Letters to the Editor
All donated blood units, thus need to be screened for MP, preferably by RDTs, to prevent and defend all suspected TTM. Naveen Agnihotri, Lokesh Kumar Pal Department of Transfusion Medicine, Fortis Hospital, Blood Bank, Shalimar Bagh, New Delhi, India Correspondence to: Dr. Naveen Agnihotri, Department of Transfusion Medicine, Fortis Hospital, Blood Bank, A-Block Shalimar Bagh, New Delhi – 110 088, India. E-mail: [email protected]
References 1. Bahadur S, Pujani M, Jain M. Use of rapid detection tests to prevent transfusion-transmitted malaria in India. Asian J Transfus Sci 2010;4:140-1. 2. Choudhury N, Jolly JG, Mahajan RC, Ganguly NK, Dubey ML, Agnihotri SK. Malaria screening to prevent transmission by transfusion: An evaluation of techniques. Med Lab Sci 1991;48:206-11. 3. Pomper GJ. Febrile, allergic, and nonimmune transfusion reactions. In: Simon TL, Snyder EL, Solheim BG, Stowell CP, Strauss RG, Petrides M, editors. Rossi’s Principles of Transfusion Medicine. 4th ed. Bethesda: Blackwell Publishing Ltd.; 2009. p. 839. 4. Choudhury NJ, Dubey ML, Jolly JG, Kalra A, Mahajan RC, Ganguly NK. Post-transfusion malaria in thalassaemia patients. Blut 1990;61:314-6. 5. Stauffer WM, Cartwright CP, Olson DA, Juni BA, Taylor CM, Bowers SH, et al. Diagnostic performance of rapid diagnostic tests versus blood smears for malaria in US clinical practice. Clin Infect Dis 2009;49:908-13. Access this article online Website: www. ajts. org
Quick Response Code:
DOI: 10.4103/0973-6247.126697
Investigating weak A subgroups in a healthy lady: The blood bank limitations Sir, Weak A subgroups such as A3, Ax, Aend, Am, Ay, and Ael are often mistyped as group O and may be potentially dangerous with regards to whole blood transfusion. These subgroups can be serologically differentiated using recommended techniques. [1,2] Special tests like serum glycosyltransferase estimation and genotyping are performed in advanced laboratories to confirm these blood groups.[3,4] We observed a discrepancy between the routine forward and 62
Table 1: Test on red cells and serum
Test on red cells Anti-A Anti-B Anti-A, B Anti-D Anti-A1 Anti-H 0 0 0 ++++ 0 ++++
Table 2: Adsorption-elution test Eluate reactivity A cells
O cells
37°C 22°C 4°C ++ ++ ++
37°C 22°C 4°C 0 0 0
Test on serum Regular Irregular Anti-B None
Final wash reactivity A cells B cells B cells O cells
0
0
0
0
reverse blood grouping of a 45-year old healthy lady. The forward group revealed ‘O’ positive and reverse showed ‘A’ group. No clerical errors and reagent problems were observed. We performed a detailed serological investigation on the lady’s red cells with both tube technique and Gel method (DiaMed, Cressier s/Morat, Switzerland) [Table 1]. Since the red cells showed no agglutination with either Anti-A and Anti-AB, we suspected a possible Am or Ay or Ael phenotype. The red cells were then subjected to adsorption – elution tests using human polyclonal Anti-A as described elsewhere.[2] To our surprise the eluate reacted with the reagent ‘A’ cells indicating the presence of ‘A’ antigen on the test red cells. The result was then validated with a) the eluate showing agglutination with two different reagent ‘A’ cells at all phases b) eluate failing to agglutinate reagent ‘O’ cells and c) the final wash solution failing to agglutinate with all the four reagent red cells ‘A’, ‘B’, ‘AB’ and ‘O’[2] [Table 2]. Blood groups of her husband and one son who were available then were confirmed to be ‘O’ positive. Saliva study showed that the lady was a secretor and carried both ‘A’ and ‘H’ substances thus excluding the probability of Ael phenotype. Serologically ‘Ay’ is almost similar to ‘Am’ and even adsorption – elution test fails to differentiate the two phenotypes. In the present study Anti-A eluted from the lady’s red cells reacted weakly with the corresponding reagent ‘A’ cells (Agglutination strength: 1+ by tube technique and 2+ by Gel) which is in favor of ‘Ay’ phenotype. In case of ‘Am’ phenotype such agglutination strength is significantly stronger.