eMedicine Specialties > Gastroenterology > Liver

Hepatorenal Syndrome: Treatment & Medication

Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Coauthor(s): Hemant K Roy, MD, Associate Professor of Medicine, Section of Gastroenterology, Feinberg School of Medicine at Northwestern University, Evanston-Northwestern Healthcare; Rowen K Zetterman, MD, Chief, Department of Medicine, Veterans Affairs Medical Center of Omaha; Director of Clinical Operation, Professor, Department of Internal Medicine, University of Nebraska Medical Center
Contributor Information and Disclosures

Updated: May 15, 2008

Treatment

Medical Care

The ideal treatment of HRS is liver transplantation; however, because of the long waiting lists in the majority of transplant centers, most patients die before transplantation. An urgent need exists for effective alternative therapies to increase survival chances for patients with HRS until transplantation can be performed. This is reinforced by a study that reported that patients successfully treated medically for HRS before liver transplantation had posttransplantation outcome and survival comparable to that of patients who underwent transplantation without being treated for HRS. Interventions that have shown some promise are drugs with vasoconstrictor effects in the splanchnic circulation and use of the transjugular intrahepatic portosystemic shunt (TIPS).

  • Pharmacological treatment  
    • Numerous medications have been used to treat HRS with little, if any, effect. In recent years, the pharmacological approach has shifted, with greater attention focused on the role of vasoconstrictors as opposed to the initial predominant use of vasodilators. The rationale for this change is that the initial event in HRS is vasodilatation of the splanchnic circulation and use of a vasoconstrictor may thus prevent homeostatic activation of endogenous vasoconstrictors. Promising results have been reported in small studies and case reports with agonists of vasopressin V1 receptors, such as ornipressin and terlipressin, which predominantly act on the splanchnic circulation.
    • Although only a few controlled trials have been conducted in this arena, the results so far are encouraging and suggest an increasing role for medical therapy, given the current shortage of the donor pool in the face of an ever-increasing demand for organs.
  • Dopamine
    • Low-dose dopamine (2-5 mcg/kg/min) is frequently prescribed to patients with renal failure in the hope that its vasodilatory properties may improve renal blood flow. Little evidence exists to support this practice; a placebo-controlled randomized trial by Bellomo and colleagues did not demonstrate any role for low-dose dopamine in early renal dysfunction.2 Five studies have evaluated the role of dopamine in HRS, and none have reported significant changes in RPF, GFR, or urine output.
    • These studies are limited by small sample size and lack of a control arm. Nonetheless, they demonstrate that dopamine administration in patients with cirrhosis, with or without HRS, does not improve renal function.
  • Misoprostol
    • Misoprostol is a synthetic analogue of PG E1, whose use in HRS was based on the observation that these patients had low urinary levels of vasodilatory PGs.
    • Five studies have assessed the role of either parenteral or oral misoprostol in HRS. None of these studies demonstrated an improvement in the GFR, sodium excretion, or renal function in patients with HRS. Although Fevery et al demonstrated reversal of HRS in 4 patients, these patients also received large doses of colloids.3 The likely scenario is that the massive administration of fluids played a predominant role here because Gines et al were unable to reproduce these findings with misoprostol alone.4
  • Renal vasoconstrictor antagonists
    • Saralasin, an antagonist of angiotensin II receptors, was used first in 1979 in an attempt to reverse renal vasoconstriction. Because this drug inhibited the homeostatic response to hypotension commonly observed in patients with cirrhosis, it led to worsening hypotension and deterioration in renal function. Poor results were also observed with phentolamine, an alpha-adrenergic antagonist, highlighting the importance of the SNS in maintaining renal hemodynamics in patients with HRS.
    • A case series by Soper et al reported an improvement in the GFR in 3 patients with cirrhosis, ascites, and HRS who received an antagonist of endothelin A receptor (BQ123).5 All 3 patients showed a dose-response improvement in inulin and para-aminohippurate excretion, RPF, and the GFR in the absence of changes in systemic hemodynamics. These 3 patients were not candidates for liver transplantation and subsequently died. More work is needed to explore this therapeutic approach as a possible bridge to transplantation for patients with HRS.
  • Systemic vasoconstrictors
    • These medications have shown the most promise for treatment of HRS in recent years and include vasopressin analogues (ornipressin, terlipressin), somatostatin analogues (octreotide), and alpha-adrenergic agonists (midodrine).
