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Dysplasia

Dysplasia (latin for 'bad form') is an abnormality in the appearance of cells indicative of an early step towards transformation into a neoplasia. It is therefore a pre-neoplastic or pre-cancerous change. This abnormal growth is restricted to the epithelial layer, not invading into the deeper tissue. Though dysplasia may regress spontaneously, persistent lesions must be removed, either with surgery, chemical burning, heat burning, burning with laser, or freezing (cryotherapy). more...

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The best know form of dysplasia is the precursor lesions to cervical cancer, called cervical intraepithelial neoplasia (CIN). This lesion is caused by an infection with the human papilloma virus (HPV). Dysplasia of the cervix is almost always unsuspected by the woman. It is usually discovered by a screening test, the pap smear. The purpose of this test is to diagnose the disease early, while it is still in the dysplasia phase and easy to cure.

Dysplasia vs carcinoma in situ vs invasive carcinoma

These terms are related since they represent the three steps of the progression towards cancer:

  • Dysplasia is the earliest form of pre-cancerous lesion recognizable in a biopsy by a pathologist. Dysplasia can be low grade or high grade (see CIS below). The risk of low grade dysplasia transforming into high grade dysplasia and, eventually, cancer is low. Treatment is usually easy.
  • Carcinoma in situ is synonymous with high grade dysplasia in most organs. The risk of transforming into cancer is high. Treatment is still usually easy.
  • Invasive carcinoma, commonly called cancer, is the final step in this sequence. It is a disease who, when left untreated, will invade the host (hence its name) and will probably kill him. It can be often, but not always, be treated successfully.

Metaplasia is a situation where cells have changed from their original mature differentiated type into another mature differentiated cell type as an adaptive response to exposure to chronic irritation, or to a pathogen or carcinogen. It also occurs where one normal cell type changes into another normal cell type as in the cervix where squamous epithelium on the exo-cervix changes to normal columnar epithelium in the endo-cervix. This area is also known as the transformation zone and is the location of many dyplastic lesions thus the sampling of this area during a pap test is critical. Metaplasia is distinct from dysplasia because in a dysplastic cell these changes have become encoded into the genome and so are heritable or passed on to daughter cells during cell replication.

Read more at Wikipedia.org


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Progression to dysplasia in Barrett's esophagus
From American Family Physician, 2/15/05 by Mark Ebell

Clinical Question: Which men with Barrett's esophagus are at greatest risk of progression to high-grade dysplasia or cancer?

Setting: Outpatient (specialty)

Study Design: Cohort (prospective)

Synopsis: The authors identified 550 patients who underwent endoscopy for any reason and were diagnosed with Barrett's esophagus between 1990 and 2003. The study took place at a Veterans Affairs hospital, 99 percent of participants were men, and 93 percent were white. Patients ranged in age from 28 to 86 years (mean age = 63 years). At the initial endoscopy, 77 percent had no dysplasia, 18 percent had low-grade dysplasia, and 5 percent had unifocal high-grade dysplasia. Helicobacter pylori infection was absent in 345 patients, present in 72 patients, and a history of H. pylori eradication was identified in 60 patients. Patients with cancer, dysplasia-associated lesion or mass, or intramucosal cancer at enrollment were excluded (n = 28).

Of the 550 patients initially identified, 28 had a diagnosis of malignancy, 173 had no follow-up endoscopy, 15 died from other causes, and 10 were lost to follow-up, leaving 324 for the study. It is unknown whether outcomes were assessed blindly. Patients with newly diagnosed low-grade dysplasia or unifocal high-grade dysplasia had optimized medical therapy and were re-endoscoped at 12 to 24 weeks (for patients with low-grade dysplasia) or four to eight weeks (for patients with high-grade dysplasia). Patients with persistent high-grade dysplasia had surveillance at three- to six-month intervals, while those with low-grade dysplasia or regression to normal had surveillance at six- to 12-month intervals. Although patients were followed for up to 130 months based on the Kaplan-Meier curves, the mean or median duration of follow-up or the number of follow-up endoscopies was not given.

Results were presented in several ways. Independent risk factors for high-grade dysplasia or cancer at the initial endoscopy were increased age, greater length of Barrett's esophagus (especially greater than 6 cm), and never having been diagnosed with H. pylori infection. The independent risk factors for progression of Barrett's esophagus to high-grade dysplasia or cancer were length, initial histology, histology at follow-up, and H. pylori status. The risk was low for patients with no dysplasia on the initial endoscopy (i.e., 2.4 percent if the length is less than 6 cm; 6.8 percent if the length is more than 6 cm) or with low-grade dysplasia only (i.e., 5.3 percent with length of less than 6 cm). All other groups had at least a 35 percent risk of progression.

Bottom Line: Patients with no dysplasia on the initial endoscopy or with low-grade dysplasia only and Barrett's esophagus length of less than 6 cm have a very low risk of progression to high-grade dysplasia or malignancy. (Level of Evidence: 2b)

Study Reference: Weston AP, et al. Risk stratification of Barrett's esophagus: updated prospective multivariate analysis. Am J Gastroenterol September 2004;99:1657-66.

Used with permission from Ebell M. Length and dysplasia predict BE progression in men. Accessed online November 24, 2004, at: http://www.InfoPOEMs.com.

COPYRIGHT 2005 American Academy of Family Physicians
COPYRIGHT 2005 Gale Group

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