Medical Care Criteria Committee, October 2006
The estimated incidence of gastrointestinal (GI) complaints among HIV-infected patients varies between 30% and 90%. HIV-related disorders may affect all structures from the mouth to the anus. Oral and esophageal lesions, hepatobiliary disorders, and diarrhea are the most common. By direct involvement of GI organs and through food avoidance associated with GI symptoms, these processes can result in malabsorption, maldigestion, or decreased intake of nutrients, thus adding to the wasting and malnutrition associated with HIV/AIDS.
In many patients with GI complaints, the cause may be elusive; therefore, diligence and perseverance are often required to establish the diagnosis. Nondiagnostic standard stool and blood tests may need to be repeated, followed by endoscopic evaluation with biopsy. During the course of a diagnostic evaluation, unusual opportunistic organisms are frequently identified, and common pathogens may be found in anatomic locations not usually associated with the pathogen. Unusual organisms should not be dismissed routinely as non-pathogens. Multiple pathogens may be found simultaneously; therefore, clinicians should be familiar with the many potential causes of GI diseases in HIV-infected patients. Diagnosis may be complicated by contributing factors, such as:
- Misidentification of non-pathogenic Entamoeba species and treating as pathogens
- Multiple concurrent GI disease processes, resulting in persistence of signs and symptoms despite adequate treatment of a single identified cause
- Adverse effects of multiple ARV medications
- Extraintestinal processes, such as pneumonia, which may be associated with diarrhea, or meningitis and central nervous system mass lesions, which may cause vomiting
- Non-HIV-related diseases that are appropriate to the patient’s age, sex, and social habits
GI complaints should not be routinely dismissed in pregnant HIV-infected women. These symptoms should be carefully considered and investigated further if necessary.
Odynophagia and dysphagia with both liquids and solids are the symptoms most frequently associated with a variety of esophageal diseases. However, esophagitis may also cause esophageal spasm that mimics angina or occasionally causes hiccups. The patient’s history may reveal potential causes of swallowing disturbances, such as medications or gastroesophageal reflux disease (GERD).
Physical examination may reveal OIs, such as pharyngeal candidiasis (thrush), herpes simplex virus (HSV), cytomegalovirus (CMV), or Kaposi’s sarcoma (KS). Pharyngeal candidiasis suggests the possibility of esophageal candidiasis. Of note, the absence of oral thrush does not exclude the diagnosis of Candida esophagitis in patients without esophageal complaints. Candida esophagitis may occur at virtually any CD4 count, although it is most commonly seen in patients with CD4 counts <200 cells/mm3. HSV and CMV esophagitis are usually seen in patients with CD4 counts <100 cells/mm3. Because functional CD4 cell-mediated immunity may be incomplete, a patient’s lowest, rather than current, CD4 count should be used to guide the relative risk for OIs in the early phase of immune reconstitution. It may take up to 1 year for immune reconstitution to occur.
Less commonly, aphthous ulcerations in the esophagus may be responsible for symptoms. Aphthous ulceration is diagnosed by exclusion. Other potential etiologies should be excluded before initiating steroids to treat aphthous ulcers (Table 1).
|Table 1: Possible HIV-Related Etiologic Agents of Esophageal Disease|
|Classification||Most Common Pathogen||Less Common Pathogens|
|Fungal||Candida species||Histoplasma capsulatum, Pneumocystic carinii|
|Viral||CMV, herpes simplex, Kaposi’s sarcoma||Papillomavirus, HIV|
|Bacterial||Rarely seen||Mycobacterium tuberculosis, Mycobacterium avium complex (MAC), Actinomyces species|
|Miscellaneous||—||Aphthous ulcers, acid reflux, pill ulcers|
Esophagitis in patients receiving antifungal therapy: When a patient receiving antifungal therapy presents with esophagitis, the clinician may prescribe increased doses of fluconazole (up to 800 mg/day); however, early endoscopy should also be strongly considered to establish the diagnosis in these cases.
CMV esophagitis: The role of maintenance therapy for CMV esophagitis is currently not known, and relapse is common, even during maintenance therapy. Cidofovir, valganciclovir, and oral ganciclovir remain of unproven efficacy.
HSV esophagitis: Recurrent HSV esophagitis may be suppressed with maintenance dosing of oral acyclovir, valacyclovir, or famcyclovir.
