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THE SOUTH AFRICAN GASTROENTEROLOGY REVIEW 2022 | VOLUME 20 | ISSUE 3 | 10 and in the event of HBsAg positivity, HDV testing should be systematically performed. However, the absence of a third-party payer is a major handicap, as the patient is unable to meet the costs. In our series, 10 patients had delta viral load, 06 were detectable (60%). Of these, 05 had a detectable B viral load but below 2000 IU/mL. In one patient, there was no B virus replication. At the same time, of the 04 patients who had no viral replication D, 02 were highly viremic for the B virus (HBV-DNA > 20000 IU/ mL), of which 01 had a B viral load < 2000 IU/mL and 01 was undetectable. The only patient in our series who was undetectable for B viral load and had achieved HDV RNA, replicated very strongly. This indicates that hepatitis B virus inhibits or decreases B virus replication. This is in agreement with the literature, since it is accepted that hepatitis delta virus leads to a decrease or even inhibition of HBV replication 24, 25, 26 . A control delta viral load in our patients could certainly shed more light on this subject and rule out the level of HBV suppression by HDV. This parameter has not been evaluated in our patients. It has been suggested by some studies that simultaneous HDV/HBV replication (although rarely observed) would lead to a more rapid and severe course of liver disease than in the absence of HDV replication. This is explained by the added pathogenic role of two viruses 20,27 . We assessed the hepatocellular function of our patients with three tests: thrombocytopenia, prothrombin level (PT), and albumin. The literature reports that among conventional liver tests, a significant diagnostic value of cirrhosis was observed for albuminemia, PT, and platelets. PT has a very good performance in the diagnosis of cirrhosis (86%) 28, 29, 30, 31 . Thrombocytopenia is an indirect sign of cirrhosis and could be explained by hypersplenism or by a defect in the production of a substance regulating thrombopoiesis in the liver, as a result of IHC 31, 32 . However, it was only observed in one patient in our study, the patient who suffered from haematemesis. The prothrombin level in this patient was 49% and the albumin level was normal. In the other patients the PT was normal as well as the albumin level. Any patient with liver activity (AST > 2N, ALT > 2N) and a detectable B viral load should receive effective, high genetic barrier antiviral therapy 28,31 with pegylated interferon if the D viral load is detectable 33 . The aim of antiviral treatment is to achieve rapid non- detectability of HBV DNA and HDV RNA reducing viral (resistance- escape) and hepatic (complication of cirrhosis) risks. In our series, all 05 patients who met the conditions for initiation of HBV treatment were put on tenofovir. Four patients were eligible for treatment for HDV. But due to the high cost (180,000 CFA francs per dose) of pegylated interferon, only 01 patient was put on treatment. He received 58 doses of IFN-peg at 180 ug/ week. This patient, due to financial difficulties, had to suspend the treatment without reaching the therapeutic objective. The two criteria for the efficacy of antiviral treatment are the biochemical response assessed by the determination of serum ALT at least once every three months and the virological response, which was assessed by the six-monthly quantification of HBV viral DNA (carried out with difficulty in some patients for financial reasons) and by the quantification of HDV-RNA (for patients treated with IFN-peg).With regard to the virological response, the objective is to obtain maximum efficacy and minimum resistance. The decrease, or rather the non-detectability, of viral DNA is a direct reflection of the efficacy of the nucleotide analogues 31 . Of the 05 patients on tenofovir, 04 had a treatment duration ≥ 03 years and complete virological response (HBV) was obtained in all (100%). Our results are superimposed on those obtained in patients treated for chronic hepatitis B in Ouagadougou in whom HBV-DNA was undetectable in 89.6% of all patients on tenofovir between one and three years and in all patients beyond five years 34 . These results were confirmed by Zouré who found that after three years of treatment, almost all patients achieved a complete virological response on tenofovir 31 . In our study, this good virological response