Development of Hypoxemia in Alcoholic Liver Disease

The aim of this study was to investigate the arterial hypoxemia in Japanese patients with alcoholic liver disease (ALD) with regard to alcohol consumption and/or disease severity. Hypoxemia was observed in 78% patients with ALD and in all 46 patients with alcoholic liver cirrhosis (ALC) and 33 (56%) of 59 patients with noncirrhotic alcoholic liver disease (NCALD) (P < 0.0001). The partial pressure of oxygen (P_aO₂) was 71.1 ± 5.2 mm Hg in ALC and 78.7 ± 6.3 mm Hg in NCALD (P < 0.0001). The oxygen consumption in ALD was significantly higher than that in control subjects (P < 0.0001), and a high oxygen consumption was seen in 88% of the patients with ALD, in all 46 ALC patients, and in 46 (78%) of 59 NCALD patients (P < 0.01). Following abstinence from alcohol, the P_aO₂ and oxygen consumption significantly recovered after day 2 (P < 0.0001), whereas the prothrombin index did not change in either NCALD or ALC patients. Multivariate analysis showed that alcohol consumption and oxygen consumption were significant independent predictors of P_aO₂. In conclusion, the present findings suggest that increased oxygen consumption due to alcohol ingestion is principally responsible for the hypoxemia in ALD patients.     

Increase in the incidence of alcoholic pancreatitis and alcoholic liver disease in Iceland: impact of per capita alcohol consumption

Abstract

Objective: To analyze the incidence of acute alcoholic pancreatitis and of severe alcoholic liver disease (ALD) and its association with per capita alcohol consumption with identification of both alcoholic cirrhosis (AC) and severe alcoholic hepatitis (AH), in a population-based setting.

Methods: A search was undertaken in diagnoses database for diagnostic codes in order to find patients hospitalized with incident acute alcoholic pancreatitis (AP) and alcoholic liver disease in Iceland in 2001–2015. Diagnoses were verified in all patients who were retrospectively reviewed. Those with ALD had either AC or AH. Alcohol sales during the study period were obtained from Statistics Iceland.

Results: Overall, 273 patients with acute AP, mean age at diagnosis 50 (14) years, 74% males and 159 patients with ALD, mean age 57 (11) years, 73% males, were identified. Mean per capita alcohol consumption was 6.95 (0.4) liters and increased by 21% over the study period. The annual incidence of AP increased from 4.2 per 100.000 to 9.5 and ALD from 1.6 to 6.1 per 100.000. Trend analysis showed a significant annual increase of 7% (RR 1.07, 95%CI 1.04–1.10) for AP and an annual increase of 10.5% (RR 1.10, 95%CI 1.06–1.15) for ALD. The increase was only significant in males.

Conclusions: Increase per capita alcohol consumption over a 15?year study period was associated with an increase in the incidence of severe alcoholic liver disease and alcohol-related acute pancreatitis in males but not in females.     

Five‐year survival predictive factors in patients with excessive alcohol intake and cirrhosis. Effect of alcoholic hepatitis,smoking and abstinence

Abstract: Aim: To evaluate 5‐year survival predictive factors in hospitalised patients with excessive alcohol intake and cirrhosis, including in a multivariate analysis the severity of the liver disease, gastrointestinal bleeding, concomitant viral B or C infection, smoking status, presence of alcoholic hepatitis at inclusion and abstinence from alcohol during follow‐up. Methods: In a non‐concurrent cohort study, 122 patients with excessive alcohol intake and cirrhosis were followed up at least five years or till death. Two patients were lost to follow‐up. Results: The 5‐year survival rates were 43% in the 122 patients and 66%, 50% and 25% in Child–Pugh class A, B and C patients, respectively. In multivariate analysis, age (P = 0.01), Child–Pugh score (P = 0.0001), gastrointestinal bleeding (P = 0.01), presence of HBs Ag and/or anti‐HCV (P = 0.03), smoking (P = 0.01), absence of histologically proven alcoholic hepatitis (P = 0.05) and persistent alcohol intake (P = 0.002) were associated with significantly increased risk ratios of death. Conclusions: In hospitalised patients with excessive alcohol intake and cirrhosis: (1) age, liver failure, gastrointestinal bleeding, concomitant viral B or C infection and persistent alcohol intake are independent poor prognostic markers, (2) smoking may contribute to the aggravation of cirrhosis, and (3) alcoholic hepatitis, being a potentially reversible cause of liver failure, has a favourable prognostic significance.     

