Síndrome de Lemmel en paciente geriátrico: a propósito de un caso / Lemmel syndrome in a geriatric patient: presentation of a case

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[STOP-BANG, a useful and easy tool for the screening of obstructive sleep apnea]. / STOP-BANG, una herramienta útil y sencilla para el cribado del síndrome de apneas hipopneas obstructivas del sueño.

The STO-BANG questionnaire, S standing for snore, T tired, O observed apneas, P pressure (arterial hypertension), B BMI (body mass index > 35 kg/ m2), A age (> 50 years old), N neck circumference (> 40 cm), G gender (male); is a simple tool that enables the detection of patients with obstructive sleep apnea syndrome (OSA). If the patient adds 3 or more points, it is considered to have a high probability of having this disease. Our goal was to evaluate the capacity of the STOP-BANG questionnaire and to compare it with the ability of a sleep trained pulmonologist in determining the probability of OSA. A retrospective analysis of 327 patients suspected of having this condition was performed. One hundred and seventy-one were males (52.3%), 49.8 years old (37.9-61.7), BMI 38.7 kg/m2 (32.5-46), neck circumference 44 cm (41-47.5), 311 snorers (95.1%), 232 with daytime sleepiness or usual tiredness (70.9%), 206 with observed apneas (63%), 169 with arterial hypertension (51.7%), normal polysomnography 42 (12.9%), mild 65 (19.9%), moderate 59 (18%), severe 161 (49.2%). The STOP-BANG's sensibility and specificity, taking as a cut-off point a respiratory disturbance index (RDI) > or = to 15, was 99.1% and 14.0% respectively, area under curve (AUC) 0.755 (0.704-0.800), the values for the PR actioner's ability were 89.1% and 58.9% respectively, AUC 0.550 (0.542-0.638). The STOP-BANG questionnaire is easy to implement as a screening tool.

STOP-BANG, una herramienta útil y sencilla para el cribado del síndrome de apneas hipopneas obstructivas del sueño / STOP-BANG, a useful and easy tool for the screening of obstructive sleep apnea

El cuestionario STOP-BANG, del acrónimo en inglés S snore (ronquido), T tired (cansancio), Oobserved apneas (apneas observadas), P pressure (hipertensión arterial), B BMI (índice de masa corporal >35 kg/m2), A age (edad > 50 años), N neck (circunferencia del cuello > 40 cm) y G gender (sexo masculino), es una herramienta sencilla que permite detectar pacientes con síndrome de apneas/ hipopneas obstructivas del sueño (SAHOS). Si el paciente suma 3 o más puntos se considera que tiene una alta probabilidad de padecerlo. El objetivo de nuestro trabajo fue evaluar la capacidad del cuestionario STOP-BANG y compararla con la habilidad del médico neumonólogo capacitado en sueño para determinar la probabilidad de tener SAHOS. Se analizaron en forma retrospectiva 327 pacientes con sospecha de esta condición. Sexo masculino 171 (52.3%), edad 49.8 (37.9-61.7) años, índice de masa corporal (IMC) 38.7 (32.5-46) kg/m², circunferencia del cuello 44 (41-47.5) cm, roncadores 311 (95.1%), con somnolencia o cansancio 232 (70.9%), con apneas observadas 206 (63%), HTA 169 (51.7%), polisomnografía (PSG) normal 42 (12.9%), leve 65 (19.9%), moderada 59 (18%) y grave 161 (49.2%). La sensibilidad y especificidad del STOP-BANG, tomando como punto de corte un índice de perturbación respiratoria (IPR) = 15, fueron 99.1% y 14.0%, área bajo la curva (ABC) 0.755 (0.704-0.800), las de la habilidad del médico fueron 89.1% y 58.9%, ABC 0.550 (0.542-0.638). El STOP-BANG es una herramienta de fácil aplicación para el cribado de pacientes con sospecha de SAHOS.

The STO-BANG questionnaire, S standing for snore, T tired, O observed apneas, P pressure (arterial hypertension), B BMI (body mass index > 35 kg/ m2), A age (> 50 years old), N neck circumference (> 40 cm), G gender (male); is a simple tool that enables the detection of patients with obstructive sleep apnea syndrome (OSA). If the patient adds 3 or more points, it is considered to have a high probability of having this disease. Our goal was to evaluate the capacity of the STOP-BANG questionnaire and to compare it with the ability of a sleep trained pulmonologist in determining the probability of OSA. A retrospective analysis of 327 patients suspected of having this condition was performed. One hundred and seventy-one were males (52.3%), 49.8 years old (37.9-61.7), BMI 38.7 kg/m² (32.5-46), neck circumference 44 cm (41-47.5), 311 snorers (95.1%), 232 with daytime sleepiness or usual tiredness (70.9%), 206 with observed apneas (63%), 169 with arterial hypertension (51.7%), normal polysomnography 42 (12.9%), mild 65 (19.9%), moderate 59 (18%), severe 161 (49.2%). The STOP-BANG´s sensibility and specificity, taking as a cut-off point a respiratory disturbance index (RDI) > or = to 15, was 99.1% and 14.0% respectively, area under curve (AUC) 0.755 (0.704-0.800), the values for the PR actioner's ability were 89.1% and 58.9% respectively, AUC 0.550 (0.542-0.638). The STOP-BANG questionnaire is easy to implement as a screening tool.

Bile acids content in brain of common duct ligated rats.

