Background Primary immunodeficiency (PID) is widely underdiagnosed in countries with high rates of infection and limited diagnostic facilities, such as Indonesia. It remains challenging to distinguish PID from other conditions predisposing children to severe, persistent, unusual, and recurrent (SPUR) infection. Such conditions include secondary immunodeficiency caused by human immunodeficiency virus (HIV) infection, allergic diseases, and chronic diseases with structural or anatomical abnormalities. Objective To evaluate children with SPUR infections for PID and to compare the clinical characteristics of children with PID to those with other underlying conditions. Methods We conducted a cross-sectional, analytic study of children aged 0-18 years presenting with SPUR infections at 10 hospitals in Jakarta, Indonesia, from July 2024 to September 2025. Clinical assessment and laboratory investigations, including immunological tests, were performed to identify the underlying cause of SPUR infections. Children were classified as healthy, PID, secondary immunodeficiency (HIV), allergy, or chronic disease/anatomical abnormalities. Results Two hundred fifty-four subjects (53% male) with a median age of 26 months were included in our study. Most of them had a history of pneumonia (72.1%), diarrhea (31.1%), and pulmonary tuberculosis (27.9%). Thirty-three (13%) subjects were diagnosed with PID, with the majority being male (60.6%). The most common PID found was antibody deficiency (27.3%), followed by immunodeficiencies combined with associated or syndromic features (24.2%), and immunodeficiencies affecting cellular and humoral immunity (21.2%). Median age of onset in the PID group was 12 (3–24) months. Severe malnutrition was most common in children with HIV. Gender, parental consanguinity, and adverse events following live vaccines did not differ significantly across groups. Conclusion The prevalence of PID among children with SPUR infection in this study was 13%, with the most common classification being antibody deficiency.
Taeniasis is a neglected tropical diseases that predominantly affects developing countries, including Indonesia. Although intestinal taeniasis can be diagnosed and treated in resource-limited settings, it is frequently underdiagnosed due to nonspecific clinical manifestations. Severe anemia is a rare complication of intestinal taeniasis.
Perinatal testicular torsion, also known as neonatal testicular torsion, is defined by some authors as occurring either prenatally or within the first 30 days of life. It is estimated that 70% of these cases happen during pregnancy or shortly after birth.1-3 It is important to note that the radiological and clinical findings, as well as the mechanisms and surgical outcomes, associated with perinatal testicular torsion differ from those observed in older age groups.1 Furthermore, a significant number of these cases occur bilaterally, vage rate in 1988 was estimated to be around 5%, but more recent pi66.1.2026.76-80 ].
Background Antibodies to factor VIII, known as inhibitors, are a major problem in hemophilia A, especially in severe cases. Certain genetic mutations are associated with a higher risk of the formation of inhibitors. This study is the first in Indonesia to report on genetic mutations of hemophilia A patients with inhibitors. Objectives To detect genetic mutations, investigate potential risk factors, and evaluate inhibitor prevalence in pediatric hemophilia A patients. Methods An observational study was conducted at the Pediatric Hemophilia Treatment Center of Cipto Mangunkusumo Hospital, Jakarta. Inhibitors were measured using the Bethesda assay and classified as low- or high titer. Inverse shifting polymerase chain reaction (IS-PCR) was performed to detect inversion mutations. Negative results for inversion were followed by Sanger sequencing. Clinical data were obtained from medical records. Results Inhibitors were detected in 17 of 114 hemophilia A patients (14.9%), most of whom (88.2%) had severe disease and had fewer than 150 days of exposure to clotting factor concentrates (CFCs), classifying them as previously untreated patients (PUPs). The genetic mutations identified in inhibitor patients were intron 22 inversion (INV-22) mutations (41.2%), intron 1 inversion (INV-1) mutations (29.4%), nonsense mutations (17.6%), large deletions (5.9%), and missense mutations (5.9%). Family history of inhibitors, previous intensive treatment for major bleeding events or surgery, and type of concentrate were potential risk factors. Conclusion Intron 22 inversion mutations were the most common mutations associated with the presence of inhibitors in hemophilia A patients.
In critical condition, sometimes continuous kidney replacement therapy (CKRT) treatment should not be held while therapeutic plasma exchange (TPE) is needed. Simultaneous use of both modalities is defined as tandem therapy, available as an option.
