GI

Should H. pylori Eradication Be Confirmed?

June 12, 2008

h-pylori.jpgCommentary by Fritz Francois, MD, MS, NYU Division of Gastroenterology

Humans are essentially the only reservoir for Helicobacter pylori, which is estimated to colonize the stomach of about half the world’s population (1). Although the bacteria generally do not invade the mucosa, attachment to the epithelium leads to an inflammatory reaction with neutrophils, lymphocytes, plasma cells, and macrophages. Over time, the persistent inflammation leads to changes in the gastric mucosa that may predispose to the development of dysplasia(2). Read more »

Class Act: Is there clinical evidence for use of probiotics in the treatment of IBS?

March 12, 2008

ibs.jpgClass act is a feature of Clinical Correlations written by NYU 3rd and 4th year medical students. These posts focus on evidenced based answers to clinical questions related to patients seen by our students in the clinics or on the wards. Prior to publication, each commentary is thoroughly reviewed for content by a faculty member.

Commentary by Alexander Jow, MSIII

Irritable bowel syndrome (IBS) is a poorly understood disorder, commonly encountered in clinical practice; IBS accounts for more than one-third of all referrals to gastroenterologists (1).  IBS is characterized by abdominal discomfort or pain occurring with changes in bowel habits (diarrhea, constipation, or mixed diarrhea and constipation) that are not explained by an established organic or biochemical abnormality (2). While management of IBS is now largely focused on treatment of the diarrhea or constipation component of IBS symptomatology, the disease’s complex pathophysiology has hindered development of optimal therapeutics. Those agents that have been marketed, Alosetron (Lotronex) and Tegaserod (Zelnorm), have since been withdrawn from the market or have seen their usage severely limited by the FDA. Further, use of a medication that controls diarrhea can precipitate constipation and vice versa. New approaches are sorely needed given the ubiquity of the disease and the significant cost, in terms of dollars and quality of life.

Many mechanisms have been proposed to explain the pathogenesis of IBS, though the most feasible invokes aberrant transmission of pain signals from the enteric to the central nervous system. Local bowel factors likely also play an important role by modulating the patients’ perception of abdominal symptoms. One such local factor, the colonic flora, has been implicated in IBS pathogenesis.  This hypothesis proposes that ‘unfavorable’ gut flora, such as gas-producing bacteria, may predispose patients to gastrointestinal symptoms, such as abdominal bloating and flatulence. In order to counter-balance the effects from potentially symptom-inducing bacteria, oral administration of probiotic bacteria as live microbial food supplements, has been proposed.  Probiotic bacteria, such as Bifidobacterium, Lactobacillus, and Streptocccus genera as well as yeasts of the Saccharomyces genus are believed to compete with, and replace “pathogenic” bacteria in the gut lumen (3). As therapeutics, probiotics would provide ease of administration with very low risk of adverse events, especially compared to those medications already marketed for IBS treatment (4).

Thus far, studies on probiotic efficacy in the treatment of IBS have yielded conflicting results. In a study done in 2000, administration of Lactobaccillus casei was not shown to improve disease symptoms (5).  However, oral supplementation with Lactobaccillus plantarum was found to be effective in reducing flatulence and abdominal pain in two double-blind, placebo-controlled studies (6,7).  A more recent study using a probiotic formulation, VSL#3, which contains a mixture of probiotic bacterial species, showed no significant differences in mean gastrointestinal transit measurements, bowel function scores, or global symptom relief, though it was effective at reducing bloating (8).

In conclusion, there is no definitive evidence showing that administration of probiotics is effective for treatment of IBS.  Our understanding of IBS pathophyisology is limited, so perhaps future studies may provide the rationale for using probiotics in a subset of IBS patients.   

References

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Meeting Perspectives: American Association for the Study of Liver Diseases

February 27, 2008

aasld_logo_bottom1.gifLast November, thousands of eager hepatologists descended on Boston to attend the AASLD Liver Meeting. While there was an enormous amount of hepatology information presented, one intrepid GI fellow, Ponni Perumalswami MD, has compiled a few of the most interesting presentations.