INTRODUCTION: Cholestasis leads to liver cell death, fibrosis, cirrhosis, and eventually liver failure. Bile duct ligated rats constitute an interesting model to study the mechanism of cholestasis, and its action on several organs and tissues, including the brain. AIM: To analyze brain bile acids individually in ligated rats to evaluate if its profile is altered towards a more toxic condition in cholestasis. MATERIAL AND METHODS: Male Wistar rats were used and separated in two groups: bile duct ligated rats and sham operated rats (n = 5 in each group). Bile acid profile was assessed in brain homogenates. Alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase determinations, bilirubin and ammonia plasma concentration were also measured in both groups. RESULTS: Although the total amount of bile acids in control animal brains showed a higher concentration than in bile duct ligated rats, the bile acid profile in this group was found more toxic composition than in controls. Lithocholic acid was present in brain in higher concentration (87.4 % of total brain bile acids) in ligated rats and absent in controls. Alkaline phosphatase, bilirubin and ammonia were significantly higher in bile duct ligated rats than in control group. CONCLUSION: It was found a toxic brain bile acid profile during hepatic cholestasis which could be one of the explanations of hepatic encephalopathy observed in cholestatic diseases.

Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress.

This review addresses recent and not so recent works that emphasize on the mechanisms by which liver damage can induce encephalopathy. Hepatic encephalopathy constitutes an intriguing complication in severe liver acute and chronic disease, whose pathophysiology is still not completely understood. In this pathology, alterations in normal brain function are associated with morphological and functional impairments of astrocytes and neurons. A wide spectrum of psychoneurological symptoms has been described and the anatomical substratum is usually associated with brain edema and intracranial hypertension, as well as with changes in the function of brain cells. An increase in blood ammonia, toxic to the brain, depends on the activity of the enzyme glutamine synthetase, the glutamine/glutamate cycle and the brain capacity to eliminate toxic substances. When the concentration of the excitotoxic neurotransmitter glutamate is increased, it acts as a toxic agent, especially when its specific transporters are altered and its uptake is decreased. Glutamine has also been recently considered a toxic substance when its concentration is high, and consequently contributes to brain edema. Finally, the formation of reactive oxygen species, basically produced by mitochondria, influence with their toxic action on membrane lipids, proteins and DNA. In conclusion we suggest that at least these four elements are involved directly in the mechanism of hepatic encephalopathy.

Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats.

AIM: To study glutamine synthetase (GS) activity and glutamate uptake in the hippocampus and frontal cortex (FC) from rats with prehepatic portal vein hypertension. METHODS: Male Wistar rats were divided into sham-operated group and a portal hypertension (PH) group with a regulated stricture of the portal vein. Animals were sacrificed by decapitation 14 d after portal vein stricture. GS activity was determined in the hippocampus and FC. Specific uptake of radiolabeled L-glutamate was studied using synaptosome-enriched fractions that were freshly prepared from both brain areas. RESULTS: We observed that the activity of GS increased in the hippocampus of PH rats, as compared to control animals, and decreased in the FC. A significant decrease in glutamate uptake was found in both brain areas, and was more marked in the hippocampus. The decrease in glutamate uptake might have been caused by a deficient transport function, significantly and persistent increase in this excitatory neurotransmitter activity. CONCLUSION: The presence of moderate ammonia blood levels may add to the toxicity of excitotoxic glutamate in the brain, which causes alterations in brain function. Portal vein stricture that causes portal hypertension modifies the normal function in some brain regions.

Involvement of serum apolipoprotein AI and B100 and lecithin cholesterol acyl transferase in alcoholic cirrhotics.

Lipoproteins are synthesized by the liver and secreted to plasma. Chronic alcoholic intoxication produces frequently cirrhosis and concomitantly alterations in liver metabolism. Thirty patients with alcoholic cirrhosis and 83 healthy controls were selected for this study. Apolipoprotein A1, B100, lecithin cholesterol acyltransferase, responsible for cholesterol esterification and seudocholinesterase enzyme activity not related to lipid metabolism, as a referent of proteins synthesized by the liver were analyzed. In 7 patients serum tiobarbituric acids, catalase, glutathione peroxidase were measured, as exponent of the presence of oxidative stress. Our results showed a significant decrease in lipoproteins, lecithin cholesterol acyltransferase and seudocholinesterase activities. An increase in serum tiobarbituric acids and a decrease in both antioxidant enzymes were found as well. In conclusion, alcohol cirrhotic liver decreases the production of liver proteins including those related to lipid metabolism, allowing the formation of steatosis and/or necrosis. Moreover oxidative stress participate possible as a major mechanism in liver damage.

Effects of six months losartan administration on liver fibrosis in chronic hepatitis C patients: a pilot study.

AIM: To evaluate the safety and efficacy of chronic administration of losartan on hepatic fibrosis in chronic hepatitis C patients. METHODS: Fourteen patients with chronic hepatitis C non-responders (n = 10), with contraindications (n = 2) or lack of compliance (n = 2) to interferon plus ribavirin therapy and liver fibrosis were enrolled. Liver and renal function test, clinical evaluation, and liver biopsies were performed at baseline and after losartan administration at a dose of 50 mg/d during the 6 mo. The control group composed of nine patients with the same inclusion criteria and paired liver biopsies (interval 6-14 mo). Histological activity index (HAI) with fibrosis stage was assessed under blind conditions by means of Ishak's score. Subendothelial fibrosis was evaluated by digital image analyses. RESULTS: The changes in the fibrosis stage were significantly different between losartan group (decrease of 0.5+/-1.3) and controls (increase of 0.89+/-1.27; P<0.03). In the treated patients, a decrease in fibrosis stage was observed in 7/14 patients vs 1/9 control patients (P<0.04). A decrease in sub-endothelial fibrosis was observed in the losartan group. No differences were found in HAI after losartan administration. Acute and chronic decreases in systolic arterial pressures (P<0.05) were observed after the losartan administration, without changes in mean arterial pressure or renal function. CONCLUSION: Chronic AT-II type 1 receptor (AT1R) blockade may reduce liver fibrosis in patients with chronic hepatitis C.