[1] Finally we reported the patient as “Weak A subgroup” Rh positive. We advised both serum glycosyltransferase estimation and genotyping of the lady for confirmation of her weak ‘A’ subgroup. We were really in a dilemma as to how the reporting should be done in the present case. We were not sure whether designating the lady as “Weak A subgroup” Rh positive was a proper reporting format. Since confirmatory tests for weak ‘A’ phenotype is beyond the scope of most blood banks, there should be a system to report these weak ‘A’ individuals. Sudipta Sekhar Das, R. U. Zaman, Md. Safi, Subrata Sen, Tirtha Pratim Sardar, Susanta Ghosh Department of Transfusion Medicine, Apollo Gleneagles Hospitals, Kolkata, India
Correspondence to: Dr. Sudipta Sekhar Das, Department of Transfusion Medicine, Apollo Gleneagles Hospitals, Kolkata - 700 054, India. E-mail: [email protected] Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014
References 1. Harmening DM, Firestone D. The ABO blood group system. In: Harmening DM, editor. Modern Blood Banking and Transfusion Practices. 3rd ed. New Delhi, Jaypee Brothers Medical Publishers (P) Ltd.; 1998. p. 86-115. 2. Bercher ME. Methods section 2: Red cell typing. AABB Technical Manual. 15th ed. Bethesda: American Association of Blood Banks; 2005. p. 735-736. 3. Heier HE, Namork E, Calkovská Z, Sandin R, Kornstad L. Expression of A antigens on erythrocytes of weak blood group A subgroups. Vox Sang 1994;66:231-6. 4. Meng QB. Genetic analysis of an individual of Ay serologic phenotype. Nan Fang Yi Ke Da Xue Xue Bao 2009;29:1615-6. Access this article online Website: www. ajts. org
Quick Response Code:
DOI: 10.4103/0973-6247.126699
Table 1: The positive IgG anti-hepatitis B core antigen among samples of donors’ blood that had been tested negative for HBsAg Male Females Total
Anti-HBc reactive n (%) 17 (10.0) 3 (7.9) 20 (9.6)
Anti-HBc non-reactive n (%) 153 (90.0) 35 (92.1) 188 (90.4)
Total n (%) 170 (81.7) 38 (18.3) 208 (100)
IgG = Immunoglobulin G, HBsAg = Hepatitis B surface antigen, HBc = Hepatitis B core antigen
Table 2: Data collected from HBe antigen and HBeAb tests from anti-HBcT-positive samples Non-reactive n (%) 20 (0) 0 (100)
HBe Antigen Anti-HBe
Reactive n (%) 0 (100) 20 (0)
HBe = Hepatitis B e antigen, HBeAb = Antibodies to Hepatitis B e antigens, HBcT = Total Hepatitis B core antigen
Table 3: A comparison between new and regular donors positive for anti-HBc IgG antibodies
Testing for hepatitis B virus core antigen and e antigen may confer additional safety of donors’ blood negative for heptitis B virus surface antigen Sir, Viral hepatitis B (HBV) is a major worldwide public health concern as it can be readily transmitted through blood transfusion, especially when blood collection would be performed during the window period.[1] The specific serologic markers for HBV testing include the hepatitis B surface antigen (HBsAg) and hepatitis B e-antigen (HBeAg), and the antibodies to hepatitis B core antigen and e-antigen (anti-HBc and anti-HBe). AntiHBc can be detected in people infected with HBV. HBeAg is associated with HBV infection and is found when there is active replication of virus.[2] This study was performed to test the positivity of serological markers in the blood of donors negative for HBsAg. Hence, the current study, performed at Hospital Tengku Ampuan Afzan, Kuantan, Malaysia, was carried out to determine the prevalence of anti-HBc, HBeAg, and anti-HBe among blood donors negative for HBsAg to detect potentially infectious blood units, and to help in deciding whether supplemental testing may result in additional safety to blood products. MONOLISA enzyme assays (MONOLISA, Bio-RAD Laboratories, France) were utilized to test for anti-HBc, HBeAg, and anti-HBe antibodies. Out of 208 HBsAg-negative blood samples, 20 samples (9.6%) were found to be anti-HBc reactive. All these 20 samples were also positive for anti-HBe and were negative for HBeAg [Tables 1 and 2]. Furthermore, the prevalence of positivity was found to be higher among regular donors compared with new donors [Table 3].
