How Long Can You Live With Fatty Liver
Gut. 2004 May; 53(five): 750–755.
Long term prognosis of fatty liver: take a chance of chronic liver disease and expiry
S Dam-Larsen
1Section of Medical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark
M Franzmann
twoDepartment of Pathology, Hvidovre Hospital, University of Copenhagen, Denmark
I B Andersen
oneDepartment of Medical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark
P Christoffersen
2Department of Pathology, Hvidovre Infirmary, University of Copenhagen, Denmark
L B Jensen
1Department of Medical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark
T I A Sørensen
3Danish Epidemiology Scientific discipline Middle at the Institute of Preventive Medicine, Copenhagen Academy Hospital, Denmark
U Becker
4Alcohol Unit, Hvidovre Infirmary, Academy of Copenhagen, Denmark
F Bendtsen
1Department of Medical Gastroenterology, Hvidovre Hospital, Academy of Copenhagen, Denmark
Abstract
Background and aims: Fatty liver is a common histological finding in human liver biopsy specimens. Information technology affects x–24% of the general population and is believed to be a marking of gamble of later chronic liver disease. The present study examined the gamble of development of cirrhotic liver disease and the risk of death in a accomplice diagnosed with pure fatty liver without inflammation.
Methods: A total of 215 patients who had a liver biopsy performed during the menses 1976–1987 were included in the study. The population consisted of 109 non-alcoholic and 106 alcoholic fat liver patients. Median follow upwardly fourth dimension was 16.vii (0.2–21.nine) years in the not-alcoholic and 9.2 (0.vi–23.i) years in the alcoholic group. Systematic data collection was carried out past review of all medical records. All members of the report cohort were linked through their unique personal identification number to the National Registry of Patients and the nationwide Registry of Causes of Death, and all admissions, belch diagnoses, and causes of death were obtained.
Results: In the non-alcoholic fatty liver grouping, 1 patient developed cirrhosis during the follow up period compared with 22 patients in the alcoholic group. Survival estimates were significantly (p<0.01) different between the ii groups, for men likewise as for women, with a higher death rate in the alcoholic fatty liver group. Survival estimates in the non-alcoholic fatty liver group were not different from the Danish population.
Conclusions: This study revealed that patients with type 1 not-alcoholic fatty liver disease take a benign clinical course without excess mortality.
Keywords: fatty liver, epidemiology, cirrhosis, mortality, liver biopsy
Fat liver or steatosis hepatitis, the accumulation of lipid within hepatocytes, is a mutual histological finding in man liver biopsy specimens and affects 10–24% of the general population.1– three
In routine clinical practice, most cases are owing to alcohol excess; however, it can also occur in association with a broad range of toxins, drugs, and diseases, such every bit morbid obesity, type 2 diabetes, hyperlipidaemia, and afterward jejunoileal bypass surgery and debilitating diseases with cachexia.4, five Non-alcoholic fatty liver disease (NAFLD) is oft histologically and clinically indistinguishable from the liver damage resulting from alcohol excess.5
The pathophysiology of NAFLD is believed to involve 2 steps.half-dozen The offset step involves insulin resistance and obesity and causes the development of steatosis; the second step is oxidative stress, activating an inflammatory response and causing non-alcoholic steatohepatitis (NASH).
The prognosis of NAFLD is uncertain. Simply a few patients have been followed prospectively in order to describe the natural history of the disease. Published follow up studies include minor numbers of patients with histological diagnoses varying from simple fatty liver to NASH and cirrhosis. Teli and colleaguesseven establish that the non-alcoholic fatty liver had a benign long term prognosis just only twoscore patients were followed in this report. Studies involving predominantly NASH patients evidence a much more than ambitious natural history, with development of cirrhosis in up to 26% of patients.eight– 13
Predictive factors that may distinguish between pure fatty liver patients with a good prognosis and those developing NASH have not withal been identified. Patients with alcoholic fatty liver illness who go on to consume large amounts of booze daily accept been found to take a risk of viii–30% of developing fibrosis or cirrhosis afterward 10 years.14, xv
The aim of this report was to examine the risk of developing cirrhosis and the risk of death in patients histologically diagnosed with pure fatty liver without inflammation (type ane NAFLD) and without other known chronic liver diseases.
