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==Overview==
==Overview==
=== Prevalence ===
* The prevalence of hypersensitivity pneumonitis varies based on exposure/occupation.
* These are as following:
**Farmers:
*** US: 8-540 cases per 100,000 persons per year among those at risk.<ref name="pmid7027852">{{cite journal |vauthors=Gruchow HW, Hoffmann RG, Marx JJ, Emanuel DA, Rimm AA |title=Precipitating antibodies to farmer's lung antigens in a Wisconsin farming population |journal=Am. Rev. Respir. Dis. |volume=124 |issue=4 |pages=411–5 |year=1981 |pmid=7027852 |doi=10.1164/arrd.1981.124.4.411 |url=}}</ref>
*** UK: 420-3000 cases per 100,000 persons per year among those at risk.<ref name="pmid8217855">{{cite journal |vauthors=Dalphin JC, Debieuvre D, Pernet D, Maheu MF, Polio JC, Toson B, Dubiez A, Monnet E, Laplante JJ, Depierre A |title=Prevalence and risk factors for chronic bronchitis and farmer's lung in French dairy farmers |journal=Br J Ind Med |volume=50 |issue=10 |pages=941–4 |year=1993 |pmid=8217855 |pmc=1035525 |doi= |url=}}</ref>
*** France: 4370 cases per 100,000 persons per year among those at risk.<ref name="pmid3420554">{{cite journal |vauthors=Depierre A, Dalphin JC, Pernet D, Dubiez A, Faucompré C, Breton JL |title=Epidemiological study of farmer's lung in five districts of the French Doubs province |journal=Thorax |volume=43 |issue=6 |pages=429–35 |year=1988 |pmid=3420554 |pmc=461305 |doi= |url=}}</ref>
*** Finland: 1400-1700 cases per 100,000 persons per year among those at risk.<ref name="pmid2220830">{{cite journal |vauthors=Terho EO |title=Work-related respiratory disorders among Finnish farmers |journal=Am. J. Ind. Med. |volume=18 |issue=3 |pages=269–72 |year=1990 |pmid=2220830 |doi= |url=}}</ref>
** Pigeon Breeders: 6000-21,000 cases per 100,000 persons per year
** Bird Fanciers: 20-20,000 cases per 100,000 persons per year
===Age===
* Hypersensitivity pneumonitis  usually affects patients in fourth to sixth decade of life.
* The mean age at diagnosis is 53 +/- 14 years.<ref name="pmid176059602">{{cite journal |vauthors=Hanak V, Golbin JM, Ryu JH |title=Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis |journal=Mayo Clin. Proc. |volume=82 |issue=7 |pages=812–6 |year=2007 |pmid=17605960 |doi=10.4065/82.7.812 |url=}}</ref>
=== Race ===
* There is no racial predilection to hypersensitivity pneumonitis.
=== Gender===
* Hypersensitivity pneumonitis affects men and women equally.
* Death due to Hypersensitivity pneumonitis is reported more in men.<ref>Adkinson NF. Hypersensitivity Pneumonitis. ''Middleton's Allergy: Principles and Practice''. 8th Ed. Saunders; 2013.</ref>


== Pathophysiology of Oral Cancer ==
== Pathophysiology of Oral Cancer ==

Revision as of 13:55, 20 February 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief:

Overview

Prevalence

  • The prevalence of hypersensitivity pneumonitis varies based on exposure/occupation.
  • These are as following:
    • Farmers:
      • US: 8-540 cases per 100,000 persons per year among those at risk.[1]
      • UK: 420-3000 cases per 100,000 persons per year among those at risk.[2]
      • France: 4370 cases per 100,000 persons per year among those at risk.[3]
      • Finland: 1400-1700 cases per 100,000 persons per year among those at risk.[4]
    • Pigeon Breeders: 6000-21,000 cases per 100,000 persons per year
    • Bird Fanciers: 20-20,000 cases per 100,000 persons per year

Age

  • Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.
  • The mean age at diagnosis is 53 +/- 14 years.[5]

Race

  • There is no racial predilection to hypersensitivity pneumonitis.

