Page 207 - AIDSBK23C

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Thromboembolic disease and deep venous thrombosis more frequent with AIDS,
particularly in persons 21 to 50 years of age. Predisposing factors include opportunistic
infections such as cytomegalovirus and AIDS-associated neoplasms. Antiretroviral therapy,
particularly regimens including protease inhibitors such as indinavir, may increase the risk for
pulmonary embolism. A hypercoagulable state may be associated with HIV infection, including
acquired protein C and protein S deficiencies, heparin cofactor II deficiency, and antithrombin
deficiency. Endothelial cell dysfunction and platelet aggregation with elevated levels of Von
Willebrand Factor and P-selectin can be found in HIV infection. Autoimmune phenomena such
as antiphospholipid syndrome may be implicated. The risk is increased for persons taking
megestrol acetate. Thrombosis is more likely to occur with clinical AIDS when the CD4 count is
less than 200/µL.[848,849]

BONE MARROW.-- A bone marrow biopsy in an HIV-infected patient is most useful
when there is a history of persistent fever along with cytopenia, and no localizing signs are
present. Marrow biopsy can be useful in the workup of lymphoma. Morphologic examination
should be combined with microbiologic culture for suspected pathogens.[850] Mycobacterial
infections (both MAC and MTB) are the most frequently identified opportunistic infections of
bone marrow with AIDS, followed by C neoformans. However, the less frequently seen
dimorphic fungi H capsulatum and C immitis, commonly involve bone marrow in cases in which
they are present. Other opportunistic agents are quite rare at this site (Table 5). Culture of bone
marrow can be useful for diagnosis of both mycobacterial and fungal infections.[425]
It is uncommon for grossly visible lesions to appear in bone marrow with any
opportunistic infections or neoplasms. Severe pancytopenia may be accompanied by a
generalized pale appearance.
Microscopically, a variety of non-specific morphologic abnormalities can occur. There
may be overall hypercellularity early in the course of AIDS, or with systemic infections, and this
is seen in about half to three fourths of cases. This is most often due to hyperplasia of
granulocytic or megakaryocytic cell lines. Debilitation leads to increasing hypocellularity and
serous atrophy of fat later in the course of AIDS. Additional non-specific microscopic findings
may include immature or dysplastic myeloid precursors (dysmyelopoietic), lymphoid aggregates,
atypical megakaryocytes, a fine reticulin fibrosis, mild vascular proliferation, histiocytosis with
or without non-specific granuloma formation, and increased hemosiderin deposition.[851,852]
A consistent finding is increased plasma cell cuffing of blood vessels, which may be
accompanied by polyclonal hypergammaglobulinemia in over 80% of patients. The presence of
giant pronormoblasts with inclusion-like nucleoli suggests parvovirus infection. Megaloblastic
features often accompany zidovudine therapy or therapy with folate antagonists. HIV can also
be demonstrated in a variety of marrow cells by in situ hybridization.[839,842]
Granulomas are infrequently present in bone marrow and may contain fungi, acid-fast
organisms, occasional parasites, or polarizable talc crystals from injection drug use. These
granulomas are typically not well formed. Localized ill-defined granulomas consisting of
collections of macrophages were more frequent than were granulomas containing organisms. Of
the dimorphic fungi, C neoformans is seen most frequently. H capsulatum, next in frequency
may produce loose lymphohistiocytic aggregates. Of the mycobacteria, Mycobacterium avium
complex (MAC) is seen more frequently than M tuberculosis.[851] The most sensitive method
for detection of MAC remains blood culture. Culture of bone marrow aspirates will be positive