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ISSN (Print) 1013-9052
EISSN 1658-3558

The Saudi Dental Journal,
P.O. Box 52500,
Riyadh 11563,
Kingdom of Saudi Arabia
Tel.
966-1-467-7328
Fax.
933-1-467-7308 /
966-1-467-7534
Email
saudidj@ksu.edu.sa

Correlation between family history of  Hepatitis B and

positive HBV serologic tests in patients attending

dental clinics in Riyadh

 

Kawkab M.A. Al -Turck, BDS, MSc
College of Applied Medical Sciences, King Saud University 

 

Abstract 

 

The aim of this study was to investigate the importance of family history in the identification of  HBV sero positive subjects. A total of 121 patients attending dental clinics were recruited for this study.  Inquiry about family history of hepatitis, if any, was obtained from each subject.  Subjects who reported family history of hepatitis or hepatitis-like conditions were called and sent for laboratory investigation for hepatitis markers using the ELISA technique. Data from 116 subjects with age range 3-60 years, mean 33.3 was analyzed.  There were 74 (63.8%) males and 42 (36.2%) females. A great majority of subjects 66 (56.8%) were in their second and third decades.  Family history of hepatitis was positive for 106 (91.4%) of the subjects. The correlation relationship of detection of HBsAg with the family history was found only marginally significant chi-square  (P=0.052). In conclusion, a positive family history of HBV infection necessitates serologic investigation to rule out sub-clinical carrier state.
 

Introduction

 

Hepatitis B virus (HBV) infection is one of the most common viral diseases worldwide.  HBV was first described in 1965.1 It is a highly infectious agent,2 capable of being transmitted sexually, perinatally, or parenterally.3,4

The frequency of HBV infection and patterns of transmission vary markedly throughout the world.3 Majority of cases of HBV infection remain sub-clinical, and most cases are anicteric in nature.5,6 Approximately 80% of all HBV infections are undiagnosed.3,7 Hepatitis B virus has been identified in almost all body fluids of infected persons including blood or saliva.8

The carrier rate of HBsAg varies worldwide. Countries that are considered highly endemic (chronic infection rates 8% - 15%) for HBV are China, Southeast Asia, Africa, Pacific Islands, parts of Middle East, and the Amazon Basin. Russia, Western block countries, India, Southern Europe, and South America are moderatly enedemic (chronic infection rates 5% - 7%). In the United States, Western Europe, New Zealand, and Australia, endemicity is low at 0.2% -0.9%.9-11

Chronic active hepatitis develops in more than 25% of carriers and often progresses to liver cirrhosis. HBV carriers have a 12 to 300 fold higher risk of developing primary liver cancer compared to the non-HBV carrier population.7

Hepatitis B has been recognizied as an occupational health hazard for the dental profession since 1975. Mosley et al.1213 The risk of HBV infection is a factor of exposure to the infected patient's blood.1415  Since in most patient's mouth, the sulcus is routinely inflamed, blood will mix with saliva, making it infectious with HBV. Therefore, the dental hygienist is equally at high risk like the dentist.12 Studies primarily directed on dental profession revealed that as high as 38.5% of oral surgeons had positive serology for HBV infection.3,15 reported at the American Dental Association Annual Session in 1972  that dentists had a higher prevalence of anti - HBs than any other health care workers. Intraorally, the greatest concentration of HBV occurs at the gingival sulcus.

Several studies ranks Saudi Arabia among the countries with high prevalence of HBV infection with a nationwide carrier prevalence that ranged from 8.3% to 10%. The prevalence reached  up to 14% in some regions with an average exposure prevalence of 50%.4,16,17 The study of Al-Sohaibani et al.18  in 1995 showed that at King Khalid University Hospital in Riyadh, the prevalence of exposure to HBV among male and female medical students was 25.3% and 19.3% respectively, and among male medical staff was 42.9%.

