Candidiasis Causing Vocal Fold Leukoplakia: Review of Clinical and Pathological Results of 289 Cases With Vocal Fold Leukoplakia.

OBJECTIVE: In laryngology practice, vocal fold leukoplakia is frequently evaluated by suspension laryngoscopy and biopsy examination upon the patient's complaints of hoarseness and dysphonia. The purpose of the present study is to investigate and analyze risk factors, diagnosis, treatment, and follow-up results of cases with Candida leukoplakia. STUDY DESIGN: Retrospective case control study. SETTING: Tertiary medical center. SUBJECTS AND METHODS: Patients with a diagnosis of vocal fold leukoplakia who underwent direct laryngoscopy and biopsy between 2007 and 2017 and diagnosed as candida or noncandida in their histopathology were assigned into 2 groups. Then they were compared in terms of their demographic characteristics, predisposing factors, diagnosis, treatment, and follow-up results. RESULTS: Of the 289 vocal fold leukoplakia cases, 36 were candida, and 253 were noncandida. The mean age of the patients with Candida leukoplakia was 60.86 years. As for the age groups, the largest group (26.1%) was in the seventh decade (P < .001). The use of inhaled corticosteroids was a significant risk factor (P < .001). For their medical therapy, the patients were administered fluconazole 200 mg per day for 3 weeks, and the treatment yielded successful results in 91.66% of them. In 5 of the patients, candida leukoplakia and superficial epithelial dysplasia were observed, and no malignant transformation was observed during a mean follow-up of 28 ± 13 months. CONCLUSION: Candidiasis causing vocal fold leukoplakia is rare, and we report the findings of the largest published case series to date. Eliminating predisposing factors and administrating oral fluconazole 200 mg for 3 weeks are sufficient for medical treatment.

Possible association between Helicobacter pylori infection and vocal fold leukoplakia.

BACKGROUND: Several studies have indicated the larynx as possible Helicobacter pylori (H. pylori) reservoirs. This study explored the association between H. pylori and vocal fold leukoplakia. METHODS: The case-control study involved 51 patients with vocal fold leukoplakia and 35 control patients with vocal polyps. Helicobacter pylori was detected in tissues by the rapid urease test, nested polymerase chain reaction (PCR), and single-step PCR. The H. pylori-specific immunoglobulin antibodies were detected in plasma by enzyme-linked immunosorbent assay (ELISA). RESULTS: Helicobacter pylori-positive rate of vocal fold leukoplakia and vocal polyps was 23.5% versus 11.4% (P = .157), 37.2% versus 14.3% (P = .020), 27.5% versus 8.6% (P = .031), and 70.6% versus 68.6% (P = .841) detected by rapid urease test, nested PCR, single-step PCR, and ELISA, respectively. Regression analysis indicated that H. pylori infection (P = .044) was the independent risk factor for vocal fold leukoplakia. CONCLUSION: Helicobacter pylori infection exists in the larynx and may be associated with vocal fold leukoplakia.

[Leucoplakia vesicae in females: diagnosis and treatment].

Sixty patients suffering from leucoplakia vesicae (LV) were examined using cystoscopy with biopsy of the urinary bladder wall, blood enzyme immunoassay for detection of antibodies to agents of sexually transmitted infections (STI), uroflowmetry, culture analysis of cervical canal and mucosa samples for STI. As shown by a pathomorphological examination of the vesical mucosa biopsy specimens, long-term persistence of pathogenic (chlamydia, trichomonades) and opportunistic (mycoplasma, ureaplasma, fungi) flora underlies development of LV. Morphogenesis of LV is characterized by hyperplastic reactions of urothelium and its metaplasy in laminated squamous keratosic epithelium, often with para- and dyskeratosis, developing in the presence of inflammatory reactions in the lamina in the presence of persisting infection. In LV, specific infection agents are often found in the urogenital tract. The spectrum of these agents is identical for samples from the cervical canal and vesical mucosa from leucoplakia foci. Vesical mucosa is most frequently contaminated with Mycoplasma hominis (57.2%), Candida albicans (51.4%), Ureaplasma urealiticum (37.1%) and Trichomonas vaginalis (22.9%). Associations of the infection agents are detected in 70% of LV patients. Persistent dysuria is a basic clinical symptom of leucoplakia. The following therapeutic measures should be taken: transurethral coagulation of the vesical mucosa, intravesical therapy, immunocorrection, antibacterial treatment by standard schemes or according to the isolated flora sensitivity.

Human oropharyngeal lesions with a defective Epstein-Barr virus that disrupts viral latency.

The Epstein-Barr virus (EBV), a human herpesvirus that is predominantly latent after infection, can be induced to replicate by deleted, rearranged EBV DNA from cultures of laboratory strain P3HR-1. Because mucosal surfaces are permissive of EBV replication, 101 oral biopsies from 70 Chinese and 5 American patients were examined for natural counterparts to tissue culture defective virus (WZhet), using as marker the abnormal juxtaposition of BamHI W and Z EBV DNA restriction fragments. Of the 49 oral biopsies that contained EBV DNA, 12 (24%) had the rearranged WZ fragment by polymerase chain reaction analysis: 3 (42%) of 7 EBV-positive epithelial dysplasias or carcinomas, 6 (38%) of 16 hairy leukoplakias, and 3 (12%) of 25 nonmalignant salivary gland biopsies. Accompanying viral replication was confirmed by in situ cytohybridization and demonstration of the linear configuration of the genome in select WZhet-positive lesions. These findings indicate that defective EBV with the unusual property of disrupting EBV latency is prevalent in natural infections and may contribute to EBV's pathogenic diversity.

Epstein-Barr virus small nuclear RNAs are not expressed in permissively infected cells in AIDS-associated leukoplakia.

Epstein-Barr virus (EBV) DNA structure and gene expression were analyzed in tissue specimens from oral hairy leukoplakia (HLP), a mucocutaneous lesion that develops in patients infected with human immunodeficiency virus (HIV). The structure of the terminal restriction enzyme fragments of EBV revealed that HLP is a permissive infection without a predominant, detectable population of EBV episomal DNA. In RNA preparations from this uniquely permissive infection, EBV replicative mRNAs could be identified by Northern analysis; however, the virally encoded small nuclear RNAs, the EBERs, were not detected in most HLP RNA preparations. In situ hybridization detected EBER expression in very rare cells. These data indicate that unlike other viral small nuclear RNAs, the EBERs are not expressed during viral replication and must participate in the complex maintenance of latent EBV infection.

Neutralizing antibody to herpes simplex virus type 1 in patients with oral cancer.

Neutralizing antibody to Herpes simplex virus type 1 (HSV-1), type 2, and measles virus was measured in the serum of patients with oral cancer, patients with oral leukoplakia, and in control subjects who were smokers and nonsmokers. Significantly higher titers to HSV-1 were found in controls who smoked than in controls who did not smoke. Patients with untreated oral cancer had HSV-1 neutralizing titers similar to those of the controls who smoked, but those with later stage tumors had higher titers than those with earlier stage tumors. In patients who were tumor free after treatment for oral cancer, higher antibody titers to HSV-1 were associated with longer survival times. No association was found between clinical status and antibody to measles virus. The data are consistent with a role for both HSV-1 and smoking in the pathogenesis of oral cancer.