Biomedical subjects

R García Robles

Publications and source records attributed to R García Robles.

13 recordsLinked to original sources

PubMed2004

Course of metabolic syndrome following the biliopancreatic diversion of Larrad.

BACKGROUND: The authors assessed the effect of Larrad's biliopancreatic diversion (BPD) on the main components of the metabolic syndrome. PATIENTS AND METHODS: Plasma concentrations of glucose, insulin, total cholesterol (TC), HDL and LDL cholesterol, triglycerides, LDL/HDL and TC/HDL ratios, and blood pressure and body weight were retrospectively evaluated in 40 patients 3-6, 12, 24 and 60 months after undergoing BPD for morbid obesity with metabolic syndrome. RESULTS: 3-6 months after BPD, glycemia and insulinemia had normalized in 97.5% of the patients and remained stable over the following 5 years. Over this period of 3-6 months to 5 years following BPD, total and LDL cholesterol levels fell by 45.2% and 53.1%, respectively. From 12 months onwards, triglyceride levels decreased appreciably, dropping by 57.4% at 5 years. HDL cholesterol concentrations failed to vary significantly or increased to normal levels in patients showing low initial values. At 5 years, high blood pressure had resolved in 75% of patients and the amount of excess weight lost was 65.5% (+/-14.6). No patient required reversal of the BPD due to severe gastrointestinal or metabolic complications. CONCLUSIONS: Technically adapted to the patient's weight, the Larrad BPD effectively stabilizes the main components of the metabolic syndrome. The BPD has low morbidity rate and should be considered a therapeutic option for patients who do not respond to medical treatment.

Adult↗

PubMed1998

Salt sensitivity: concept and pathogenesis.

Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, was described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the kidneys to excrete the whole intake of sodium until renal perfusion pressure (mean blood pressure) attains a level that is able to restore pressure-natriuresis relationship to values that enable the kidney to excrete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin system or endothelial function. It is also relevant that organ damage secondary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be significantly higher when compared with that of salt-resistant animals or humans. Interestingly, in humans, salt sensitivity has been shown to correlate with microalbuminuria, an important predictor of cardiovascular morbidity and mortality, which correlates with most of the cardiovascular risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high blood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypertensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanisms underlying the increase in BP, when salt intake is increased. Furthermore, therapy must preferably improve the diminished insulin sensitivity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk.

Animals↗

PubMed1998

Therapeutic implications and new perspectives for essential hypertension and renal damage.

The kidney can suffer the consequences of a persistently elevated blood pressure. In fact end-stage renal failure caused by essential hypertension appears to be one of the most prevalent etiologies in patients entering a dialysis program. Blood pressure control is needed in order to prevent the progressive loss of renal function. Target blood pressure control has been established at values as low as 125/75 mm Hg for patients with proteinuria above 1 g/day. Attainment of this target level usually requires the combination of two or more drugs. However, the possibility that differences exist among the different classes of antihypertensive drugs beyond their capacity to simply lower blood pressure remains to be clearly elucidated. The fact that the presence of chronic renal failure is also accompanied by an enhanced cardiovascular risk potentiates the need to explore the renoprotective and cardiovascular protective capacity of the different classes of antihypertensive drugs, in patients with essential hypertension and some degree of renal involvement, characterized by the presence of microalbuminuria, proteinuria and/or an elevated serum creatinine.

Antihypertensive Agents↗

PubMed1998