Studies have shown that HBV can be transmitted by various parental and non-parental routes. Common factors which lead to increased HBV prevalence include contact with  HBsAg carriers or patients with chronic liver disease.4  Traditionally, Saudis are accustomed to living under strong family bond.16

The aim of this study was to investigate the role of family history in detecting seropositive subjects among patients attending dental clinics.

    

Materials and Methods

 

Using a questionnaire, patients who attended Oral Diagnosis Clinic at the College of Dentistry, King Saud University, Riyadh were routinely asked about history of hepatitis and/or jaundice. Subjects who indicted a history of such diseases were sent for laboratory investigation screening test to rule out carrier state prior to dental treatment. Patients with positive response to inquiries with or without previous symptoms were referred for hepatitis B profile of HBV markers in addition to HBsAg. This profile was performed at the University Hospitals laboratory using Organon Teknikew Hepanostica HBsAg Uni-form II of Microelisa system. This system is an enzyme-linked immunosorbent assay (ELISA) for the qualitative determination of HBsAg in human serum or plasma.

A total of 121 patients were included in the study. The data was analyzed using Statistical Package for Social Sciences using (SPSS version 10). Descriptive statistics was used. The relationship between the positive family or personal history of liver disease, and present investigation with hepatitis markers was studied using the Chi-square test and Fisher exact test for small sample. Statistical significance was defined at the level of P < 0.05.

 

Results

 

Data from 116 subjects were used for analysis. Five cases were excluded due to unrelated data (two cases were reactive to anti-HAV alone and three cases were reactive to anti-HCV alone).  The demographic findings of the subjects is shown in Table 1. Age range was 3 - 60 years with a mean of 33.3  years. Male subjects constituted the majority. The highest percentage of subjects was in the second and third decades, each comprised 28.4% of the total sample. Positive response of history of hepatitis/or jaundice on health questionnaire was indicated in 72 subjects (62.1%), although 36 subjects (31%) confirmed  previously associated symptoms. Majority of the subjects (91.4%) recorded positively for family history of hepatitis.

The relationship of hepatitis markers with case history are discussed in Table 2. More than fifty percent of the subjects with positive findings from case history were found reactive to HBsAg. The statistical relationship of HBsAg with family history was found marginally significant by both Chi-square and Fisher's Exact tests (P=0.052). The relationship with patient history was also found marginally significant by Chi-square test only. Previously associated symptoms did not show any statistically significant relationship.

Relationship of anti-HBs with case history findings indicated a statistically significant result with family history (P = 0.006). Other findings did not show any significant relationship. Whereas HBeAg indicated a marginally significant relationship with previously associated symptoms by Chi-square test (P=0.052), no statistically significant relationship was found between anti-HBc, anti-HBe and any of the positive case history findings (Table 2).

   

Discussion

 

This study was conducted in the Oral Diagnosis Clinic at the College of Dentistry in Riyadh. In this clinic the dental patients are screened for health problems and related conditions. The potential impact of the HBV carrier state to the dental professional is significant.7 The HBV carrier state develops more commonly by means of asymptomatic sub-clinical HBV infection, during which  clear symptoms of the disease is not obvious.19 Moreover, these asymptomatic sub-clinical carriers are more likely to be HBeAg positive, being in a more infectious and contagious state and, at risk of transmitting the disease.20 Therefore, it is the responsibility of the dentist to identify patients who may transmit the infection via contaminated saliva and/or blood.

The present study confirmed male preponderance,21-24 indicating high exposure rate to HBV infection than females. This could be due to the fact that males in Saudi Arabia are more active socially with greater hygiene implication. This finding agrees with the results reported from other parts of the world.4 In this study majority of subjects were in the second and third decade which coincide with the findings of Talukder et al.25 and Arya et al.23 who described two peaks for HBV exposure in Saudi Arabia. One is in infancy and early childhood and the other is around 30 years of age. The later is reflected in the findings of this study.