In a late-breaking abstract, major results were presented by Dr. Di Bisceglie from the HALT-C trial. This study is designed to examine the effect of prolonged antiviral therapy with peginterferon in prevention of the complications of advanced liver disease associated with hepatitis C. This has been a randomized, controlled trial of patients with chronic hepatitis C who received peginterferon alfa-2a (90mcg per week) for 3.5 years versus those who received no treatment. The patients, in addition to their chronic hepatitis C infection had to have advanced fibrosis and were non-responders to prior therapy with peginterferon and ribavirin. A total of 1,050 patients were randomized (517 treatment, 533 control). While treatment resulted in a significant decrease in serum ALT, HCV RNA levels and inflammation on liver biopsy, the authors found no significant effect on the most important endpoints of death, decompensation of their liver disease, development of hepaticellular carcinoma or an increase in hepatic fibrosis. Therefore, they were forced to conclude that long-term therapy with peginterferon did not reduce the rate of disease progression and that these findings do not support maintenance therapy with peginterferon in patient with chronic hepatitis C and advanced fibrosis who are nonresponders to a course of peginterferon/ribavirin therapy.

Another important presentation was given by Dr. Terrault who discussed the unique aspects of liver disease management in women. While the authors described a number of important observations, the most interesting were the findings that the risk of amenorrhea is increased in women with cirrhosis. Furthermore, in pregnant women with cirrhosis, portal hypertension is a major complication, and variceal bleeding occurs in 25-40% of such patients. He therefore concluded that prophylactic endoscopic variceal banding should be considered in anticipation of pregnancy or if bleeding occurs. TIPS should also be considered. Dr Terrault also stated that women with chronic hepatitis C have slower rates of fibrosis progression as compared to men, and that when they are treated for their disease, they are more likely to attain a sustained virologic response. All is not optimistic, though, because during their post-menopause years their HCV disease and progression to fibrosis tends to accelerate. Once these women hit the post-menopausal period, their risk of developing hepatocellular carcinoma also increases.

The natural history of hepatitis B infection is also different in women. Women with chronic HBV who are e antigen positive and who have a high viral load have increased prophylaxis failure in studies where lamivudine was used in the third trimester. During pregnancy, the patients HBV liver disease may also flare, so patients have to be followed closely. In pregnant women with primary biliary cirrhosis (PBC), there is an increased risk of developing jaundice, perhaps related to increases in estrogen. These patients also experience an increased rate of still births and premature labor with increased cholestasis.

Treatment of these patients with ursodiol seems safe, though patients may require fat soluble vitamin replacement and consideration for early delivery. In pregnant women with autoimmune hepatitis, flares are more common in the first trimester, and while treatment with prednisone seems to be well tolerated, cyclosporine may increase the risk of premature labor and low birth weight infants.

In a final presentation, Dr. Fallon described some of the pulmonary vascular complications of liver disease. He stated that pulmonary vascular complications of liver disease comprise two distinct entities: hepatopulmonary syndrome (HPS, microvascular dilatation) and portopulmonary hypertension (POPH), which involves vasoconstriction and vascular remodeling in resistance vessels. These are important entities for the following reasons, HPS is found in 15-30% of patients with cirrhosis and appears to increase mortality and risks of liver transplantation, particularly when hypoxemia is present. Furthermore, no medical therapies are available, although liver transplantation has been effective in reversing this syndrome in some patients. There are no reliable screening tests or clinical predictors for HPS and screening protocols should be a future area of development. In comparison, POPH is found rarely; but in patients undergoing liver transplantation, it is associated with a significantly increased perioperative mortality. Transthoracic echocardiography is recommended for screening and right heart catheterization is required to establish the diagnosis. Medical therapies are increasingly effective in improving pulmonary vascular hemodynamics in POPH and may result in better perioperative outcomes.

