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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the US, and obesity is the most common cause of NAFLD. Obesity and NAFLD are associated with hyperlipidemia, type 2 diabetes, and hypertension, all components of the metabolic syndrome. The purpose of this study was to examine the incidence of NAFLD among morbidly obese patients undergoing bariatric surgery and to determine if advanced liver disease can be predicted by demographics, comorbidities, and/or preoperative biochemical profiles. 135 nonconsecutive patients (109 female, average age 46) with mean body mass index (BMI) 50 (SD 7.6) who underwent liver biopsies during bariatric surgery were studied. Patient data including age, BMI, comorbidities, and preoperative liver function tests were analyzed against liver biopsy pathology. 86% of patients had abnormal liver biopsy results. 60% of patients had steatosis, and 27% had advanced liver disease (7% steatohepatitis, 16% fibrosis, and 4% cirrhosis). Patients were grouped according to liver biopsy pathology. Group A included patients with normal results and steatosis only. Group B included those patients with advanced liver disease:steatohepatitis, fibrosis, and cirrhosis. Of 37 patients in group B, 27% had abnormal preoperative liver function tests (LFTs) compared to 10% of patients in group A (p = 0.022). Patients in group B were more likely to have preoperative hyperlipidemia (p = 0.020) and were also found to have a significantly higher BMI (p = 0.042). Diabetes mellitus, male gender, and age were not predictive of advanced liver disease on liver biopsy, with p = 0.056, p = 0.074, p = 0.26, respectively. Liver disease is common in the morbidly obese. More than one quarter of morbidly obese patients undergoing bariatric surgery have advanced liver disease. Patients with increased preoperative LFTs, hyperlipidemia, and increased BMI are more likely to have non-alcoholic steatohepatitis, fibrosis, or cirrhosis on liver biopsy during weight loss surgery. Diabetes, male gender, and age did not predict advanced liver disease.
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PMID:Laparoscopic bariatric surgery: what else are we uncovering? Liver pathology and preoperative indicators of advanced liver disease in morbidly obese patients. 1747 22

Pulmonary hypertension (PH) has been partially reclassified during the 2003 Third World Symposium on Pulmonary Arterial Hypertension held in Venice. PH is a common disorder that may complicate a variety of cardiopulmonary diseases, including severe COPD, left ventricular failure and chronic thromboembolic obstruction of the pulmonary arteries. Pulmonary arterial hypertension (PAH) is an increase in pulmonary arterial pressure which is not due to classical coexistent cardiopulmonary disease. PAH usually occurs in the absence of an evident cause (idiopathic or familial) or it may be associated with connective tissue disease, HIV infection, chronic liver disease, congenital systemic-to-pulmonary shunts, venous or capillary involvement, thyroid or myeloproliferative disorders as well as a result of the use of toxic agents and anorexigens. The actuality of developed disease-specific treatments over the past decade, emphasises the importance of an early screening and detection of PH which, even optimally treated in advanced stages, still remains a progressive lethal disease in most of its forms. Early identification represents a real challenge for the clinician: in fact, it is believed that an early recognition and, thus, an early treatment, might be associated with improved survival. In this review, after a short introduction on disease prognosis, we will focus on screening and early recognition of some categories of PH, based on a sequential approach that includes clinical suspicion, detection and differentiation of pulmonary hypertension. This strategy should consent to reach an assessment of severity, ultimately providing the best selective use of therapies.
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PMID:Prognosis, screening, early detection and differentiation of arterial pulmonary hypertension. 1762 2