Urinary excretion of catecholamines in patients with primary aldosteronism before and after unilateral adrenalectomy

The authors compared urinary excretion of noradrenalin (NA), adrenalin (A) and dopamine (DA) in 12 patients with primary aldosteronism (PA), 54 healthy controls and 17 patients with fixed benign essential hypertension (BEH), and in PA investigated the changes occurring in the catecholamine spectrum after removal of aldosterone-producing adrenal adenoma. The patients with PA before adrenalectomy differed from the controls and patients with BEH by low NA excretion and high DA excretion. After unilateral adrenalectomy, patients with PA presented simultaneously with BP, aldosterone and renin normalization a rise in NA excretion and a drop in urinary DA to similar or lower values than those found in the controls and BEH. The results show that changes in urinary catecholamines excretion in A may be a secondary consequence of hypermineralocorticism. High DA may be the consequence of a mobilization of contra-regulatory natriuretic mechanisms in the course of aldosterone-induced sodium retention. Low NA and A may participate in lowering the plasma renin activity which in PA in suppressed, sometimes disproportionately to the actual body sodium content.     

The lifestyle influence on alcoholic pancreatitis versus alcoholic liver disease: a case-control study

Objective: To evaluate the association of lifestyle with the development of alcoholic liver disease (ALD) or alcoholic pancreatitis (AlcP).

Methods: A case-control study was conducted on 80 patients attending a tertiary university hospital, subdivided into three groups: ALD (n?=?34), AlcP (n?=?21) and a control (CT) group (n?=?25) of alcohol abusers without clinical evidence of hepatic or pancreatic disease. Participants were interviewed regarding alcohol consumption, tobacco use and diet. A physical examination was concomitantly performed and we had access to their complementary investigation.

Results: We included 10 females and 70 males (mean age 57?±?10 years). The pure amount of alcohol consumed by the ALD group was significantly higher than the AlcP group, regarding both daily (grams/day) and lifetime (kilograms) consumptions (p?=?.018 and p?=?.009, respectively); no statistically significant differences were seen with the CT group. We found no differences regarding the beverage type or drinking outside meals. Smoking was very common in every study group, with higher consumptions and a significantly higher prevalence of ever smokers in the AlcP group, in comparison with ALD and CT patients (p?=?.033 and p?=?.036, respectively). There were significant differences in the patients’ eating habits before the onset of disease between groups (p?Conclusion: We found differences in lifestyle between ALD and AlcP, not considered sufficient to explain the subjects’ susceptibility to one disease or the other.     

Histochemical Study of Hyaluronate in Alcoholic Liver Disease

Recently, it has been reported that serum hyaluronate (hyaluronic acid; HA) concentrations increase in various liver diseases, especially in alcoholic liver disease (ALD), and serum HA concentration has been used as a marker for hepatic fibrosis. However, it is unknown whether hepatic HA contents in ALD increase by alcohol or not. In this study, we histochemically stained HA in liver biopsy specimens obtained from ALD patients while actively drinking and after abstinence to clarify the effects of alcohol on hepatic HA contents. Liver biopsy specimens were obtained from 13 patients with ALD and 10 patients with non-ALD. In ALD patients, liver biopsy was performed twice within 3 days, and 4 to 8 weeks after abstinence when serum levels of AST and ALT normalized. HA in biopsy specimens was stained histochemically with biotinylated HA binding protein. Staining intensity of HA in liver tissue was also determined by computer-assisted imaging analyzer. HA staining was clearly observed in sinusoidal wall and fibrous regions around the portal tract and central vein in liver diseases. HA staining intensities in patients actively drinking with ALD increased markedly, compared with those in patients with non-ALD, and these intensities decreased with abstinence. These results clearly suggest that hepatic HA contents in ALD may be increased by alcohol in addition to hepatic fibrosis, and, therefore, increased HA deposition in the liver may be reversible by abstinence of alcohol.     