Treatment of obesity with bariatric surgery: evidence and implications

November 15, 2007

vertical_banded_gastroplasty.jpgCommentary by Jatin Roper MD PGY-3 and Christine Ren MD Associate Professor, Department of Surgery

Bariatric procedures to treat obesity involve the restriction of the gastric reservoir, bypass of part of the gastrointestinal tract, or both. Worldwide, an estimated 300 million people are obese, and in the United States, the percentage of adults who are obese increased from 15% in 1995 to 24% in 2005. (Obesity is defined as a Body Mass Index or BMI of 30 or more, measured as kg / m2; for example, a woman 5 feet, 4 inches tall weighing 175 pounds.) Obesity is associated with, but not limited to, increased risk of coronary artery disease, stroke, diabetes, obstructive sleep apnea, osteoarthritis, several forms of cancer, and depression, as well as decreased quality of life.

Non-surgical therapy for obesity

Therapy for obesity has included dieting, exercise, and medications. However, reduction in caloric intake combined with exercise typically results in 5-10% reduction in weight (roughly 10-15 pounds) over a number of months, which is rarely sustained. There are no truly effective pharmacologic therapies for obesity; the only currently FDA-approved compounds, sibutramine (trade name Meridia), orlistat (trade name Xenical), and phentermine are limited by side effects and rebound weight gain after discontinuation.

Types of bariatric surgery

Surgical modalities of bariatric surgery can be grouped by their intended physiologic effects: Vertical-banded gastroplasty and adjustable gastric banding involve gastric restriction, while jejunoileal bypass and bilio-pancreatic diversion induce malabsorption; Roux-en-Y gastric bypass contains components of both of these basic types. Adjustable gastric banding and Roux-en-Y gastric bypass are now the favored procedures, and are often performed laproscopically. In gastric banding, a band is placed around the proximal portion of the stomach. In gastric bypass, the stomach is divided into a small proximal gastric pouch and the remaining main stomach is bypassed. The gastric pouch is connected to the small bowel by a jejunal segment, called a Roux limb.

Clinical evidence

A meta-analysis of 136 studies involving 22,094 patients by Buchwald et al. (JAMA 2004;292(14):1724-37) found a peri-operative mortality of 0.1% of purely restrictive procedures and 0.5% for gastric bypass. Almost all patients pooled in the study were followed for approximately two years. Bariatric surgery resulted in resolution of co-morbidities such as diabetes (77% of patients), hypertension (62%), hyperlipidemia (70%), and obstructive sleep apnea (86%). They report an overall excess weight loss of 48% for gastric banding and 62% for gastric bypass.

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Why Does Hypertriglyceridemia Lead to Pancreatitis?

October 4, 2007

fat_triglyceride_shorthand_formula.pngCommentary by Daniel Frenkel, PGY-2

Case: A 46 year old male with diabetes on oral hypoglycemic medications is admitted to the hospital with one day of constant epigastric pain, nausea, vomiting, and an inability to tolerate oral intake. You are concerned about pancreatitis but laboratory analysis reveals amylase levels that are within the normal reference range. You notice that his glucose level is 410mg/dL and that the specimen is described as lactescent. Should you still be concerned about acute pancreatitis?

Lactescent or lipemic blood samples are indicative of elevated fatty substances usually in the form of triglycerides. Such samples may interfere with amylase assays and produce false negative results to the extent that acute pancreatitis may actually be the correct diagnosis in a patient with normal amylase levels. While gallstones and alcohol account for roughly 80% of cases of pancreatitis, hypertriglyceridemia is the next most common etiology, accounting for roughly 1-4% of cases (sometimes noted up to 7%). An association between elevated triglyceride levels and pancreatitis exists where mild to moderate elevations are considered to be an epiphenomenon, while elevations greater than 1,000mg/dL can lead to pancreatitis. Despite the frequency of hypertriglyceridemia causing pancreatitis, it remains unclear how to predict which patients with triglyceride levels greater than 1,000mg/dL will actually develop this disorder.

