the extrinsic hypercoagulation mainly through FVIIa, FXa or FIIa inhibition. Therefore, anticoagulants turn off the thrombosis-inflammation circuit, offering not only antithrombotic but anti-inflammatory significance in the prevention of cardiovascular complications.
PMID: 15617024 [PubMed - indexed for MEDLINE]
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- ISAC Panel (Fibrinogen Activity, Prothrombin Fragment 1+2, Thrombin/Antithrombin Complex, PA by Flow)320020 – Hypercoagulation Panel (No Meds) (Antithrombin Activity, Protein C Activity, Protein S Activity, Activated Protein C Resistance, Fibrinogen Activity, Prothrombin Time/INR, Activated Partial Thromboplastin Time, Dilute Russell’s Viper Venom Time Screen, Dilute Russell’s Viper Venom Time Confirm, Lipoprotein (a), Homocysteine, Factor II Mutation, Platelet Activation by Flow) Note: May include PNP, PT Mixing Study, and/or aPTT Mixing Study
Source
Also See: Original Hypercoagulation Study on Gulf War Veterans
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