Epithelial lesions

ML Margall, N., Matias-Guiu, X., Chilton, M., Coll, P., Alejo, M., Nunes, V., Quilez, M., Rabella, N., Prats, G., and Prat, J., Detection of human papilloma virus 16 and 18 DNA in epithelial lesions of the lower genital tract by in situ hybridization and polymerase chain reaction. J. Clin. Microbiol. 31, 924-930 (1993). 

A study was conducted to examine proliferative nasal epithelial lesions in F344 rats following subchronic inhalation of 1,2-dibromoethane at concentrations of 0, 3, 10, or 40 ppm (Nitschke et al. 1981). The study incorporated serial sacrifices and sacrifices after an 88-89-day postexposure period. Rats in the mid - and high-dose groups had hyperplasia of nasal turbinate epithelium rats at the highest dose also exhibited nonkeratinizing squamous metaplasia of respiratory epithelium of the nasal turbinates. 

Altered vitamin A homeostasis, primarily manifested as decreased hepatic storage of vitamin A, is another established effect of PBBs in animals. Vitamin A is essential for normal growth and cell differentiation, particularly differentiation of epithelial cells, and some PBB-induced epithelial lesions resemble those produced by vitamin A deficiency. Because it is the primary storage site for vitamin A, the liver has a major role in retinol metabolism. Esterification of dietary vitamin A, hydrolysis of stored vitamin A, mobilization and release into the blood of vitamin A bound to retinol-binding protein, and much of the synthesis of retinol-binding protein occurs in the liver. 

Radovic S, Selak I, Babic M, Pasic F, Carcinoembryonic antigen (CEA) in colonic inflammatory-regenerative and dysplastic epithelial lesions, Croat. Med. J., 39 15-18, 1998. 

Sakata T, Smith RA, Garland EM, et al. 1989. Rat urinary bladder epithelial lesions induced by acrolein. J Environ Pathol Toxicol Oncol 9 159-170. 

Persistent acute body zinc loss has resulted in many symptoms in addition to taste and smell dysfunction if losses continue at significant levels for periods of 14 days or more. These symptoms Include mental confusion, cerebellar dysfunction, including intention tremor and ataxia, an erythrematous, Intracrural rash, buccal epithelial lesions and ulcers, and acute toxic psychosis (,6). The altered mental state of these patients can be related to the rapid depletion of the relatively high zinc content in the limbic system of the brain (16.17), demonstrating that zinc can cross the blood brain barrier bidirectionally, dependent upon the gradient, and that it can be readily mobilized from brain tissue. 

Because sulfur mustard is a highly corrosive agent, the subcommittee believes that epithelial lesions at the point of entry into the stomach are... 

After RCE, the epithelial lesion heals rapidly, usually within 5 days with no visible sequelae.At some later time the symptoms suddenly recur. The mean time to recurrence in one study of 80 patients was 18 months. Although the time from initial injury to recurrence was reported to range from 2 days to 16 years, 63% of recurrences were noted within the first 4 months. Although RCEs can start at any age, depending on the underlying corneal etiology, early adulthood to middle age is the common age at onset. 

External examination reveals erythema and swelling of the affected skin areas. Slit-lamp examination reveals diffuse conjunctival injection and pimctate epithelial erosions of the cornea with corresponding NaFl staining. If the epithelial lesions are extensive and if lacrimation is profuse, corneal edema also may be noted. 

The conjunctivitis and symptoms last 7 to 16 days, with a mean between 8.6 and 10 days. A diffuse superficial epithelial keratitis usually develops in the first week and may be cansed by proliferation of live virus within the corneal epithelium. In approximately 1 week this fine keratitis progresses to become deeper, positively staining, slightly elevated focal epithelial lesions. These epithelial lesions fede slowly, usually disappearing by 4 weeks. 

Granular or fluffy subepithelial opacities typically develop under the focal epithelial lesions 11 to 15 days after the onset of symptoms (Figure 26-45).These lesions likely represent antigen-antibody complexes that form in response to the viral antigen. Subepithelial infiltrates occur in 10% to 90% of cases depending on the serotype of the causative agent. Severe subepithelial infiltrates may decrease the patient s visual acuity to 20/200 or worse. They can last from 3 months to 2 years and may cause permanent focal anterior stromal scars. 

Recurrent HSK has accompanying lid and conjunctival involvement in about 31% of cases. This involvement typically appears as unilateral follicular conjunctivitis with moderate to severe diffuse conjunctival hyperemia. The initial epithelial lesions of HSK are small vesicles that are generally described as punctate epithelial keratopathy. Although dendritic or ameboid keratitis is the most common manifestation of HSK (Figure 26-47), a diffuse... 

Hubert P, Evrard B, Maillard C, et al. Delivery of granulocyte-macrophage colony-stimulating factor in bioadhesive hydrogel stimulates migration of dendritic cells in models of human papillomavirus-associated (pre)neoplastic epithelial lesions. Antimicrob Agents Chemother 2004 48(11) 4342 348. 

With a predominantly epithelial origin, CRC phenotypically consists of a broad spectrum of epithelial lesions ranging from adenoma to adenocarcinoma, evolving from benign growth to invasive stages often over a period of 10-20 years. A multi-step sequence of... 

Considerable research effort has therefore been focused on the association of contaminant exposure and hepatic lesions. Epithelial lesions and neoplasms have, in... 

Several studies have histologically examined nasal biopsy specimens in formaldehyde-exposed workers and observed epithelial lesions that are consistent with the irritant and reactive properties of formaldehyde (Ballarin et al. 1992 Boysen et al. 1990 Edling et al. 1988 Holmstrom et al. 1989c). 

Histological scores did not increase with increasing employment duration in the exposed group. The authors reported that there was no difference in average histological scores between the exposed workers from the particle board plants, where confounding exposure to wood dust occurred, and those from the laminate plant without wood dust exposure. This observation supports the hypothesis that the observed nasal epithelial lesions were caused by formaldehyde and not by an interaction between formaldehyde and wood dust. 

Upper respiratory tract epithelial lesions similar to those observed in rats have been observed in Rhesus monkeys exposed to 6 ppm, 6 hours/day, 5 days/week for 1 week the regional distribution of these lesions was not restricted to the nasal cavity, as they were in rats exposed to 6 ppm (Monticello et al. 

Wistar rats]), Kamata et al. (1997) reported that some F344 rats, after 28 months of exposure, displayed a mild response at 2 ppm and even at 0.3 ppm. A statistically significantly increased incidence for nasal epithelial squamous metaplasia without hyperplasia was observed in rats exposed to 2 ppm compared with control rats (5/32 versus 0/32) the incidence for nasal epithelial cell hyperplasia with squamous metaplasia was also significantly elevated compared with controls (7/32 versus 0/32). In rats exposed to 0.3 ppm, incidences of the same respective nasal epithelial lesions were also greater than control incidences (1/32 versus 0/32 and 4/32 versus 0/32), but not to a statistically significant degree. 

Many of the tumors of the nasal cavity and paranasal sinuses fall under the category of round cell neoplasms. Among these are olfactory neuroblastoma, sinonasal undifferentiated carcinoma, malignant melanoma, neuroendocrine carcinoma-small cell neuroendocrine carcinoma, malignant lymphoma, extramedullary plasmacytoma, invasive-ectopic pituitary adenoma, rhabdomyosarcoma, and Ewing s sarcoma (ES)-peripheral neuroectodermal tumor (ES/ PNET). But there is also a host of other epithelial lesions that are unique to the sinonasal tract. 

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