Similar to cholesterol, triglycerides have both exogenous and endogenous sources. When triglycerides are obtained from dietary sources they are initially packaged in chylomicrons while endogenous triglycerides synthesized by the liver are packaged in VLDL. These two lipoproteins are the predominant source of triglycerides in blood and interact with lipoprotein lipase in peripheral tissue in order to store triglycerides in muscle and adipose tissue. Therefore, the development of hypertriglyceridemia is dependent on a balance between the synthesis and catabolism of these lipoproteins. Primary hypertriglyceridemia is a category of rare hereditary diseases that can cause elevated triglycerides which include Familial Chylomicronemia (Type I Hyperlipidemia), Familial Hypertriglyceridemia (Type IV Hyperlipidemia), and Familial Combined Hyperlipidemia (Type V Hyperlipidemia). Secondary hypertriglyceridemia has numerous common etiologies such as alcohol, diabetes, diet, obesity, estrogen, pregnancy, CRF, hypothyroidism, and drugs (thiazides, beta-blockers, protease inhibitors). The primary hereditary disorders are capable of producing triglyceride levels greater than 1,000mg/dL, while secondary causes require a baseline defect in triglyceride catabolism which is then subjected to the precipitating insult to achieve similar levels.

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X Ray Visions Mystery Quiz- The Answer

August 30, 2007

Before you read the answer, you may want to review the initial Mystery Quiz posted last week.

Commentary by Andrew Hardie MD, Fellow, NYU Department of Radiology

Although this patient’s symptoms were not the most typical of this entity, the CT findings in this case are diagnostic of a perforated anterior duodenal ulcer. The most essential observation, and the one that alters management, is the presence of intraabdominal free air (arrows). The small collections of air in this case are not unusual for bowel perforations, especially proximally. One can see how occasionally these small volumes of free air may not be able to be seen on plain films, especially inadequately positioned films.

The specific location of the free air in this case directs one to suspect a duodenal perforation. Air is seen in the periportal region, around the duodenum (green arrows), and in this case, at the site of the perforation in the duodenal wall (red arrow).

ansewr2.jpganswer1.jpg

A point of interest is that only the anterior duodenal bulb wall is intraperitoneal. Therefore, this must be an anterior wall ulcer. A posterior wall ulcer will lead to gastrointestinal bleeding, because, if you remember your anatomy, the gastroduodenal artery lies directly posterior to the duodenal bulb. Although very rare, a perforated posterior wall ulcer would cause retroperitoneal air, not intraperitoneal air.

The patient in this case reported severe epigastric pain, which could be indicative of peptic ulcer disease. However, physical exam was not suggestive of peritonitis. It is important to remember that atypical presentations of perforated ulcers can occur, although this is more commonly seen in elderly patients. Also, in this case, the perforation could have occurred in the interval between admission and abdominal imaging. The patient was taken to the OR for immediate repair of the perforation and postoperative clinical course was uneventful. Upon further questioning, he did admit to heavy weekend alcohol use as well as recent increased NSAID use for some low back pain.

Are beta blockers indicated in cirrhotics with small varices?

August 1, 2007

evarices.jpgCommentary by Bani Chander MD, PGY-2

Esophageal varices are a common complication of cirrhosis and approximately one-third of all cirrhotic patients with varices will develop a variceal bleed [1]. Each episode of variceal hemorrhage is associated with a 15 to 20 percent risk of mortality in patients with severe liver dysfunction.  The risk of bleeding is related to the location, size, and appearance of the varix, presence of red wale markings, variceal pressure, prior history of variceal bleeding, as well as the severity of hepatic dysfunction (classified by Child-Pugh class.)

