Background: The high incidence of duodenal ulcer and perforated duodenal ulcers in this part of the country prompted us to test the hypothesis that, duodenal ulcer perforations may be associated with Herpes simplex virus infection. There is apparent absence of risk factors in DU perforation. Also it is associated with very short duration of pre-perforation dyspepsia in a significant number of perforated duodenal ulcers. It appeared that there is a high possibility that atleast a subset of these perforations could be due to Herpes simplex virus I or 2 infections.

Aim: To assess the role of Herpes Simplex Virus type I and II in duodenal- ulcer perforation.

Materials and Methods: This was a case-control study with three groups of 65 patients. Controls were formed by patients with no symptoms of upper gastrointestinal diseases who were admitted for non-gastrointestinal disorders. Case group again subdivided to a Second group of patients with acute duodenal ulcer perforation and a third group with chronic duodenal ulcer perforation.

Results: Significant statistical difference in seropositivity for HSV I & II was found in patients with both acute and chronic duodenal perforation vs controls. (P<0.05) For both HSV I and HSV II, there was a significant association between the seropositivity rates and size of acute DU perforation. P <0.05. Statistically significant difference in seropositivity to both HSV I and HSV II was seen in NSAID users. However, in the case of alcoholics and non- alcoholics, significant difference was noticed for seropositivity to HSV I only. In the case of smokers and non-smokers, there was no significant difference in the seropositivity to HSV I and II in all cases. There was a significant trend to higher seropositivity in patients with shorter pre-perforation duration and dyspepsia, for both HSV I and HSV II. There is a trend towards higher HSV titres in perforated DU compared to controls, which is statistically significant.

Keywords: herpes simplex virus (HSV), duodenal ulcer (DU).

1. Rosenow E. The causation of gastric and duodenal ulcer by Streptococci. Journal of Infectious Diseases 1916; 19- 332-362.
2. Neumann HH. Herpes simplex in peptic ulceration? Lancet 1967; 2: 779.
3. Knyvett AF. Herpes simplex in peptic ulceration. Lancet 1967; 2: 779.
4. Alexiu 0, David S, Cajal N, Grugia M, Gologain R, Nicolescu P. Experimental herpes virus inoculation. Virology 1976; 27: 61-62.
5. Borg 1, Andren L, Herpes simplex as a cause of peptic ulcer. Scandinavian Journal of Gastroenterology 1980; 15(Suppl 63): 56-59. 6. Anonymous. Viruses and duodenal ulcer. Lancet 1981; 1: 705-708. 7. Docherty JJ, Chopan M. The latent herpes simplex virus. Bacteriological Reviews 1974; 38: 337-355.
6. [No authors listed] Viruses and duodenal ulcer. 1981 Mar 28;1(8222):705-6.
7. Gesser RM, Valyi-Nagy T, Altschuler SM, Frazer NW. Oral-esophageal inoculation of mice with herpes simplex virus type 1 causes latent infection of the vagal sensory ganglia (Nodose ganglia). Journal of General Virology 1994; 75: 2379-2386
8. Alexiu, Caijal N, Niculascu, David S, Carnat ML, Gologan R. Herpetic etiology of gastric and duodenal ulcer. 11. Study in humans (Romanian). Revista de Chirugie, Oncologie, Radiologie. Ofthalmologie, Stomatologie, Ch.irugie 1977; 26(1): 73-80
9. Rand KH, Jacobson DG, Cottrell CR, Koch KL, Guild RT, Mcguigan JE. Antibodies to Herpes simplex type I in patients with active duodenal ulcer. Archives of Internal Medicine 1983; 143(10): 19171920.
10. Kemker BP, Docherty JJ, Lucia AD, Ruf W, Lewis RD. Herpes Simplex Virus: A possible etiologic agent in some gastroduodenal ulcer disease. American Surgeon 1992; 58(12): 775-778.
11. Kottaridis SD, Irene Goula, Mihas AA, Mihas TA. Herpes viruses and duodenal ulcer disease. Journal of Medical Virology 1989; 29: 224226.
12. Krishnakumar G. A study of factors contributing to releak after surgical closure in perforated duodenal ulcers. Dissertation, Pondicherry University, 2000.
13. Pai D, Sharma A, Kanungo R, Jagdish S, Gupta A. Role of abdominal drains in perforated duodenal ulcer patients: A prospective controlled study. Australian and New Zealand Journal of Surgery 1999; 69(3): 210-213.
14. Khoursheed M, Fuad M, Safar H, Dashti II, Behbenhani A. Laparoscopic closure of perforated duodenal ulcer. Surgical Endoscopy 2000; 14(1): 56-58.
15. Watkins RM, Demison AR, Colin J. What happened to perforated peptic ulcer? British Journal of Surgery 1984; 71: 774-776.
16. Vestergaard BF, Rune Sf. Type specific herpes simplex antibodies in patients with recurrent duodenal ulcer. Lancet 1980; 14:1(8181): 1273-1274.
17. Archimandritis A, Markoulatos P, Tjivras M, Alexiu A, Kordossi A, Kordossis T, Ferkatis A. Herpes Simplex Virus Types 1 and, 2 and cytomegalo virus in peptic ulcer disease and non-ulcer dyspepsia. Hepato-gastr6enterology 1992; 39: 540-541.
18. Fleming DT, McQuilan GM, Johnson RE. Herpes simplex virus type 2 in the United States 1976-1994. New England Journal of Medicine 1997; 337- 1105-1111.
19. Nahass GT, Goldstein BA, Shu WY. Comparison of Tzank smear, viral cultures and DNA diagnostic methods in detection of Herpes simplex and varicella-zoster infection. Journal of American Medical Association 1992; 268: 2541-2544.

Dr Premlal A.P

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