Mesothelioma Cancer: Diagnosis Of Mesothelioma Cancer

Jan 25, 2009 – Beginning with diagnosis mesothelioma with a review of the patient's medical history, including any history of asbestos exposure. A complete physical examination including x-rays of the chest or abdomen and lung function tests is performed. A CT (or CAT) scan or an MRI may also be useful. A CT scan is a series of detailed pictures of areas inside the body created by a computer linked to an x-ray machine. In an MRI, a powerful magnet linked to a computer is used to make detailed pictures of areas inside the body. These pictures are viewed on a monitor and can also be printed.
Such sophisticated imaging procedures as MRIs and CT scans usually offer a fairly clear diagnosis, but doctors almost always recommend one more test before coming to a definitive conclusion about any type of cancer. That test is known as a biopsy.

A biopsy, derived from the Greek word meaning "view of the living", involves removing a sample of fluid or tissue from the affected area and sending it to a pathologist for examination. The biopsy is done by inserting a thin needle into the area in question.

In a biopsy, a surgeon or a medical oncologist (a doctor who specializes in diagnosing and treating cancer) removes a sample of tissue for examination under a microscope by a pathologist. A biopsy may be done in different ways, depending on where the abnormal area is located. If the cancer is in the chest, the doctor may perform a thoracoscopy. In this procedure, the doctor makes a small cut through the chest wall and puts a thin, lighted tube called a thoracoscope into the chest between two ribs. Thoracoscopy allows the doctor to look inside the chest and obtain tissue samples. If the cancer is in the abdomen, the doctor may perform a peritoneoscopy. To obtain tissue for examination, the doctor makes a small opening in the abdomen and inserts a special instrument called a peritoneoscope into the abdominal cavity. If these procedures do not yield enough tissue, more extensive diagnostic surgery may be necessary.

If the diagnosis is mesothelioma cancer, the doctor will want to learn the stage (or extent) of the disease. Staging involves more tests in a careful attempt to find out whether the cancer has spread and, if so, to which parts of the body. Knowing the stage of the disease helps the doctor plan treatment.

If the cancer is found only on the membrane surface where it originated the mesothelioma symptom is described as localized. It is classified as advanced if it has spread beyond the original membrane surface to other parts of the body, such as the lymph nodes, lungs, chest wall, or abdominal organs.

Mesothelioma Treatments

We've compiled the most comprehensive and updated information on, including traditional and unconventional treatments, and the latest in clinical trials, and more.

Radiation & chemotherapy are common mesothelioma treatment options.

Highlighting topics such as, associated tests, and our treatment section offers the most helpful information available to mesothelioma victims.

Recent clinical studies have found that caffeine may prove to be beneficial in mesothelioma treatment and that the efficacy of current chemotherapy options is not as effective as once presumed. Make sure check back frequently for current research and advancements in mesothelioma treatments.

Mesothelioma Cancer

Mesothelioma is an uncommon form of cancer in which the average life span of a patient from the time of diagnosis until death is less than 6 months. Therefore, it is considered as one of the deadliest diseases known to man. According to The National Cancer Institute, "Malignant mesothelioma, a rare form of cancer, is a disease in which cancer (malignant) cells are found in the sac lining the chest (the pleura), the lining of the abdominal cavity (the peritoneum) or the lining around the heart (the pericardium)."

The only known cause for this disease is exposure to the deadly mineral, Asbestos. When particles of asbestos dust are inhaled, they decay inside the lungs, eating away at the mesothelial cells that make up the mesothelium – the outer lining that protects the body’s major organs such as the heart, stomach and lungs. Mesothelial cells protect these organs by producing a minute amount of lubricating fluid that helps the lungs expand and allows movement of the abdominal organs against one another freely. Mesothelioma occurs when these cells grow and spread uncontrollably. The tumor continues to grow around the lungs (pleurae), beginning first as a flat white plaque, and may also originate around the abdominal cavity.

Mesothelioma is still a relatively rare cancer though reported incidence rates have increased in the past 20-30 years. Mesothelioma occurs more often in men than in women and risk increases with age. However, this disease can appear in either children or women at any age too. The cause of the disease is not very well understood in the latter two groups, but evidence of possible asbestos exposure does exist for some of these cases as well.

