Time to reconsider hepatitis A vaccination policy in Bangladesh
Authors
- Rubaiyat AlamDepartment of Pediatric Gastroenterology and Nutrition, Bangladesh Medical University, Dhaka, Bangladesh
- Khan Lamia NahidDepartment of Pediatric Gastroenterology and Nutrition, Bangladesh Medical University, Dhaka, Bangladesh
- Md. RukunuzzamanDepartment of Pediatric Gastroenterology and Nutrition, Bangladesh Medical University, Dhaka, Bangladesh
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Published by Bangladesh Medical University (former Bangabandhu Sheikh Mujib Medical University).
Hepatitis A virus (HAV) remains a major cause of acute viral hepatitis in Bangladesh [1]. Traditionally, high endemicity ensured early childhood exposure, resulting in asymptomatic infection and lifelong immunity [2]. However, improvements in sanitation, hygiene, and socioeconomic conditions are altering this pattern [3]. Increasingly, exposure is delayed to adolescence and adulthood, where infection is more likely to be symptomatic and severe. This transition creates a “window of susceptibility,” where individuals are neither protected by natural immunity nor vaccinated, making them vulnerable to clinically significant disease. This phenomenon, often described as the “paradox of development,” has been observed across several low- and middle-income countries undergoing epidemiological transition.
Recent hospital-based surveillance in Bangladesh supports this epidemiological shift. A multicenter study found that nearly one-fifth of suspected acute hepatitis cases were anti-HAV IgM positive, confirming hepatitis A virus as a major contributor. Although most cases occurred in children, adolescents and adults were also affected, often with more severe disease and greater healthcare needs [1]. This study reported that HAV accounted for 76.6% of hospitalised paediatric acute viral hepatitis cases, with 41.1% developing complications such as prolonged cholestasis, ascites, acute liver failure, and encephalopathy, and a mortality of 6.3%. A large laboratory-based study from Dhaka reported anti-HAV IgM positivity in nearly 30% of suspected acute viral hepatitis cases, indicating sustained transmission, particularly among children and adolescents [4]. Similar epidemiological changes have been reported globally, including in Asia and Africa, [5] where declining early-life exposure has led to increased susceptibility in older populations. These findings highlight that Bangladesh is part of a broader global transition, reinforcing the need for timely policy adaptation.
The burden of HAV extends beyond clinical outcomes. Indirect economic costs are substantial but often underrecognised. Caregiver burden is significant because parents often miss work to care for affected children. Additionally, infection in adults, particularly primary income earners can result in prolonged work absenteeism and financial hardship. A “double burden” may also emerge, where improved living conditions in urban or higher-income groups delay exposure, while continued transmission in lower-income settings sustains infection risk. This dynamic can exacerbate health inequities and complicate disease control efforts. Outbreaks among susceptible older populations may therefore become increasingly costly, both in terms of healthcare expenditure and productivity losses, underscoring the need for preventive strategies.
The World Health Organization recommends tailoring hepatitis A vaccination strategies according to endemicity and population susceptibility. In countries transitioning from high to intermediate endemicity, routine childhood immunization has proven effective in reducing disease incidence and generating herd protection [6, 7]. In Bangladesh, the expanded programme on Immunization provides a robust delivery platform; however, the ongoing epidemiological shift necessitates a reassessment of hepatitis A vaccination policy. This should be guided by age-stratified seroprevalence data, comprehensive cost-effectiveness analyses incorporating both direct and indirect costs, and evaluation of optimal strategies (targeted versus universal). Prioritization of high-risk groups, such as individuals with chronic liver disease, immunocompromised populations, and susceptible adults should also be considered.
Hepatitis A thus represents a dynamic and increasingly consequential public health challenge in Bangladesh. The convergence of shifting epidemiology, sustained morbidity, and economic impact underscores the urgency of revisiting vaccination policy through a strategic, evidence-based lens to reduce preventable disease and improve population-level outcomes.