Aphthous ulcers: Steroids are the first-line therapy for aphthous ulcers. Thalidomide has been shown to be effective for the treatment of non-resolving aphthous ulcers in HIV-infected patients; however, there are serious documented teratogenic effects associated with thalidomide in pregnant women. Central nervous system toxicity and peripheral neuropathy may occur as well. Because of these potential side effects, thalidomide should only be used as second-line therapy. In adolescent and adult women capable of bearing children, thalidomide should only be used when the woman is known not to be pregnant and is using effective methods of birth control.
Diagnostic evaluation of patients with HIV-associated gastric disease is no different than that used in diagnosing peptic or duodenal ulcers or gastritis in non-HIV-infected populations. Although the full range of non-HIV-associated gastric disorders may be encountered in patients with HIV disease, opportunistic gastric processes may also be seen but are uncommon. The two most common infectious agents, CMV and Kaposi’s sarcoma, are usually seen in the context of severe disseminated disease. CMV, like Kaposi’s sarcoma, can cause episodes of hematemesis. Kaposi’s sarcoma and antral lymphoma may cause gastric outlet obstruction and/or symptoms of early satiety.
Symptoms of dyspepsia or peptic ulcer disease should be thoroughly studied, including serology for Helicobacter pylori and/or endoscopy for urea test. If H. pylori infection is diagnosed, ARV medications may need to be stopped for the duration of H. pylori treatment to prevent drug-drug interactions.
The symptoms of nausea, vomiting, and general dyspepsia commonly occur in the early stages of ARV therapy. Zidovudine, didanosine, tenofovir, and the protease inhibitors (PIs) are the most common ARV drugs associated with GI side effects. In addition, other therapeutic agents may cause stomach upset, especially when the daily pill burden is high. Discussing the possible ARV medication side effects on the GI system before they arise, as well as their potential impact on adherence, is critical.
Treatment of infectious gastric pathogens is the same as those outlined for esophageal disease (see Esophageal Disease). For moderate to severe or intractable vomiting ascribed to HAART, the more potent 5-hydroxytryptamine-3 (5-HT3) receptor antagonists (e.g., ondansetron hydrochloride, dronabinol) may be required. Dronabinol is also helpful for nausea and anorexia.
Because of a poorly understood mechanism underlying hypochlorhydria, gastritis and peptic ulcer disease may respond better to a mucosal protective agent such as sucralfate than to histamine-2 blockers or proton pump inhibitors. Hypochlorhydria has not been fully demonstrated to be a significant effect of HIV disease. In addition, peptic ulcer disease occurring despite hypochlorhydria would be more likely to be infectious in etiology.
Table 2 shows the hepatotoxicity of the available ARV drugs. For recommendations regarding treatment of viral hepatitis, see the individual guidelines for HAV, HBV, HCV.
|Table 2: Hepatotoxicity of Antiretrovial Drugs|
|NRTI Agents||Hepatotoxicity||Usual Time Frame|
|Abacavir (ABC)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Didanosine (ddI)||Modest nonspecific ALT, AST elevations; rare clinical hepatitis||LFT elevations develop by week 4; fulminant hepatitis within 8 to 12 weeks|
|Emtricitabine (FTC)||Rare, except may cause LFT elevations when discontinued with HBV (similar to lamivudine)||—|
|Lamivudine (3TC)||Rare, except when discontinued in HBV (see text)||—|
|Stavudine (d4T)||Modest nonspecific ALT, AST elevations; rare steatosis/lactic acidosis syndrome||LFT elevations develop by week 4; fulminant hepatitis within 8 to 12 weeks and steatosis at generally >18 weeks|
|Tenofovir (TDF)||Rare, except may cause LFT elevations when discontinued in HBV (similar to lamivudine)||—|
|Zalcitabine (ddC)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Zidovudine (ZDV)||Modest nonspecific ALT, AST elevations; rare clinical hepatitis; rare steatosis/lactic acidosis syndrome||LFT elevations develop by week 4; fulminant hepatitis within 8 to 12 weeks and steatosis generally at >18 weeks|
