Cases reported "Leukoplakia, Hairy"

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1/16. Oral hairy leukoplakia in a patient with acute lymphocytic leukemia.

    The first case of oral hairy leukoplakia (OHL) in an HIV-negative 56-year-old patient with acute lymphocytic leukemia (ALL) is reported. A white plaque was observed while the patient was in complete remission which followed the chemotherapeutic scheme. The clinical and histopathologic findings were typical for OHL and the polymerase chain reaction method was positive for Epstein-Barr virus dna. Underdiagnosis and underreporting of OHL in patients with a malignant haematological disease and the apparent different environmental factors to which these non-AIDS patients have been exposed, probably constitute some of the reasons for the very few OHL cases reported in these patients. ( info)

2/16. Oral hairy leukoplakia: an ultrastructural study and review of the literature.

    A 39-year-old, homosexual, Caucasian man with a 9-month history of acquired immunodeficiency syndrome by reduced cd4 lymphocyte count alone was found to have extensive, asymptomatic, nonremovable, corrugated, white patches on the lateral borders and ventral aspects of the tongue typical of oral hairy leukoplakia (OHL). Histologically, irregular hyperparakeratosis, acanthosis, and clusters of ballooned keratinocytes in the stratum spinosum were present in the biopsied lateral tongue. Some of the superficial ballooned keratinocytes had peripherally beaded nuclei, whereas others had ground glass intranuclear inclusions. Ultrastructurally, the ballooned keratinocytes had three important findings of diagnostic significance. First, frequent herpesvirus nucleocapsids were largely confined to superficial ballooned keratinocytes having marginated and condensed chromatin. In searching for herpesvirus nucleocapsids, the marginated and condensed chromatin was an invaluable marker for cells harboring the virions. Second, the marginated and condensed chromatin frequently had a distinctive punched-out or cribriform appearance. Third, the ground glass intranuclear inclusion bodies consisted of central, medium electron-dense, finely granular material containing frequent herpesvirus nucleocapsids and partially surrounded or capped by prominent, clumped chromatin. The patient died with progressive multifocal leukoencephalopathy 24 months after OHL was diagnosed. ( info)

3/16. Oral hairy leukoplakia: a manifestation of primary infection with Epstein-Barr virus?

    Oral hairy leukoplakia (OHL) is a characteristic lesion presumably secondary to Epstein-Barr virus (EBV) reactivation. It is frequently seen in individuals infected with the human immunodeficiency virus (HIV) and less often in other immunosuppressed individuals. The frequent association of this lesion with HIV infection and its rare occurrence in normal individuals usually motivates the search for immunosuppression, particularly secondary to HIV, when this lesion is found. We describe here a healthy HIV-negative individual with OHL and clinical and laboratory data suggestive of acute EBV infection. ( info)

4/16. Oral hairy leukoplakia in two children with perinatally acquired hiv-1 infection.

    We report on two children with acquired immunodeficiency syndrome (AIDS), a 5-year-old girl and a 9-year-old boy, who presented with oral hairy leukoplakia (OHL) as a late clinical manifestation of perinatally acquired human immunodeficiency virus type 1 (hiv-1) infection. The reasons why OHL is a rare symptom in hiv-1-infected children, compared with hiv-1-infected adults, are discussed. ( info)

5/16. Case report on a rare lesion in an HIV-infected child: hairy leukoplakia.

    This report describes a case of hairy leukoplakia in an HIV-infected child, and the treatment adopted. It was diagnosed by clinical and laboratory examinations, using exfoliative cytology (staining by the Papanicolaou method) and additional information was obtained by optical microscope analysis. In view of the lack of painful symptoms, of the innocuous nature of the lesion and large amount of medicines used by the patient, we decided to preserve and monitor the lesion. ( info)

6/16. Secondary syphilis simulating oral hairy leukoplakia.

    We describe a case of secondary syphilis of the tongue in which the main clinical presentation of the disease was similar to oral hairy leukoplakia. In a man who was HIV seronegative, the first symptom was a dryness of the throat followed by a feeling of foreign body in the tongue. Lesions were painful without cutaneous manifestations of secondary syphilis. IgM-fluorescent treponemal antibody test and typical serologic parameters promptly led to the diagnosis of secondary syphilis. We initiated an appropriate antibiotic therapy using benzathine penicillin, which induced healing of the tongue lesions. The differential diagnosis of this lesion may include oral squamous carcinoma, leukoplakia, candidosis, lichen planus, and, especially, hairy oral leukoplakia. This case report emphasizes the importance of considering secondary syphilis in the differential diagnosis of hairy oral leukoplakia. Depending on the clinical picture, the possibility of syphilis should not be overlooked in the differential diagnosis of many diseases of the oral mucosa. ( info)

7/16. Oral hairy leukoplakia in a child with AIDS.

    A case of a 9-year-old boy with AIDS and severe hairy leukoplakia on the tongue is reported. Clinically it appears as a bilateral whitish-grey, nonremovable lesion on the lateral margins of the tongue with characteristic vertical corrugations. The lesion failed to respond to topical and systemic antifungal treatment. In contrast, it completely disappeared after treatment with 600 mg acyclovir per day for 1 month. During the hairy leukoplakia development the CD4-lymphocytes count was 95/microL. ( info)

8/16. Oral hairy leukoplakia in an HIV-negative woman with Behcet's syndrome.

    The first case of oral hairy leukoplakia in an HIV-negative patient with Behcet's syndrome is reported. The patient was a 47-year-old woman with bilateral lesions on the tongue. The clinic and histologic appearances were typical of hairy leukoplakia, and Epstein-Barr virus was demonstrated in the epithelial cells by dna in situ hybridization. The patient had been on systemic steroid therapy for 15 years to control lesions of Behcet's syndrome. The literature now records 30 HIV-negative patients with hairy leukoplakia. ( info)

9/16. Epstein-Barr virus coinfection and recombination in non-human immunodeficiency virus-associated oral hairy leukoplakia.

    Human immunodeficiency virus-associated oral hairy leukoplakia (HLP) is characterized by coinfection with multiple types and strains of Epstein-Barr virus (EBV) and recombination within the EBV genome. HIV-seronegative immunosuppressed and immunocompetent patients with HLP were examined to determine the pathogenic contribution of EBV coinfection and recombination to the development of HLP. Multiple coinfecting EBV strains were detected in both HLP specimens and peripheral blood lymphocytes (PBL) of HIV-seronegative persons with HLP. One specific EBV strain was detected in HLP specimens from 3 of 4 patients. Also, viral recombination during productive replication within HLP generated variants of the latent membrane protein-1 (LMP-1) and nuclear antigen-2 (EBNA-2) genes. Some variants were also detected within PBL. Thus, EBV coinfection and recombination are consistent findings in persons with HLP regardless of immune status. Virally mediated determinants may be important features of EBV pathogenesis. ( info)

10/16. Oral hairy leukoplakia in nonimmunosuppressed patients. Report of four cases.

    Hairy leukoplakia was first described in association with HIV infection. Today hairy leukoplakia has come to represent a sign of immunosuppression and not just of HIV infection. Although molecular mechanisms have not been fully elucidated, Epstein-Barr virus appears to play a significant role in its etiopathogenesis. We present four cases that illustrate that HL may be seen in non-HIV and nonimmunocompromised patients. The use of high potency topical steroids for the treatment of oral vesiculoerosive diseases seems to have been a contributing factor in two of these cases. ( info)
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