Dimension | Illustrative attributes |
Core values | • Equity and inclusivity – valuing all forms of knowledge and participation |
Guiding principles | • Co-production of knowledge – integrating disciplinary, professional, and experiential expertise |
Defining characteristics | • Integration – weaving diverse epistemologies and perspectives |
Operationalizing practices | • Co-design and co-planning – joint problem definition, goal setting, and methodology development |




Variables | Frequency (%) |
Indication of colposcopy |
|
Visual inspection of the cervix with acetic acid positive | 200 (66.7) |
Abnormal pap test | 13 (4.3) |
Human papilloma virus DNA positive | 4 (1.3) |
Suspicious looking cervix | 14 (4.7) |
Others (per vaginal discharge, post-coital bleeding) | 69 (23.0) |
Histopathological diagnosis | |
Cervical Intraepithelial Neoplasia 1 | 193 (64.3) |
Cervical Intraepithelial Neoplasia 2 | 26 (8.7) |
Cervical Intraepithelial Neoplasia 3 | 32 (10.7) |
Invasive cervical cancer | 27 (9.0) |
Chronic cervicitis | 17 (5.6) |
Squamous metaplasia | 5 (1.7) |
Groups based on pre-test marks | Pretest | Posttest Marks (%) | Difference in pre and post-test marks (mean improvement) | P |
Didactic lecture classes | ||||
<50% | 36.6 (4.8) | 63.2 (9.4) | 26.6 | <0.001 |
≥50% | 52.8 (4.5) | 72.4 (14.9) | 19.6 | <0.001 |
Flipped classes | ||||
<50% | 36.9 (4.7) | 82.2 (10.8) | 45.4 | <0.001 |
≥50% | 52.8 (4.6) | 84.2 (10.3) | 31.4 | <0.001 |
Data presented as mean (standard deviation) | ||||
Background characteristics | Number (%) |
Age at presentation (weeks)a | 14.3 (9.2) |
Gestational age at birth (weeks)a | 37.5 (2.8) |
Birth weight (grams)a | 2,975.0 (825.0) |
Sex |
|
Male | 82 (41) |
Female | 118 (59) |
Affected side |
|
Right | 140 (70) |
Left | 54 (27) |
Bilateral | 6 (3) |
Delivery type |
|
Normal vaginal delivery | 152 (76) |
Instrumental delivery | 40 (20) |
Cesarean section | 8 (4) |
Place of delivery |
|
Home delivery by traditional birth attendant | 30 (15) |
Hospital delivery by midwife | 120 (60) |
Hospital delivery by doctor | 50 (25) |
Prolonged labor | 136 (68) |
Presentation |
|
Cephalic | 144 (72) |
Breech | 40 (20) |
Transverse | 16 (8) |
Shoulder dystocia | 136 (68) |
Maternal diabetes | 40 (20) |
Maternal age (years)a | 27.5 (6.8) |
Parity of mother |
|
Primipara | 156 (78) |
Multipara | 156 (78) |
aMean (standard deviation), all others are n (%) | |
Background characteristics | Number (%) |
Age at presentation (weeks)a | 14.3 (9.2) |
Gestational age at birth (weeks)a | 37.5 (2.8) |
Birth weight (grams)a | 2,975.0 (825.0) |
Sex |
|
Male | 82 (41) |
Female | 118 (59) |
Affected side |
|
Right | 140 (70) |
Left | 54 (27) |
Bilateral | 6 (3) |
Delivery type |
|
Normal vaginal delivery | 152 (76) |
Instrumental delivery | 40 (20) |
Cesarean section | 8 (4) |
Place of delivery |
|
Home delivery by traditional birth attendant | 30 (15) |
Hospital delivery by midwife | 120 (60) |
Hospital delivery by doctor | 50 (25) |
Prolonged labor | 136 (68) |
Presentation |
|
Cephalic | 144 (72) |
Breech | 40 (20) |
Transverse | 16 (8) |
Shoulder dystocia | 136 (68) |
Maternal diabetes | 40 (20) |
Maternal age (years)a | 27.5 (6.8) |
Parity of mother |
|
Primipara | 156 (78) |
Multipara | 156 (78) |