PATIENTS AND METHODS
Patient population
Liver biopsy specimens obtained in 243 patients during the period 1976–1987 with a histological diagnosis of pure fatty liver without inflammation were identified (the alphabetize liver biopsy) through a computerised pathology register at the Section of Pathology, Hvidovre Hospital, University of Copenhagen, Denmark.
The 243 patients were examined with respect to the post-obit exclusion criteria: (one) presence of acute or chronic liver affliction during follow upwardly, modifying the index liver biopsy: hepatitis B, hepatitis C, principal biliary cirrhosis, autoimmune hepatitis, α1 antitrypsin deficiency, haemochromatosis, other types of infectious hepatitis, and human immunodeficiency virus; (2) jejunoileal bypass operation during the follow upwardly catamenia; (iii) full parenteral diet at the fourth dimension of the index liver biopsy; (4) use of methotrexate, amiodarone, tamoxifen, or loftier doses of corticosteroids; and (5) malignancy at the time of the index liver biopsy.
During the inclusion flow, several obesity research projects were performed at the Department of Endocrinology, Hvidovre University Hospital. Seventy five (35%) patients described in this study had their index liver biopsy performed equally part of these research projects and all were morbidly obese. The indication for the index liver biopsy in the rest of the cohort was either incidental finding of abnormalities in liver role tests, mainly elevated serum aspartate aminotransferase, and/or hepatomegaly, or suspicion of alcoholic liver affliction.
Data collection
The unique personal identification number assigned to all inhabitants in Kingdom of denmark was found through record linkage to the pathology register at Hvidovre Hospital. Systematic data collection was carried out by review of all 243 medical records. Age, pinnacle, and weight were documented at baseline (fourth dimension of index liver biopsy). Body mass index (BMI) was calculated and divers as weight/pinnacle2 (kg/mii). History of diabetes mellitus, hyperlipidaemia, liver diseases, malignancy, or other chronic medical atmospheric condition was recorded at baseline (fourth dimension of alphabetize liver biopsy) when available, together with data on drug and alcohol intake, as noted in the medical records. Nonetheless, at that place was no systematic testing for diabetes or hyperlipidaemia at baseline.
Laboratory data at baseline included the following variables when available: serum aspartate aminotransferase (ASAT), serum lactate dehydrogenase (LDH), serum alkaline phosphates, serum bilirubin, serum albumin, plasma prothrombin time, blood glucose, urine glucose, serum sodium, serum potassium, serum creatinine, platelet count, serum cholesterol, serum triglycerides, and hepatitis B surface antigen.
The Danish National Registry of Patients (LPR)16 contains information on all patients admitted to non-psychiatric hospitals in Denmark since 1977. This includes appointment of birth, the unique personal identification number, sex, hospital, section, date of admission, and discharge diagnoses. Diagnoses were coded according to the WHO International Nomenclature of Diseases, eighth edition (ICD-8)17 from 1 January 1977 to 31 December 1993, and from one January 1994 according to 10th edition (ICD-10).xviii
All members of the study accomplice were linked through their personal identification number to the LPR and the nationwide Registry of Causes of Decease,19 and all admissions, discharge diagnoses, and causes of death in the report population were obtained. Patients were followed until death or 31 December 1999 in the LPR and Registry of Causes of Death; information regarding time of death for survival statistics was until i May 2001, thus allowing follow up for upwards to 23 years. Patients were excluded if they were lost to follow up in the registries.
Liver cirrhosis was accustomed as present in patients who had a discharge diagnosis, decease certificate diagnosis, or a histological finding in the follow up period consistent with cirrhosis. The first registered appointment of diagnosis was used in the statistical analysis.
Patients with an alcohol intake in a higher place the sensible drinking limits ready past the Danish National Board of Health (21 drinks per week for men (one potable = 12 g alcohol) and 14 drinks per week for women) or an alcohol related diagnosis at whatever time from biopsy to 31 December 1999 were considered to take alcoholic fatty liver. Alcohol related diagnoses used were: alcohol corruption (ICD-8 codes 303.20 + 294.30 + 780.nineteen + 979.xix + 979.29 + 979.49; ICD-x codes F10.x + E51.2 + Z72.one), alcoholic polyneuropathy (ICD-8 code 303.91; ICD-10 code G62.1), alcoholic cardiomyopathy (ICD-x code I42.six), and alcoholic pancreatitis (ICD-10 code K86.0).
The Danish Data Protection Agency and the regional scientific ethics commission approved the written report.
