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Abstrak :
ABSTRAK
Latar belakang. Di Sumatera Barat didapatkan peningkatan kasus infeksi virus dengue. Beberapa kasus juga terjadi pada bayi ≤ 1 tahun. Bayi mempunyai karakteristik klinik yang unik dan tidak banyak penelitian mengenai hal ini di Indonesia. Tujuan. Mengetahui profil klinis, laboratorium dan serologi infeksi virus dengue pada bayi yang di rawat di RSUP Dr. M Djamil Padang dari tahun 2012-2014 Metode. Penelitian cross-sectional, menggunakan data rekam medic bayi IVD yang dirawat di RSUP Dr M Djamil Padang dari 1 Januari 2012-31 Desember 2014. Data yang dianalisis mencakup usia, jenis kelamin, hari demam saat diagnosis, suhu, demam, batuk, diare, muntah, kejang, hematemesis, melena, syok, ptekie, and hepatomegali. Hasil. 12 bayi digunakan sebagai sampel. Usia termuda bayi DBD adalah 3 bulan, dengan usia terbanyak 5 bulan (5 bayi). Muntah merupakan gejala tambahan yang paling banyak ditemukan (9 dari 12 bayi), diikuti oleh ptekie dan syok (masing-masing 6 bayi), serta batuk (5 bayi). 8 dari 12 bayi menunjukkan infeksi primer Kesimpulan. Rerata usia dan kelompok usia terbanyak setara dengan penelitian sebelumnya.

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ABSTRACT
Background. In West Sumatera, cases of dengue virus infection is increasing. Some occur in infants below 1 year old. Babies has unique clinical characteristic and only few researchs take place on this subject in Indonesia. Objection. Describing the clinical, laboratory, and serology profile of dengue virus infection in infants taken care at Dr. M Djamil Hospital in Padang, West Sumatera from 2012 to 2014. Methods. This is a cross-sectional study based on medical record data on baby who were treated in Dr M Djamil Padang from January 1st, 2012 to December 31st, 2014. The data analyzed were age, gender, fever duration at diagnosis, body temperature, fever, cough, diarrhea, vomit, seizure, hematemesis, melena, shock, ptekie, and hepatomegaly. Results. 12 babies were collected as sample. Youngest baby had DHF was 3 months old, while the oldest was 5 months old (5 infants). Vomit is the additional symptom most commonly found (9 of 12 infants), followed by ptekie and shock (6 babies each), and cough (5 infants). Eight of 12 infants showed primary infection. Conclusion. The mean for age and mode for age group were similar to previous studies

Abstrak :
ABSTRAK
Pada operasi koreksi penyakit jantung bawaan PJB dengan teknik pintas jantung paru PJP , proses sindrom respons inflamasi sistemik SRIS sering menjadi penyulit pascaoperasi. Disfungsi mitokondria pada SRIS diawali dengan pelepasan mediator inflamasi TNF-. Dampak cedera neurologis pascabedah belum dapat dihindari. Biomarker Brain derived protein S100B dapat digunakan sebagai penanda hipoksia serebral akibat disfungsi mikrosirkulasi dan mitokondria pada operasi PJB. Pemantauan keadaan hipoksia serebral diperlukan karena kejadian awal defisit neurologis sering tidak menimbulkan manifestasi klinis. Near infrared spectroscopy NIRS merupakan salah satu alat yang dapat memantau penghantaran oksigen ke otak dengan mengukur saturasi oksigen serebral SctO 2 . Penelitian ini bertujuan untuk mengevaluasi peran S100B, sTNFR-1, laktat, saturasi vena cava superior dan saturasi oksigen serebral sebagai prediktor kejadian defisit neurologis pada operasi koreksi PJB. Penelitian ini bersifat kohort propsektif. Kriteria inklusi adalah pasien anak dengan PJB usia 1 bulan minus;6 tahun yang menjalani operasi koreksi. Kriteria eksklusi adalah pasien anak dengan sindrom Down, dengan arteri koroner tunggal, dan yang orang tuanya menolak berpartisipasi dalam penelitian. Dalam analisis, subjek dibagi menjadi 2 kelompok yakni kelompok 1 mengalami defisit neurologis dan kelompok 2 tidak mengalami defisit neurologis . Semua subjek dipantau selama perawatan di ICU, dan tetap diikuti sampai keluar rumah sakit. Pemeriksaan darah dilakukan dalam tiga kali pemantauan: pra-operasi, akhir PJP, dan 4 jam pasca-PJP. Monitoring NIRS dilakukan selama 24 jam pascabedah di ICU. Selama periode Maret 2015 minus;Oktober 2015, didapatkan 51 pasien yang diteliti. Terdapat perbedaan proporsi yang bermakna antara konsentrasi S100B, sTNFR-1, laktat, dan NIRS AUC 20 baseline saturasi serebral pasien PJB pascabedah koreksi dengan PJP pada kelompok berdasarkan defisit neurologis. Parameter tersebut dapat dipakai sebagai model prediktor kejadian defisit neurologis pascabedah jantung dengan PJP. Nilai S100B, sTNFR-1, laktat, dan nilai NIRS AUC 20 dari baseline saturasi serebral dapat digunakan sebagai prediktor kejadian defisit neurologis pascabedah pada operasi PJB dengan mesin PJP.