New donors Regular donors Total
Anti-HBc reactive n (%) 7 (5.6) 13 (15.9) 20 (9.6)
Anti-HBc nonreactive n (%) 119 (94.4) 69 (84.1) 188 (90.4)
Total n (%) 126 (60.6) 82 (39.4) 208 (100)
HBc = Hepatitis B core,
temporarily. Furthermore, it can be suggested that testing for antiHBc be introduced routinely for all blood samples, especially in Asian countries where the prevalence of HBV infection is generally higher than that in European and North American countries.[3] The high frequency of post-transfusion hepatitis is apparently because HBsAg circulates at undetectable levels for current screening assays; hence, screening for anti-HBc antibody is necessary.[4] This will increase the safety and reduce the risk of disease transmission during blood transfusion; however, it has a drawback in that it may also lead to a sharp increase in the rejection rates and may be responsible for an increase in the total costs. Thus, such a screening program can be substantiated by long-term follow-up of donors deferred for this reason, to monitor them for viral loads and/or development of clinical disease. Fawwaz Shakir Al-Joudi, Maimunah Binti Mohd Arif1, Zulaikha Binti Mohamed1, Ismarulyusda Ishak2, Suhair A. Ahmed3 Department of Microbiology, Royal College of Medicine Perak, University of Kuala Lumpur, Ipoh, Perak, 1Unit of Haematology, Tengku Ampuan Afzan Hospital, Kuantan, 2 Faculty of Allied Health Sciences, University Kebangsaan Malaysia, Kuala Lumpur, 3 Department of Haematology and Transfusion Medicine, School of Medical Sciences, University of Science of Malaysia, Kota Bharu, Malaysia
Although exposure to HBV may be followed by full recovery, it is still advisable to defer these anti-HBc-positive donors, at least
Correspondence to: Prof. Fawwaz Shakir Al-Joudi, Department of Microbiology, Royal College of Medicine Perak, University of Kuala Lumpur, 3 Jalan Greenwood, 30450 Ipoh, Perak, Malaysia. E-mail: [email protected]
Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014
63
Copyright of Asian Journal of Transfusion Science is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
All donated blood units, thus need to be screened for MP, preferably by RDTs, to prevent and defend all suspected TTM. Naveen Agnihotri, Lokesh Kumar Pal Department of Transfusion Medicine, Fortis Hospital, Blood Bank, Shalimar Bagh, New Delhi, India Correspondence to: Dr. Naveen Agnihotri, Department of Transfusion Medicine, Fortis Hospital, Blood Bank, A-Block Shalimar Bagh, New Delhi – 110 088, India. E-mail: [email protected]
References 1. Bahadur S, Pujani M, Jain M. Use of rapid detection tests to prevent transfusion-transmitted malaria in India. Asian J Transfus Sci 2010;4:140-1. 2. Choudhury N, Jolly JG, Mahajan RC, Ganguly NK, Dubey ML, Agnihotri SK. Malaria screening to prevent transmission by transfusion: An evaluation of techniques. Med Lab Sci 1991;48:206-11. 3. Pomper GJ. Febrile, allergic, and nonimmune transfusion reactions. In: Simon TL, Snyder EL, Solheim BG, Stowell CP, Strauss RG, Petrides M, editors. Rossi’s Principles of Transfusion Medicine. 4th ed. Bethesda: Blackwell Publishing Ltd.; 2009. p. 839. 4. Choudhury NJ, Dubey ML, Jolly JG, Kalra A, Mahajan RC, Ganguly NK. Post-transfusion malaria in thalassaemia patients. Blut 1990;61:314-6. 5. Stauffer WM, Cartwright CP, Olson DA, Juni BA, Taylor CM, Bowers SH, et al. Diagnostic performance of rapid diagnostic tests versus blood smears for malaria in US clinical practice. Clin Infect Dis 2009;49:908-13. Access this article online Website: www. ajts. org
Quick Response Code:
DOI: 10.4103/0973-6247.126697
Investigating weak A subgroups in a healthy lady: The blood bank limitations Sir, Weak A subgroups such as A3, Ax, Aend, Am, Ay, and Ael are often mistyped as group O and may be potentially dangerous with regards to whole blood transfusion. These subgroups can be serologically differentiated using recommended techniques. [1,2] Special tests like serum glycosyltransferase estimation and genotyping are performed in advanced laboratories to confirm these blood groups.[3,4] We observed a discrepancy between the routine forward and 62