|NNRTI Agents||Hepatatoxicity||Usual Time Frame|
|Delavirdine (DLV)||Modest nonspecific ALT, AST elevations||LFT elevations develop by 4th week|
|Nevirapine (NVP)||Modest nonspecific ALT, AST elevations; common GGT elevations; rarely hepatitis||LFT and GGT elevations develop by week 4; fulminant hepatitis within 12 weeks|
|PI Agents||Hepatatoxicty||Usual Time Frame|
|Amprenavir (APV)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Atazanavir (ATV)||Rare; hyperbilirubinemia without abnormal LFTs common||Indirect bilirubin elevations develop by week 6|
|Darunavir (DRV)||No data||—|
|Fos-Amprenavir (FPV)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Indinavir (IDV)||Hyperbilirubinemia; hepatitis in the setting of chronic HBV or HCV (see text)||Indirect bilirubin elevations develop by week 6|
|Lopinavir/r (LPV/r)||Modest nonspecific ALT, AST, and GGT elevations||LFT elevations develop by week 4|
|Ritonavir (RTV)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Saquinavir (SQV)||Modest nonspecific ALT, AST elevations||LFT elevations develop by week 4|
|Tipranavir (TPV)||Modest nonspecific ALT, AST, and GGT elevations||LFT elevations develop by week 4|
|Fusion Inhibitor||Hepatatoxicty||Usual Time Frame|
|Rare, nonspecific ALT, AST elevations||—|
Liver disease is common among HIV-infected patients. Frequently asymptomatic, it may be identified by elevations of either serum transaminases (i.e., AST or ALT) or alkaline phosphatase and gamma-glutamyltranspeptidase (GGTP) levels. A satisfactory marker of hepatic fibrosis or fibrogenesis other than needle biopsy is not yet available, particularly for early-to-mid-stage disease. Abdominal imaging studies (CT scan, MRI, or ultrasound) may help assess advanced cirrhosis, portal hypertension, peri-portal disease (schistosomiasis), echinococcal disease, and hepatocellular carcinoma.
Alkaline phosphatase and GGTP elevations are indicative of intrahepatic or cholestatic disease. The most common causes of cholestatic disease include disseminated mycobacterial, fungal, or protozoal infections; drug-induced hepatotoxicity; and biliary tract disorders. In addition to the classic viral hepatitides, hepatobiliary pathogens encountered in the setting of HIV infection include HSV, tuberculosis, Bartonella, and histoplasmosis, as well as ascending cholangitis caused by OIs, such as CMV, MAC, Cryptosporidium, and microsporidia ascending from the gut via the common bile duct. When treating a patient with advanced immunosuppression, clinicians should conduct a thorough search for the offending organism(s). In the setting of HIV disease, organisms that are generally regarded as of little clinical significance should not be routinely dismissed as non-pathogenic. Serum lactate also should be considered as a cause of increased serum liver enzymes.
Although the benefits of ART are readily apparent, use of these complex regimens has multiplied the risk of potential medication interactions and hepatotoxicity. The potential for such toxicity is exacerbated by the presence of acute or chronic viral hepatitis, ethanol use/abuse, and hepatic steatosis.
Treatment for liver disease should be directed to the suspected or specific pathogen. Standard treatment for pathogens found in the liver, such as fungi and mycobacteria, should be initiated; however, suboptimal outcomes, even after multiple and prolonged regimens, are not uncommon. Treatment of an offending organism may be further complicated by the overlapping toxicities of the regimen with the patient’s underlying liver function and HAART. If a component of the patient’s HAART regimen must be discontinued and a suitably potent ARV agent cannot be substituted, then all components of the HAART regimen should be discontinued temporarily to prevent the development of HIV resistance. HAART should be restarted after the abnormal laboratory values have returned to the patient’s baseline values. An alternative HAART regimen may be necessary.