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In congenital heart disease CHD surgery using cardiopulmonary bypass CPB machine, systemic inflammation response syndrome SIRS process often causes post-operation complication. Mitochondria dysfunction in SRIS starts with the release of inflammation mediator TNF-? and sTNFR-1. Neurological injury after pediatric congenital heart surgery still cannot be avoided. Study about brain derived protein S100B as a biomarker for cerebral hypoxia caused by microcirculation and mitochondria disfunction as SRIS consequence in PJP in pediatric CHD surgery has yet to be conducted. Observation to find cerebral hypoxia is needed because the early stages of cerebral hypoxia often not show any symptoms. NIRS is one of the tools for observing oxygen delivery to the brain by measuring the cerebral oxygen saturation SctO 2 . In Indonesia, NIRS is still not common to be used and there are no studies about it yet. This study aimed to evaluate the role of S100B, sTNFR-1, lactate, saturation of superior vena cava and cerebral saturation as the predictor of neurological deficiency incidence on correction of CHD. This was a prospective cohort research. Inclusion criteria were children with CHD aged 1 month minus;6 years old who underwent corrective operation. Exclusion criterias were children with Down syndrome, with single coronary artery, and whose parents declined to participate in this study. In analysis, subjects were divided into 2 groups; group 1 with neurological deficit and group 2 without neurological deficit. All subjects were observed closely while they were in ICU, observed until they discharge from hospital. Blood examination were done 3 times: before surgery, after CPB, and 4 hours after CPB. Monitoring of NIRS was done during 24 hours after surgery in ICU. During March minus;October 2015, there were 51 patients included. There are significant difference for value of S100B, STNFR-1, lactate, and NIRS AUC 20 baseline of cerebral saturation between groups based on neurological deficit occurrence. Those parameters could be used as predictor of neurologic deficiency incidence post operation using CPB in CHD children. In CHD patients who underwent corrective operation with CPB, S100B value, sTNFR1, lactate, and AUC 20 baseline of cerebral saturation could be used as predictor of neurologic deficit after corrective operation.

