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CMV infection is clusters of small lymphocytes. These lymphocytes do not form reactive
follicles. Small hemorrhages may also be present along with isolated small areas of necrosis.
Whenever any of these changes are present, a careful search for CMV should be made. The
greater the degree of necrosis, inflammation, or fibrosis, the more likely electrolyte or hormonal
abnormalities will become apparent clinically.[419,867]
The CMV inclusions in adrenal are similar to those elsewhere, with large violaceous,
dark red, or mauve intranuclear inclusion bodies surrounded by a clear halo beneath the thin
nuclear membrane. An extensive amount of basophilic finely reticulated cytoplasm (basophilic
inclusions) may draw attention to the CMV cell at low or medium power magnification. Cells
with characteristic basophilic stippling are rare. The inclusions are larger than the nucleoli of
medullary ganglion cells.
Adrenal involvement with other opportunistic infections and neoplasms usually occurs
with widespread dissemination and is only diagnosed at autopsy. Malignant lymphomas are seen
at autopsy in adrenal in one third of cases, followed by Cryptococcus neoformans infection in
one fourth, and Mycobacterium tuberculosis in one fifth. Mycobacterium avium-complex,
usually more common than M tuberculosis, is seen less frequently in adrenal (Table 5). In many
cases the adrenal is only involved through superficial capsular infiltration from periadrenal
deposits of these agents or tumors. Thus, adrenal enlargement with these diseases is uncommon.
Despite the presence of adrenal CMV in over a third of all AIDS patients at autopsy,
despite involvement of the adrenal with mycobacterial or fungal infections that microscopically
are associated with necrosis and inflammation, and despite frequent clinical evidence for adrenal
dysfunction, adrenal failure leading to demise is rare. Adrenal insufficiency accounts for less
than 2% of all deaths in AIDS.[419]
THYROID AND PARATHYROID.—A clinical appearance similar to "sick euthyroid"
state in debilitated and/or hospitalized AIDS patients is common. This condition is characterized
by decreased triiodothyronine levels secondary to diminished peripheral conversion of thyroxine.
Patients with advancing HIV infection are noted to have elevated concentrations of thyroid
binding globulin and a progressive decline in reverse triiodothyronine concentration.
Hypocalcemia has been observed as a complication of pentamidine isethionate therapy. Therapy
with foscarnet may also reduce serum calcium.[864,865]
Patients receiving antiretroviral therapy may have subclinical hypothyroidism with
laboratory findings of increased TSH and low thyroxine. The serum total thyroxine (T4) and
triiodothyronine (T3) concentrations may be increased because of an increase in thyroxine-
binding globulin, the cause of which is unknown. Late in the course of AIDS, the T4 and T3
may fall slightly. Conversely, some patients on antiretroviral therapy with immune restoration
may have laboratory evidence of Graves disease.[865,868]
Thyroid and parathyroid glands are rarely the site of involvement for any opportunistic
infections or neoplasms diagnostic for AIDS (Table 5). Occasional CMV inclusions may be
found at these sites when there is widely disseminated CMV. The same is true for Pneumocystis
jiroveci (carinii) and pathogenic fungi. However, significant organ enlargement, atrophy, or
failure does not usually ensue, probably because of the focal nature of involvement and because
widespread involvement of a more critical organ--such as lung or brain--causes demise of the
patient first.[864]
The whole blood calcium tends to be lower in patients with HIV infection, and both basal
and maximal secretion of parathyroid hormone is reduced in patients with AIDS.[869]