Asymptomatic and clinically insignificant hyperbilirubinemia (total bilirubin >2.5 mg/dL) may occur with the use of indinavir and atazanavir therapy. Indinavir has been implicated as a rare cause of significant symptomatic hepatitis (elevated total bilirubin with a greater than 5-fold increase in serum transaminase levels) when given to patients with preexisting chronic viral hepatitis. These patients should be observed closely after the initiation of indinavir therapy.
|Table 3: Evaluation of Diarrhea Based on CD4 Count|
|Common pathogen with CD4 count <100 cells/mm3||Method of identification|
|Cryptosporidium||Antigen assay or modified Kinyoun|
|Enterocytozoon bieneusi||Biopsy with Giemsa stain or electron microscopy|
|Septata intestinalis||Biopsy with Giemsa stain or electron microscopy|
|Cyclospora||No fecal leukocytes, AFB smear of stool for oocytes|
|CMV||Biopsy demonstrating intranuclear inclusion bodies|
|Histoplasma capsulatum||Blood culture and urine antigen assay|
|Giardia||Antigen assay and/or stool examination for ova and parasites|
|Common pathogens with CD4 count <200 cells/mm3||Method of identification|
|Salmonella||Fecal leukocytes, stool and blood cultures|
|Shigella species||Fecal leukocytes, stool cultures|
|Campylobacter jejuni||Fecal leukocytes, stool cultures|
|Giardia||Antigen assay and/or stool examination for ova and parasites|
|Common pathogen with any CD4 count||Method of identification|
|Clostridium difficile||Fecal leukocytes, antigen assay for toxin a and b|
Diarrhea is a prevalent complaint among HIV-infected patients. It is defined as >250 mL of stool per day. The primary process may occur in the large or small intestine, or both. Attempting to localize the source based on specific characteristics of the diarrhea may allow the clinician to narrow the list of potential pathogens (see below), select appropriate diagnostic studies, and prescribe the most effective therapy.
Characteristics of large bowel diarrhea:
- Small, frequent bowel movements with tenesmus
- Sense of incomplete evacuation
- Blood that may or may not be present in the stool
Characteristics of small bowel diarrhea:
- Particularly symptomatic at night
- Large volume, watery bowel movements
- Increase throughout the day
Clinicians should perform distal duodenal biopsy in patients with large volume diarrhea (>2L/24hr) of suspected small bowel origin. If microsporidia is suspected, electron microscopy or PCR should be used to confirm and identify the microsporidia. If the results of small bowel biopsy are negative, the possibility of pancreatic insufficiency should be considered and quantitative or qualitative stool testing for fecal fat after a 100-gram fat challenge should be performed.
Most patients with diarrhea will have a specific pathologic process or infection identified by use of readily available studies, including endoscopy with biopsies when necessary. If initial stool studies are negative, the tests may be repeated. If repeated stool studies are negative, an empiric trial of metronidazole may be given for 1 to 2 weeks before endoscopy is performed. If the patient’s stool examination is positive for fecal leukocytes, a colonic pathogen is more likely. Clostridium difficile diarrhea is common in HIV-infected patients, sometimes even in the absence of antibiotic therapy. The routine use of loperamide for symptomatic treatment should be avoided in HIV-infected patients until C. difficile is excluded by obtaining stool C. difficile toxin assay.
Another common cause of diarrhea in HIV-infected patients is the use of ARV agents. Although all ARVs may be associated with diarrhea, the class of drugs most likely to cause diarrhea is the PIs, especially nelfinavir, amprenavir, and any ritonavir-enhanced regimen. The titration of over-the-counter psyllium products may offer symptomatic relief for the PI-induced diarrhea and may obviate the need for prescription agents.
Tenesmus or proctitis may occur as part of the infectious diarrheal symptom complex, hemorrhoids, or more commonly as the result of an infection with an STI (herpes simplex, HPV, syphilis). More information about STI-related symptoms can be found in Atypical Presentations of STIs and Anal Dysplasia.