In patients with cirrhosis, elevated portal pressure develops as a result of both increased portal inflow due to splanchnic arteriolar vasodilatation in combination with an elevated resistance to outflow through hepatic sinusoids.  Varices develop when the hepatic venous pressure gradient or HVPG (pressure between the portal and hepatic veins) rises above 12 mmHg, as a compensatory mechanism to decompress the portal vein and return blood to the systemic circulation. In a review of 12 studies, including 943 patients, D’Amico and colleagues showed that reducing HPVG<12mmHg significantly reduced the risk of variceal bleeding in cirrhotics. [2]

Non-selective beta-blockers impair the formation of varices by decreasing the β-2 receptor mediated vasodilatory tone in mesenteric arterioles.  This results in unopposed alpha vasoconstriction and therefore a decrease in portal venous inflow. In addition, the systemic effects of beta blockers on cardiac output via β-1 receptor blockade also contributes to the reduction of portal venous inflow.

It is well known that non-selective beta- blockers prevent variceal bleeding in patients with moderate to large varices [3-9], however, primary prophylaxis in cirrhotics without varices has not been shown to be beneficial nor does it appear to prevent the formation of varices [10]. 

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A Case of Celiac Disease and Diagnostic Clues

July 12, 2007

Commentary by Josh Olstein MD, Chief Resident NYU Internal Medicine

Mr. J is a 56 year old Caucasian gentleman who presented with complaints of “I just can’t do what I used to be able to do. I just don’t have the energy.” He describes himself as a hearty fellow who had never had a problem with his energy level until around a year ago. Though he has not noticed any weight loss, he denied any weight gain despite the lumberjack-like portions he eats (no disrespect meant to the lumberjack audience). He denied any other systemic complaints. His past medical and social history is noncontributory and he does not provide any pertinent family history of illness, in particularly denying any history of neoplasia. Physical examination reveals a well-developed individual with nothing out of the normal range except some slight conjunctival pallor. Laboratory examination reveals a significant microcytic anemia and mild transaminitis. Three stool samples sent to assess for occult blood were negative. Despite this, he underwent a colonoscopic exam, which revealed a 3mm sigmoid polyp, and an esophagogastroduodenoscopy, which appeared normal, except for mild gastric erythema. Biopsies were taken from his gastric antrum and the mid-body, greater curve of his stomach, as well as from the normal-appearing duodenal mucosa. The histologic appearance of the gastric biopsies were normal, but the duodenal biopsies revealed severe blunting of the villi, crypt hypertrophy, with lymphocytic infiltration of the mucosa. The pathologist suggested that the findings were consistent with celiac disease, a diagnosis that was confirmed by a positive IgA tissue transglutaminase antibody. Upon repeat questioning, the patient continued to deny any gastrointestinal symptomatology.

The variability and non-specific nature of symptoms experienced by patients with celiac disease frequently lead to delayed and missed diagnoses of this common condition. As many as 85% of cases go undiagnosed and thus many patients are subject to the increased morbidity and mortality of untreated disease. Likely the largest obstacle to diagnosing celiac disease is failure to consider and test for the condition. Recently, a study published in the British Medical Journal described and validated a clinical decision tool that was highly sensitive at detecting celiac disease. Before discussing this article, let’s briefly review some of the background on celiac disease.

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Should All Patients with Hepatitis C Be Screened for Hepatocelluar Carcinoma?

July 3, 2007

Should patients with Hepatitis C (HCV) with no evidence of cirrhosis undergo screening for hepatocellular carcinoma (HCC)? Is there any reason to check for HCC when the liver associated enzymes (LAEs) are normal?

-Sandeep Mangalmurti, PGY-2

Commentary by Mike Poles MD, Associate Editor Clinical Correlations and Assistant Professor, Division of Gastroenterology

