Lester Daron Robert Thompson, MD
Lymphoid changes of the nasopharyngeal
and palatine tonsils that are indicative of human immunodeficiency
virus infection. A clinicopathologic study of 12 cases.
Wenig BM, Thompson LD, Frankel SS, Burke AP, Abbondanzo SL,
Sesterhenn I, Heffner DK.
Am J Surg Pathol. 1996 May;20(5):572-87.
We report 12 cases in which the histomorphologic changes of the
nasopharyngeal tonsils (adenoids) or palatine tonsils suggest
infection with the human immunodeficiency virus (HIV). The patients
included 10 men and two women, aged 20 to 42 years (median, 33
years). The clinical presentation included airway obstruction,
pharyngitis, fever, and a tonsillar or adenoidal mass lesion.
Histologic evaluation of the excised adenoids or tonsils in 10 of
the cases demonstrated a spectrum of changes including florid
follicular hyperplasia, follicle lysis, attenuated mantle zone, and
the presence of multinucleated giant cells (MGC). The latter
characteristically localized adjacent to the surface or tonsillar
crypt epithelium. Two of the 12 cases showed marked lymphoid
depletion with absent germinal centers, plasmacytosis, and stromal
vascular proliferation. Immunohistochemical evaluation for HIV p24
core protein showed reactivity in 10 of 12 cases localized to
follicular dendritic cell network (FDC), the MGC, scattered
interfollicular lymphoid cells, and cells identified within the
surface or crypt epithelium. Localization of viral RNA by in situ
hybridization paralleled the HIV p24 immunohistochemical findings.
Additional significant findings included the presence of both CD-68
and S-100 protein in the MGC and the presence of S-100 protein in
dendritic cells. Other than HIV, no microorganisms were identified.
At the time of presentation, eight patients were not known to be a
risk for HIV infection, nor were they known to be HIV infected or
suffering from AIDS. In these patients, HIV infection was suspected
on the basis of the histologic changes seen in the resected
tonsillar and adenoidal tissue. Serologic evaluation (by
enzyme-linked immunosorbent assay), confirmed the presence of HIV
infection. Our findings suggest the possibility of HIV dissemination
through the upper aero-digestive tract mucosa via target cells, such
as intraepithelial dendritic cells, submucosal macrophages, and
T-lymphocytes. Subsequent presentation of viral antigens to the
tonsillar and adenoidal lymphoid tissues results in enlargement of
these structures that clinically may simulate a neoplastic
proliferation but causes histomorphologic changes that are highly
suspicious for HIV infection even in asymptomatic HIV-positive
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Tonsillar lymphangiomatous polyps: a
clinicopathologic series of 26 cases.
Kardon DE, Wenig BM, Heffner DK, Thompson LD.
Mod Pathol. 2000 Oct;13(10):1128-33.
BACKGROUND: Lymphangiomatous polyps are uncommon benign tumors of
METHODS: Twenty-six cases of lymphangiomatous polyps diagnosed
between 1980 and 1999 were retrieved from the files of the
Otorhinolaryngic-Head and Neck Tumor Registry of the Armed Forces
Institute of Pathology. Hematoxylin and eosin-stained slides were
reviewed to characterize the histologic features of these tumors.
Immunohistochemical stains were performed on 15 cases. Clinical
follow-up data were obtained.
RESULTS: The patients included 13 males and 13 females, ages 3 to 63
years (mean, 25.2 years). Patients experienced dysphagia, sore
throat, and the sensation of a mass in the throat. Symptoms were
present from a few weeks to years. The tonsillar masses were
unilateral in all cases. Clinically, the lesions were frequently
mistaken for a neoplasm (n = 18 patients). Grossly, all of the
lesions were polypoid and measured 0.5 to 3.8 cm (mean, 1.6 cm).
Histologically, the polyps were covered by squamous epithelium
showing variable epithelial hyperplasia, dyskeratosis, and
lymphocytic epitheliotropism. The masses showed a characteristic
submucosal proliferation of small to medium-sized,
endothelial-lined, lymph-vascular channels lacking features of
malignancy. Collagen, smooth muscle, and adipose tissue were present
in the stroma. Intravascular proteinaceous fluid and lymphocytes
were noted. Immunohistochemical findings confirmed the endothelial
origin of the vascular proliferation and a mixed lymphoid
population. The differential diagnosis included fibroepithelial
polyp, lymphangioma, juvenile angiofibroma, and squamous papilloma.
In all patients with follow-up, complete surgical excision was
curative (mean follow-up, 5.4 years; range, 1 mo to 14 years).