Possible HIV-related etiologic agents of diarrhea in HIV-infected patients:
- Small intestine: Cryptosporidium, microsporidia, Isospora belli, MAC, Salmonella species, Campylobacter species, Giardia lamblia
- Large intestine: CMV, Cryptosporidium, MAC, shigella, C. difficile, C. jejuni, H. capsulatum, Adenovirus, HSV (rare), P. carinii (rare)
- Miscellaneous: Drugs, alcohol, lactose intolerance, pancreatic insufficiency
|Table 4: Symptomatic Treatment for Patients with Diarrhea|
|Loperamide||2-4 mg 4x/day||Moderate to severe ARV-related diarrhea; should only be used after bacterial or amoebic etiology has been excluded|
|Diphenoxylate||2 tablets 4x/day||Moderate to severe ARV-related diarrhea; should only be used after bacterial or amoebic etiology has been excluded|
|Paregoric||30 mL po every 4h||Moderate to severe ARV-related diarrhea; should only be used after bacterial or amoebic etiology has been excluded|
|Deodorized tincture of opium||10-20 drops po every 3-4h|
|Bismuth subsalicylate||—||Mild, noninfectious diarrhea|
|Aluminum antacids||—||Mild, noninfectious diarrhea|
|Cholestyramine||—||Mild, noninfectious diarrhea|
|Fiber supplement||—||Mild, noninfectious diarrhea|
|Calcium carbonate pills*||—||ARV-related diarrhea|
|Glutamine supplementation*||—||ARV-related diarrhea|
|*Anectdotally noted to be useful for ARV-related diarrhea.|
Relapse of parasitic and bacterial pathogens is common, and maintenance therapy may be required, especially when accompanied by low CD4 counts. The role of maintenance therapy for CMV infection is currently not known and relapse is common, even during maintenance therapy. Cidofovir, valganciclovir, and oral ganciclovir remain of unproven efficacy.
Octreotide 100 to 500 µg administered subcutaneously or intravenously every 8 hours has been advocated for treatment of diarrhea, especially in severe situations not responsive to oral agents. However, the efficacy of this agent is largely untested in controlled trials.
The signs and symptoms of biliary disease do not differ between HIV-infected and non-HIV-infected patients except jaundice is less common in patients with HIV. Right upper quadrant or epigastric pain, fever, and cholestasis are presenting symptoms in >90% of patients. Nausea and/or vomiting occur in approximately 50% of patients with biliary disease, but pruritus is rare.
Many pathogens causing opportunistic biliary disease can be isolated from the stool; therefore, obtaining stool specimens may assist in establishing a probable diagnosis. Elevations in alkaline phosphatase and GGTP are suggestive of cholestatic disease. Common causes of cholestatic disease include disseminated mycobacterial infections, HIV cholangiopathy, and other OIs (Cryptosporidium and microsporidia) that affect the biliary tract; traditional biliary tract disease would include gallstones, acalculous cholecystitis, and cholangitis. Abdominal ultrasound is a sensitive (at least 75%) procedure for diagnosing gallbladder disease. Acalculous cholecystitis is a common finding on ultrasound and should be confirmed by hepatoiminodiacetic acid (HIDA) scan. The etiologic organisms of cholecystitis are similar to those that cause cholangitis, and the two processes often co-exist.
Endoscopic retrograde cholangiopancreatography (ERCP) may be required as an adjunct to ultrasound in diagnosing bile duct pathology. Bacterial septic cholangitis may complicate ERCP or occur superimposed on cholecystitis because of other causes. The latter is seen in advanced HIV infection when CD4 counts are <100 cells/mm3. If papillary stenosis is present, sphincterotomy may reduce pain, but serum liver enzyme elevations often persist post-sphincterotomy. The most common opportunistic pathogens implicated in cholangitis are Cryptosporidium (biliary involvement in up to 20% of intestinal infections), CMV, and microsporidia, especially Enterocytozoon bieneusi. Rare causes include Isospora, MAC, lymphoma, and Kaposi’s sarcoma. In addition, medications used to treat HIV or associated OIs may produce a cholestatic hepatitis (e.g., efavirenz, nevirapine, and clarithromycin) or steatohepatitis (e.g., NRTIs).
Treatment of biliary disease should be aimed at the underlying pathogen. Pain should be treated when indicated, and narcotics may be used if necessary.
Although abdominal discomfort may be vague or mild during early pancreatitis, the characteristic steady, boring epigastric pain of acute pancreatitis with its radiation to the back and the associated signs and symptoms of nausea, vomiting, and abdominal distension should be expected as frequently in the HIV-infected population as in the non-HIV-infected population.
The usual causes of pancreatitis are alcohol and pancreatotoxic medications. Pentamidine, trimethoprim-sulfamethoxazole, dideoxyinosine, dideoxycytidine, stavudine, hydroxyurea, megesterol acetate, and octreotide have all been reported as pancreatotoxins. Hypertriglyceridemia, either as a result of HIV infection or as a common consequence of PI therapy, is another inciting cause of pancreatitis. Opportunistic pathogens also may be associated with the development of pancreatitis. Biopsy is usually not an option in pancreatic disease; therefore, ascribing an infectious etiology, other than through blood culture isolation of CMV, mycobacteria, or fungi, usually will require supporting clinical evidence of end-organ disease elsewhere. The most common infectious etiology in an autopsy series was CMV, followed by Cryptococcus and toxoplasmosis.