Hepatitis C virus (HCV) is the most common cause of chronic liver disease in patients with end-stage renal disease. It is more prevalent in hemodialysis (HD) patients than the general population but the exact routes of transmission are not clear. In this study, the current situation of HCV infection was assessed in eleven dialysis centers in Tehran, Iran. A total of 548 patients on maintenance HD with a mean age of 45.4 +/- 16.8 years were studied. Most of the patients were dialysed 3 times/week, each session lasting 4 to 4.5 hours. About 15% of patients had a history of having received peritoneal dialysis prior to maintenance HD and 23.6 of patients had received blood transfusion(s). The most common cause of renal failure was hypertension in 29.7% followed by diabetes mellitus in 23.2%, failed renal transplant in 19.4% and glomerulonephritis in 9.7%. HCV antibodies were measured by ELISA-III. All positive sera were tested for HCV RNA by RT-PCR. Positive HCV antibody tests were present in 19.6% of patients. In these seropositive patients, 48.6% had detectable HCV RNA. Prevalence of HCV antibody seropositivity was not different in patients with or without history of blood transfusion. The prevalence of positive HCV antibody in this study was higher than reports from Europe but lower than other countries in the region. Only 48.6% of seropositive cases were confirmed by PCR, which is lower than expected values. It seems that nosocomial transmission is the main route of infection in Iran.
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PMID:Prevalence of hepatitis C infection and its risk factors in hemodialysis patients in tehran: preliminary report from "the effect of dialysis unit isolation on the incidence of hepatitis C in dialysis patients" project. 1766 Jun 69

Nine patients with hepatocellular carcinoma (HCC) in nonalcoholic steatohepatitis (NASH) (six men and three women, median age 71.5 years) and one patient with intrahepatic cholangiocarcinoma (ICC), a 50-year-old man, in NASH are described. Most patients were associated with obesity, diabetes, hypertension, hypercholesterolemia, or hypertriglyceridemia. Seven patients showed insulin resistance and hyperinsulinemia. All patients except one met the criteria for metabolic syndrome. An HCC or ICC diagnosis was confirmed by tumor biopsy, surgery or autopsy except in two patients, who were diagnosed by computed tomography or hepatic angiography. The underlying liver disease was liver cirrhosis in six patients and chronic liver disease including mild hepatic fibrosis in four patients. The treatment of liver cancers consisted of surgery, radio-frequency ablation (RFA), transcatheter arterial embolization and transcatheter arterial infusion. Although the follow-up period was relatively short (median 27.5 months, average 32.1 months), all postoperative and post-RFA patients have not had a recurrence of HCC to date, except for one patient who had a palliative operation with intra-arterial infusion of anticancer drugs through an implanted reservoir port. Older age and liver cirrhosis are considered risk factors for HCC in NASH, and regular screening of these patients is necessary. Diabetes may contribute to the development of ICC in NASH. Curative therapy (surgery or RFA) and weight loss by the active therapeutic intervention (nutritional care and exercise therapy) after curative therapy may help us improve the prognosis of HCC in NASH.
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PMID:Primary liver cancers with nonalcoholic steatohepatitis. 1787 5

Pulmonary hypertension is a common complication of sickle cell anemia. Despite the fact that the elevations in pulmonary artery pressures are slight, morbidity and mortality are high. In adult sickle cell anemia patients, pulmonary hypertension is emerging as a major risk factor for death. The pathogenesis of sickle cell anemia-related pulmonary hypertension is multifactorial, including hemolysis, impaired nitric oxide bioavailability, chronic hypoxemia, thromboembolism, chronic liver disease and asplenia. In the majority of patients, pulmonary arterial hypertension is the main cause of elevated pulmonary artery pressures. However, pulmonary venous hypertension also plays a role in a subgroup of patients. Specific data on the effects of treatment modalities for pulmonary hypertension in patients with sickle cell anemia are scarce. It is likely that all patients would benefit from maximization of sickle cell anemia therapy, and that patients with the severe form of the disease would benefit from treatment with selective pulmonary vasodilators and antiproliferative agents. Large trials evaluating the effects of treatment for pulmonary hypertension in the sickle cell anemia population are underway.
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PMID:Sickle cell anemia-associated pulmonary arterial hypertension. 1802 58