Sixty-two percent of the subjects responded positively to family history of hepatitis and/ or jaundice, yet only  half of those diagnosed with hepatitis was confirmed. These findings are in agreement with Hoofnagle5 who reported in 1980 that majority of HBV infections were sub-clinical and most cases were anicteric in nature. Jaundice, a known pathognomonic sign of hepatitis is rarely evident for diagnosis confirmation.5,26 Thus, approximately 80% of all HBV infections are undiagnosed. Only about 20% of patients had clinical symptoms, which subsided in two to four weeks. Therefore, patients medical histories were unreliable and insufficient in identifying exposure to HBV infection.21, 26

Positive family history of hepatitis and/or jaundice was evident in more than ninety percent of the subjects in our study which included both clinical and sub-clinical cases. This was reflected when HBsAg was assayed showing marginally significant association with both family and patients' medical history. This finding demonstrated that household and sexual contacts of HBV carriers are risks for HBV infection.27

The HBV marker, anti-HBs in this group revealed statistically significant association with family history(P = 0.006) which may indicate previous HBV-vaccination following HBV infection of a  family member. The HBeAg is considered an important marker for infection in a given population. The prevalence in this study was 8.3% which was in agreement with previous report of HBeAg prevalence that didn't exceed 9%.28

The positivity of HBV marker demonstrates a high exposure rate. In Saudi Arabia, it was suggested that in addition to worldwide recognized mode of transmission, folk medicine practices, the large house holds, low standards of hygiene are among factors which contributed to increased prevalence of HBV infection.4

In this study, the sub-clinical cases were discovered through previous routine laboratory investigations. This was for blood donation in case of male subjects or due to pregnancy in case of female subjects. Almost all cases revealed a previous contact with a household member who was a HBV carrier. These patients are potential source of HBV infection for the dental team. Relative to occupational transmission, it is estimated that dental health care worker have a three to five times higher rate of HBV infection than the general population.27

In conclusion, all clinical records for dental patients should include questions on possible family history of hepatitis and/or jaundice. Contact with a chronic HBsAg carrier may lead to a sub-clinical carrier status. Therefore, a positive family history of HBV infection necessitates serologic investigations to rule out carrier state.  

 

Acknowledgement

 

The author would like to express her thanks to Dr. Nazeer Khan, a statistician of the Research Center, Dental College for his help on the data analysis. The author is also thankful to her son, Ammar Al-Turck, for typing the manuscript.

  

References

 