Gender

  • Hypersensitivity pneumonitis affects men and women equally.
  • Death due to Hypersensitivity pneumonitis is reported more in men.[6]

Pathophysiology of Oral Cancer

Tumor suppressor genes (TSGs)

  • It is understood that oral cavity cancer is the result of allelic imbalance which is caused by chromosomal changes particularly in chromosome 3,9,11 and 17.
  • These changes lead to mutation in tumor suppressor genes (TSGs).
  • Normally TSGs modulate normal growth.
  • Mutation of these TSGs leads to dysfunctional growth control.
  • Mutation most commonly occurs in either of the following:
    • Short arm of chromosome 3
    • TSG termed P16 on chromosome 9
    • TSG termed TP53 on chromosome 17
  • Cytochrome P450 genotypes is related to mutations in some TSGs and lead to oral squamous cell carcinoma.
  • In western countries (eg, United Kingdom, United States, Australia) TP53 mutations are the most common molecular change that leads to oral squamous cell carcinoma.

Oncogenes

  • Cancer may also occur if there is mutation to other genes that control cell growth, mainly oncogenes.
  • Oncogenes most commonly involved are:
    • Chromosome 11 (PRAD1)
    • Chromosome 17 (Harvey ras [H-ras])
  • In eastern countries (eg, India, Southeast Asia), ras oncogenes is a more common cause of oral squamous cell carcinoma.

Carcinogen-metabolizing enzymes

  • Carcinogen-metabolizing enzymes are known to cause cancer in some patients.
  • Cytotoxic enzymes such as alcohol dehydrogenase result in the production of:
    • Free radicles
    • DNA hydroxylated bases
  • These cytotoxic enzymes especially predispose oral squamous cell carcinoma.

Alcohol

  • Alcohol dehydrogenase oxidizes ethanol to acetaldehyde which is cytotoxic in nature.
  • cytochrome P450 IIEI (CYP2E1) also metabolizes ethanol to acetaldehyde.
  • Alcohol dehydrogenase type 3 genotype predisposes to oral squamous cell carcinoma.
  • Carcinogenic potential increases when combined with tobacco use.

Tobacco

  • Cigarette smoke has various carcinogens which can lead to oral cancers.
  • Low reactive free radicals in cigarette smoke interact with redox-active metals in saliva.
  • This makes saliva to loose its antioxidant potential and become a potent pro-oxidant milieu.[7]

Gross Pathological Findings

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology

{{#ev:youtube|inSkXkNK_dE}}

References

  1. ↑ Gruchow HW, Hoffmann RG, Marx JJ, Emanuel DA, Rimm AA (1981). "Precipitating antibodies to farmer's lung antigens in a Wisconsin farming population". Am. Rev. Respir. Dis. 124 (4): 411–5. doi:10.1164/arrd.1981.124.4.411. PMID 7027852.
  2. ↑ Dalphin JC, Debieuvre D, Pernet D, Maheu MF, Polio JC, Toson B, Dubiez A, Monnet E, Laplante JJ, Depierre A (1993). "Prevalence and risk factors for chronic bronchitis and farmer's lung in French dairy farmers". Br J Ind Med. 50 (10): 941–4. PMC 1035525. PMID 8217855.
  3. ↑ Depierre A, Dalphin JC, Pernet D, Dubiez A, Faucompré C, Breton JL (1988). "Epidemiological study of farmer's lung in five districts of the French Doubs province". Thorax. 43 (6): 429–35. PMC 461305. PMID 3420554.
  4. ↑ Terho EO (1990). "Work-related respiratory disorders among Finnish farmers". Am. J. Ind. Med. 18 (3): 269–72. PMID 2220830.
  5. ↑ Hanak V, Golbin JM, Ryu JH (2007). "Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis". Mayo Clin. Proc. 82 (7): 812–6. doi:10.4065/82.7.812. PMID 17605960.
  6. ↑ Adkinson NF. Hypersensitivity Pneumonitis. Middleton's Allergy: Principles and Practice. 8th Ed. Saunders; 2013.
  7. ↑ Nagler R, Dayan D (2006). "The dual role of saliva in oral carcinogenesis". Oncology. 71 (1–2): 10–7. doi:10.1159/000100445. PMID 17344667.

Template:Metabolic pathology

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