References Consulted and Further Reading
Aceti A, Pasquazzi C, Zechini B, et al. Hepatotoxicity development during antiretroviral therapy containing protease inhibitors in patients with HIV: the role of hepatitis B and C virus infection. JAIDS 2002;29:41-48.
Benhamou Y, Katlama C, Lunel F, et al. Effects of lamivudine on replication of hepatitis B virus in HIV-infected men. Ann Intern Med1996;125:705-712.
Call SA, Heudebert G, Saag M, et al. The changing etiology of chronic diarrhea in HIV-infected patients with CD4 cell counts less than 200 cell/mm3. Am J Gastroenterol 2000;95:3142-3146.
Carr A, Cooper DA. Adverse effects of antiretroviral therapy. Lancet 2000;356:1423-1430.
Carr A, Morey A, Mallon P, et al. Fatal portal hypertension, liver failure and mitochondrial dysfunction after HIV-1 nucleoside analogue-induced hepatitis and lactic academia. Lancet 2001;357:1412-1414.
Cohen J, West AB, Bini EJ. Infectious diarrhea in HIV. Gastroenterol Clin North Am 2001;30:637-664.
Coyle CM, Wittner M, Kotler DP, et al. Prevalence of microsporidiosis due to Enterocytozoon bieneusi and Encephalitozoon (Speptat) intestinalis among patients with AIDS-related diarrhea: determination by polymerase chain reaction to the microsporidian small-subunit rRNA gen. Clin Infect Dis 1996;23:1002-1006.
Chen XM, Keithly JS, Paya CV, et al. Cryptosporidiosis. NEJM 2002;346:1723-1731.
Dascomb K, Clark R, Aberg J, et al. Natural History of intestinal microsporidiosis among patients infected with human immunodeficiency virus. J Clin Microbiol 1999;37:3421-3422.
Dassopoulos I, Ehrenpreis ED. Acute pancreatitis in human immunodeficiency virus-infected patients: a review. Am J Med 1999;107:78-84.
Dieterich DT, Kotler DP, Busch DF, et al. Ganciclovir treatment of cytomegalovirus colitis in AIDS: a randomized double-blind, placebo-controlled multicenter study. J Infect Dis 1993;167:278-282.
Dieterich DT, Poles MA, Lew E. Gastrointestinal manifestations of HIV disease. In: Textbook of AIDS. (Broder, Merigan, Bolognesi, eds.) Baltimore: Williams & Wilkins; 1993.
Dieterich DT, Wilcox CM. Gastroenterology. Diagnosis and treatment of esophageal diseases associated with HIV infection. Am J Gastroenterol1996;91:2265-2269.
Eyster ME, Diamondstone LS, Lien JM, et al. Natural history of hepatitis C virus infection in multitransfused hemophiliacs: effect of coinfection with human immunodeficiency virus. The Multicenter Hemophilia Cohort Study. J Acquir Immune Defic Syndr 1993;6:602-610.
Falco V, Rodriguez D, Ribera E, et al. Severe nucleoside-associated lactic acidosis in human immunodeficiency virus-infected patients: report of twelve patients and review of the literature. Clin Infect Dis 2002;34:838-846.
Fellay J, Boubaker K, Ledergerber B, et al. Prevalence of adverse events associated with potent antiretroviral treatment: Swiss HIV Cohort Study.Lancet 2001;358:1322-1327.
Guido M, Rugge M, Fattovich G, et al. Human immunodeficiency virus infection and hepatitis C pathology. Liver 1994;14:314-319.
John M, Moore CB, James IR, et al. Chronic hyperlactemia in HIV-infected patients taking antiretroviral therapy. AIDS 2001;15:717-723.
Laine L, Bonacini M, Sattler F, et al. Cytomegalovirus and candida esophagitis in patients with AIDS. J Acquir Immune Defic Syndr 1992;5:605-609.
Lew E, Dieterich D, Poles M, et al. Gastrointestinal emergencies in the patient with AIDS. Crit Care Clin 1995;2:531-560.