CONCLUSIONS: We detail the clinical and pathologic features of
tonsillar lymphangiomatous polyps. These tumors are uncommon and may
clinically be mistaken for a malignant neoplasm. The characteristic
histologic features should allow for its correct diagnosis and
differentiation from similar appearing tonsillar lesions.
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A clinicopathologic series of 22 cases of
Kardon DE, Thompson LD.
Laryngoscope. 2000 Mar;110(3 Pt 1):476-81.
OBJECTIVES: Tonsils are uncommonly affected by granulomatous
inflammation, often with an obscure cause. This study attempts to
elucidate the nature of tonsillar granulomatous inflammation.
DESIGN: Retrospective clinicopathologic review.
METHODS: Twenty-two cases of tonsillar granulomas diagnosed between
1940 and 1999 were retrieved from the files of the Armed Forces
Institute of Pathology. H&E slides and a series of histochemical
stains were reviewed, and patient follow-up was obtained.
RESULTS: There were 11 males and 11 females, aged 7 to 64 years
(mean, 29.9 y). Most of the cases presented bilaterally (n = 19)
with sore throat, dysphagia, and/or nasal obstruction. The clinical
differential included chronic tonsillitis, tuberculosis, nonspecific
infection, sarcoidosis, and a neoplasm. Histologically, the
granulomas were focal and scattered, or diffuse, identified in the
interfollicular zones (n = 16) and/or the germinal centers (n = 13),
and occasionally associated with necrosis (n = 6). Based on
histochemical and clinical follow-up information, the etiology of
the granulomas included sarcoidosis (n = 8), tuberculosis (n = 3),
Hodgkin's lymphoma (n = 2), toxoplasmosis (n = 1), squamous cell
carcinoma (n = 1), and no specific known cause (n = 7). Twelve
patients were either alive at last follow-up or had died with no
evidence of disease (mean, 12.4 y), and 9 were either alive at last
follow-up or had died with disease (mean, 24.9 y). One patient was
alive with unknown disease status (lost to follow-up after 13.3 y).
CONCLUSIONS: Although a cause for tonsillar granulomas is frequently
identified, a number may not develop an identifiable etiology, with
the granulomas probably representing an exaggerated immune response
to chronic tonsillitis. However, a careful work-up must be conducted
to exclude specific causes and avoid clinical mismanagement.
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Routine histologic examination is
unnecessary for tonsillectomy or adenoidectomy.
Randall DA, Martin PJ, Thompson LD
Laryngoscope. 2007 Sep;117(9):1600-4
OBJECTIVE: To determine whether the current practice and incurred
cost of histologic examination of tonsillectomy and adenoidectomy
specimens is warranted.
STUDY DESIGN: Review article based on medical literature.
SUBJECTS AND METHODS: A retrospective PubMed review of all pertinent
literature regarding tonsillectomy, adenoidectomy, and related
surgical pathology was conducted. References of the articles
obtained were reviewed for additional sources.
RESULTS: Twenty studies report 54,901 patients and found 54
malignancies (0.087% prevalence). Of these, 48 (88% of the patients)
had suspicious features such as tonsillar asymmetry, cervical
lymphadenopathy, or abnormal tonsil appearance, preoperatively. The
remaining six patients without any suspicious features (better
representing true occult malignancy) were 0.011% of the total cases.
CONCLUSION: Submission of tonsillectomy, adenoidectomy, or both
specimens is warranted only when patients demonstrate findings
associated with malignancy: tonsillar asymmetry, history of cancer,
neck mass, tonsil firmness or lesion, weight loss, and
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Tonsil with Tangier disease.
Nelson BL, Thompson LD.
Ear Nose Throat J. 2003 Mar;82(3):178.
FIRST PARAGRAPH: Tangier disease is a rare autosomal-recessive
inherited disorder that is caused by a defect in chromosome 9q31. It
is characterized by a severe deficiency or absence of high-density
lipoproteins in plasma. A defect in cellular cholesterol removal
results in the massive, abnormal accumulation of cholesterol esters
in macrophages in many tissues. Although this accumulation is most
conspicuous in the tonsils, progressive accretion of these esters
also occurs in nerves (neuropathy) and vessels (atherosclerosis).
The pathognomonic finding is a low plasma cholesterol concentration
accompanied by normal or elevated triglyceride levels and large,
lobulated, hyperplastic, bright orange-yellow tonsils and adenoid
tissue. Affected families have been identified on Tangier Island,
Va., in Chesapeake Bay as well as in Missouri, Kentucky, and Europe.
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