Oxidative stress and redox signaling mechanisms of alcoholic liver disease: updated experimental and clinical evidence

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality in the United States and Europe. The spectrum of ALD ranges from fatty liver to alcoholic hepatitis and cirrhosis, which may eventually lead to hepatocellular carcinoma. In developed countries as well as developing nations, ALD is a major cause of end-stage liver disease that requires liver transplantation. The most effective therapy for ALD is alcohol abstinence; however, for individuals with severe ALD and those in whom alcohol abstinence is not achievable, targeted therapies are absolutely necessary. In this context, advances of our understanding of the pathophysiology of ALD over the past two decades have contributed to the development of therapeutic modalities (e.g., pentoxifylline and corticosteroids) for the disease although the efficacy of the available treatments remains limited. This article is intended to succinctly review the recent experimental and clinical findings of the involvement of oxidative stress and redox signaling in the pathophysiology of ALD and the development of mechanistically based antioxidant modalities targeting oxidative stress and redox signaling mechanisms. The biochemical and cellular sources of reactive oxygen and nitrogen species (ROS/RNS) and dysregulated redox signaling pathways associated with alcohol consumption are particularly discussed to provide insight into the molecular basis of hepatic cell dysfunction and destruction as well as tissue remodeling underlying ALD.     

Changes in the excretion of catecholamines and their metabolites in patients with essential hypertension during sodium intake restriction

Excretion of noradrenaline (NA), adrenaline (A), dopamine (DA) and their metabolites vanillylmandelic acid (VMA), methoxycatecholamines (MNA + MA) as well as 3-methoxy-4-hydroxy-phenylglycol (MHPG) was studied in 95 patients with essential hypertension and in 25 normal subjects on normal and low sodium diets. The patients were divided into 3 groups according to NA excretion under basal conditions. NA excretion was increased during sodium intake restriction, the highest values of this increase being found in patients whose basal NA excretion was diminished. At low sodium intake the high and the low NA excretors responded with significant increases of DA excretion. The mean excretion of VMA increased significantly on low sodium diet in all 3 groups of patients. The MNA + MA excretion decreased significantly during sodium intake restriction in patients with normal NA excretion. At low sodium intake the excretion of MHPG was highest in patients with low basal NA excretion. These data suggest that in patients with essential hypertension subjected to sodium restriction the excretion and metabolism of catecholamines are related to basal sympathetic activity.     

Microheterogeneity with Concanavalin A Affinity of Serum Transferrin in Patients with Alcoholic Liver Disease

Microheterogeneity of transferrin (Tf) with concanavalin A (ConA) affinity was investigated by sensitive lectin-affinity electrophoresis and antibody-affinity blotting technique of sera obtained from patients with alcoholic liver disease (ALD) and normal subjects. Serum Tf was separated by ConA into three bands–a strongly ConA-reac-tive major band (C1), a weakly reactive minor band (C2), and a non-reactive trace band (C3). The C3 fraction was significantly increased in patients with ALD before alcohol abstinence, compared with normal subjects and patients with ALD after 4 weeks of abstinence. Furthermore, a significant correlation was found between the C3 fraction and serum carbohydrate-deficient transferrin or γ-glutamyl-transpeptidase. These results indicate that the microheterogeneity of serum Tf in patients with ALD may be a more complex abnormality of elongation and processing on the glycans than merely a loss of terminal sialic acids. Determination of the C3 fraction is a useful marker for ALD.     

Study of Mitochondrial DNA Deletion in Alcoholics

Background: Recently, it has been reported that single or multiple mitochondrial DNA (Mt-DNA) deletions have been observed frequently in liver tissue and white blood cells (WBC) obtained from patients with alcoholic liver disease (ALD). In this study, we investigated the deletion of the Mt-DNA encoding adenosine triphosphatase (ATPase) region in WBC to clarify whether Mt-DNA heteroplasmy caused by alcohol drinking is reversible. Methods: Blood samples were obtained from 4 healthy volunteers, 56 patients with ALD, and 106 nonalcoholic healthy controls. The Mt-DNA encoded ATPase region was amplified by polymerase chain reaction (PCR) by using two primers: forward primer, 5‘-AACCAACACCTCTTTACAGTGA; and reverse primer; 5‘-TTGGTGGGTCATTATGTGTTGT. Results: Heteroplasmy was observed in one volunteer on day 3 and in the remaining persons on day 4 after the start of alcohol consumption. Heteroplasmy was observed for another 6 days after alcohol consumption stopped, but on the 7th day it had disappeared in all volunteers. In WBC Mt-DNA obtained from ALD patients within 3 days of abstinence, heteroplasmy was observed in 38 of the 56 patients (67.9%), whereas heteroplasmy was not detected in any healthy subjects. In 10 of the 18 ALD patients (56%) who had heteroplasmy within 3 days of abstinence, heteroplasmy disappeared after 4 weeks of abstinence. Conclusion: An acquired mutation of Mt-DNA, at least in the encoding ATPase region, may result from alcohol drinking and may be reversed by stopping drinking.     

