Anak Agung Ngurah Ketut Putra Widnyana
Department Of Child Health, Universitas Udayana Medical School/Sanglah Hospital, Denpasar, Bali

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Kadar Feritin Serum Terhadap Fungsi Paru pada Pasien Talasemia β Mayor Luh Gde Ayu Pramitha Dewi; Ayu Setyorini Mestika Mayangsari; Ida Bagus Subanada; Putu Siadi Purniti; AANKP Widnyana
Sari Pediatri Vol 21, No 3 (2019)
Publisher : Badan Penerbit Ikatan Dokter Anak Indonesia (BP-IDAI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14238/sp21.3.2019.183-8

Abstract

Latar belakang. Talasemia merupakan penyakit anemia hemolitik herediter akibat defek genetik pembentukan rantai globin. Tata laksana talasemia dengan transfusi darah dapat menimbulkan penumpukan besi di berbagai jaringan seperti paru. Tujuan. Untuk mengetahui korelasi kadar feritin serum terhadap fungsi paru pada anak talasemia β mayor.Metode. Studi analitik potong lintang dilakukan di RSUP Sanglah sejak Juli-Agustus 2017. Subjek diambil secara konsekutif dengan kriteria inklusi semua anak talasemia usia ≥6 tahun, mendapatkan transfusi darah rutin dan kelasi besi. Kriteria eksklusi adalah anak penderita talasemia dengan penyakit paru kronis dan tidak kooperatif saat spirometri.Hasil. Dari total 31 pasien talasemia di RSUP Sanglah, 28 subjek memenuhi kriteria inklusi dan tidak ada yang memenuhi kriteria eksklusi. Pada penelitian ini median usia pasien talasemia 12,5 tahun dengan kadar rerata feritin serum 3196,5 g/dL. Hasil spirometri dengan median vital capacity (VC) 75%, force vital capacity (FVC) 82,5%, force expiratory volume in one second (FEV1) 80,6%, FEV1/FVC 101,9%. Korelasi kadar feritin serum terhadap semua parameter fungsi paru yaitu VC, FVC, FEV1, dan FEV1/FVC adalah sangat lemah dengan masing-masing nilai r adalah (r=0,016; p=0,936), (r=0,181; p=0,357), (r=0,305; p=0,114), (r=0,158; p=0,42).Kesimpulan. Korelasi kadar feritin serum terhadap semua parameter fungsi paru didapatkan korelasi lemah dan tidak bermakna secara statistik.
Triiodothyronin (T3) as a parameter of mortality in sepsis patients in the PICU Sri Wahyuni Djoko; Nyoman Budi Hartawan; Bagus Ngurah Putu Arhana; Eka Gunawijaya; Anak Agung Ngurah Ketut Putra Widnyana; Dyah Kanya Wati
Paediatrica Indonesiana Vol 59 No 6 (2019): November 2019
Publisher : Indonesian Pediatric Society

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (246.333 KB) | DOI: 10.14238/pi59.6.2019.298-302

Abstract

Background Thyroid hormone stimulates the regulation of β-adrenergic receptors in order to increase the inotropic effect of the heart myocardium. Euthyroid sick syndrome is a disorder of non-metabolic thyroid function, which is characterized by a decrease in triiodothyronine (T3) levels in patients with non-thyroid systemic disease, such as sepsis. Low serum T3 hormone level is a potentially high-risk factor for mortality from sepsis. Objective To assess for a relationship between decreased serum T3 levels and mortality in pediatric sepsis patients admitted in the PICU. Methods This study used a nested case-control design. The subjects were children aged 1 month-18 years who were diagnosed with sepsis in the pediatric intensive care unit at Sanglah Hospital, Denpasar, Bali, from September 2017 to January 2019. Results A total of 90 children were included, of whom 44 died and 46 survived. Median age was 10.5 (IQR 44) months in subjects who died and 9 (IQR 50) months in those who survived. The majority of subjects in both groups had well-nourished nutritional status. Bivariate analysis revealed that significantly more subjects who died had low serum T3 (≤1 ng/dL), PELOD-2 score ≥5, than subjects who survived. Multivariate analysis revealed that serum T3 £1 ng/dL (OR 55.1; 95%CI 9 to 334.8; P<0.001) and PELOD-2 score ³5 (OR 6.5; 95%CI 1.6 to 26.7; P=0.01) were significant risk factors for sepsis mortality. Conclusion Low serum T3 level and high PELOD-2 score are risk factors for death in sepsis.
Plasma NT-proBNP and pulmonary to systemic blood flow ratio in congenital heart defects with left-to-right shunts Eko Kristanto Kunta Adjie; Ni Putu Veny Kartika Yantie; Made Gede Dwi Lingga Utama; Eka Gunawijaya; Ketut Ariawati; Ida Bagus Subanada; Anak Agung Ngurah Ketut Putra Widnyana
Paediatrica Indonesiana Vol 60 No 6 (2020): November 2020
Publisher : Indonesian Pediatric Society