aMean (standard deviation), all others are n (%) | |
Mean escape latency of acquisition day | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
Days |
|
|
|
|
|
1st | 26.2 (2.3) | 30.6 (2.4) | 60.0 (0.0)b | 43.2 (1.8)b | 43.8 (1.6)b |
2nd | 22.6 (1.0) | 25.4 (0.6) | 58.9 (0.5)b | 38.6 (2.0)b | 40.5 (1.2)b |
3rd | 14.5 (1.8) | 18.9 (0.4) | 56.5 (1.2)b | 34.2 (1.9)b | 33.8 (1.0)b |
4th | 13.1 (1.7) | 17.5 (0.8) | 53.9 (0.7)b | 35.0 (1.6)b | 34.9 (1.6)b |
5th | 13.0 (1.2) | 15.9 (0.7) | 51.7 (2.0)b | 25.9 (0.7)b | 27.7 (0.9)b |
6th | 12.2 (1.0) | 13.3 (0.4) | 49.5 (2.0)b | 16.8 (1.1)b | 16.8 (0.8)b |
Average of acquisition days | |||||
5th and 6th | 12.6 (0.2) | 14.6 (0.8) | 50.6 (0.7)b | 20.4 (2.1)a | 22.4 (3.2)a |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.05; bP <0.01. | |||||
Categories | Number (%) |
Sex |
|
Male | 36 (60.0) |
Female | 24 (40.0) |
Age in yearsa | 8.8 (4.2) |
Education |
|
Pre-school | 20 (33.3) |
Elementary school | 24 (40.0) |
Junior high school | 16 (26.7) |
Cancer diagnoses |
|
Acute lymphoblastic leukemia | 33 (55) |
Retinoblastoma | 5 (8.3) |
Acute myeloid leukemia | 4 (6.7) |
Non-Hodgkins lymphoma | 4 (6.7) |
Osteosarcoma | 3 (5) |
Hepatoblastoma | 2 (3.3) |
Lymphoma | 2 (3.3) |
Neuroblastoma | 2 (3.3) |
Medulloblastoma | 1 (1.7) |
Neurofibroma | 1 (1.7) |
Ovarian tumour | 1 (1.7) |
Pancreatic cancer | 1 (1.7) |
Rhabdomyosarcoma | 1 (1.7) |
aMean (standard deviation) | |



Test results | Disease | Sensitivity (%) | Specificity (%) | PPV (%) | NPV (%) | ||
Yes | No | ||||||
Reid’s score ≥ 5 | Positive | 10 | 15 | 37.0 | 94.5 | 40.1 | 93.8 |
Negative | 17 | 258 |
|
|
|
| |
Swede score ≥ 5 | Positive | 20 | 150 | 74.1 | 45.0 | 11.8 | 94.6 |
Negative | 7 | 123 |
|
|
|
| |
Swede score ≥ 8 | Positive | 3 | 21 | 11.1 | 92.3 | 12.5 | 91.3 |
Negative | 24 | 252 |
|
|
|
| |
a High-grade indicates a score of ≥5 in both tests; PPV indicates positive predictive value; NPV, negative predictive value | |||||||
Test | Sensitivity (%) | Specificity (%) | Positive predictive value (%) | Negative predictive value (%) |
Reid’s score ≥ 5 | 37.0 | 94.5 | 40.0 | 93.8 |
Swede score ≥ 5 | 74.1 | 45 | 11.8 | 94.6 |
Swede score ≥ 8 | 11.1 | 92.3 | 12.5 | 91.3 |
Test | Sensitivity (%) | Specificity (%) | Positive predictive value (%) | Negative predictive value (%) |
Reid’s score ≥ 5 | 37.0 | 94.5 | 40.0 | 93.8 |
Swede score ≥ 5 | 74.1 | 45 | 11.8 | 94.6 |
Swede score ≥ 8 | 11.1 | 92.3 | 12.5 | 91.3 |
Narakas classification | Total 200 (100%) | Grade 1 72 (36%) | Grade 2 64 (32%) | Grade 3 50 (25%) | Grade 4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7, 8, 9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Narakas classification | Total 200 (100%) | Grade-1 72 (36%) | Grade-2 64 (32%) | Grade-3 50 (25%) | Grade-4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7,8,9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Variables in probe trial day | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
Target crossings | 8.0 (0.3) | 7.3 (0.3) | 1.7 (0.2)a | 6.0 (0.3)a | 5.8 (0.4)a |
Time spent in target | 18.0 (0.4) | 16.2 (0.7) | 5.8 (0.8)a | 15.3 (0.7)a | 15.2 (0.9)a |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.01. | |||||
Pain level | Number (%) | P | ||
Pre | Post 1 | Post 2 | ||
