Acute human parvovirus B19 infection triggers immune-mediated transient bone marrow failure syndrome, extreme direct hyperbilirubinaemia and acute hepatitis in patients with hereditary haemolytic anaemias: multicentre prospective pathophysiological study.

A total of 244 patients with hereditary haemolytic anaemias (HHA) were screened for acute symptomatic human parvovirus B19 infection (HPV-B19) in a prospective study. To assess the risks associated with HPV-B19 infection, patients were classified into Group I and Group II according to presence or absence (symptoms, signs and specific serology) of acute HPV-B19 infection respectively. In all, 131 (53·7%) patients had ß-thalassaemia, 75 (30·7%) hereditary spherocytosis (HS), 27 (11·1%) sickle cell anaemia (SCA) and 11 (4·5%) glucose-6-phosphate dehydrogenase (G6PD) deficiency. Of 33 (13·5%) patients who presented with symptomatic HPV-B19 infection, 19 (57·5%) had HS, nine (27·3%) had ß-thalassaemia and five (15·2%) had SCA. In Group I, there were significant differences in the mean white blood cell, red blood cell and platelet counts, haemoglobin concentration, total bilirubin (TB), alanine aminotransferase, aspartate aminotransferase and serum creatinine (all P < 0·001) compared to Group II. In all, 27 (81·8%) patients had arthropathy and bone marrow failure (BMF); 13 (39·4%) had acute kidney injury (AKI), more in SCA (80%); and 12 (36·4%) patients had hepatitis, more in HS (66·8%). Five (15·2%) patients with HS had BMF, AKI, nervous system involvement and extreme hyperbilirubinaemia (TB range 26·3-84·7 mg/dl). Five (15·2%) patients had haemophagocytic syndrome. Two patients with HS combined with Type-I autoimmune hepatitis presented with transient BMF. Complete recovery or stabilisation was noted at 12 months in every patient except for one patient with SCA who died during the infection. HPV-B19 must be suspected and screened in patients with HHA with typical and atypical presentations with careful follow-up.

Ectopic atrial tachycardia in an infant with transient erythroblastopenia of childhood.

Transient erythroblastopenia of childhood is a self-limited anemia occurring in previously healthy children, secondary to temporary cessation of erythrocyte production. Although the precise etiology is unclear, most cases are associated with a viral illness. The anemia may be severe, with associated pallor, tachypnea, and tachycardia; treatment is supportive. We present an unusual case of a child with viral-induced transient erythroblastopenia of childhood and associated ectopic atrial tachycardia, requiring therapy with antiarrhythmics.

Acute pericarditis and transient erythroblastopenia associated with human parvovirus B19 infection.

We report on an eight-year-old girl with acute pericarditis and transient erythroblastopenia associated with human parvovirus B19 (PVB19) infection. The patient presented with complaints of fever, chest pain, fatigue, and shortness of breath. On physical examination, she had tachycardia, hepatomegaly, and muffled heart sounds. Teleradiography exhibited cardiomegaly and echocardiography showed a pericardial effusion of 25 mm. Serum anti-PVB19 IgM and PVB19 DNA were positive. The patient developed anemia and reticulocytopenia in the second week, both of which persisted for two weeks then resolved spontaneously. At the end of three months, pericardial effusion resolved, hemoglobin and hematocrit levels were normal, and serum anti-PVB19 IgM was negative. This case represents the first report of acute pericarditis associated with PVB19 infection in a pediatric patient.

Prevalence of hepatitis B, hepatitis C and human immune deficiency virus markers among patients with hereditary haemolytic anaemias.

To determine the prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) markers among Bahraini children with hereditary haemolytic anaemias, a cross-sectional study was conducted at the paediatric outpatient clinic of Sulimaniya Medical Center in the State of Bahrain. A total of 242 patients with hereditary haemolytic anaemias were enrolled in the study: 171 (71%) with sickle cell syndromes, 59 (24%) with beta thalassaemia major and 12 (5%) with alpha thalassaemia. Among the 191 multi-transfused patients, 39 (20.5%) had one or more markers for HBV, 78 (40%) were seropositive for HCV antibody, and three (1.6%) were seropositive for HIV antibody. In contrast, none of the 51 non-transfusion group was seropositive for HBV and HIV antibodies but one patient was seropositive for HCV antibody. HBV, HCV and HIV infections therefore remain a major hazard for children with hereditary haemolytic anaemias, despite blood donor screening. More refined and sensitive tests which would detect infection in all stages of the disease are required. Hepatitis B vaccine should be given to all children with hereditary haemolytic anaemias.