Only one or two months of exposure to asbestos can result in mesothelioma 30 or 40 years later. Hence, workers in factories and mines, constantly exposed to the dust and fibers from the asbestos, are most susceptible to this form of cancer. People exposed to this mineral 30 or 40 years ago are now being diagnosed with mesothelioma. This long latency period also makes this form of cancer very difficult to diagnose.

Malignant mesothelioma is divided into three main types. About 50% to 70% of mesothelioma occurrences are the epithelioid (relating to the membranous cellular tissue that covers free surface or lines of a tube or cavity) type. This type has the best prognosis (outlook for survival). The other two types are the sarcomatoid (resembling a malignant tumor arising from connective tissues) type (7%-20%), and the mixed/biphasic (having two phases) type (20%-35%). These are the variations associated with mesothelioma - Pleural mesothelioma, which affects the lining of the lungs, and the most common variation of this cancer. Symptoms include breathing and swallowing difficulties, coughing, shortness of breath, fever and weight loss. The abdomen is another area affected by this cancer, and this variation is known as peritoneal mesothelioma. Symptoms of peritoneal mesothelioma can include nausea and vomiting, weight loss and loss of appetite, fever, bowel obstruction and pain or swelling of the stomach area. The last variation of the cancer is pericardial mesothelioma, which is where the cancer affects the heart and the tissue surrounding it. This variation is rare, and symptoms can include palpitations, breathing difficulties, and persistent coughing.

Mesothelioma was recognized as a tumor of the pleura, peritoneum and pericardium in the late 1700's. However it was only in the 1960s, that this particular type of tumor was described in more detail. This was the period when J.C.Wagner described 32 cases of workers in the Asbestos Hills in South Africa.

Symptoms associated with mesothelioma are very similar to a number of other diseases which are more common. Therefore, it is not unusual for patients to be misdiagnosed when they display any or all of mesothelioma symptoms. The current treatments for mesothelioma include surgery, radiation therapy, palliative therapy and chemotherapy. Unfortunately, these treatments do not have a high success rate particularly on patients in whom the cancer is in its later stages. Like most cancers, the faster it is diagnosed and treated, the higher the chances of recovery. Treatment for mesothelioma is still being investigated through clinical trials and research, but as a rule, it responds poorly to the treatments that are currently used.

Lung cancer after treatment for Hodgkin's lymphoma: a systematic

Developments in modern chemotherapy and radiotherapy mean that most patients with Hodgkin's lymphoma can now be cured. However, the long-term effects of anticancer treatment include an increased risk of a second malignant disease. We have done a systematic review of studies reporting long-term complications of the treatment of Hodgkin's lymphoma published in English since 1985. These studies show that risk of lung cancer is significantly increased in patients treated for Hodgkin's lymphoma, with a reported mean relative risk of 2·6—7·0 and a significantly increased absolute excess risk. The absolute excess risk increases with time from treatment, for as long as 20—25 years, and is highest in patients treated at age 45 years or older. Both chemotherapy and radiotherapy contribute to the risk, and evidence suggests that the effects are additive. Cigarette smoking seems to multiply the risk associated with both chemotherapy and radiotherapy. In the high-risk group of patients, 50—150 patients per 1000 are expected to develop lung cancer by 10—20 years after treatment. The role of screening in this group of patients has not yet been assessed, but an international study combining CT with genomic and proteomic assessment is planned.

Treatment of Advanced Non-Small-Cell Lung Cancer: A Review of Current Randomized Clinical Trials and an Examination of Emerging Therapies

Abstract and Introduction

Abstract

Background:

Lung cancer continues to be the leading cause of cancer-related deaths for Americans. As most patients present with nonsurgically curable disease, major efforts have been made in the treatment of advanced non-small-cell lung cancer (NSCLC) with chemotherapy. Several new agents and new combinations of chemotherapy are available.

Methods:

The author reviews randomized clinical trials investigating chemotherapy for advanced NSCLC in chemotherapy-naive patients, in patients who present with relapsed or progressive disease, and in elderly patients. Therapies that incorporate new biological agents to target specific aberrations in lung cancer are discussed.

Results:

Several clinical trials demonstrate improvement in overall survival as well as quality of life with chemotherapy treatment of advanced NSCLC. Better options are available for patients who have relapsed after first-line chemotherapy, and treatment of elderly patients with chemotherapy has demonstrated benefit in survival and quality of life. New agents that target molecular pathways are being tested in patients with early-stage disease.