Mean (SD)a pain score | 4.7 (1.9) | 2.7 (1.6) | 0.8 (1.1) | <0.001 |
Pain categories | ||||
No pain (0) | - | 1 (1.7) | 31 (51.7) | <0.001 |
Mild pain (1-3) | 15 (25.0) | 43 (70.0) | 27 (45.0) | |
Moderete pain (4-6) | 37 (61.7) | 15 (25.0) | 2 (3.3) | |
Severe pain (7-10) | 8 (13.3) | 2 (3.3) | - | |
aPain scores according to the visual analogue scale ranging from 0 to 10; SD indicates standard deviation | ||||
Surgeries | Number (%) | Satisfactory outcomes n (%) |
Primary surgery (n=24) |
|
|
Upper plexus | 6 (25) | 5 (83) |
Pan-palsy | 18 (75) | 6 (33) |
All | 24 (100) | 11 (46) |
Secondary Surgery (n=26) |
|
|
Shoulder deformity | 15 (58) | 13 (87) |
Wrist and forearm deformity | 11 (42) | 6 (54) |
All | 26 (100) | 19 (73) |
Primary and secondary surgery | 50 (100) | 30 (60) |
Mallet score 14 to 25 or Raimondi score 2-3 or Medical Research grading >3 to 5. | ||
Narakas classification | Total 200 (100%) | Grade-1 72 (36%) | Grade-2 64 (32%) | Grade-3 50 (25%) | Grade-4 14 (7%) |
Complete recoverya | 107 (54) | 60 (83) | 40 (63) | 7 (14) | - |
Near complete functional recovery but partial deformitya | 22 (11) | 5 (7) | 10 (16) | 6 (12) | 1 (7) |
Partial recovery with gross functional defect and deformity | 31 (16) | 7 (10) | 13 (20) | 10 (20) | 1 (7) |
No significant improvement | 40 (20) | - | 1 (1.5) | 27 (54) | 12 (86) |
aSatisfactory recovery bGrade 1, C5, 6, 7 improvement; Grade 2, C5, 6, 7 improvement; Grade 3, panpalsy C5, 6, 7,8,9, Grade 4, panpalsy with Hornon’s syndrome. | |||||
Trials | Groups | ||||
NC | SC | ColC | Pre-SwE Exp | Post-SwE Exp | |
1 | 20.8 (0.6) | 22.1 (1.8) | 41.1 (1.3)b | 31.9 (1.9)b | 32.9 (1.8)a, b |
2 | 10.9 (0.6) | 14.9 (1.7) | 37.4 (1.1)b | 24.9 (2.0)b | 26.8 (2.5)b |
3 | 8.4 (0.5) | 9.9 (2.0) | 32.8 (1.2)b | 22.0 (1.4)b | 21.0 (1.4)b |
4 | 7.8 (0.5) | 10.4 (1.3) | 27.6(1.1)b | 12.8 (1.2)b | 13.0 (1.4)b |
Savings (%)c | 47.7 (3.0) | 33.0 (3.0) | 10.0 (0.9)b | 23.6 (2.7)b | 18.9 (5.3)b |
NC indicates normal control; SC, Sham control; ColC, colchicine control; SwE, swimming exercise exposure. aP <0.05; bP <0.01. cThe difference in latency scores between trials 1 and 2, expressed as the percentage of savings increased from trial 1 to trial 2 | |||||


Lesion-size | Histopathology report | Total | |||||
CIN1 | CIN2 | CIN3 | ICC | CC | SM | ||
0–5 mm | 73 | 0 | 0 | 0 | 5 | 5 | 83 |
6–15 mm | 119 | 18 | 1 | 4 | 0 | 0 | 142 |
>15 mm | 1 | 8 | 31 | 23 | 12 | 0 | 75 |
Total | 193 | 26 | 32 | 27 | 17 | 5 | 300 |
CIN indicates cervical intraepithelial neoplasia; ICC, invasive cervical cancer; CC, chronic cervicitis; SM, squamous metaplasia | |||||||
| Histopathology report | Total | ||||||
CIN1 | CIN2 | CIN3 | ICC | CC | SM | |||
Lesion -Size | 0-5 mm | 73 | 0 | 0 | 0 | 5 | 5 | 83 |
6-15 mm | 119 | 18 | 1 | 4 | 0 | 0 | 142 | |
>15 mm | 1 | 8 | 31 | 23 | 12 | 0 | 75 | |
Total | 193 | 26 | 32 | 27 | 17 | 5 | 300 | |
CIN indicates Cervical intraepithelial neoplasia; ICC, Invasive cervical cancer; CC, Chronic cervicitis; SM, Squamous metaplasia | ||||||||
Group | Didactic posttest marks (%) | Flipped posttest marks (%) | Difference in marks (mean improvement) | P |
<50% | 63.2 (9.4) | 82.2 (10.8) | 19.0 | <0.001 |
≥50% | 72.4 (14.9) | 84.2 ( 10.3) | 11.8 | <0.001 |
Data presented as mean (standard deviation) | ||||








