Gac Med Mex
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Sepsis continues to be a major cause of morbidity and mortality. Evidence is emerging from observational studies and basic science research that statins might be associated with reduced mortality in sepsis. Statins have diverse immunomodulatory and antiinflammatory properties independent of their lipid-lowering ability. ⋯ It suggests an urgent need to investigate the pharmacology of these drugs and reappraise their therapeutic indications in critically ill patients. If this finding is supported by prospective controlled trials, statins may play an important role in sepsis related mortality. By the other hand statins are significantly cheaper than other therapies that have been shown to improve outcome in sepsis, and the demonstration of mortality benefit would have enormous cost-benefit implication.
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Review Comparative Study
[Pulmonary complications of hepatic cirrhosis: portopulmonary hypertension and hepatopulmonary syndrome. The paradox of pulmonary vasoconstriction and vasodilation].
Cardiopulmonar complications in chronic liver diseases were described 100 years ago. Altough both hepatopulmonary sindrome and portopulmonary hypertension originates from liver damage, clinical findings and diagnosis are very different. ⋯ In this review we analyze the most important issues on hepatopulmonary sindrome and portopulmonary hypertension. These complications,under the cornerstone of portal hypertension are characterized by pulmonary constriction and dilatation, respectively.
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Review Comparative Study
[Hepatic fibrosis: role of matrix metalloproteases and TGFbeta].
Liver fibrosis and cirrhosis involve multiple cellular and molecular events that lead to deposition of an excess of extracellular matrix proteins and increase the distortion of normal liver architecture. Etiologies include chronic viral hepatitis, alcohol abuse and drug toxicity. Degradation of these matrix proteins occurs predominantly as a result of a family of enzymes called metalloproteases (MMPs) that specifically degrade collagenous and non-collagenous substrates. ⋯ This molecule blocks the conversion of plasminogen into plasmin, and the MMP cannot be activated. At a second level, the inhibition is possible by binding to inhibitors called TIMP that can inhibit the proteolitic activity even when the MMPs had been previously activated by plasmin. During abnormal conditions, overexpression of these inhibitors is directed by the transforming growth factor-beta that in a fibrotic disease acts as an extremely important adverse factor.
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Arginine-vasopressin (VP), also known as the antidiuretic hormone, is essential for water homeostasis. Its synthesis and liberation depends on regulation of osmotic, hypovolemic, hormonal, and nonosmotic stimuli. ⋯ Shock state with refractory vasodilation seen in sepsis, systemic inflammatory response, hypovolemia, cardiac arrest, polytrauma, etc., is characterized by an initial phase of liberation and increased levels of VP followed by a second phase characterized by inappropriately low levels of this hormone that are associated with refractoriness to management with volume, inotropics, and vasopressors. It has been demonstrated in clinical and experimental studies that exogenous VP treatment under this condition increases systemic vascular resistance, perfusion pressure, and oxygen supply to peripheral tissues, which makes it possible to decrease and to suspend vasopressors and also to increase survival.
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Cardiovascular disease is the leading cause of mortality in Mexico, as well as in other Western countries. Conventional risk factors for atherosclerosis, such as cigarette smoking, systemic hypertension, diabetes mellitus, and hypercholesterolemia, do not explain this association completely. ⋯ Elevated plasma levels of this amino acid (higher than 15 mmol/L or lower in the presence of other cardiovascular risk factors) promote the development of atherosclerosis. Folic acid and vitamin B6 and B12 supplements decrease plasma levels of homocysteine effectively and may play an important role in the prevention and treatment of atherosclerotic vascular disease.