Alzheimer's disease is the most prevalent and common form of cognitive impairment, ie, dementia, in the elderly followed in second place by vascular dementia due to the microangiopathy associated with poorly-controlled hypertension. Besides blood pressure elevation, advancing age is the strongest risk factor for dementia. Deterioration of intellectual function and cognitive skills that leads to the elderly patient becoming more and more dependent in his, her, activities of daily living, ie, bathing, dressing, feeding self, locomotion, and personal hygiene. It has been known and demonstrated for many years that lowering of blood pressure from a previous hypertensive point can result in stroke prevention yet lowering of blood pressure does not prevent the microangiopathy that leads to white matter demyelinization which when combined with the clinical cognitive deterioration is compatible with a diagnosis of vascular dementia. It is known from many large studies, ie, SHEP, SCOPE, and HOPE, that lowering of blood pressure gradually will not and should not worsen the cognitive impairment. However, if the pressure is uncontrolled a stroke which might consequently occur would further worsen their cognitive derangement. So an attempt at slow reduction of blood pressure since cerebral autoregulation is slower as age increases is in the patient's best interest. It is also important to stress that control of blood glucose can also be seen as an attempt to prevent vascular dementia from uncontrolled hyperglycemia. Vascular dementia is not considered one of the reversible causes of dementia. Reversible causes of cognitive impairment are over medication with centrally acting drugs such as sedatives, hypnotics, antidepressants, and antipsychotics, electrolyte imbalance such as hyponatremia, azotemia, chronic liver disease, and poor controlled chronic congestive heart failure. Criteria for the clinical diagnosis of vascular dementia include cognitive decline in regards to preceding functionally higher level characterized by alterations in memory and in two or more superior cortical functions that include orientation, attention, verbal linguistic capacities, visual spacial skills, calculation, executive functioning, motor control, abstraction and judgment. Patients with disturbances of consciousness, delirium (acute confusional states), psychosis, serious aphasia, or sensory-motor alterations that preclude proper execution of neuro-psychological testing are also considered to have probably vascular dementia. Furthermore, these are ten of the other essential cerebral or systematic pathologies present that would be able to produce a dementia syndrome.
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PMID:Hypertension and cognitive function in the elderly. 1809 Aug 79

Non-alcoholic fatty liver disease is present in 15-25% of the general population. The fundamental derangement in non-alcoholic fatty liver disease is insulin resistance, a key component of the metabolic syndrome, which includes type 2 diabetes mellitus, dyslipidemia, hypertension, and obesity. The natural history of non-alcoholic fatty liver disease is not always benign, and causality for chronic liver disease and cirrhosis is well known in clinical practice and sometimes it is accompanied by hepatocellular carcinoma. Non-alcoholic fatty liver disease is likely to be associated with increased cardiovascular disease risk, and it raises the possibility that non-alcoholic fatty liver disease may be not only a marker but also an early mediator of atherosclerosis. Therapy is currently directed at treating components of the metabolic syndrome which may be beneficial also for the liver.
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PMID:[Non-alcoholic fatty liver disease and cardiovascular risk]. 1861 57

Chronic liver disease results from a variety of causes such as hepatitis virus infections, autoimmune processes and alcohol consumption. Its complications include fat deposition, hemodynamic changes and fibrosis. Clinically there may be progression to portal-hypertension and porto-systemic encephalopathy. Pioneering research from the laboratory of Kunos at NIH has stressed the importance of endocannabinoids (ECs) as mediators of some of the pathological processes in chronic liver disease. The present review summarizes the literature on the association between ECs and liver disease, as well as the therapeutic potential of ECs and exogenous cannabinoids in liver disease with emphasis on hepatic encephalopathy.
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PMID:Endocannabinoids in liver disease and hepatic encephalopathy. 1878 86