was not associated with a good biochemical response. Indeed, of the 04 patients with a good virological response, 02 had fluctuating transaminases after more than 4 years of tenofovir treatment but remained < 2N with sometimes a return to normal. Several studies in HBV mono-infected patients found that a good virological response was associated with a good biochemical response 35,36 . Our results can probably be explained either by the HDV infection or by an unacknowledged exogenous factor (e.g. traditional medication). The patient treated for HDV had a B viral load of 45 IU/ mL and a D viral load of 600,000 IU/mL at control. These incomplete virological responses were also associated with a poor biochemical response (AST 54 and ALT 52 IU/mL). The same observation has been made by other authors. In a study evaluating the efficacy and safety of IFN-peg in patients treated for 12 months (48 weeks), Castelnau found a normalisation of transaminases in only 57% of patients and a good virological response (6 to 42 months with an average of 16 months after treatment) in 47% of patients37. In a similar study, Niro found that only 37.5% of patients achieved a good biochemical response and virological response was achieved in 21% at the end of 72 weeks of IFN-peg treatment 25 . Although the findings on the only patient in our series do not allow us to draw conclusions on the efficacy of IFN-peg, the literature concludes that even if IFN-peg remains the currently recommended treatment against delta virus, it is disappointing in 30% of cases, with high relapse rates 15 , hence several encouraging clinical trials are currently being evaluated: Myrcludex has obtained the AMM in France and is currently used • Input inhibitor: Myrcludex B • Assembly inhibitor: Lonafarnib • Nucleic acid polymers: NAPs . Conclusion The results of our study add to the still very limited data in the literature on the prevalence of delta virus infection in Burkina Faso. It appears to be low. The delta virus leads to a more rapid cirrhogenic evolution compared to mono-infection and even increases the risk of hepatocellular carcinoma. The prevention of B-delta infection involves prevention, but also treatment of hepatitis B. The best strategy to combat viral hepatitis B-delta remains the search for viral markers (HBV and HDV) during health check-ups, the prevention of mother-to-child transmission of HBV and the vaccination of uninfected adults. References 1. Hepatitis B [internet]. Geneva: World Health Organization; 2021. Available from: https:// www .who .int/ news -room/ fact -sheets/ detail/ hepatitis -b [cited 2021 Jul 15]. 2. Ghorachi Mint Mohamed Mahmoud. Impact of delta virus infection on the natural history of hepatitis B in Mauritania. REVIEW The results of the biological tests performed by the patien s are presented in table 4. Table 4: Distribution according to biological characteristics of patients Reviews Minimum value Average value Maximum v lu Total pati nts Prothrombin rate (%) 85 59 100 09 Albumin (g/l) 40.8 30 48 05 ASAT (IU) 202,7 13 2269 11 ALAT (IU) 270 08 2403 11 White blood cells (/mm3) 6194 3516 14000 09 Haemoglobin (g/dl) 13 9,7 16 09 Platelets (/mm3) 155000 48000 233000 09 Alpha fetoprotein (IU/ml) 3.4 1 9 04 Of the 11 patients, 06 were treated against HBV. Of these, 01 patient was treated against HDV. The cirrhotic patient with oesophageal varices presented three episodes of haematemesis and received four sessions of oesophageal variceal ligation. The average duration of treatment was 4.5 years with extremes of 04 months and 11 years. One patient had a treatment duration of 04 months. The other patients had a treatment duration ≥ 3 years. The biological evolution under treatment is presented in Table 5. Table 5: Distribution of patients according to virological and biochemical results Treatment Duration of treatment HBV DNA (IU/mL) AST (IU/ mL) ALAT (IU/ mL) Detectable Undetectable Patient 1 TDF* 04 years < 10 53 59 Patient 2 IFN-peg* 04 years 45 54 52 Patient 3 TDF 03 years < 10 20 10 Patient 4 TDF 05 years < 10 31 50 Patient 5 TDF 04 months 82 104 Patient 6 TDF 11 years < 10 28 15 TDF* : Tenofovir 300 mg/d, IFN-peg*: Pegylatedinterferon The patient treated with IFN-peg for 58 weeks was 39 years old and showed improvement in ALT (from 80 to 52 IU/ML), HDV-RNA (from 7.7 to 5.7 log) and HBV-DNA/ IU/mL (385 to 45 IU/mL). Discussio It is estimated that 5-10% of HBsAg carriers are