Histological cess
Formalin fixed paraffin embedded alphabetize liver biopsies were cutting into 4–5 µm sections, approximately 50 sections per biopsy. Sections were stained with haematoxylin and eosin, Van Gieson Hansen, periodic acid, periodic acid with diastase, Pearls iron, and for reticulum.
Ii pathologists reviewed the histological slides without knowledge of the patient's clinical or biochemical data, and morphological findings were recorded in a semi-quantitative way (0 to +++) regarding steatosis and fibrosis. Furthermore, the location of steatosis (centrilobular, periportal, or lengthened) and fibrosis (periportal or diffuse, perisinusoidal or pericellular) were recorded. The size of the steatotic vesicles (macrovesicular, microvesicular, or mixed) was also recorded.
Statistical assay
Results are presented as medians (ranges) unless otherwise stated. The Isle of mann-Whitney U test was used to test for differences betwixt groups. A p value of <0.05 was considered statistically pregnant.
The master end point was death from all causes and the secondary finish point was cirrhosis. Survival curves were constructed based on the Kaplan-Meier method. We performed our statistical analysis using delayed entry, taking into business relationship both the age of the patient and fourth dimension of entry at diagnosis, and compared survival between the groups in a Cox model. Survival curves for the whole Danish population as a comparison were estimated from data from Statistics Denmark for 1982–83.
Statistical tests were performed using SPSS software (version 10.ane for Windows) and SAS software (version 8 for Windows).
RESULTS
Clinical and biochemical results
Numbers of patients and reasons for exclusion are shown in fig 1 ▶. The medical records of the 243 patients initially identified as having fatty liver were traced and the biopsies reviewed. 2 index biopsies were misclassified; four patients had an jejunoileal bypass functioning performed in the follow up menses due to obesity; 13 were excluded owing to specific hepatic diseases diagnosed in the follow up period that could have modified the index biopsy (3 biopsies shortly after acute hepatitis B, one hepatitis C, iv primary biliary cirrhosis, two haemochromatosis, one α1 antitrypsin deficiency, ane autoimmune hepatitis, one histologically verified cirrhosis diagnosed prior to the alphabetize liver biopsy); ii received methotrexate handling; three had malignant illness at the time of biopsy; and 4 were lost to follow upwards.
Details of patients studied, showing reasons for exclusions.
No patient was receiving drugs known to be associated with the development of steatosis. All biopsies were without histological signs of viral hepatitis.
Table 1 ▶ shows the clinical characteristics at the time of the alphabetize liver biopsy in 215 patients in the ii groups. Median follow up fourth dimension was xvi.7 (0.2–21.nine) years in the non-alcoholic and 9.ii (0.half-dozen–23.i) years in the alcoholic group.
Table 1
Clinical and biochemical information
| Non-alcoholic fatty liver (north = 109) | Alcoholic fatty liver (n = 106) | |
| Sex (F/M) | 76/33 | 31/75 |
| Age (y) | 39 (19–80) | 50 (26–72)*** |
| Obesity (%) | 81 (n = 101) | xxx** (n = 76) |
| BMI (kg/m2) | 42 (19–72) (n = 82) | 26 (18–fifty)*** (n = 31) |
| Daily alcohol intake drinks† | 0 (0–3) (northward = 95) | 10 (0–fifty)*** (n = 95) |
| ASAT (x–40 U/l)‡ | 25 (9–201) | 43 (10–576)*** |
| LDH (200–450 U/l) | 393 (165–948) | 361 (177–747) |
| Bilirubin (5–17 U/l) | seven (2–49) | 10 (three–57)** |
| Alkaline phosphatases (lxxx–275 U/l) | 212 (100–6360) | 226 (99–1037) |
| Prothrombin (0.lxx–one.xxx) | 1.09 (0.62–ii.01) | ane.15 (0.49–1.99) |
| Albumin (540–800 µmol/l) | 630 (407–754) | 584 (303–726)*** |
| Platelets (135–400 109/l) | 277 (121–638) | 255 (102–624) |
| Cholesterol (3.v–8.0 mmol/fifty) | 5.13 (2.22–eight.84) | five.35 (three.32–7.97) |
Information on BMI was available in 53% of the total population; 75% in the non-alcoholic and 29% in the alcoholic fatty liver grouping. The non-alcoholic fatty liver group had a significantly higher BMI which in role reflected the fact that they comprised a selected group from the ongoing obesity research projects at that time. If, in the present context, obesity was defined equally BMI ⩾30 or a clinical description of obesity in the patient tape by the dr., 81% were obese in the non-alcoholic group and 30% in the alcoholic group. 4 patients (of 106 patients with alcoholic fatty liver) had their initial alphabetize liver biopsy performed due to participation in an obesity research project simply were later classified as having alcoholic fatty liver because of excessive alcohol intake at the time of the index liver biopsy. None developed cirrhosis or had an alcohol related diagnosis registered during the follow up period.