Nonalcoholic fatty liver disease (NAFLD), first described in 1980, is now recognized as one of the most common causes of elevated liver enzymes and chronic liver disease in Western countries. The incidence of NAFLD in both adults and children is rising, in conjunction with the burgeoning epidemics of obesity and type 2 diabetes mellitus. NAFLD often coexists with other sequelae of the metabolic syndrome: central obesity, type 2 diabetes, hypertension, and hyperlipidemia. NAFLD encompasses a spectrum of pathologic liver diseases ranging from simple hepatic steatosis to a predominant lobular necro-inflammation, with or without centrilobular fibrosis (called nonalcoholic steatohepatitis or NASH). NASH can progress to cirrhosis, decompensated liver disease, and hepatocellular carcinoma. Though the natural history of NASH is still not clearly defined, it has been observed to progress to cirrhosis in 15%-220% of those affected. Insulin resistance is nearly universal in NASH and is thought to play an important role in its pathogenesis leading to dysregulated lipid metabolism. The prevalence of insulin resistance is reported in the general population to be approaching 45%, suggesting that NAFLD and NASH will contin nue to be an important public health concern. To date, NASH has proven to be a difficult disease to treat. Front-line therapy with lifestyle modifications resulting in weight loss through decreased caloric intake and moderate exercise is generally believed to be beneficial in patients with NASH, but is often difficult to maintain long term. Given that insulin resistance plays a dominant role in the pathogenesis, many studies have examined the use of insulin sensitizers: the biguanides (metformin), thiazolidinediones (pioglitazone, troglitazone, and rosiglitazone), glucagon-like peptide-1-receptor agonists, or incretins (exenatide)in NASH. This review will provide an overview of insulin resistance in NAFLD and provide a detailed summary on the clinical data regarding the use of insulin sensitizers in NASH.
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PMID:Insulin sensitizers in nonalcoholic fatty liver disease and steatohepatitis: Current status. 1992 Nov 18

Alzheimer's disease is the most prevalent and common form of cognitive impairment, ie, dementia, in the elderly followed in second place by vascular dementia due to the microangiopathy associated with poorly-controlled hypertension. Besides blood pressure elevation, advancing age is the strongest risk factor for dementia. Deterioration of intellectual function and cognitive skills that leads to the elderly patient becoming more and more dependent in his, her, activities of daily living, ie, bathing, dressing, feeding self, locomotion, and personal hygiene. It has been known and demonstrated for many years that lowering of blood pressure from a previous hypertensive point can result in stroke prevention yet lowering of blood pressure does not prevent the microangiopathy that leads to white matter demyelinization which when combined with the clinical cognitive deterioration is compatible with a diagnosis of vascular dementia. It is known from many large studies, ie, SHEP, SCOPE, and HOPE, that lowering of blood pressure gradually will not and should not worsen the cognitive impairment. However, if the pressure is uncontrolled a stroke which might consequently occur would further worsen their cognitive derangement. So an attempt at slow reduction of blood pressure since cerebral autoregulation is slower as age increases is in the patient's best interest. It is also important to stress that control of blood glucose can also be seen as an attempt to prevent vascular dementia from uncontrolled hyperglycemia. Vascular dementia is not considered one of the reversible causes of dementia. Reversible causes of cognitive impairment are over medication with centrally acting drugs such as sedatives, hypnotics, antidepressants, and antipsychotics, electrolyte imbalance such as hyponatremia, azotemia, chronic liver disease, and poor controlled chronic congestive heart failure. Criteria for the clinical diagnosis of vascular dementia include cognitive decline in regards to preceding functionally higher level characterized by alterations in memory and in two or more superior cortical functions that include orientation, attention, verbal linguistic capacities, visual spacial skills, calculation, executive functioning, motor control, abstraction and judgment. Patients with disturbances of consciousness, delirium (acute confusional states), psychosis, serious aphasia, or sensory-motor alterations that preclude proper execution of neuro-psychological testing are also considered to have probably vascular dementia. Furthermore, these are ten of the other essential cerebral or systematic pathologies present that would be able to produce a dementia syndrome.
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PMID:Hypertension and cognitive function in the elderly. 2018 99


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