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Antimycobacterial Agents

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Historically, mycobacterial infections have been associated with signifi cant morbidity and mortality worldwide. In particular, Mycobacterium tuberculosis is a highly successful human pathogen, infecting one-third of the world’s population and leading to approximately 3 million deaths worldwide annually (1). The organism is unique in its ability to establish persistent infection, requiring prolonged treatment with antimicrobials in order to achieve clinical cure. In general, the goals of antituberculosis therapy include rapid reduction of the massive numbers of actively multiplying bacilli in the diseased host, prevention of acquired drug resistance, and sterilization of infected host tissues to prevent clinical relapse. In order to achieve these goals, currently accepted guidelines recommend administration of multiple active drugs for a minimum duration of 6 months (2). In areas where drug resistance is prevalent and resources permit, M. tuberculosis clinical isolates should be
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Antibacterials

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Antibacterial: Anything that destroys bacteria or suppresses their growth or their ability to reproduce. Heat, chemicals such as chlorine, and antibiotic drugs all have antibacterial properties. Many antibacterial products for cleaning and handwashing are sold today. Such products do not reduce the risk for symptoms of viral infectious diseases in otherwise healthy persons. This does not preclude the potential contribution of antibacterial products to reducing symptoms of bacterial diseases in the home. Cultures and antibiotic sensitivity testing are essential for selecting a drug for serious infections. However, treatment must often begin before culture results are available, necessitating selection according to the most likely pathogens (empiric antibiotic selection). Whether chosen according to culture results or not, drugs with the narrowest spectrum of activity that can control the infection should be used. For empiric treatment of serious infections that may involve any on
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Pharmacologic Treatment of Dyslipidemia

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Dyslipidemias are disorders of lipoprotein metabolism, including lipoprotein overproduction or deficiency. These disorders may be manifested by elevation of the serum total cholesterol, low-density lipoprotein (LDL) cholesterol and triglyceride concentrations, and a decrease in the high-density lipoprotein (HDL) cholesterol concentration. Epidemiologic, angiographic and postmortem studies have documented a causal relationship between elevated serum cholesterol levels and the genesis of coronary heart disease. Angiographic studies show that aggressive cholesterol reduction by a variety of methods, as opposed to dietary modifications alone, results in increased rates of plaque regression and stabilization. Treatment with cholesterol-lowering drugs appears to be accompanied by a reduction in the lipid content of atherosclerotic plaques, thereby making them more stable and less prone to rupture. The Scandinavian Simvastatin Survival Study demonstrated a 30 percent reduction in t
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Pharmacologic Treatment of Diabetes

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Patients with diabetes mellitus have a higher risk for cardiovascular heart disease (CHD) than does the general population, and once they develop CHD, mortality is higher. Good glycemic control will reduce CHD only modestly in patients with diabetes. Therefore, reduction in all cardiovascular risks such as dyslipidemia, hypertension, and smoking is warranted. The focus of this article is on therapy for dyslipidemia in patients with type 2 diabetes. Patients with the metabolic syndrome (insulin resistance) share similarities with patients with type 2 diabetes and may have a comparable cardiovascular risk profile. Diabetic patients tend to have higher triglyceride, lower high-density lipoprotein cholesterol (HDL), and similar low-density lipoprotein cholesterol (LDL) levels compared with those levels in nondiabetic patients. However, diabetic patients tend to have a higher concentration of small dense LDL particles, which are associated with higher CHD risk. Current recommendation
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Pharmacologic Treatment of Asthma

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The current concept of asthma therapy is based on a stepwise approach, depending on disease severity, and the aim is to reduce the symptoms that result from airway obstruction and inflammation, to prevent exacerbations and to maintain normal lung function. β 2 ‐Adrenoceptor agonists and glucocorticoids are at present the most effective drugs for the treatment of airway obstruction and inflammation, with theophylline, leukotriene receptor antagonists and anticholinergics as second- or third-line therapy. There are, to date, no additional or newly developed drugs available that add substantially to the current strategies or even replace β 2 ‐adrenoceptor agonists or glucocorticoids. New approaches in asthma therapy recommend drug combinations of inhaled steroids, primarily with long-acting β 2 ‐adrenoceptor agonists, based on their improved efficacy and the potential for a steroid-sparing effect. Although existing drug entities are able to control the vast majority of patients w
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Anticoagulants, Procoagulants, Fibrinolytics

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The haemostatic profile of 46 healthy, adult female llamas was evaluated and compared to a human reference plasma. The results indicate that standard laboratory reagents and procedures are suitable for the determination of procoagulant, anticoagulant and fibrinolytic analytes in llama plasma. Human recombinant tissue factor is an effective reagent for the prothrombin time assay. With this reagent, llama plasma exhibited a clotting time similar to human reference plasma. The activated partial thromboplastin time results were shorter for llama plasma than for human plasma, and there was a significant (p<0.05) increase, in the order of tenfold, in factor VIII:C activity when human plasma was used as the reference standard. The activities of other procoagulant proteins, including factor VII, IX, X and Xl, were similar irrespective of whether llama or human reference standards were used. The anticoagulant or inhibitory activity, as determined by the amounts of α2-macroglobulin
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Antiplatelet Agents

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Antiplatelet agents inhibit platelet aggregation and prevent formation of the platelet plug. Platelet plug forms in places of vascular injury to stop bleeding, and it can also cause pathological artherosclerosis and thrombosis. There are two classes of antiplatelet agents: glycoprotein platelet inhibitors and platelet aggregation inhibitors. These drugs work by different mechanisms to inhibit platelet function. Antiplatelet agents are used as treatment and prophylaxis in patients who have had myocardial infarctions or are at a high risk of other thromboembolic disorders such as stroke.
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