HIV-associated polymyositis Head
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This is quite common and does not appear to be due
to direct infection of myocytes by HIV. This entity can occur in AIDS,
AIDS-related complex or in the earlier stages.
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Its pathogenesis includes a major
histocompatibility complex (MHC)-1-restricted
T8 cytotoxicity, as in polymyositis of seronegative individuals. They are
histologically indistinguishable from other polymyositis except that there are
less T4 cells and almost total absence of B cells.
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Iron pigments tend to be found in macrophages but
are not diagnostic.
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It responses to steroid treatment.
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They significantly deviate from the HIV-associated
polymyositis picture although some overlap may occur. In some cases, there are
variable amount of interstitial inflammation without a full-blown picture of
polymyositis. In other cases, scattered or clusters of necrotic fibers
suggesting infarcts are present.
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Tubuloreticular
structures and/or cylindrical confronting cisternae
are found in virtually all HIV patients with morphological changes in muscle.
HIV-associated non-inflammatory
myopathy
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This form is characterized by accumulation of
nemaline bodies, largely in type I fibers and associated type 1 atrophy. The
rods tend to be relatively small, up to 1 mm.
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There are also loss of thick filaments in areas
where rods are found and in some cases, loss of thick filament is not associated
with rod formation.
Neurogenic atrophy associated with
HIV-related neuropathy
Opportunistic infection of skeletal muscle: These are seldom recognized.
They include focal pyogenic infection (so-called pyomyositis), usually due to
Staphylococcus aureus, infection by cytomegalovirus, Mycobacterium avium
intracellulare, Cryptococcus neoformans, Toxoplasma gondii, and microsoporidia.
AIDS cachexia:
This includes the HIV wasting syndrome which occurs in the absence of
intercurrent opportunistic infections and indicates per se a stage IV of the disease according to the CDC criteria.
Zidovudine (AZT) myopahty
Mechanism:
AZT is a thymidine analogue that can inhibit viral reverse transcriptase. Higher
levels of AZT also inhibit g-DNA
polymerase of mitochondria and a-DNA
polymerase of nucleus. AZT treatment may result in damage of mitochondria.
Clinical:
Zidovudine myopathy is a dose-related, painful, amyotrophic myopathy associated
with mitochondria abnormalities, which may resolve after withdrawal of the drug.
Histology:
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Damaged fibers contain masses of mitochondria that
is best demonstrated by oxidative enzymes. At the same time cytochrome C oxidase
negative fibers are found.
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There is lipid accumulation in the muscle fibers
and artifactual cracks due to increased lipid content may be seen in frozen
sections.
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Myofibrillar changes such as cytoplasmic bodies are
common in damaged fibers.
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Antibodies to cytokines show interleukin-1 in a
reticular pattern in their cytoplasm; this is a phenomenon that is not seen in
noniatrogenic mitochondrial cytopathies (a small amount could be seen).
Other myopathies