GI manifestations of HIV

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GI manifestations of HIV :

GI manifestations of HIV

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By : Ephrem Bekele (MSC fellow in clinical infectious disease at MU) April,2012

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Oropharyngial diseases Esophageal disease Diarrhea Hepatobiliary disease

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Oropharyngial disease Oral thrush Oral hairy leukoplekia Aphthous ulcer Oral Kaposi sarcoma

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Oropharyngial candidiasis Caused by candidia albicans There are two major forms pseudomembranous form is the most common and appears as white plaques on the buccal mucosa, palate, tongue easily scrachable and bleeding base , or the oropharynx Atrophic form denture stomatitis It is often found under dentures and is characterized by erythema without plaques Fairly indicative of advanced immunologic decline(59% goes to AIDS in next yr)

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DX Clinical (distinguish from hairy leukoplakia) KOH exam of scrapings Culture Rx Topical therapy with clotromazole , Nystatin , or miconazole jel 2% BID for 2-3wks or Oral fluconazole 100mg/d for 2wks is considered drug of choice

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Oral hairy leukoplakia EBV mediated hyperplasia of sequamous epith not considered premalignant condition lesions are described as white corrugated painless plaques commonly on lateral aspect of tangue unlike candida , cannot be scraped Relatively specific to HIV infection RX- HAART or topical podophylin or isotretinoin

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Aphthous ulcer painful oral lesions that appear as localized, shallow, round, to oval ulcers with a grayish base Pathogenesis is not well defined, alteration of local cell mediated immunity Risk Factors- stress immun supr. HIV food hypersensitivity, & familial tendency vitamin deficieny (B.1,2,6,12, Fe, folic acid & Zink)

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Rx Symptomatic relief with triamcinolone oralbase , fluocinoide jel,amlexanox paste Intraleisional or oral corticosteroids for sever cases Thalidomide 200mg po bid for 5days,then 200mg/d for 8wks -for HIV positive

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Oral kap osi sarcoma is a multicentric neoplasm consisting of multiple vascular nodules appearing in the mucous membranes skin or visera HHV8 is strongly implicated in pathogenesis Incidence is decreased due to HAART, in 1997 <1% Can occur at any stage or at normal CD4 count Lesions - reddish to purple to brown raised maqules

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Dx Biopsy- proliferation of spindle cells and endothelial cells, extravasation of red blood cells, hemosiderin -laden macrophages Rx Majority showed spontaneous regresion with HAART Other options- radioterapy,or cryothearapy

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Other oral lesions Non- hudgkins lymphoma( swelling or ulcer) Oral warts

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esophageal disease( Dysphagia & Odenophagia ) One third of Aids pts.develop dysphagia and odynophagia In ART neive pts. With CD4+ count <200, oesophagitis is due to OI Only 4% normal endoscopy, 1.6% has oesophagial reflux disease

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Most common causes are: Oesophagial candidiasis Herpetic oesophagitis CMV infection Aphtous ulceration

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Oesophagial candidiasis At CD4 count <200 Can Present with oral thrush or alone Symptoms- odynophagia , dysphagia and substernal chest pain Odynophagia is less sever than other causes Dx - Endoscopy-small white plaque with erythema and ulceration(for refractory cases) Barium swallow- coblestone apearance

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Treatment Fluconazole 200mg/d for 7-14days Failure to improve early or after 7days of treatment calls for endoscopy for alternative dx or fluconazole resistance Others – itraconazole *, newer antifungals ( caspofungin,voriconazole,posaconazole *, micofungin )

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Ulcerative oesophagitis Is associated with CMV HSV infection Hiv induced Aphtuos ulceration and oesophageal reflux disease Characterized by prominent odynophagia , substernal chest pain and limiting oral intake and cause wt. loss Of patients fail emperical antifungal thearapy , 1/3 have CMV ulerations

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CXI of CMV ulcration Solitary(single) or multiple diffuse ulcerations Involving middle to distal oesophagus Histology- inclusion bodies in endothelial cell nucles and immflamatory cell rxn Definitive diagnosis is made by biopsy and culture

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Treatment Induction and maintenance Ganciclovir or Foscarnet Gancyclovir 5 mg/kg IV every 12 hr for 14 days, then 5mg/d for 4wks or Valganciclovir 900 mg po every 12 h for 21 days, then 600mg/d for 3wks Pt. monitering - CBC(2x/wk), creatinine (monthly), Electrolytes

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HSV esophagitis Accounts for 8-16% Occur at CD4 count<100 On endoscopy Smaller and confulent ulceration Culture & PCR are diagnostic Treatment is IV acyclovir 200mg 5x/d for 7days or valcyclovir 500mg po BID for 7days Empirically for HSV & CMV coverage, foscarnet,cidofovir or galcyclovir can be used

