Tabaco y peso corporal / Smoking and body weight

Resumen En esta revisión, se analiza la literatura existente en relación al tabaco y el peso corporal, su rol en el cambio de peso corporal según el consumo de tabaco o cesación de este y las diferentes alternativas farmacológicas validadas para el manejo de este problema, cada vez más prevalente.

This review analyses the existing literature regarding tobacco and body weight, its role in the change of body weight according to smoking consumption or cessation and the different pharmacological alternatives validated used to address this issue, which is everyday more prevalent

Síndrome metabólico: bases clínicas y fisiopatológicas para un enfoque terapéutico racional / Metabolic Syndrome: clinical and pathophysiological basis for a rational therapeutical approach

Regardless of the diagnostic criteria, the metabolic syndrome is found at least in 20 percent of the population. The adipose tissue plays an important role in the insulin resistance found in this syndrome. Free fatty acids released by intra-abdominal adipocytes produce an inflammatory and pro-thrombotic response and the persistence of the insulin resistance state, phenomenon termed lipotoxicity. This altered phenotype explains the development of the different components of the metabolic syndrome, such as hypertension, dyslipidemia and altered glucose metabolism. The treatment is based on weight loss and healthy lifestyle. A balanced diet, physical activity and avoidance of smoking are key management features. The use of drugs with pleiotropic effects, which inhibit the renin angiotensin aldosterone axis or acts on the peroxisome proliferators-activated receptors (PPAR) seems promising.

Hipercolesterolemia familiar heterocigota: diagnóstico molecular y terapia combinada. Caso clínico / Molecular diagnosis and combined lipid lowering therapy of heterozygous familial hypercholesterolemia: Report of one case

Heterozygous familial hypercholesterolemia affects one every 400 individuals, is caused by mutations in the LDL receptor gene and is associated with premature coronary artery disease. Nowadays, LDL cholesterol can be efficiently reduced with the new therapies to reduce blood lipids. We report a female patient who consulted in 1975, when she was 46 years old, for severe hypercholesterolemia. In 2003, a sample of leukocyte DNA was obtained and the uncommon 1705 + 1G >A mutation of the LDL receptor gene was detected. No mutations in the apolipoprotein B gene were found. The patient was treated successfully with simvastatin 80 mg/day and ezetimibe 10 mg/day and LDL cholesterol levels were reduced below 200 mg/dl.