Table 1: Test on red cells and serum
Test on red cells Anti-A Anti-B Anti-A, B Anti-D Anti-A1 Anti-H 0 0 0 ++++ 0 ++++
Table 2: Adsorption-elution test Eluate reactivity A cells
O cells
37°C 22°C 4°C ++ ++ ++
37°C 22°C 4°C 0 0 0
Test on serum Regular Irregular Anti-B None
Final wash reactivity A cells B cells B cells O cells
0
0
0
0
reverse blood grouping of a 45-year old healthy lady. The forward group revealed ‘O’ positive and reverse showed ‘A’ group. No clerical errors and reagent problems were observed. We performed a detailed serological investigation on the lady’s red cells with both tube technique and Gel method (DiaMed, Cressier s/Morat, Switzerland) [Table 1]. Since the red cells showed no agglutination with either Anti-A and Anti-AB, we suspected a possible Am or Ay or Ael phenotype. The red cells were then subjected to adsorption – elution tests using human polyclonal Anti-A as described elsewhere.[2] To our surprise the eluate reacted with the reagent ‘A’ cells indicating the presence of ‘A’ antigen on the test red cells. The result was then validated with a) the eluate showing agglutination with two different reagent ‘A’ cells at all phases b) eluate failing to agglutinate reagent ‘O’ cells and c) the final wash solution failing to agglutinate with all the four reagent red cells ‘A’, ‘B’, ‘AB’ and ‘O’[2] [Table 2]. Blood groups of her husband and one son who were available then were confirmed to be ‘O’ positive. Saliva study showed that the lady was a secretor and carried both ‘A’ and ‘H’ substances thus excluding the probability of Ael phenotype. Serologically ‘Ay’ is almost similar to ‘Am’ and even adsorption – elution test fails to differentiate the two phenotypes. In the present study Anti-A eluted from the lady’s red cells reacted weakly with the corresponding reagent ‘A’ cells (Agglutination strength: 1+ by tube technique and 2+ by Gel) which is in favor of ‘Ay’ phenotype. In case of ‘Am’ phenotype such agglutination strength is significantly stronger.[1] Finally we reported the patient as “Weak A subgroup” Rh positive. We advised both serum glycosyltransferase estimation and genotyping of the lady for confirmation of her weak ‘A’ subgroup. We were really in a dilemma as to how the reporting should be done in the present case. We were not sure whether designating the lady as “Weak A subgroup” Rh positive was a proper reporting format. Since confirmatory tests for weak ‘A’ phenotype is beyond the scope of most blood banks, there should be a system to report these weak ‘A’ individuals. Sudipta Sekhar Das, R. U. Zaman, Md. Safi, Subrata Sen, Tirtha Pratim Sardar, Susanta Ghosh Department of Transfusion Medicine, Apollo Gleneagles Hospitals, Kolkata, India
Correspondence to: Dr. Sudipta Sekhar Das, Department of Transfusion Medicine, Apollo Gleneagles Hospitals, Kolkata - 700 054, India. E-mail: [email protected] Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014
References 1. Harmening DM, Firestone D. The ABO blood group system. In: Harmening DM, editor. Modern Blood Banking and Transfusion Practices. 3rd ed. New Delhi, Jaypee Brothers Medical Publishers (P) Ltd.; 1998. p. 86-115. 2. Bercher ME. Methods section 2: Red cell typing. AABB Technical Manual. 15th ed. Bethesda: American Association of Blood Banks; 2005. p. 735-736. 3. Heier HE, Namork E, Calkovská Z, Sandin R, Kornstad L. Expression of A antigens on erythrocytes of weak blood group A subgroups. Vox Sang 1994;66:231-6. 4. Meng QB. Genetic analysis of an individual of Ay serologic phenotype. Nan Fang Yi Ke Da Xue Xue Bao 2009;29:1615-6. Access this article online Website: www. ajts. org
Quick Response Code:
DOI: 10.4103/0973-6247.126699
Table 1: The positive IgG anti-hepatitis B core antigen among samples of donors’ blood that had been tested negative for HBsAg Male Females Total
Anti-HBc reactive n (%) 17 (10.0) 3 (7.9) 20 (9.6)
Anti-HBc non-reactive n (%) 153 (90.0) 35 (92.1) 188 (90.4)
Total n (%) 170 (81.7) 38 (18.3) 208 (100)
IgG = Immunoglobulin G, HBsAg = Hepatitis B surface antigen, HBc = Hepatitis B core antigen