  1. Blumberg BS, Alter HJ, Visnich S: A ‘new' antigen in leukemia sera. JAMA 1965; 191:541.
  2. Glick M. Know thy hepatitis: A through TT. Certified Dental Assistant J 1999; 27(5): 376-385.
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  4. Al-Faleh FZ, Fachar ZT. Hepatitis B infection in Saudi Arabia. Ann Saudi Med 1988; 8:474-480.
  5. Hoofnagle JH. Type B hepatitis: Virology, serology, and clinical course. Semin Liver Dis 1980; 1(1):7-14.
  6. Tullman MJ, Boozer CH. Past infection with hepatitis B virus in patients at a dental school. J Am Dent Assoc 1978; 97:477-478.
  7. Cottone JA. Hepatitis B current status in dentistry. Dent Clin North Am 1991; 35(2):269-272.
  8. Petersdorf RG, Adams RD, Braunwald E, Isselbacher KJ, Martin JB, Wilson JD. Harrison's principles of internal medicine, 13th ed. Auckland: McGraw - Hill, 1997; 1789.
  9. Simon J. Hepatitis. In: Beers M, Berkos R, editors. The Merck manual of dignosis and therapy, 17th ed. West Point (PA): Merck Research Laboratories 1999 ; 377-386.
  10. Centers for Disease Control and Prevention. Health information for international travel. CDC. Atlanta: HHS Publication, 1989; 89-8280.
  11. Gilcrist J. Hepatitis viruses A, B, C, D, E, and G: Implication for dental personnel. J Am Dent Assoc 1999; 130: 509 - 520.
  12. Mosley JW, Edwards VM, Casey G, Redeker AG, White E. Hepatitis B virus infection in dentists. N Engl J Med1975; 293(15):729-734.
  13. Lodi G, Porter SR, Teo CG, Scully C. Prevalence of HCV infection in health care workers of an UK dental hospital. Br Den J 1997; 183(9):329-335.
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  15. Sampson E. Hepatitis B - Protection of patient, dentist, and staff. Proceedings of a symposium on hepatitis B: Risk, prevention and the vaccine. 123rd Annual Session of American Dental Association, Las Vegas, 1982; 16-20.
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  17. Coode PE, Hossain J, Ibrahim MB. Hepatitis B virus prevalence in a liver biopsy series in Jeddah, Saudi Arabia. Saudi Med J 1993; 14(1):36-39.
  18. Al-Sohaibani MO, Al-Sheikh EH, Al-Ballal SJ, Mirghani MAM, Ramia S. Occupational risk of hepatitis B and C infection in Saudi medical staff. J Hosp Inf 1995; 31:143-147.
  19. Koff RS. Management of hepatitis B surface antigen (HBsAg) carrier. Semin Liver Dis 1980; 1: 33-43.
  20. Cottone JA, Goebel WM. Hepatitis B : The clinical detection of the chronic carrier dental patient and the effects of immunization via vaccine. Oral Surg 1983;56:449-454.
  21. Tullman MJ, Barrett RA, Boozer CH, Hamrich JT, Rayson JH. Prevalence of hepatitis B surface antigen in a dental school patient population. J Public Health Dent 1975; 38: 4 - 9
  22. Jamjoom GA, Ramia S, Bakir T, Buckley P, George M, Kurien CR, Al-Swailem A. A two - year survey of diagnostic virus laboratory services of King Saud University Hospitals, Riyadh. Saudi Med J 1986; 7 (2): 166 - 175.
  23. Arya SC, Ashraf SJ, Parande CM, El-Sayed M, Sahay R, Ageel AR, Tobeiqi MS. Hepatitis B virus in Gizan, Saudi Arabia. J Med Viral 1985; 17 (3): 267 - 274.
  24. Jamjoom GA, Higham R. Prevalence of viral hepatitis type B surface antigen (HBsAg) in patients with liver disease and in the general patient population at King Abdulaziz Hospital, Riyadh. Proceedings of the 5th Saudi Medical Meeting, Riyadh, 1980; 331-339.
  25. Talukder MA. Gilmore R, Bacchus RA. Prevalence of hepatitis B surface antigen among male Saudi Arabians. J Infect Dis 1982 ; 146 (3) : 446.
  26. Goebel WM. Reliability of medical history in identifying patients likely to place dentists at an increased hepatitis risk. J Am Dent Assoc 1979; 98: 907 - 913.
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Address reprint requests to:

Dr. K.M.A.Al-Turck

Dental Health Department

College of Applied Medical Sciences

King Saud University

P.O. Box 10219, Riyadh 11433, Saudi Arabia

E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

   

Tables


Table 1. Demographic data on 116 subjects

Descriptions

n

%

Gender

   Male

   Female

74

42

63.8

36.2

Age

   0 – 10

   11 – 20

   21 – 30

   31 – 40

   41 – 50

   51 – 60

7

11

33

33

20

12

6

9.5

28.4

28.4

17.2

10.3

History of Liver Disease

   Yes

   No

72

44

62.1

37.9

History of symptoms

   Yes

   No

36

80

31.0

69.0

Family History

   Yes

   No

106

10

91.4

8.6

 

 

 

Table 2. Correlation of positive HBV serology and case history

HBV marker

Case history findings

 

History of

Hepatitis

Symptoms

Family history

n

%

n

%

n

%

HBsAg

40

55.6

19

52.8

55

51.9*

Anti – HBs

29

40.3

14

38.9

38

35.8**

HBe Ag

3

4.2

3

8.3*

4

3.8

Anti – HBc

33

45.8

14

38.9

42

39.6

Anti – HBe

21

29.2

11

30.6

33

31.1

* marginally significant (P = 0.052)
** statistically significant (P = 0.006)

 
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