There were no correlations between the prevalence of cirrhosis and obesity in the alcoholic group. Simply four of 22 patients diagnosed with alcoholic cirrhosis were also characterised as obese. There was no deviation in the amount of alcohol consumed in the obese alcoholic patients diagnosed with cirrhosis compared with non-obese alcoholic patients with cirrhosis.
At the time of the index liver biopsy, 2% and i% of patients had known type 1 diabetes in the not-alcoholic and alcoholic groups, respectively. Type 2 diabetes was present in seven% and 2% in the non-alcoholic and alcoholic groups, respectively.
ASAT and bilirubin were significantly higher, and albumin significantly lower, in the alcoholic group at the time of the alphabetize liver biopsy. Other biochemical results were not significantly different (table 1 ▶). Serological markers for hepatitis B were examined in 27% of the accomplice at the time of the index liver biopsy and none was positive for hepatitis B surface antigen. No patient was diagnosed with hepatitis B subsequently the index liver biopsy. None was tested for hepatitis C at the time of the index liver biopsy but 1 patient had a diagnosis of hepatitis C registered in the follow upwardly period and was excluded from the study.
Histological end points
In the non-alcoholic fatty liver group, one patient (ane%) developed cirrhosis during the follow up period compared with 22 (21%) in the alcoholic fatty liver group (table ii ▶). 2 of 22 patients diagnosed with alcoholic cirrhosis denied booze intake at the time of the index liver biopsy but had booze related diagnoses registered during the follow upward period.
Table 2
Development of chronic liver diseases and expiry
| Non-alcoholic fatty liver (n = 109) | Alcoholic fatty liver (n = 106) | |
| Cirrhosis | 1 (one) | 22 (21) |
| Expiry | 27 (25) | 79 (74) |
Values are number (%).
Of 23 patients diagnosed with cirrhosis in our cohort, seven had a histologically verified diagnosis, either by ways of a second liver biopsy during the follow up period or at autopsy, 12 had a diagnosis registered in the LPR, and four patients were classified as having cirrhosis based simply on the information on the expiry certificate. In viii of the 12 patients, the diagnosis in the LPR was based on the post-obit clinical signs: bleeding oesophageal varices (n = ane); oesophageal varices and ascites (n = 1); hepatic coma (n = i); hepatic coma and ascites (northward = 1); hepatic coma and coagulopathy (north = 3); and compensated cirrhosis (n = i). The last 4 patients were admitted to other hospitals and nosotros do not know whether the diagnosis was based on histology or clinical criteria lone.
A total of 13 patients in the alcoholic and six patients in the non-alcoholic group were autopsied. Another 19 in the alcoholic and 20 patients in the non-alcoholic grouping had at to the lowest degree one follow up biopsy during the study catamenia.
Two patients were diagnosed with NASH in a second liver biopsy less than one yr subsequently the index liver biopsy. Both were obese women (BMI >38 kg/m2) and ane had diabetes at the fourth dimension of the alphabetize liver biopsy. None died in the follow up menses. The iv patients with alcoholic steatohepatitis diagnosed in some other liver biopsy during the follow up flow were all men. Ii died of causes unrelated to liver illness.
Bloodshed
A total of 106 patients died during the follow upwardly period; 44 women and 62 men (table 2 ▶). Of these, 20 were liver related in the alcoholic group while 59 died from other causes. The only patient in the non-alcoholic group diagnosed with cirrhosis died of liver illness; 26 died of causes unrelated to liver disease. Comparing the 2 groups in a Cox model, survival was institute to exist significantly higher (p<0.01) in the not-alcoholic fatty liver group for men besides every bit for women. Survival estimates of those with non-alcoholic fatty liver were not unlike from the Danish population (according to the confidence intervals for the survival curve for patients) (fig ii ▶).
Survival probability for women (A) and men (B) with histologically verified non-alcoholic and alcoholic fatty liver in comparing with the general population.