Table 2: Data collected from HBe antigen and HBeAb tests from anti-HBcT-positive samples Non-reactive n (%) 20 (0) 0 (100)
HBe Antigen Anti-HBe
Reactive n (%) 0 (100) 20 (0)
HBe = Hepatitis B e antigen, HBeAb = Antibodies to Hepatitis B e antigens, HBcT = Total Hepatitis B core antigen
Table 3: A comparison between new and regular donors positive for anti-HBc IgG antibodies
Testing for hepatitis B virus core antigen and e antigen may confer additional safety of donors’ blood negative for heptitis B virus surface antigen Sir, Viral hepatitis B (HBV) is a major worldwide public health concern as it can be readily transmitted through blood transfusion, especially when blood collection would be performed during the window period.[1] The specific serologic markers for HBV testing include the hepatitis B surface antigen (HBsAg) and hepatitis B e-antigen (HBeAg), and the antibodies to hepatitis B core antigen and e-antigen (anti-HBc and anti-HBe). AntiHBc can be detected in people infected with HBV. HBeAg is associated with HBV infection and is found when there is active replication of virus.[2] This study was performed to test the positivity of serological markers in the blood of donors negative for HBsAg. Hence, the current study, performed at Hospital Tengku Ampuan Afzan, Kuantan, Malaysia, was carried out to determine the prevalence of anti-HBc, HBeAg, and anti-HBe among blood donors negative for HBsAg to detect potentially infectious blood units, and to help in deciding whether supplemental testing may result in additional safety to blood products. MONOLISA enzyme assays (MONOLISA, Bio-RAD Laboratories, France) were utilized to test for anti-HBc, HBeAg, and anti-HBe antibodies. Out of 208 HBsAg-negative blood samples, 20 samples (9.6%) were found to be anti-HBc reactive. All these 20 samples were also positive for anti-HBe and were negative for HBeAg [Tables 1 and 2]. Furthermore, the prevalence of positivity was found to be higher among regular donors compared with new donors [Table 3].
New donors Regular donors Total
Anti-HBc reactive n (%) 7 (5.6) 13 (15.9) 20 (9.6)
Anti-HBc nonreactive n (%) 119 (94.4) 69 (84.1) 188 (90.4)
Total n (%) 126 (60.6) 82 (39.4) 208 (100)
HBc = Hepatitis B core,
temporarily. Furthermore, it can be suggested that testing for antiHBc be introduced routinely for all blood samples, especially in Asian countries where the prevalence of HBV infection is generally higher than that in European and North American countries.[3] The high frequency of post-transfusion hepatitis is apparently because HBsAg circulates at undetectable levels for current screening assays; hence, screening for anti-HBc antibody is necessary.[4] This will increase the safety and reduce the risk of disease transmission during blood transfusion; however, it has a drawback in that it may also lead to a sharp increase in the rejection rates and may be responsible for an increase in the total costs. Thus, such a screening program can be substantiated by long-term follow-up of donors deferred for this reason, to monitor them for viral loads and/or development of clinical disease. Fawwaz Shakir Al-Joudi, Maimunah Binti Mohd Arif1, Zulaikha Binti Mohamed1, Ismarulyusda Ishak2, Suhair A. Ahmed3 Department of Microbiology, Royal College of Medicine Perak, University of Kuala Lumpur, Ipoh, Perak, 1Unit of Haematology, Tengku Ampuan Afzan Hospital, Kuantan, 2 Faculty of Allied Health Sciences, University Kebangsaan Malaysia, Kuala Lumpur, 3 Department of Haematology and Transfusion Medicine, School of Medical Sciences, University of Science of Malaysia, Kota Bharu, Malaysia
Although exposure to HBV may be followed by full recovery, it is still advisable to defer these anti-HBc-positive donors, at least
Correspondence to: Prof. Fawwaz Shakir Al-Joudi, Department of Microbiology, Royal College of Medicine Perak, University of Kuala Lumpur, 3 Jalan Greenwood, 30450 Ipoh, Perak, Malaysia. E-mail: [email protected]
Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014
63
Copyright of Asian Journal of Transfusion Science is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