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Aphtuos ulcer esophagitis Occurs in the same population,with the same frequency as CMV esophagitis On endoscopy exam., large ulcers with raised indurated margins Diagnosis is difficult needs culture – ve and histology Treatment is with prdonsolone 40mg,followed by daily tapering over 2-3wks

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Diarrhea is the most common GI symptom prevalence of diarrhea ranged from 0.9 to 14% in out pt In hospitalized individuals with advanced HIV, >50% of all patients had diarrhea Around 26% acounts chronic diarhea

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common Causes Infectious etiologies HIV enteropathy Neoplasms

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Infectious ethiologies Bacterial Viral Fungal protozoal

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Bacterial causes Type of pathogen involved based on level of immunosupresion In HIV causes more sever or persistant diarrhea Systemic infections are common Salmonela ( s.typhi ) Shigela (s. flexineri ) Campylobacter ( c.Jejuni ) MAC( Avium or intracellulare )- dissiminated or localized E.coli ( Enteroagrasive E.coli ) Clustridium difficles

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Viral cause CMV Entritis (accounts for 4% of GI CMV infection, Abd . Pain and watery diaria ) Colitis ( second most common next to CMV retinitis) Decreased with advent of HAART C/m- low grade fever, abdominal pain, non bloody watery diarrhea, wt. loss, - small frequent diahhrea , tenismus and/or hematochezia (large bowel) Complications- mucusal hemorhage and perforation Dx - LGI endoscopy – multiple ulcerations, biopsy revile intranuclear inclusion bodies or intracytoplasmic enclusion bodies Treatment is with either ganciclovir ( prefered )or foscarnet for 3–6 weeks and Optimizine HAART Others- HSV, Adenovirus, Rotavirus

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Fungal infections Histoplasmosis coccidioidomycosis , and penicilliosis have all been identified as a cause of fever and diarrhea in patients with HIV infection

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Protozoal infections Cryptosporidia microsporidia , and Isospora belli Cyclosporadia

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Cryptosporidiasis Epidemiology Causes self limitted diarrhea in healthy individuals severe, life-threatening diarrhea in severely immunodeficient individuals Individual at high risk are those with CD4 count of <100cells/ Incidence rate is 1per 100 person -year Etiology cryptosporadium parvum Cryptosporidium oocysts are highly infectious, requiring only 10 to 1000 oocysts to cause human disease Immidiatly infectious after excretion Commenly involve small bowel Advanced cases caninvolve large bowel and biliary truct

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Clinical Manifestations acute or subacute onset of profuse, nonbloody , watery diarrhea nausea, vomiting, and lower abdominal cramping Fever is present in one third of patients and malabsorption is common Diagnosis Modified* AFB stain Others- direct immunofluorescence,ELISA , or PCR

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Treatment supportive (rehydration) HAART Nitazoxanide *(FDA approved) 500-1000mg/d po for 14d Privention Avoid exposure to infected contacts Contact with diarrhea Potential oral exposure to feces during sex Direct contact with farm animals, stool from pets Use gloves and wash hands if exposure unavoidable

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Microsporidia Epidemiology Ubiqiutious , Zoonotic ,and waterborn In pre-ART era prevalence was 2-70% in HIV + ve Prevalence decreased with widespread use of HAART Clinical signs observed when CD4+ cell count is <100

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C/M Diarrhea(common) malabsorption,cholangitis,Hepatitis or dissiminated disease(based on spc .) Dx * Light microscopy can be used to differentiate spores of microsporadium from cells or debrids / tholedine stain/ As microsporadium is small in size(1-5mm) needs 1000x magnification Chromotrope 2R, calcofluor white (a fluorescent brightener), and Uvitex 2B (a fluorescent brightener) are useful as selective stains for microsporidia in stool and other body fluids (

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Rx Albendazole 400mg po BID for 2-4wk HAART- help for resolusion of symptomes Pts. With CD4 count of <200cell should avoid drinking untreated water

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Isospora beli Share same prevalence, symptoms and clinical manifestation with crypotosporadial infection Dx - modified AFB Rx TMP-SMX 1DS tab po QID for 10days followed by 1DS tab po BID for 3wks

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Cyclosporiasis One of causes of persistant diarrhea in AIDS Contaminated water is source of infection Oocysts are not immidiaty infectious, thus person to person transmision is not likely Dx - modified AFB( reviles Oocyst ) Rx-TMP- SMX(as above)