Long-term survival and predictors of relapse and survival after liver transplantation for alcoholic liver disease

Objective: Studies of predictive factors of alcohol recidivism and survival post-LT are not up-to-date. With evolving LT activity and with longer-term outcomes becoming increasingly available, re-evaluating post-LT outcomes is imperative. We analyzed recent data on survival, alcohol recurrence and predictive factors.

Methods: We compared long-term survival among 159 consecutive ALD patients transplanted 2003–2016 with 159 propensity-score matched controls transplanted for non-ALD. Alcohol ‘slips’ (occasional lapse) and relapse to moderate or harmful drinking were assessed from medical records and structured forms filled in by home-district physicians, and analyzed by competing-risk and multivariate Cox regression analyses.

Results: Patient and graft survival at 10 years were 75 and 69% in the ALD group and 65 and 63% in the control group (p=.06 and .36). In ALD patients, the 10-year cumulative rate of alcohol slip was 52% and of relapse, 37%. Duration of pre-LT abstinence (HR 0.97, 95% CI 0.94–0.99) and a history of prior alcohol relapses (HR 3.05, 95% CI 1.41–6.60) were significant predictors of relapse, but failed to predict death/graft loss. Patients with <6 months abstinence relapsed sooner than those with 7–24 months abstinence, but 10-year relapse rates were similar (40–50%). Ten-year relapse rate with 2–5-year pre-LT abstinence was 21%, and with >5-year abstinence, 0%. In patients with <6 months pre-LT abstinence, years of heavy drinking, prior addiction treatments, and lack of children predicted inferior survival.

Conclusions: Although 37% of our ALD patients relapsed to drinking by 10 years post-LT, 14-year survival was not significantly different from survival in non-ALD patients. Short duration of pre-LT abstinence and prior relapses predicted post-LT relapse.     

Roles of gender, obesity, and lifestyle-related diseases in alcoholic liver disease: Obesity does not influence the severity of alcoholic liver disease

Aim: To elucidate gender differences and the influence of obesity and/or metabolic syndrome‐related fatty liver on alcoholic liver disease (ALD), we analyzed characteristic features of ALD. Methods: We investigated 266 ALD patients (224 males and 42 females) without hepatocellular carcinoma stratified by gender and the presence of cirrhosis. Male and female patients matched for age and total ethanol intake were also analyzed. A diagnosis of ALD was based on alcohol intake (>70 g daily for more than 5 years), clinical features, and exclusion of other liver diseases. The prevalence of obesity, lifestyle‐related diseases, and psychological disorders were assessed. Results: The prevalence of psychological disorders showed a significant gender difference among all ALD patients (12% in males versus 43% in females, P < 0.001), as well as in patients matched for age and total ethanol intake. There were 156 cirrhotic patients. Absence of dyslipidemia, presence of diabetes, and high total ethanol intake were selected as independent predictors of cirrhosis in males by multivariate analysis after excluding laboratory data of liver function tests. The prevalence of obesity was significantly lower in cirrhotic male patients than in non‐cirrhotic male patients (34% vs. 20%, P = 0.023). Among females, there were no significant predictors of cirrhosis on multivariate analysis after eliminating liver function tests. The prevalence of obesity and diabetes was similar in non‐cirrhotic and cirrhotic female patients. The prevalence of psychological disorders was 47% in cirrhotic females with ALD. Conclusions: Obesity was not common in cirrhotic ALD. Psychological disorders seem to be important for female ALD.     

Cellular cytotoxicity against autologous hepatocytes in alcoholic liver disease

ABSTRACT— We tested lymphocyte cytotoxicity against autologous hepatocytes in patients with alcoholic liver disease (ALD). The following cytotoxicity values were found (mean ± SEM): alcohol-induced steatosis with or without fibrosis 16.5±2% (n = 29), alcoholic cirrhosis 28±4% (n = 13), controls with normal liver histology or minimal changes 6±2% (n = 11). The differences were statistically significant (both forms of ALD versus controls p<0.005). T-cell as well as non-T-cell-enriched lymphocyte fractions showed increased cytotoxicity in ALD. We did not observe a correlation between cellular cytotoxicity and the degree of biochemical or histological alterations within the groups tested. Thus, our study demonstrating enhanced cellular cytotoxicity against autologous hepatocytes in ALD further supports the hypothesis that cellular immune reactions are involved in the pathogenesis of ALD, especially of alcoholic cirrhosis.     