HCC continues to be one of the most common solid malignancies worldwide. Further, almost all cases of HCC occur in the background of a histologically-abnormal liver; approximately 90% of cases of HCC occur in the background of cirrhosis. It is important to note that cirrhosis due to any etiology can result in the development of HCC, though cirrhosis due to the viral hepatitides is the most common causes. In the Far East, where HBV is highly endemic, it is the most common cause of cirrhosis-related HCC. On the other hand, in the U.S. and Western Europe, HCV-related cirrhosis is more commonly associated with HCC development. As noted above, approximately 10% of patients with HCC do not have cirrhosis. Worldwide, the majority of those with HCC, but without cirrhosis, are infected with HBV, which is believed to be oncogenic, in part, by virtue of its ability to integrate its DNA into the human genome. HCV, on the other hand, is a RNA virus that is not capable of integration, but nonetheless can probably rarely cause HCC through its effect on hepatic inflammation and increased hepatocyte activation and proliferation. A recent article in the Annals of Internal Medicine (Ikeda K et al. Antibody to Hepatitis B Core Antigen and Risk for HCV-Related HCC: A Prospective Study. Ann Int Med. 2007;146(9):649-656) [http://www.annals.org/cgi/content/full/146/9/649]supports past studies that have shown that the development of HCC in HCV-infected patients may also be related to occult (latent) HBV infection in which the patient has been exposed to HBV and has integrated HBV in the liver, but no signs of infection in the periphery except for antibody against the HBV Core antigen. Thus, in HCV-infected patients without cirrhosis, the development of HCC may be related to co-existent HBV infection. So, is this risk of development of HCC in non-cirrhotic HCV patients enough to trigger us to perform surveillance for HCC? It is generally accepted that it is not cost-effective to screen for HCC if it is not expected to occur at a rate of greater than 0.2% per year (Di Bisceglie AM. Issues in Screening and Surveillance for Hepatocellular Carcinoma. Gastroenterology. 2004;127:S104-S107). This threshold is exceeded in patients with established cirrhosis, who have a rare of development of HCC at 1-4% per year. Since the risk of development of HCC in patients with chronic HCV, but without cirrhosis is very low (below 0.2% yearly), surveillance is not cost-effective in such patients. Whether this recommendation would be modified by the presence of anti HBV Core antibody requires more study.

In response to the second question, it is important to realize that patients with chronic HCV, but without abnormal LAEs can still have significantly abnormal liver histology, including development of cirrhosis, though the risk of development of significant liver damage is decreased in this population. Thus, evidence for the presence of cirrhosis is far more pertinent with regard to HCC risk than is the presence of abnormal LAEs.

Meeting Perspectives: Digestive Disease Week (DDW) 2007

June 20, 2007

Commentary by Milini Sahu, MD Fellow, Division of Gastrotenterology, Gina Sam-DeRiggs, Fellow, Division of Gastroenterology, and Michael Poles MD,  Assistant Professor, NYU Division of Gastroenterology and Associate Editor, Clinical Correlations

Close to 17,000 gastroenterologists attended Digestive Disease Week (DDW) from May 19-24 in Washington DC. While I stayed behind (someone has to help with emergency endoscopies), the majority of NYU’s gastroenterology fellows and attendings were there for a week of learning, presenting, and making NYU proud.  Two of our fellows, Malini Sahu and Gina Sam-DeRiggs were there and have provided the majority of the information in this update.

As always, there is an immense amount of information presented at this meeting, where the world’s experts in gastroenterology present their most recent observations. A handful of important studies are presented below:

In a study examining the interaction between body weight and erosive esophagitis, Koo et al. performed a cross-sectional study. They enrolled 3801 patients in Korea who had routine EGD, of which 9.9% were found to have esophageal erosions. They found that BMI was higher in patients with esophageal erosions, though the average BMI of each group was less than 25. Waist circumference was also significantly higher in patients with erosive esophagitis. This study therefore suggests that, even in patients with fairly unimpressive BMIs, abdominal obesity is a risk factor for erosive esophagitis

As endoscopists, we are often faced with patients with melena for whom a diagnosis is not revealed by EGD and colonoscopy. A study examined 41 patients who received either capsule endoscopy or mesenteric angiogram as the next step in the diagnostic work-up. The authors showed that capsule endoscopy revealed the likely source of bleeding 55% of the time, while the angiogram only showed the source 9.5% of the time. A drawback of this study was the exclusion of further examination of the upper GI tract using enteroscopy, given that many lesions were found in the stomach (missed with the first endoscopy) and proximal small bowel (potentially within the reach of a longer endoscope). While therapy cannot be rendered with the capsule as opposed to angiography, it appears that it may be a important diagnostic modality in patients with obscure GI bleeding.