    • In 1956, Hecker and Sherlock used norepinephrine to treat patients with cirrhosis who had HRS; they were the first to describe an improvement in arterial pressure and urine output. However, no improvement was observed in biochemical parameters of renal function, and all patients subsequently died.
    • Octapressin, a synthetic vasopressin analogue, was first used in 1970 to treat type 1 HRS. RPF and the GFR improved in all patients, all of whom subsequently died from sepsis, gastrointestinal bleeding, and liver failure. Because of these discouraging results, the use of alternate vasopressin analogues, particularly ornipressin, attracted attention. Three important studies by Lenz and colleagues demonstrated that short-term use of ornipressin resulted in an improvement in circulatory function and a significant increase in RPF and the GFR.6,7,8  
    • The combination of ornipressin and albumin was subsequently tried by Guevera in patients with HRS.9,10 This was based on data suggesting that the combination of plasma volume expansion and vasoconstrictors normalized renal sodium and water handling in patients who have cirrhosis with ascites. In this important paper, 8 patients were originally to be treated for 15 days with ornipressin and albumin. Treatment had to be discontinued in 4 patients after fewer than 9 days because of complications from ornipressin use that included ischemic colitis, tongue ischemia, and glossitis. Although a marked improvement in the serum creatinine level was observed during treatment, renal function deteriorated upon treatment withdrawal. In the remaining 4 patients, the improvement in RPF and the GFR was significant and was associated with a reduction in serum creatinine levels. These patients subsequently died, but no recurrence of HRS was observed.
    • Due to the high incidence of severe adverse effects with ornipressin, the same investigators used another vasopressin analogue with fewer adverse effects, namely terlipressin. In this study, 9 patients were treated with terlipressin and albumin for 5-15 days. This was associated with a marked reduction in serum creatinine levels and improvement in mean arterial pressure. Reversal of HRS was noted in 7 of 9 patients, and HRS did not recur when treatment was discontinued. No adverse ischemic effects were reported, and, according to this study, terlipressin with albumin is a safe and effective treatment of HRS.
    • Since this early study, terlipressin has become the most studied vasopressin analogue in HRS. When used in conjunction with albumin, improvement in GFR and reduction in serum creatinine levels to below 1.5 mg/dL occur in 60-75% of patients with type 1 HRS. This may take several days, and although recurrent HRS after treatment discontinuation is uncommon (<15%), a repeat course of terlipressin with albumin is usually effective. Ischemic complications are also rare (<5%), but one limitation of terlipressin is its unavailability in many countries, including the United States. Under these circumstances, such agents as octreotide, albumin, and alpha-adrenergic agonists may be considered.
    • Angeli et al showed that long-term administration of midodrine (an alpha-adrenergic agonist) and octreotide improved renal function in 8 patients with type 1 HRS.11 All patients also received albumin, and this approach was compared to dopamine at nonpressor doses. Not surprisingly, none of the patients treated with dopamine showed any improvement in renal function, but all 8 patients treated with midodrine, octreotide, and volume expansion had improvement in renal function. No adverse effects were reported in these patients. A study of 14 patients by Wong et al reported improvement in renal function in 10 patients. Three of these patients subsequently underwent liver transplantation.12
    • These studies demonstrate several important points. First, vasoconstrictors play an important role in the treatment of HRS, but further work is needed to identify the ideal agent and to determine if the addition of albumin is necessary. Another important conclusion of these studies is that patients may maintain relatively preserved renal function once therapy is discontinued. This suggests that if the precipitating factor, such as SBP, is not readily identified, an irreversible decline in renal function ensues.
    • N- acetylcysteine (NAC): In 1999, the Royal Free group reported their experience with NAC for the treatment of HRS. This was based on experimental models of acute cholestasis, in which administration of NAC resulted in an improvement in renal function. Twelve patients with HRS were treated with intravenous NAC, without any adverse effects, and the survival rates were 67% and 58% at 1 month and 3 months, respectively (this included 2 patients who received liver transplantation after improvement in renal function). The mechanism of action remains unknown, but this interesting study encourages further optimism for medical treatment of a condition that once carried a hopeless diagnosis in the absence of liver transplantation. Controlled studies with longer follow-up may help answer these pressing questions.