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HIV Enteropathy chronic diarrheal syndrome for which no etiologic agent other than HIV can be identified Can occur from acute phase of infection to advanced stage It is characterised by diarrhoea , increased GIT inflammation, increased intestinal permeability, malabsorption of bile acids, vitamin B12, wt. loss

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Mechanisms are poorly understood Proposed mechanisms are HIV direct “ virotoxic ” effect on the enterocyte * Local activation of the GIT immune system* Histologically , inflammatory infiltrates of lymphocytes and damage to the GIT epithelial layer (which includes villous atrophy, rypt hyperplasia and villous blunting) In pts. diagnostic evaluation is nonrevealing , a presumptive diagnosis of HIV enteropathy can be made if the diarrhea has persisted for >1 month Initiation of HAART is the only option for improvement

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Hepatobiliary disease Diseases of the hepatobiliary system are a major problem in patients with HIV infection Causes HIV virus itself Ois Hepatitis viruses co-infection HAART

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HIV virus related HIV can involve the liver directly presence of HIV p24 within Kupffer cells &hepatic endothelial cells and HIV messenger RNA within hepatocytes . It remains unclear, however, whether HIV itself directly damages the liver The quantity of HIV antigens in immunohistochemical studies does not correlate with the degree of histologic abnormalities, and normal histology can be seen

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OIS Granulomatous hepatitis may be seen as a consequence of mycobacterial or fungal infections, particularly MAC infection Hepatic masses may be seen in the context of TB, or fungal infection( C. immitis and Histoplasma capsulatum )are those most likely to involve the liver Biliary tract disease in the form of papillary stenosis or sclerosing cholangitis has been reported in the context of cryptosporidiosis, CMV infection, and KS

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Hepatitis virus coinfection Hepatitis B Around 90% of HIV infected pts. Have positive serologic marker for a past HBV infection Co-infection outcomes Decrease the chance of clearing during acute infection(risk of chronicity ) 5-10% VS >50% Accilerate the chance of liver disease in chronic hepatitis Complicate HIV thearapy (IRIS)

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C/m Abrupt onset of malaise,fever , anorexia,nausia and headach and abd . Pain Joundice acompanied by dark urine and acholic stool Serologic finding during acute phase- HBSAg , IgM anti- HBc,HBH DNA, Hbe Raise in tranaminase level(5to 20xUNL) and moderate elivatin of A.phsphatase (2 to 10x) Around 20% of HIV pts. Fail to produce Antibody to HBSAg and chronic infection with complain of chronic fatigue and extrahepatic manstn .

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Treatment Based on decision algorism with lamivudine , emtricitabine , or adefovir / tenofovir and entecavir alone or in combination If Both HIV and HBV Rx is indicated TDF+ 3Tc or FTC

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HCV coinfection 3.5% of patients are co-infected with HCV(16.1% HIV RG) is more severe in the patient with HIV infection HCV coinfected pts. Progress more rapidely , higher risk of liver cirrosis & hepatic failure Dignosis HCV antibodies test with EIA PCR HCV RNA Liver biopsy Treatment pegylated IFN- α 2a alone or with ribavirin for 24-48wks

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Pancreatitis pancrease is common site of imflamatory sd in HIV Autopsy studies revealed lesions in 90% of AIDS pts. Common causes are: Dissiminated infections(CMV,MAC cryptococus ) or infiltrative disease(lymphoma or kaposi sarcoma) or Drugs HAART(DDI,PIS,D4T…) cotri …,steroids, pentamidine , Alcohol etc) C/m- Abdominal pain radiating to the back associted with nausia and vomiting with elivated Amilase and lipase level Treatment Treat or remove the offending drug Pain relief with Opoids Fliud and electrolyte replacment Keep NPO for moderate Debridment of necrotic area for severe cases

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Cholecystitis & AIDS cholangiopathy Infectious disease of the billiary tree and gallblader are more common in HIV infected pts. Cause acalcules cholesystitis Occur at low CD4 count(<50) Major pathogens are: Cryptosporadia , Microsporadia MAC.& CMV Cholecystitis is due to obstruction of cystic duct by immflamation induced with OIS

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C/M Rt. Upper quadrant pain or epigastric pain,fever nausia , vomiting Joundice is rare Marked alkaline phosphatase elivation Thickened or dilated gallblader (U/S) Presentation of AIDS cholangiopathy is same as acalcules chlecystitis Endoscopic choleangiopancreatography is more sensitive than CT or MRI Treatment of HIV related billiary sx is same as non HIV

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References CDC OI treatment giudeline,2008 Uptodate 17.3, 2009 Harrisons ,2007

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