**16. Medical illnesses**

#### **16.1 Inflammatory bowel disease**

The incidence of VTE among hospitalized medical patients with ulcerative colitis was 1.9% and the incidence with Crohn disease was lower (1.2%).200 Among medical patients who had neither ulcerative colitis nor Crohn disease the incidence was 1.1%.200 The relative risk of VTE among patients with ulcerative colitis compared with patients who did not have inflammatory bowel disease was 1.9 and with Crohn disease it was 1.2. Among patients younger than 40 years with ulcerative colitis, the relative risk of VTE compared with patients who did not haveinflammatory bowel disease was 2.96 and in patients younger than 40 years with Crohn disease the relative risk was 2.23.200

#### **16.2 Liver disease**

Patients with chronic liver disease (both alcoholic and nonalcoholic) seem to have a lower risk of PE than patients without liver disease,43,201 but data are inconsistent.202 Chronic liver disease may result in impaired production of vitamin-K dependent procoagulant factors.203 However, decreased production of vitamin-K dependent endogenous anticoagulants, such as protein C, protein S, and antithrombin III, may counter the hypocoagulability in such patients.203 Other prothrombotic factors may counteract the impaired production of vitamin Kdependent procoagulant factors including lupus anticoagulant, activated protein C resistance, PT20210A mutation, Factor V Leiden, MTHFR

Risk Factors of Deep Vein Thrombosis 17

From 1979 to 2005, 925,000 patients were discharged from short-stay hospitals with nephrotic syndrome and 14,000 (1.5%) had DVT (relative risk 5 1.72).211 In patients aged 18 to 39 years the relative risk for DVT was 6.81.211 Renal vein thrombosis was so uncommon that too few were reported to calculate its prevalence. Therefore, PE, if it occurs, is likely to

Sickle cell disease does not seem to be a risk factor for DVT.212 Among 1,804,000 patients hospitalized in short-stay hospitals with sickle cell disease from 1979 to 2003, 11,000 (0.61%) had a discharge diagnosis of DVT, which was not more than in African Americans without sickle cell disease (0.81%).212 Among patients with sickle cell disease, a discharge diagnosis of PE was made in 0.50% compared with 0.33% who did not have sickle cell disease. Regarding patients younger than 40 years, 0.44% had PE, whereas among patients who did not have sickle cell disease, 0.12% had PE.212 The higher prevalence of apparent PE in patients with sickle cell disease compared with African American patients the same age who did not have sickle cell disease, and the comparable prevalence of DVT in both groups, is

Systemic lupus erythematosus is believed to be independently associated with the risk of developing DVT.61 The odds ratio for DVT in patients with systemic lupus erythematosus,

Behcet disease is a rare multisystem inflammatory disorder of unknown cause.213 VTE

Review of 13 retrospective studies of patients with paroxysmal nocturnal hemoglobinuria showed a 30% prevalence of venous thrombotic events in patients from Western nations.214

PE associated with thromboangiitis obliterans (Buerger disease) is rare, and to our

Initiation of coagulation takes place when TF is exposed, such as by fibroblasts, when there is tissue damage or by cytokine-stimulated monocytes and endothelial cells216, as in sepsis. While TF is the major initiator of coagulation, endotoxin, foreign bodies, and negatively charged particles may initiate coagulation via contact system activation. TF binds to factor

be due to emboli from the lower extremities and not the renal vein.

compatible with the concept that thrombosis in situ may be present in many.

**16.7 Nephrotic syndrome** 

**16.8 Sickle cell disease** 

**16.9 Systemic lupus erythematosus** 

**16.10 Behçet disease** 

**16.12 Buerger disease** 

**17. Sepsis** 

compared with those without it, was 4.3.61

**16.11 Paroxysmal nocturnal hemoglobinuria** 

knowledge, limited to a case report.215

occurs in about one-fifth of patients with Behc¸ et disease.213

The majority was within the hepatic and mesenteric veins.214

mutation, and increased levels of factor VIII.204 Based on data from the National Hospital Discharge Survey, among 4,927,000 hospitalized patients with chronic alcoholic liver disease from 1979 to 2006, the prevalence of VTE was 0.6% and among 4,565,000 hospitalized patients with chronic nonalcoholic liver disease it was 0.9%.201 The prevalence of VTE was higher in those with chronic alcoholic liver disease than with nonalcoholic liver disease, but the difference was small and of no clinical consequence.201

Both showed a lower prevalence of VTE than in hospitalized patients with most other medical diseases. It may be that both chronic alcoholic liver disease and chronic nonalcoholic liver disease have protective antithrombotic mechanisms although the mechanisms differ.