co- infected or superinfected with HDV worldwide8. In the present study, the prevalence of B-delta infection among chronic B virus carriers was 2.2%. This rate is close to that (3.38%) found by Sawadogo and al in a 2016 study f 177 HBsAg positive blood donors in Bobo-Dioulasso 9 . In Senegal, Vray and al found similar results among blood donors: 3.2% 10 . However, our prevalence is higher than that found by Méda and coll agues 7 in 2010 in the general population of Burkina Faso, which was 0.10%. We can note that t e prevalence of delta infection in our study is very low compared to African series. Thus in Mauritania the prevalence was 39% and 33% respectively in 2010 and 2012 11 , in Niger 29% 12 , Cameroo : 17.6% 5 , in B nin among pregnant women: 11.4% 13 , in Ghana: 11.3% in 2014 14 , in orth Cameroon: 7.3% 15 and Djebbi in Tunisia who found a prevalence of HDV of 6.8% among 176 asymptomatic HBV carri r 6 . It should be no d hat in France, very high preval ces we e noted in 1980 (70% f drug addicts and 15% of homosexuals) in contrast to recent studi which found a r valenc of 4% in the gen ral population 17 . In Taiwan, rates of 74.4%, 43.9%, 11.4%, 11.1% and 4.4% ere resp ively found in HIV positive drug users, HIV n gative drug users, homosexual women (Men), HIV inf ct d heterosexual women and the g neral HBsAg positive population 18 . The e results show that, although the hepatitis delta virus circulates in Burkina Faso, its prevalence remains low despite a relatively high prevalence f HBV: 9.1% 7 . The prevalence f B-delta infe tion i relat d to a number of epidemiological factors including family istory, his ory of i v sive care and risk behaviours (hom sexuali y, i ravenous drug use) 19,20,21 . In our s ries, we did not find n explanation for this prevalence wh ch i l w (2.2%) compared t othe African series. The mean age of the delta-positive patients was 42.5 y ars +/- 7.9 ye rs. Th age ra ge above 40 y ars was th m st representative, as s ven patients in our series were over 40 years old. In Burkina Faso, Sawadogo et al found a much lower ave age age (22 years) than in our study. Howe er, our results are compar ble to those of Mansour in Mauritani with a averag ge of 41±11.5 years and El Gorach in Mauritania (46 ±11.5 years) 22,23 . According to Mansour, the presenc of Ac-anti-del a was as oci ted with age nd sex. However, according to Moatter 20 , HDV can inf ct at any age and we did not find any other studies showing a predilectio for delta infection ccordi g to age. The gender distribution of patient in our study shows a slight mal predominance. The sex ratio was 1.75. This slight male predominance has also been reported i other studies conduct d in Algeria in 2008 7 and in Pakistan in 2007 20 . This may b explained by the fact that HBV becomes chronic more often in me than in w men. However, while the predomi ance was male in the r vious series, in the Djebbi et al study the sex ratio was 0.2 17 . Hepatitis B was disc vered during the sessment of jaundice in three patients. In three others, the d scovery was fo tuitous during a he lth check- p and one c s was discovered duri g the follow-up of a haematemesis. This result s ows that HBV screening is not done systematical the population, but on the occasion of a symptomatology that is generally a complication of hepatitis B. The clinical examination was normal in 10 patients. Cirrho is was found in three pati nts, two of whom were confirm d by PBH, and severe fibrosis (F3) assessed by the FibroMeter® w s found in 02 patients. Th Fibr Scan® performed n three patients showed a hepatic elasti ity of 5.2 kpa; 11.8 kpa and 15 pa. The nly p tient wh h d a clinical argument (ha m temesis) did not und rgo PBH or non-inv siv evaluation of fibrosis. These observations show that despite a normal clinic l examination, a patient with HBV /or HDV ca develop complications (in particular cirr osis) and the patient will most often only come to see a clinical sign of decompensation of cirrhosis, which is the most frequent stage of discovery of chronic viral hepatitis in our context as reported in the literature. Thes findings reinforc the importance of early detection and management of chro ic hepatitis B before the stage of compli ations. In principle, HBsAg testing should be systematically perf rmed during routine consultations and ny health check-up in our context, REVIEW
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