Introduction: the causal linkCardiovascular diseases (CVDs) are a major cause of morbidity and mortality throughout the world. In the United States, CVDs affect many racial or ethnic groups, and this fact has an extremely high cost that is estimated around $200 billion annually in healthcare services, drugs, and loss of productivity. Much of this burden is due to insufficient implementation of prevention strategies and poor control of atherosclerotic cardiovascular disease (ASCVD) risk factors in many adults (1,2). According to World Health Organization data, smoking determines 10% of all CVDs (3). Tobacco smoking usage causes approximately 6 million death per year throughout the world, in the United States almost 500,000 deaths can be attributed to smoking and about 10% of these deaths are caused from second-hand smoke exposure. Epidemiologic studies have supported the assumption that cigarette smoking increases the incidence of myocardial infarction and fatal coronary artery diseases (4). The increased risk of cardiovascular events has also been shown for low-tar cigarettes and smokeless tobacco. Even passive smoking is responsible for a 30% increased risk of ASCVD, a little less than half of the risk increase in active smokers that is around 80% (5,6). Ever since the Framingham study, the epidemiologic investigations have tried to identify people with a high likelihood for a future cardiovascular events in order to make actionable interventions to reduce the risk. The concept of "risk factors" was made popular by Kannel et Review Article on Improving Outcomes in Lung Cancer Through Early Diagnosis and Smoking Cessation

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Warm-type idiopathic autoimmune hemolytic anemia (AIHA) is a relatively common hematologic disorder resulting from autoantibody production against red blood cells. Steroids represent the first-line therapeutic option, and immunosuppressive agents as well as splenectomy are used for refractory cases. Recently, the anti-CD20 monoclonal antibody rituximab has been shown to control autoimmune hemolysis in patients with refractory chronic disease. We report results from a retrospective analysis of 11 adult patients receiving rituximab for steroid-refractory AIHA of the warm type at a mean age of 55 yr (range 23-81 yr). All patients were given methyl-prednisolone as first-line treatment and some of them also received azathioprine and intravenous high-dose immunoglobulins. One patient underwent splenectomy. All patients were considered refractory to steroids and/or immunosuppressive drugs and all were then given weekly rituximab (375 mg/m(2)) for four consecutive weeks. An increase in hemoglobin (Hgb) levels in response to rituximab, with a mean increment of 3.3 g/dL (95% CI 2.1-4.4), was observed in all cases. Four patients required packed red cell transfusions before starting rituximab and all became transfusion-free. At a mean follow-up of 604 d (range 30-2884 d) since the treatment of AIHA with rituximab, all patients are alive, eight (73%) of them in complete remission (CR) and three (27%) in partial remission (PR). A moderate hemolysis still persisted in six (54%) patients. In conclusion, our experience clearly demonstrates that anti-CD20 monoclonal antibody rituximab is an effective and safe alternative treatment option for idiopathic AIHA, in particular, for steroid-refractory disease.

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