Lowther SA, Dworkin MS, Hanson DL, Entamoeba histolytica/Entamoeba dispar infections in human immunodeficiency virus-infected patients in the United States. Clin Infect Dis 2000;30:955-959.
Manfredi R, Calza L, Chiodo F. Enteric and disseminated Campylobacter species infection during HIV disease. Am J Gastroenterol 2002;97:510-511.
Martinez E, Blanco JL, Arnaiz JA, et al. Hepatotoxicity in HIV-1-infected patients receiving nevirapine-containing antiretroviral therapy. AIDS2001;15:1261-1268.
Miao YM, Awad-El-Kariem FM, Franzen C, et al. Eradication of cryptosporidia and microsporidia following successful antiretroviral therapy. J Acquir Immune Defic Syndr 2000;25:124-129.
Manocha AP, Sossenheimer M, Martin SP, et al. Prevalence and predictors of severe acute pancreatitis in patients with AIDS. Am J Gastroenterol1999;94:784-789.
Nunez M, Lana R, Mendoza JL, et al. Risk factors for severe hepatic injury after introduction of highly active antiretroviral therapy. J Acquir Immune Defic Syndr 2001;27:426-431.
Orenstein J, Dieterich D, Kotler D. Biopsy diagnosis of intestinal microsporidiosis. AIDS 1993;7(Suppl):S49-S54.
Palefsky J, Gonzalez J, Greenblatt R, et al. Anal intraepithelial neoplasia and anal papillomavirus infection among homosexual males with group IV HIV disease. JAMA 1990;263:2911-2916.
Patterson DL, Georghou PR, Allwoth AM, et al. Thalidomide as treatment of refractory aphthous ulceration related to human immunodeficiency virus infection. Clin Infect Dis 1995;20:250-254.
Perez-Rodriguez E, Gonzalez L, Kopp B. The role of calcium supplements in the treatment of nelfinavir-induced diarrhea. 39th Interscience Conference on Antimicrobial Agents and Chemotherapy 1999;San Francisco, CA.
Poles MA, Dieterich DT, Schwarz ED, et al. Liver biopsy findings in 501 patients infected with human immunodeficiency virus (HIV). J Acquir Immune Defic Syndr Hum Retrovirol 1996;11:170-177.
Schmidt W, Schneider T, Heise W, et al. Stool viruses, coinfections and diarrhea in HIV-infected patients. J Acquir Immune Defic Syndr Hum Retrovirol 1996;13:33-38.
Sherman DS, Fish DN. Management of of protease inhibitor-associated diarrhea. Clin Infect Dis 2000;30:908-914.
Soriano V, Garcia-Samaniego J, Bravo R, et al. Efficacy and safety of alpha-interferon treatment for chronic hepatitis C in HIV-infected patients. HIV-Hepatitis Spanish Study Group. J Infect Dis 1995;31:9-13.
Sulkowski MS, Thomas DL, Chaisson RE, et al. Hepatotoxicity associated with antiretroviral therapy in adults infected with human immunodeficiency virus and the role of hepatitis C or B virus infection. JAMA 2000;283:74-80.
Thomas DL, Shih JW, Alter HJ, et al. Effect of human immunodeficiency virus on hepatitis C virus infection among injecting drug users. J Infect Dis 1996;174:690-695.
Wilcox CM, Straub RF, Alexander LN, et al. Etiology of esophageal disease in human immunodeficiency virus-infected patients who fail antifungal therapy. Am J Med 1996;101:599-604.
Wilcox CM, Schwartz DA. Etiology, response to therapy, and long-term outcome of esophageal ulcerations associated with human immunodeficiency virus infection. Ann Intern Med 1995;122:143-149.
Zylberberg H, Pol S. Reciprocal interactions between human immunodeficiency virus and hepatitis C virus infections. Clin Infect Dis 1996;23:1117-1125.
Medical Care Criteria Committee, October 2006
|ALL RECOMMENDATIONS: GASTROINTESTINAL COMPLICATIONS|
Esophageal Disease Diagnosis and Treatment
Gastric Disease Diagnosis and Treatment
Liver Disease Diagnosis and Treatment
Diarrhea Diagnosis and Treatment
Biliary Disease Diagnosis and Treatment
Pancreatic Disease Diagnosis and Treatment