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Morning Report-How Do You Approach a Patient with a Significant Transaminitis?

March 23, 2007

Bellevue 1Consultant: Robert Raicht, MD Professor of Medicine, Chief Division of Gastroenterology

Clinical Vignette:
The patient is a 50 year old male with a past medical history notable for type II diabetes, hypertension and recently treated right foot cellulitis and c.difficile colitis who presented to the emergency room with the complaint of fevers and malaise for 1 week. His labs were notable for a significant transaminitis (AST 1997, ALT 1620, alkaline phosphatase 365, total bilirubin 3.1), INR wnl. An abdominal ultrasound was ordered with outpatient follow-up arranged in GI clinic. He returned to the ER one day later complaining of persistent fever, malaise, vomiting and decreased oral intake. He reported taking up to 6 tabs per day of acetaminophen for the past week. Physical exam was significant for temperature of 101.4, scleral icterus and mild hepatomegaly. Labs revealed AST/ALT 1719/1583, alk phos 311, t.bili 4.1, and acetaminophen level <1. Hepatitis serologies were significant for positive HBsAg, HBcIgM and 7 million copies of HBV DNA. A right upper quadrant ultrasound showed hepatomegaly and normal portal and hepatic venous blood flow. The patient was treated supportively and his hospital course was significant for peak AST/ALT 2562/2033, INR 2 with subsequent slow resolution of transaminitis. Pt was discharged to outpatient follow-up when the AST and ALT fell below 1000.

Teaching Points Regarding the Differential Diagnosis of this Case:

  1. hepatitis A generally takes >30 days from exposure to present with abnormal liver function tests, risk factors include food, travel, sexual contact, fecal-oral transmission
  2. hepatotoxicity from acetaminophen is generally not dose related except in cases of overdose
  3. the three most probable causes of an ast/alt in the 1000 range-viral hepatitis, drugs, ischemia
  4. the risk of seroconversion after a needlestick from a patient with hepatitis b is ~25%
  5. cholangitis can result in a transaminitis
  6. alcoholic hepatitis usually presents with a transaminitis <1000
  7. hepatitis a is the most cholestatic of the viral etiologies-it generally induces the synthesis of alkaline phosphatase
  8. in fulminant hepatic failure always give vit k for the small possibility that the patient is deficient
  9. the best prognostic factors to follow in fulminant hepatic failure are the inr and the mental status
  10. outcomes of hepatitis B infection include (1) fulminant hepatic failure-send for early transplant, (2)recovery 95%, (3)chronic hep b
  11. consider starting lamivudine when patient with chronic hepatitis B and even patients who are hbsab+ start chemotherapy
  12. even patients that are hepbsab + can still relapse, and likely still have a small amount of virus present in their liver

Image: Bellevue Hospital as viewed from the East River circa 1880. Courtesy of Ehrman Medical Library NYU Medical Center Archives

Should patients with Anemia and a Normal Ferritin Undergo Colonoscopy?

February 16, 2007

Endoscope

Commentary By: Joshua Olstein PGY-3

Second only to lung cancer, colon cancer claimed an estimated 55,000 lives in the United States in 2006. In an effort to reduce colon cancer morbidity and mortality, multiple screening tests have been developed to detect early disease among asymptomatic individuals. The 2003 American Gastroenterology Associations guidelines for screening asymptomatic individuals recommended colonoscopy as a preferred method of screening.

Due to a higher risk of colonic neoplasm, patients with unexplained iron-deficiency anemia are not included in these guidelines. However, consensus opinion recommends that these patients be considered for colonoscopy to exclude colonic neoplasm. Patients with anemia who are not iron-deficient represent a group for which risk of colonic neoplasm is not well known and no recommendations exist. These questions were recently addressed in an article authored by Sawhney et al. published in the American Journal of Gastroenterology. Read more »