Conclusions:

Despite progress with newer agents for the treatment of advanced NSCLC, only 14% of patients with the disease are alive at 5 years after initial diagnosis. New therapies are needed.

Introduction

Lung cancer continues to be the leading cause of cancer-related deaths for Americans.^[1] Despite nearly twice the estimated cases of prostate cancer in men,estimated deaths from lung cancer are nearly 3-fold higher. Similarly for women, estimated cases of breast cancer are nearly 2.5-fold higher than lung cancer, but the estimated death rate for lung cancer is nearly 2-fold higher. While age-adjusted cancer rates for lung cancer have fallen in the past decade for men, the same is not true for women. Overall, the 5-year relative survival rate for lung cancer is 14% for the years 1989-1995,which is significantly, albeit minimally, increased from 13% for the years 1974-1976 and 1980-1982.

Approximately 75% to 80% of cases are of the non-small-cell histology, and the majority of patients present with either locally advanced disease (stage III)or metastatic disease (stage IV). Importantly, patients who undergo curative surgical resection for apparent localized disease have survival rates ranging between 50% and 80%, implying the need for better systemic treatment to cure occult micrometastatic disease.Therefore, the majority of patients either present with advanced disease requiring chemotherapy or require chemotherapy at the time of relapse after surgical resection. While efforts to reduce smoking are crucial to the eventual control of the disease,newer treatments for patients who currently have the disease are critical.

For some time,the treatment of non-small-cell lung cancer (NSCLC) with cytotoxic chemotherapy remained controversial, given the unclear impact on patient survival. A review of chemotherapy for lung cancer in 1992 identified the active agents as cisplatin,mitomycin, ifosfamide, etoposide, and the vinca alkaloids vinblastine and vindesine.^[2] Response rates to single agents were approximately 20% and, while combination chemotherapy suggested improvements in response rates, the impact of chemotherapy on patient survival was unclear. This review concluded that the impact of chemotherapy on survival for patients with NSCLC was not demonstrated and "it is difficult to recommend incorporating chemotherapy into the standard care of patients with disseminated NSCLC."^[2]

Support of treating patients with advanced NSCLC came from an international collaborative meta-analysis using updated data on patients from 52 randomized clinical trials.^[3] Eleven trials examined best supportive care vs best supportive care plus chemotherapy. Two trials used long-term alkylating agents, one trial used etoposide as a single agent, and the remaining eight trials used cisplatin-based chemotherapy. All except one trial enrolled patients with locally advanced disease (stage III) as well as metastatic disease (stage IV). Use of long-term alkylator therapy was associated with an increased rate of death, although given the limited number of trials, confidence intervals were wide and statistical significance was not reached. Patients treated with cisplatin-containing regimens demonstrated a 27% reduction in the risk of death. This was equivalent to an absolute improvement in survival of 10% at 1 year with a modest improvement in median survival of 1.5 months. Further analysis did not demonstrate that any grouping based on sex, age, histology,performance status, or stage benefited any more or any less than others. The demonstration that patients who received cisplatin-based chemotherapy in addition to surgery or radiotherapy also had improved outcomes gave more support to the idea that cisplatin plays an important role in the treatment of NSCLC. It was not clear which cisplatin combination regimen was superior,but the majority of combinations consisted of cisplatin plus either a vinca alkaloid or etoposide.

This study concluded that cisplatin-based chemotherapy programs may provide a 10% absolute benefit in 1-year survival. Although the results were modest, they were nonetheless important from a public health perspective,given the large numbers of patients with nsclc who potentially would receive benefit. While cisplatin demonstrated an improvement in patient survival,its use was still greeted with a degree of unease due to its toxicity profile and difficulty in administration.The analog carboplatin was then developed, and two trials compared carboplatin to cisplatin. The first performed by the Eastern Cooperative Oncology Group(ECOG) compared three cisplatin-based regimens to single-agent carboplatin.^[4] The results demonstrated that carboplatin-treated patients had better overall survival and less toxicity compared with cisplatin-containing regimens. The second trial performed by the European Organization for Research and Treatment of Cancer(EORTC) compared cisplatin and etoposide vs carboplatin and etoposide and concluded that no significant differences in survival were apparent but that patients treated with carboplatin had significantly less leukopenia,nausea and vomiting, and diarrhea.^[5]

