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cytologic abnormality to predict any degree of anal dysplasia is 95%.[721] Lesions are treated
with excision.[711]
An epidermodysplasia verruciformis-like (AEV) syndrome occurs in HIV-infected
persons co-infected with HPV. AEV is characterized by hypopigmented macules or
erythematous flat-topped papules on the face, trunk, and arms. AEV most commonly occurs
with HPV types 5, 8, 17, and 20.[722]
AIDS ENTEROPATHY.-- Despite extensive clinical workup and laboratory testing,
some AIDS patients with chronic diarrhea, weight loss, and/or malabsorption cannot be found to
have an infection or etiologic factor that can explain the symptomatology, even after biopsy.
Endoscopic biopsies in such cases may show prominent villus atrophy, crypt architectural
distortion, decrease in crypt/villus ratio, and increased IgM containing but decreased IgA
lymphocytes within the lamina propria. However, AIDS patients without diarrhea may also have
endoscopic biopsies that show villous atrophy. The term "AIDS enteropathy" has been used to
describe this condition. The malabsorption is out of proportion to the degree of pathologic
changes present. Octreotide and nutrional support have been recommended for patients with
AIDS enteropathy.[723]
The pathogenesis of this enteropathy may be related directly to local HIV infection, and
antiretroviral therapy leads to statistically significant improvements in gastrointestinal
symptoms. Several theories have been postulated to explain this enteropathy. HIV may have an
effect upon mucosal ion flux that is cytokine mediated to alter transepithelial resistance by
changes in transcellular or intercellular (paracellular) permeability. A decreased staining of
acetylated tubulin has been observed in small bowel and colonic epithelial cells from HIV-
infected subjects, implying microtubular depolymerization and cytoskeletal alterations.
Incubation of the intestinal cell line, HT-29, with gp120, applied to the basolateral side, led to an
increase in cytosolic calcium, which was associated with both tubulin depolymerization and
decreased epithelial resistance, suggesting that HIV enteropathy is a pathophysiological
consequence of gp120 exposure, and is independent of epithelial cell HIV infection.[724]
HIV WASTING SYNDROME.-- Progressive, involuntary weight loss is a common
accompaniment to HIV infection. Poor diet from lack of sufficient care or economic resources
certainly plays a role, as well as malabsorption from concomitant AIDS-associated infections or
neoplasms, particularly those affecting the GI tract. However, there are persons with HIV
infection and AIDS who do not have a concurrent illness or condition other than HIV infection
that explains a weight loss of >10% of baseline body weight plus either chronic diarrhea or
chronic weakness and fever, which are the CDC criteria for HIV wasting syndrome that satisfy
definitional criteria for a diagnosis of AIDS.[392] Additional criteria that adjust for changes in
baseline weight with advancing HIV illness include unintentional loss of >10% body weight, a
body mass index decreasing to <20, or unintentional loss of 15% body weight in 6 months that
persists for at least 1 year. About a third of HIV-infected persons may be affected by this
wasting syndrome.[725]
Several causative factors probably contribute to the development of wasting syndrome.
These can include hypermetabolic or altered metabolic states, production of cytokines such as
tumor necrosis factor and interleukin-1 because of macrophage infection by HIV, and endocrine
dysfunction. Also, progression of HIV infection may play a role in the appearance of wasting