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14238/pi60.6.2020.310-5

Abstract

Background Cardiac left-to-right shunts changes to the pulmonary-to-systemic blood flow ratio (Qp/Qs ratio). This ratio can be used to monitor the hemodynamics of the heart. Left-to right-shunts cause the release of amino terminal proB-ty natriuretic peptide (NT-proBNP) that can be utilized as a specific marker for the presence of heart failure in children with congenital heart defects (CHDs). Early intervention such as defect closure in CHD is important to prevent heart failure. Objective To assess for a correlation between the level of NT pro-BNP and Qp/Qs ratio in CHD patients with left-to-right shunts. Methods This cross-sectional, analytical study was conducted in 32 children who underwent cardiac catheterization at Sanglah General Hospital, Denpasar, Bali, and were recruited by consecutive sampling. NT-proBNP levels were measured by ELISA with a two-step sandwich assay system; Qp/Qs ratio using Fick rules. Statistical analyses included Shapiro-Wilk test, descriptive analysis for subject characteristics, and Pearson’s correlation analysis. A P value of <0.05 was considered to be statistically significant. Age and defect size were analyzed as confounding factors by partial correlation test. Results The correlation value between NT-proBNP and Qp/Qs ratio was r=0.384 (P<0.05), after controlling for age and defect size as cofounding factors. Conclusion There is a weak positive correlation between NT-proBNP levels and pulmonary-to-systemic blood flow ratio in patients with left-to-right shunt, after controlling for age and defect size as confounding factors.
Hemolytic anemia in a 2-years old caused by Glucose 6 Phosphate Dehydrogenase Deficiency (G6PD): a case report Paulus Arief Budiman; Ketut Ariawati; Anak Agung Ngurah Ketut Putra Widnyana
Intisari Sains Medis Vol. 12 No. 3 (2021): (Available online: 1 December 2021)
Publisher : DiscoverSys Inc.

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (295.444 KB) | DOI: 10.15562/ism.v12i3.1159

Abstract

Background: Glucose-6-Phosphate-Dehydrogenase (G6PD) deficiency is an enzyme abnormality related to sex chromosomes (x-linked), which is inherited. The activity or stability of the G6PD enzyme decreases, thus causing the breakdown of red blood cells when an individual is exposed to exogenous substances that can cause oxidative damage. This case study aims to describe a rare case of hemolytic anemia caused by glucose 6 phosphate dehydrogenase deficiency in a two-year-old boy. Case Presentation: A two-year-old boy presented with agitated, pale, yellowish eyes and body and projectile vomiting after consuming fava beans. He had a prior history of packed red cell transfusion. Physical examination found the conjunctivae were pale with the icteric sclera. Laboratory examination revealed leukocytosis, moderate normochromic normocytic anemia, increased reticulocytes count, and elevated total and unconjugated bilirubin. Peripheral blood smear examination found microcytes, spherocytes, fragmentocytes, and burr cells. Coomb test was negative with decreased G6PD result. Conclusion: G6PD deficient patients have no symptoms until exposed to oxidizing drugs, infections or after fava beans ingestion which may cause hemolytic anemia and jaundice. Several methods of screening and diagnosis of G6PD can be performed to avoid morbidity and mortality.