At the time of the index biopsy, nine patients had an alcohol consumption lower than the limits defined by the Danish National Board of Health simply had an alcohol related diagnosis registered in the LPR during the follow up period and were characterised as having alcoholic fatty liver. Seven of these died; ii from cirrhosis and two from alcohol related causes.
Word
In this large cohort report, we found that patients diagnosed with alcohol induced fatty liver illness had a loftier risk of developing cirrhosis and premature death, for both men and women. In contrast, patients with type one NAFLD9 seemed to take the same life expectancy as the average normal population and the chance of progressing to cease stage liver affliction was small-scale.
The report was based on register, clinical, and histological data. The LPR is a unique source of information for monitoring long term outcome, every bit in this cohort of patients, and record linkage using the unique personal identification number ensures complete follow up.
The belch diagnosis in the LPR may vary in validity but is more often than not high.20– 22 We minimised this problem further by a thorough examination of the medical records and a search in the pathology annals supplementing the diagnostic information bachelor in the LPR. The index diagnosis, alcoholic versus not-alcoholic, was made from the information on alcohol intake in the medical record at the time of the index biopsy and before we requested data from the LPR and Registry of Causes of Death. However, if the patient had an alcohol related diagnosis at any time during the follow up catamenia, they were characterised as having alcoholic steatosis, regardless of alcohol intake. The ICD diagnoses from the registries were not altered or interpreted.
The majority of patients had not moved from the uptake surface area of Hvidovre Infirmary and medical records from the follow up catamenia were available. Information technology cannot be excluded that some patients with clinical cirrhosis were treated by their general practitioner and thereby not registered in the LPR. Even so, the structure of the Danish wellness service makes it likely that patients with clinically significant liver disease are admitted to hospital and the long follow upwardly period makes this fifty-fifty more than probable.
Death is recorded without errors in the Registry of Causes of Expiry while the cause of death may exist misclassified. Misclassifications in the death certificates may over or underestimate the risk of death from liver cirrhosis. In the group of patients with known excessive alcohol intake, a trend towards overestimation of cirrhosis as the cause of decease might be expected while patients with non-alcoholic fatty liver are less likely to be suspected of chronic liver diseases. This would underestimate the prevalence of the cirrhosis diagnosis for this group of patients both in the LPR and Registry of Causes of Death. In the four patients who did not die in infirmary, it is likely that a general practitioner completed the death certificate. In Kingdom of denmark, it is the patient'due south local general practitioner who writes the death certificate in cases of death outside hospital. This makes the document more valid considering of their knowledge of the patient. In the inclusion period, a high percentage of patients, who died during hospitalisation, had an dissection performed. We believe that information on liver disease finish points in this report are sufficiently valid even though histological verification could not be obtained in all cases.
Patients were classified as having not-alcoholic or alcoholic fatty liver on the data given to the doctor on booze intake at the time of the index liver biopsy. As this was not a prospective study, the validity of self reported alcohol intake can be questioned and was well-nigh likely underreported; potentially patients with high alcohol consumption may be misclassified every bit belonging to the non-alcoholic group. Because of the lack of a sensitive and specific mark of alcoholism, it is impossible to prove the not-drinking status of patients with NAFLD. Nosotros tried to recoup for this misclassification by examining all discharges registered in the LPR. If the patient was discharged from a hospital during the follow up period with an alcohol related diagnosis, they were classified as having alcoholic fat liver, regardless of when this hospitalisation took place. Ix patients would take been classified as non-alcoholic, based solely on information on alcohol consumption in the medical report at the time of the index liver biopsy merely had an alcohol related diagnosis registered during the follow upward menses and were after reclassified into the alcoholic group. Two of these adult cirrhosis. Thereby, the prevalence of cirrhosis was lowered in the non-alcoholic group and is probable to have increased the validity of the classification.
Patients may have stopped drinking alcohol subsequently the alphabetize liver biopsy and these individuals may not have the same take chances of developing chronic liver disease as individuals who go along to drink.xiv, xv All the same, the design of the written report did not allow us to analyse this aspect further. The same method has been used in other follow up studiesseven, 15 but past using the unique data from the registries, we believe classification into the 2 groups, non-alcoholic and alcoholic, is even more than valid.
Not all patients were examined for hepatitis B, and hepatitis C tests were non bachelor at the time of the index liver biopsy. However, none of these patients had whatever known risk factors for the development of hepatitis C, and the clinical follow up did non suggest viral hepatitis; furthermore, liver biopsies in all patients were consistent with NAFLD or alcoholic fat liver and did non show the typical findings of chronic hepatitis C infection.23, 24 Also, Denmark is a low prevalence area for infectious hepatitis in the full general population (0.08%).25, 26 However, we recognise that hepatitis C may exist present and that we could not control for this potential confounder in the follow up study.