Surgical Care

  • Peritoneovenous shunting  
    • Peritoneovenous shunting (PVS) seems attractive in theory because it leads to plasma volume expansion and improvement of circulatory function. However, very few studies evaluating the role of PVS in this area have been performed because PVS has been used predominantly for treating refractory ascites.
    • This may be important for patients with type 2 HRS, who often develop refractory ascites, are not candidates for orthotopic liver transplantation, and do not tolerate frequent LVPs.
    • PVS has no role in type 1 HRS.
  • Surgical shunts  
    • No description on the treatment of HRS is complete without a brief review of the role of portacaval shunts, particularly with the introduction of TIPS.
    • Despite the theoretical benefit of improving portal hypertension and thus HRS with a portosystemic shunt, only a few scattered case reports have shown some benefit.
    • Currently, no indication exists for portacaval shunts in this setting.
  • Liver transplantation 
    • Liver transplantation is the ideal treatment of HRS but is limited by the availability of donors.
    • Patients with HRS have a higher risk of postoperative morbidity, early mortality, and longer hospitalization. Gonwa et al reported that at least one third of patients require hemodialysis postoperatively, with a smaller percentage (5%) requiring long-term hemodialysis.13
    • Because renal dysfunction is common in the first few days following transplantation, avoiding nephrotoxic immunosuppressants generally is recommended until recovery of renal function. However, the GFR gradually improves and reaches an average of 40-50 mL/min by the sixth postoperative week. The systemic and neurohumoral abnormalities associated with HRS also resolve in the first postoperative month.
    • Long-term survival rates are excellent, with the survival rate at 3 years approaching approximately 60%. This is only slightly lower than the 70-80% survival rate of transplant recipients without HRS and is markedly better than the survival rate of patients with HRS not receiving transplants, which is virtually 0% at 3 years.

Consultations

  • Nephrologist  
    • The importance of a nephrologist in the multidisciplinary management of patients with HRS cannot be overemphasized. Nephrologists play a critical role in assisting hepatologists and liver transplant surgeons in the management of these critically ill patients.
    • No controlled studies evaluating the role of dialysis in this setting have been performed, but most centers dialyze patients with HRS who are on a waiting list.
    • Continuous arteriovenous or venovenous hemofiltration has also been used, but the efficacy of these 2 measures has yet to be determined.
    • Variations of hemodialysis include the recently described molecular adsorbent recirculating system. This is a modified dialysis method that uses an albumin-containing dialysate that is recirculated and perfused online through charcoal- and anion-exchanger columns. A prospective, randomized, controlled trial showed improvement of type 1 HRS with this method, although long-term survival remained very poor, with survival of more than 1 month in only 1 of 8 patients in the treatment arm.
    • If transplantation is not available, hemodialysis probably will continue to be performed for patients on the waiting list.
  • Interventional radiologist  
    • The use of TIPS in the treatment of HRS has yet to be established. Due to its ability to reduce portal hypertension in patients with variceal bleeding and refractory ascites, its role in HRS initially seemed logical, particularly in view of isolated reports of renal function improvement following surgical shunts in the 1970s. However, TIPS quickly fell out of favor because of high morbidity and mortality rates.
    • Small, uncontrolled studies indicate that TIPS may improve RPF and the GFR and reduce the activity of the RAAS and SNS in patients who have cirrhosis with types 1 and 2 HRS. Improvement in renal function is usually slow and occurs in approximately 60% of patients. However, the effects on renal function can be variable, and some patients fare worse. As a result, the role of TIPS in the treatment of HRS remains investigational because of the lack of prospective studies and the known risks of the procedure.

Diet

  • Institute a low-salt (2 g) diet.
  • Do not restrict protein intake unless patient has severe encephalopathy.

Activity

  • No restrictions are necessary.

Medication

The pharmacological approach to the treatment of HRS continues to evolve, with several possible effective treatments. However, readers should be aware that none of these medications (including the addition of albumin) has been validated in randomized controlled trials. A brief review of only the most promising (but yet unproven) medications will be described because not only is this historical list extensive, but most of the trials for the medications were conducted outside the United States.

Vasopressin analogues

Improve circulatory dysfunction secondary to splanchnic vasodilatation. Also improve RPF, the GFR, and urine output.


Ornipressin (POR-8)

Not available in the United States. Synthetic vasopressin analogue with a short half-life that requires continuous IV administration. V1 vasopressin receptors are abundantly expressed in the mesenteric arteries as compared with other vascular areas. Has been used in conjunction with albumin to treat HRS but is associated with ischemic complications.

Adult

2-6 IU/h IV

Pediatric

Not established

Documented hypersensitivity; coronary artery disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Treatment discontinuation usually due to ischemic reactions (eg, colitis, tongue ischemia, ulcers), which have occurred in as many as 33% of patients in Guevera's study


Terlipressin

Not available in United States. Nonselective V1 vasopressin agonist that has similar vasoconstrictor potency to ornipressin but a lower incidence of ischemic complications. Inactive by itself but is transformed into a biologically active form (lysine-vasopressin) by the action of tissue endopeptidases and exopeptidases. Due to its longer half-life (2-10 h) compared to ornipressin, may be administered as a bolus. Has lower incidence of adverse ischemic effects, with <5% of cases reported in a series of 1258 patients receiving it for variceal bleeding.

Adult

0.5-2 mg/4h IV

Pediatric

Not established

Documented hypersensitivity; coronary artery disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia

Sympathomimetic agents

Improve renal artery perfusion.


Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on dose. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses. Described for its historical interest because it has no role in monotherapy for HRS. However, reversal of HRS has been described when used at low doses in conjunction with ornipressin.

Adult

2-3 mcg/kg/min IV

Pediatric

Not established

Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Should be administered through central line, although risks of phlebitis are increased at higher doses; patients should be on cardiac monitor when administered because it is a proarrhythmic agent at higher doses

Somatostatin analogs

Improvement in splanchnic circulation may improve renal hemodynamics.


Octreotide (Sandostatin)

Synthetic derivative of somatostatin. Potent physiological inhibitor of several gastrointestinal functions, one of which is a reduction in intestinal blood flow by splanchnic vasoconstriction.

Adult

25-50 mcg/h IV; alternatively, 250 mcg SC bid for up to 3 mo

Pediatric

Not established

May reduce effects of cyclosporine; patients on insulin, oral hypoglycemics, beta-blockers, and calcium channel blockers may need dosage adjustments

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Role in treatment of HRS remains investigational; well tolerated and no adverse effects reported; long-term administration for other conditions (eg, neuroendocrine tumors) associated with development of cholelithiasis in up to 60% of patients

Antioxidants

Experimental evidence demonstrates improvement of renal function in acute cholestasis and renal failure.


N-acetylcysteine (Mucomyst)

Traditionally used to treat acetaminophen overdose. Replenishes low hepatic glutathione stores to prevent synthesis of toxic epoxide intermediates. Does not have a role in the treatment of non–acetaminophen-related liver failure. Exact mechanism of action in HRS remains unclear.

Adult

150 mg/kg IV over 2 h followed by continuous infusion of 100 mg/kg/d for 5 d

Pediatric

Not established

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

GI distress may occur

Antibiotics

Are only indicated in the treatment of HRS if renal dysfunction is precipitated by an infection. Prophylactic antibiotics may play a role in preventing SBP, which, in turn, is also a risk factor for the development of type 1 HRS in patients with type 2 HRS. The efficacy and safety of prophylactic antibiotics remains to be established because of reports of emergent resistant bacteria. May play an important role in selected patients, such as those awaiting liver transplantation, although the duration (long-term vs cyclic) remains to be determined.


Cefotaxime (Claforan)

Because the most common cause of type 1 HRS is SBP, IV cefotaxime is the DOC.

Adult

1-2 g IV q8h for 5 d (1 dose q12h recommended when CrCl 30-50 mL/min)

Pediatric

<50 kg: 50-180 mg/kg IV qd divided qid for 5 d
>50 kg: Administer as in adults

Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or with repeated therapy; has been associated with severe colitis


Ciprofloxacin (Cipro)

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth.

Adult

750 mg PO single dose qwk

Pediatric

Not established

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


Norfloxacin (Noroxin, Chibroxin)

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth.

Adult

400 mg PO qd

Pediatric

Not established

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Septra, Septra DS)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Adult

1 tab (Bactrim DS) 5 d/wk

Pediatric

Not established

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in persons with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation

Plasma volume expanders

Indicated for the correction of abnormal hemodynamic parameters.


Albumin (Albunex, Albuminar, Albumisol)

Useful for plasma volume expansion and maintenance of cardiac output.

Adult

20-60 g/d IV

Pediatric

Not established

Documented hypersensitivity; pulmonary edema; protein load of 5% albumin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

While theoretically attractive, no proven benefit exists for colloid resuscitation over isotonic crystalloids

More on Hepatorenal Syndrome

Overview: Hepatorenal Syndrome
Differential Diagnoses & Workup: Hepatorenal Syndrome
Treatment & Medication: Hepatorenal Syndrome
Follow-up: Hepatorenal Syndrome
References
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Further Reading

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Keywords

HRS, hepato-renal syndrome, acute renal failure, renal dysfunction, renal disorder, chronic liver disease, liver failure, fulminant hepatitis, ascites, portal hypertension, cirrhosis, end-stage liver disease, liver transplantation, renin-angiotensin-aldosterone system, RAAS, sympathetic nervous system, SNS, renal prostaglandins, spontaneous bacterial peritonitis, SBP, renal vasoconstriction, renal hypoperfusion, type 1 HRS, type 2 HRS

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Contributor Information and Disclosures

Author

Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Coauthor(s)

Hemant K Roy, MD, Associate Professor of Medicine, Section of Gastroenterology, Feinberg School of Medicine at Northwestern University, Evanston-Northwestern Healthcare
Disclosure: Nothing to disclose.

Rowen K Zetterman, MD, Chief, Department of Medicine, Veterans Affairs Medical Center of Omaha; Director of Clinical Operation, Professor, Department of Internal Medicine, University of Nebraska Medical Center
Rowen K Zetterman, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Ann Ouyang, MBBS, Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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