Tongue cancer primary prevention

Revision as of 18:22, 30 November 2017 by Medhat (talk | contribs)
Jump to navigation Jump to search

Tongue cancer Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Tongue cancer from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Staging

History and Symptoms

Physical Examination

Laboratory Findings

Chest X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Tongue cancer primary prevention On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Tongue cancer primary prevention

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Tongue cancer primary prevention

CDC on Tongue cancer primary prevention

Tongue cancer primary prevention in the news

Blogs on Tongue cancer primary prevention

Directions to Hospitals Treating Tongue cancer

Risk calculators and risk factors for Tongue cancer primary prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

Effective measures for the primary prevention of tongue cancer include avoiding the use of tobacco and excessive use of alcohol.

Primary Prevention

  • As some of the risk factors of the tongue cancer include age, gender and family history, which cannot be controlled, not all cases of tongue cancer can be prevented. However, avoiding known risk factors such as the use of tobacco and excessive use of alcohol is the best method of tongue cancer prevention.
  • The best way to prevent tongue cancer recurrence is to quit tobacco and/or drinking of alcohol. While quitting alcohol and tobacco does not guarantee that you will never develop tongue cancer, it greatly reduces the risk.
  • Patients suitable for a chemoprevention trial may have a documented precancerous lesion or have a known risk factor for developing malignancy without having a premalignant lesion. A third group of patients are those with previously treated malignancy who are at a significant risk for developing a second primary tumor [45]. [46,47]. Most of the completed chemoprevention trials for premalignant lesions of the oral cavity and oropharynx have studied either naturally occurring compounds (vitamin A, vitamin E, beta-carotene) or synthetically derived retinoids [48-50]. Vitamin A, vitamin E, and beta-carotene  The interest in the antioxidants vitamin A, vitamin E, and beta-carotene as chemopreventive agents is due to their apparent efficacy in inducing regression of oral leukoplakia. Although these agents have been studied relatively extensively, both for primary and secondary chemoprevention, none has an established role.
  • the protective effect of diets rich in fresh fruits and vegetables, but with a substantial minority without these established risk factors. The protective effect of diets rich in trace elements and antioxidant vitamins is well demonstrated in many countries.
  •  Reports on the utility of vitamin A to treat oral leukoplakia date back to 1957, when a 90 percent response rate was described in 20 patients [51]. Subsequent trials supported the activity of vitamin A in oral leukoplakia in populations likely to be deficient in vitamin A and at risk based upon tobacco or betel nut chewing [52,53]. The applicability of these results to disease in relatively developed nations where vitamin deficiency is rare is unclear. High response rates have also been described with the administration of beta-carotene, a precursor of vitamin A, to patients with oral leukoplakia [54-56]. In one series of 24 patients, for example, there were 15 partial and 2 complete responses with no significant toxicity [54]. However, toxicity was particularly severe in patients dosed at the higher dose of isotretinoin (2 mg/kg per day), with 47 percent of patients requiring dose reduction. Patients treated at the lower dose level (1 mg/kg per day) had less toxicity and did not require dose reduction, although most noted xeroderma and 29 percent developed conjunctivitis. Furthermore, over 50 percent of responders relapsed within three months of treatment cessation.

References

Template:WikiDoc Sources