Treatment Gives Lung Cancer Patients With Inoperable Tumors Two Years Or More, Study Shows

ablation (RFA)—an interventional treatment that “cooks” and kills lung cancer tumors with heat—greatly improves survival time from primary or metastatic inoperable lung tumors, according to a new study. Of the 244 patients suffering from lung metastases (195 patients) or primary non-small cell lung cancer (49 patients), 70 percent were still alive at two years, including 72 percent for lung metastases and 64 percent for primary lung cancer

These survival results are similar to surgical results from other studies, but the interventional treatment is less invasive and has far fewer side effects and less recovery time. The researchers found that RFA often can completely destroy the primary tumor and, therefore, extend a patient’s survival and greatly improve his or her quality of life. Survival thus becomes dependent on the extent of disease elsewhere in the body.

Of the 49 patients (ages 27–85) with non-small cell primary lung cancer who were treated with RFA, 85 percent had no viable lung tumors after one year on imaging, and 77 percent had no viable lung tumors after two years, which indicates a cure. This study was conducted in tumors four centimeters in diameter or smaller, and even better results were obtained for tumors smaller than two centimeters.

“About two-thirds of patients diagnosed with non-small cell lung cancer are ineligible for surgery and typically have less than 12 months to live. A subset of these patients ineligible for surgery can be treated with RFA with the intention of curing the primary tumor. Thus, 70 percent of my patients gained at least another two years. This new outpatient treatment is effective, allowing us to treat patients who historically have only palliative options, such as chemotherapy or radiation therapy,” said Thierry de Baere, M.D., interventional radiologist with the Institut Gustave Roussy in Villejuif, France.

These results are similar to studies in the United States and add to the growing body of evidence for RFA in extending survival time.

RFA is effective for local control of lung cancer, providing an attractive option for patients who may not be ideal surgical candidates, who wish to avoid conventional surgery or who have failed conventional treatments. A trial is needed to define if RFA can replace surgery in a subset of patients.

By the time lung cancer becomes symptomatic, 85 percent of patients are incurable, often due to serious coexisting health conditions or poor respiratory function. Most patients who are diagnosed with non-small cell lung cancer are not surgical candidates at the time of diagnosis. For these patients, minimally invasive interventional radiology procedures can improve survival, reduce pain and improve quality of life. Interventional radiologists are uniquely skilled in using imaging guidance to deliver targeted cancer treatments throughout the body.

the treatment of alcoholic liver disease

Over the past 20 years we have moved from a situation in which we had no therapy for alcoholic liver disease, through a period when any therapy we had was purely empirical, to an era where we have specific therapies for different aspects of this disease based upon sound pathogenic principles. In this short review, an attempt has been made to summarize these advances in the understanding of the pathogenesis of alcoholic liver disease. In particular, they explain why patients with severe acute alcoholic hepatitis continue to deteriorate in hospital despite withdrawal from alcohol, why they respond to corticosteroids, why only a small percentage of patients develop cirrhosis, and why propylthiouracil may offer Protection.

Antioxidant supplements for non-alcoholic fatty liver disease and/or steatohepatitis

Non-alcoholic fatty liver disease (NAFLD) is characterised by fatty deposition in the hepatocytes of patients with minimal or no alcohol intake and without other known cause. NAFLD includes a wide spectrum of histologic abnormalities ranging from hepatic steatosis to non-alcoholic steatohepatitis (NASH), or even cirrhosis. Antioxidant supplements, therefore, could potentially protect cellular structures against oxidative stress and the resulting lipid peroxidation.

Objectives

To systematically evaluate the beneficial and harmful effects of antioxidant supplements versus no intervention, placebo, or other interventions for patients with NAFLD or NASH.

Search strategy

We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (June 2006), the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 2, 2006), MEDLINE (1966 to June 2006), EMBASE (1980 to June 2006), and The Chinese Biomedical Database (1978 to June 2006). No language restrictions were applied.

Selection criteria

Randomised clinical trials evaluating any antioxidant supplements versus no intervention, placebo, or other interventions in patients with NAFLD or NASH. Our inclusion criteria for NAFLD or NASH were based on history of minimal or no alcohol intake, imaging techniques showing hepatic steatosis, and/or histological evidence of hepatic damage (including simple steatosis, fatty infiltration plus nonspecific inflammation, steatohepatitis, fibrosis, and cirrhosis), and by exclusion of other causes of hepatic steatosis.