Interrelationships Between the Renin-Angiotensin-Aldosterone System and Sympathetic and Dopaminergic Activities in Elderly Subjects

The interrelationships between the renin-aldosterone system and the sympathetic and dopaminergic activities were studied by measuring the plasma renin activity (PRA), plasma aldosterone concentration (PAC), serum prolactin (PRL) concentration, and 24 hr-urinary excretions of adrenaline (Ad), noradrenaline (NA) and dopamine (DA) in elderly normotensive subjects aged 60 to 90 yrs.

The PAC showed a significant correlation with NA in the urine (γ = 0.694, n = 24, p < 0.001). The PRA also tended to correlate with NA in the urine, although the degree was weak and not significant. The serum PRL concentration showed a significant correlation with DA in the urine (γ = 0.447, n = 24, p < 0.05). No significant correlation was observed between DA and PRA or PAC, and between the serum PRL concentration and PRA or PAC.

From these results, it is shown that the renin-aldosterone system has a relation to urinary NA excretion, and the existence of an interrelationship between the central dopaminergic activity and urinary DA excretion is suggested.     

Non-invasive monitoring of oxidant stress in alcoholic liver disease

Objective. In alcoholic liver disease (ALD), progression from initial steatosis, through hepatitis to cirrhosis is well described, resulting in 20,000 deaths in the UK annually. However, pathological mechanisms are not well understood and drug trials have led to conflicting results. It has been established that alcohol consumption increases hepatic free radical production and oxidant stress has been implicated in the disease process.Material and methods. Markers of lipid peroxidation, antioxidant status, hepatic fibrogenesis, inflammation and liver function were measured in blood and urine from 24 patients with established alcoholic cirrhosis and in 49 age- and sex-matched controls.Results. In the ALD group, lipid peroxidation markers 8-isoprostane and malondialdehyde were significantly increased (p <0.001), as was the ratio of oxidized to reduced glutathione (p=0.027). The antioxidants selenium, glutathione (whole blood and plasma) and vitamins A, C and E were all significantly decreased (p<0.001); median plasma glutathione levels were only 19% of control levels. Type III procollagen peptide (PIIINP), a serum marker of hepatic fibrogenesis, and C-reactive protein (CRP) were both increased (p<0.001). Urinary 8-isoprostane correlated positively with PIIINP, CRP and markers of cholestasis (alkaline phosphatase and bilirubin) and negatively with glutathione (whole blood), vitamins A and E and albumin.Conclusions. Oxidant stress, as reflected in blood and urine by a wide range of pro- and antioxidant markers, is a significant feature of alcoholic cirrhosis, providing a mechanism by which alcohol intake may be linked to hepatic inflammation and fibrosis. Non-invasive markers could prove valuable in monitoring response to treatment during clinical trials.     

Incidence,survival and cause-specific mortality in alcoholic liver disease: a population-based cohort study

Objective: We studied the incidence of severe ALD requiring hospitalization in Finland, and survival and causes of death among the ALD patients.

Methods: A cohort of 11,873 persons (8796 men and 3077 women) with diagnosis of ALD during the years 1996–2012 was identified from Finnish national Inpatient Register. The annual incidence of alcoholic hepatitis (AH) and alcoholic liver cirrhosis was calculated. The cohort was combined with the data from national Cause of Death Register of Statistics Finland.

Results: The incidence of alcoholic liver cirrhosis increased from 8.8/100,000 in year 2001 to 14.6/100,000 in year 2012 among men and from 2.4 to 4.2/100,000 among women. The incidence of AH increased from 3.7 to 6.5/100,000 among men and from 1.3 to 2.7/100,000 among women. The relative 5-year survival ratios of patients with alcoholic liver cirrhosis and AH were 29 and 50% among men and 38 and 52% among women, respectively. Out of 8440 deaths, 65% were due to alcoholic-related causes. The risk of death among ALD patients was increased in malignancies (SMR 6.82; 95% CI: 6.35–7.29), cardiovascular diseases (6.13; 5.74–6.52), respiratory diseases (7.86; 6.70–9.10), dementia (3.31; 2.41–4.44) and accidents and violence (11.12; 10.13–12.15).

Conclusions: The incidence of AH and alcoholic liver cirrhosis is increasing. The survival is poor. Most deaths are alcohol-related and other common causes of excess deaths are cancers especially in the upper aerodigestive tract and cardiovascular, digestive and respiratory diseases as well as violence and accidents.     