Bouchier and colleagues27 observed a 75% survival charge per unit later 10 years in patients diagnosed with alcoholic fatty liver. Patients with this histological diagnosis had the best survival rate in the spectrum of alcoholic liver diseases. However, they estimated survival in the diverse groups of patients from the time of diagnosis, regardless of the age at diagnosis. We performed our statistical analysis with delayed entry, taking into account both the age of the patient and time of entry at diagnosis. Thereby the age distribution was not a bias. We found significantly college mortality in patients with alcoholic fatty liver in comparison with both type 1 NAFLD patients and the general population, as previous observed by Orholm and colleagues28 in patients with alcohol related liver diseases. Patients in our cohort with NAFLD had a benign course as but ane of 109 patients developed cirrhosis after the 16.7 year follow upwardly and the survival rate did not appear to differ from that of the general population when survival curves were compared. We did non compare the survival estimate statistically with the full general population but the survival curve of the general population was inside the confidence interval of the non-alcoholic fatty liver group for both men and women (fig 2 ▶).
Our findings are in contrast with previous reports on the prognosis for NAFLDane, vi, 9, eleven, 29– 33 and the risk of developing chronic liver diseases. This discrepancy may have several explanations. Other studies mainly comprised selected patients with NASH, which accounts for the college incidence of chronic liver diseases. Still, the patient accomplice in our report was the aforementioned as in other studies, mainly obese women, and we would accept expected that the natural history was the aforementioned, with development of NASH and a high prevalence of cirrhosis. It seems that factors other than obesity contribute to the evolution of chronic liver illness in patients with blazon i NAFLD. It may exist speculated whether pure non-alcoholic fatty liver predisposes to NASH and the evolution of chronic liver illness or if NASH develops primarily without the presence of fatty liver, which could explain the apparent different prevalence rates of cirrhosis in the report. Teli and colleaguesvii also found a skilful prognosis for patients with pure non-alcoholic fatty liver. Insulin resistance and hyperlipidaemia are other well known factors that predispose to fatty liver but we accept no data to substantiate this hypothesis. The natural history may also exist influenced by hitherto unknown genetic or nutritional differences, which could explain the dissimilar findings in studies from the United states of america in item.
It has previously been shown that obesity in both alcoholic34 and non-alcoholic patients predisposes to the evolution of fat liver and chronic liver affliction.35, 36 Obesity could be a contributing factor in patients in our cohort with alcoholic fatty liver, fifty-fifty though the observed number of cirrhosis among the 106 patients was comparable and not higher than in other reports on non-obese patients with alcoholic fatty liver.15 Non-alcoholic patients in our cohort had an extremely high median BMI of 42 kg/yard2. This makes our population a selected group, only was also a unique opportunity to study the natural history of NAFLD in a large accomplice with a long term follow up. Fifty-fifty though they were very obese, only i developed cirrhosis in the 16.7 years of follow upward.
In decision, in this long term follow up study, we demonstrated a loftier prevalence of cirrhosis in patients with alcoholic fatty liver, in contrast with a benign clinical grade in patients with type 1 NAFLD with no excess mortality. Information technology is important for clinicians to realise that fatty liver is one of the almost common causes of liver dysfunction, but few non-alcoholic individuals seem to develop chronic liver disease. However, more data on the natural history of NAFLD in large prospective follow up studies is needed to guide future decisions about diagnostic strategy and identification of subgroups with a risk of developing chronic liver disease and the potential demand for future specific treatments.
Acknowledgments
Financial back up was from the Liver Foundation at Hvidovre Hospital, University of Copenhagen, Denmark; Gerda and Aage Haenschs Foundation, Denmark; and the Danish Medical Association Inquiry Fund/The Vibe A Linholter Estate. The Danish National Enquiry Foundation supports the Danish Epidemiology Science Middle at the Institute of Preventive Medicine.
Abbreviations
-
NAFLD, non-alcoholic fatty liver disease
-
NASH, non-alcoholic steatohepatitis
-
BMI, torso mass index
-
LPR, the national registry of patients
-
ICD, International Classification of Diseases
-
ASAT, aspartate aminotransferase
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774026/
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