Data collection and analysis

We extracted data from the identified trials and contacted authors. We used a random-effects model and fixed-effect model with the significant level set at P = 0.05. We evaluated the methodological quality of the randomised trials by looking at how the generation of allocation sequence, allocation concealment, blinding, and follow-up were performed. We made our analyses following the intention-to-treat method by imputing missing data.

Main results

We identified six trials: two were regarded of high methodological quality and four of low methodological quality. None of the trials reported any deaths. Treatment with antioxidant supplements showed a significant, though not clinically relevant, amelioration of aspartate aminotransferase levels, but not of alanine aminotransferase levels, as compared to placebo or other interventions. Gamma-glutamyl-transpeptidase was decreased, albeit not significantly, in the treatment arm. Radiological and histological data were too limited to draw any definite conclusions on the effectiveness of these agents. Adverse events were non-specific and of no major clinical relevance.

Authors' conclusions

There is insufficient data to either support or refute the use of antioxidant supplements for patients with NAFLD. It may be advisable to carry out large prospective randomised clinical trials on this topic.

Treatment of alcoholic liver disease

INTRODUCTION — There are at present few specific therapies available for patients with alcoholic liver disease. There is, however, one extremely important intervention — abstinence — since continued alcohol ingestion is the single most important risk factor for progression in patients with alcoholic liver disease. Abstinence is also critical for those patients with advanced disease who may eventually require liver transplantation; in this setting, continued drinking will remove the patient from consideration. Referral to a rehabilitation program is usually necessary in combination with family support and counseling.

Alcoholic Liver Disease

Alcohol causes a spectrum of liver injury that can progress from fatty liver to alcoholic hepatitis (often considered an intermediate stage) to cirrhosis.

Alcohol consumption is high in most Western countries. In the US, annual ingestion is estimated at 10 L of pure ethanol equivalent per person; 15 million people abuse or are dependent on alcohol. The male:female ratio is 11:4.

Risk Factors

The major causative factors in alcoholic liver disease are quantity of alcohol consumed, duration of alcohol abuse (usually > 8 yr), nutritional status, and genetic and metabolic traits. Among susceptible people, a linear correlation generally exists between the amount and duration of alcohol use and the development of liver disease. As little as 20 g of alcohol in women or 60 g in men can cause serious liver damage when consumed daily for several years. Consuming more than 60 g/day for 2 to 4 wk produces fatty liver even in otherwise healthy men; 80 g/day may lead to alcoholic hepatitis; and 160 g/day over a decade can lead to cirrhosis. Alcohol content is estimated to be the beverage volume (in mL) multiplied by its percentage of alcohol. For example, 16 mL of alcohol is contained in roughly 40 mL of an 80‑proof (40% alcohol) beverage. Each mL of alcohol contains about 0.79 g. Although values can vary, the percentage of alcohol is about 2 to 7% for most beers and 10 to 15% for most wines.

Only 10 to 20% of alcoholics develop cirrhosis. Women are more susceptible than men (even when adjusting for smaller body size), probably because women have less alcohol dehydrogenase in their gastric mucosa, which lessens the first-pass oxidation of alcohol. Alcoholic liver disease often runs in families, suggesting genetic factors (eg, deficiency of cytoplasmic enzymes that eliminate alcohol). Malnutrition, particularly protein-energy malnutrition, increases susceptibility. Other risk factors include a diet high in unsaturated fat, iron deposition in the liver, and concomitant hepatitis C virus infection.

Pathophysiology

Alcohol is readily absorbed from the stomach and small intestine. It cannot be stored; > 90% is metabolized through oxidation. The first breakdown product is acetaldehyde, which is produced by three enzymatic pathways: alcohol dehydrogenase (responsible for about 80% of metabolism), cytochrome P‑450 2E1 (CYP2E1), and catalase.

Acetaldehyde is converted to acetate by mitochondrial aldehyde dehydrogenase. Chronic alcohol consumption enhances acetate formation. The processes generate hydrogen, which converts nicotinamide-adenine dinucleotide (NAD) to its reduced form (NADH), increasing the redox potential in the liver. This replaces fatty acids as a fuel, lowers fatty acid oxidation, and allows triglycerides to accumulate, causing fatty liver and hyperlipidemia. The excess hydrogen also converts pyruvate to lactate, which decreases glucose production (hypoglycemia can result), causing renal acidosis, reduced urate excretion, hyperuricemia, and thus gout.