Perceptions of post-transplant recidivism in liver transplantation for alcoholic liver disease

Although alcoholic liver disease (ALD) is regarded as a common indication for liver transplantation (LT), debatable issues exist on the requirement for preceding alcoholic abstinence, appropriate indication criteria, predictive factors for alcoholic recidivism, and outcomes following living-donor LT. In most institutions, an abstinence period of six months before LT has been adopted as a mandatory selection criterion. Data indicating that pre-transplant abstinence is an associated predictive factor for alcoholic recidivism supports the reasoning behind this. However, conclusive evidence about the benefit of adopting an abstinence period is yet to be established. On the other hand, a limited number of reports available on living-donor LT experiences for ALD patients suggest that organ donations from relatives have no suppressive effect on alcoholic recidivism. Prevention of alcoholic recidivism has proved to be the most important treatment after LT based on the resultant inferior long-term outcome of patients. Further evaluations are still needed to establish strategies before and after LT for ALD.     

The Influence of Alcoholic Liver Disease on Serum PIVKA-II Levels in Patients without Hepatocellular Carcinoma

Background/AimsProthrombin induced by vitamin K deficiency or antagonist II (PIVKA-II) is a widely used diagnostic marker for hepatocellular carcinoma (HCC). We evaluated the correlation between alcoholic liver disease (ALD) and serum PIVKA-II levels in chronic liver disease (CLD) patients.MethodsWe retrospectively reviewed the medical records of 2,528 CLD patients without HCC. Among these patients, 76 exhibited serum high PIVKA-II levels of >125 mAU/mL (group 1). We categorized 76 control patients matched by age, sex, and the presence of liver cirrhosis from the remaining patients who were negative for serum PIVKA-II (group 2).ResultsGroup 1 revealed increased antibiotic usage (23.7% vs 2.6%, p<0.001) and incidence of ALD (60.5% vs 14.5%, p<0.001) as well as elevated aspartate aminotransferase (52.5 IU/L vs 30.5 IU/L, p=0.025) and γ glutamyl transpeptidase (67.5 IU/L vs 36.5 IU/L, p=0.005) levels compared with group 2. Further, group 1 was significantly associated with a worse Child-Pugh class than group 2. In the multivariate analysis, ALD (odds ratio [OR], 7.151; p<0.001) and antibiotic usage (OR, 5.846; p<0.001) were significantly associated with positive PIVKA-II levels.ConclusionsOur study suggests that ALD and antibiotics usage may be confounding factors when interpreting high serum PIVKA-II levels in patients without HCC. Therefore, serum PIVKA-II levels in patients with ALD or in patients administered antibiotics should be interpreted with caution.     

双环醇与多烯磷脂酰胆碱治疗酒精性脂肪肝的临床病理比较

观察双环醇与多烯磷脂酰胆碱治疗酒精性脂肪肝的临床病理差异。55例患者随机分为两组,治疗组29例给予双环醇,对照组26例给多烯磷脂酰胆碱,疗程36周。两组各20例治疗前后肝组织学比较。治疗36周,双环醇组完全应答率50％,部分应答率30％,多烯磷脂酰胆碱组分别为45％和15％,双环醇组在改善ALT、ALP、GGT和肝纤维化积分优于多烯磷脂酰胆碱,双环醇组血清GST—Px治疗后升高,两组治疗后MDA均下降。     

CHANGES IN PLASMA CATECHOLAMINE LEVELS DURING HEMODIALYSIS

The plasma concentrations of dopamine (DA), adrenaline (AD) and noradrenaline (NA) were measured during 29 routine hemodialysis (HD) treatments on 13 patients to determine whether any changes occurred in the concentrations of these substances during HD. All of the 13 patients studied demonstrated a fall in mean arterial pressure (MAP) when HD was commenced. Decreased concentrations of all three catecholamines were also demonstrated after the first hour of dialysis. Plasma AD rose after two hours, but NA and DA were still significantly lower than pre-dialysis values at the end of HD. Study of 12 further patients during the first hour of HD confirmed that the NA level had fallen significantly by the fifteenth minute of HD, while the DA and AD levels took somewhat longer to fall. Both NA and DA were present in the dialysate in substantial amounts. Although the fall in MAP which accompanies HD is probably multifactorial, the loss of plasma catecholamines during HD may possibly contribute to the hemodynamic changes.