Alcohol metabolism may also make the liver hypermetabolic, causing hypoxia and free radical–induced lipid peroxidative damage. Alcohol and undernutrition deplete antioxidants, such as glutathione and vitamins A and E, which predispose to such damage.

Acetaldehyde initiates much of the inflammation and fibrosis of alcoholic hepatitis. It transforms the stellate (Ito) cells lining liver blood channels (sinusoids) into fibroblasts that develop myocontractile elements and actively produce collagen. The sinusoids narrow and fill, limiting transport and blood flow. Gut endotoxins, which the impaired liver can no longer detoxify, lead to production of inflammatory cytokines. Acetaldehyde and lipid peroxidation products recruit leukocytes, resulting in production of more inflammatory cytokines. This elicits a vicious circle of inflammation that culminates in fibrosis and loss of hepatocytes.

Fat is deposited throughout the hepatocytes, a result of increased input from peripheral adipose tissue, elevated triglyceride synthesis, decreased lipid oxidation, and reduced lipoprotein production that impairs fat export from the liver.

Diagnosis and Treatment of Non-alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent condition affecting adults and children, leading to significant morbidity. It is often associated with the metabolic syndrome, although multiple pathogenetic mechanisms have been suggested. In the coming decades, it promises to be the leading cause of liver disease in industrial countries.
Aim: To provide a comprehensive, updated review of diagnosis and management of NAFLD and to appraise the evolution of new modalities in these areas.
Methods: An Ovid MEDLINE search was performed to identify pertinent original research and review articles. Selected references in these articles were also evaluated.
Results: The diagnosis of hepatic steatosis and steatohepatitis or non-alcoholic steatohepatitis (NASH) is not yet possible without liver biopsy. This is impractical given the large numbers affected by the condition. Current therapy has focused on improving insulin resistance and mediators of inflammation, factors probably associated with disease progression.
Conclusions: There are no proven non-invasive diagnostic modalities to distinguish NAFLD and NASH, but new biomarker panels are approximating the liver biopsy in accuracy. Therapeutic targets of drug development are in early stages, but a multifaceted approach will probably yield several treatment options in the years to come.

Introduction

Fatty liver disease is not a new condition, and indeed, alcohol-induced liver injury dates back thousands of years. The entity of non-alcoholic fatty liver disease (NAFLD) is also not a new condition, but was not appreciated in early reports. In the 1950s, livers consistent with non-alcoholic steatohepatitis (NASH) were described in obese individuals, but surreptitious alcohol use was suspected.^[1] In the now famous report of Ludwig et al. in 1980, the term NASH was coined.^[2] It was not until the 1990s, however, that the prevalence and increasing incidence of the condition brought it into the limelight. It was not coincidence that the recognition of NAFLD paralleled the alarming increase in body mass index (BMI) in the American population^[3] (Figure 1). The umbrella term of NAFLD embodies simple steatosis, NASH and advanced fibrosis or cirrhosis related to this pathological entity.

Non-alcoholic fatty liver disease: natural history, pathogenesis and treatment

Norma C Mcavoy

Liver Unit, Royal Infirmary of Edinburgh, Edinburgh, UK

James W Ferguson

Medical Unit, Royal Victoria Hospital, Kirkcaldy, UK

Ian W Campbell

Medical Unit, Royal Victoria Hospital, Kirkcaldy, UK

Peter C Hayes

Liver Unit, Royal Infirmary of Edinburgh, Edinburgh, UK

Non-alcoholic fatty liver disease (NAFLD) is the term used to describe the alcohol-like liver injury that occurs in the absence of alcohol abuse. It embraces a range of histological abnormalities including simple steatosis or fatty liver, non-alcoholic steatohepatitis (NASH) and NAFLD induced cirrhosis. The predominant risk factor for NAFLD appears to be insulin resistance. Simple steatosis and NASH are generally asymptomatic and it is only the development of cirrhosis that has clinical consequence. At present, therapy in NAFLD concentrates on managing risk factors but in the future clinical trials may provide robust evidence for the use of insulin sensitising agents and other potential therapies.