Abstrak :
Latar belakang: Rekomendasi Centers for Disease Control and Prevention (CDC) 2010 (revisi 2002) tidak spesifik memberi panduan dalam pencegahan sekunder sepsis awitan dini (SAD) pada neonatus cukup bulan (NCB), asimtomatik lahir dari ibu yang mengalami KPD < 18 jam. Tujuan: Didapatnya model determinan SAD pada NCB sesuai masa kehamilan (SMK), asimtomatik lahir dari ibu yang mengalami KPD lebih dari 12 jam. Metodologi: penelitian observasional potong lintang untuk mendapatkan model determinan sepsis neonatorum awitan dini (SNAD) yang dilakukan dari Februari 2013 sampai bulan Mei 2014 di RSAB Harapan Kita, RSUD Tarakan, RSIA Budi Kemuliaan. Determinan yang diteliti adalah jenis persalinan, petanda infeksi saluran kemih (ISK) pada ibu, petanda infeksi intra amnion (IIA) seperti demam intrapartum, ibu takikardia, janin takikardia, adanya perubahan warna dan bau cairan ketuban, leukosit darah ibu, dan petanda infeksi darah tali pusat (peningkatan jumlah total leukosit, neutrofil, peningkatan rasio I/T, hs-CRP dan IL-6). Diagnosis sepsis ditegakkan berdasarkan catatan medis bayi yang dipastikan berdasarkan hasil positif biakan darah tali pusat. Model determinan SNAD yang dihasilkan adalah suatu persamaan regresi logistik yang digunakan untuk menentukan probabilitas terjadinya SNAD sebagai acuan terapi antibiotik. Hasil: model determinan SAD pada NCB SMK, asimtomatik lahir dari ibu KPD > 12 jam berupa kalkulator dan sistem skor yang dibentuk dari determinan persalinan per vaginam, perubahan warna dan bau cairan ketuban, leukosit darah ibu, leukosit darah tali pusat, kadar hs-CRP darah tali pusat dan kadar IL-6 darah tali pusat. Model determinan SNAD memiliki dua varian, varian lengkap digunakan untuk fasilitas pelayanan neonatus subspesialistik dan varian alternatif digunakan untuk fasilitas pelayanan spesialistik. Titik potong ideal penentuan probabilitas terjadinya SNAD memiliki sensitivitas di antara 24,2 – 40,3 % dan spesifisitas 87,1 - 94,5 %. Nilai diskriminasi dengan nilai AUC berkisar di antara 0,743 – 0,816 dengan kalibrasi baik berdasarkan uji Hosmer-Lemeshow. Simpulan: Hasil penelitian ini adalah model determinan SAD pada NCB SMK asimtomatik lahir dari ibu yang mengalami KPD > 12 jam, berbentuk kalkulator dan sistem skor yang memiliki varian lengkap dan alternatif untuk menentukan probabilitas terjadinya SNAD sebagai dasar pemberian terapi antibiotik empiris secara rasional. ......Background: Centers for Disease Control and Prevention (CDC) 2010 (revised 2002) recommendations does not specifically provide guidance in secondary prevention of asymptomatic early-onset sepsis (EOS) on term infant born to mother experiencing PROM < 18 hours. Objective: to develop early-onset neonatal sepsis (EONS) determinant model as a rational basis for determining the empirical antibiotic therapy in asymptomatic, term infant born to mother with PROM > 12 hours. Method: A cross-sectional observational study to obtain an EONS determinant model which was conducted from February 2013 to May 2014 in RSAB Harapan Kita, Tarakan Hospital, RSIA Budi Kemuliaan. The determinant factor is the type of delivery, marker of maternal urinary tract infection (UTI), intra-amniotic infection markers (intrapartum fever, maternal tachycardia, fetal tachycardia, change in the color and odor of amniotic fluid, maternal blood leukocytes), and umbilical cord blood infection marker (increased the total number of leukocytes, neutrophils, an increase in the ratio of I / T, hs-CRP and IL-6). Early-onset neonatal sepsis was diagnosed base on infant medical record on 72 hours afeter birth and confirmed by the positive results of umbilical cord blood cultures. The resulting of EONS determinants model is a logistic regression equation used to determine the probability of the occurrence of EONS as reference rational basis empirical antibiotic therapy. Results: The EOS determinants model on asymptomatic term infant born to mothers with PROM> 12 hours is a calculator and scoring system that is formed from the determinant of vaginal delivery, change the color and odor of amniotic fluid, maternal blood leukocytes, cord blood leukocytes, the levels of hs-CRP and IL-6 umbilical cord blood level. Early-onset neonatal sepsis determinant model has two variants, the full variant used for subspecialty neonatal care facilities and alternative variant is used for specialty neonatal care facilities. Ideal cutoff point probability of occurrence SNAD has sensitivity range of 24.2 to 40.3% and specificity of 87.1 to 94.5%. The model performe is good based on Hosmer-Lemeshow test anda discrimination value AUC in in range of 0.743 to 0.816. Conclusion: The EOS determinant model of asymptomatic term infant born to mothers with PROM > 12 hours is a calculator and scoring system that is used to determine the probability of EONS occurrence as the basis of determining the rational empirical antibiotic therapy.

Abstrak :
ABSTRAK
Patomekanisme dermatitis atopik melibatkan interaksi yang kompleks antara genetik dan lingkungan. Satu gen yang secara konsisten berhubungan dengan DA adalah mutasi gen Filaggrin yang dapat mengganggu agregasi sitoskeleton epidermis. Beberapa usaha pencegahan telah dilakukan antara lain dengan pemberian ASI eksklusif dan suplementasi LCPUFA, tetapi studi klinis dan meta-analisis tidak menunjukkan hasil yang konsisten. Inkonsistensi ini dapat disebabkan adanya variasi aktivitas enzim desaturase yang dapat memodulasi metabolisme PUFA, yang diatur oleh gen FADS1 dan FADS2, serta usia saat intervensi dilakukan. Diperkirakan periode in-utero memegang peran penting untuk keberhasilan intervensi. Penelitian ini bertujuan mengetahui peran mutasi gen FLG dan polimorfisme gen FADS1 dan FADS2 terhadap timbulnya DA pada usia satu tahun. Tujuan Khusus yaitu mengetahui frekuensi mutasi gen FLG dan polimorfisme gen FADS1 dan FADS2, mengetahui peran polimorfisme gen FADS1 dan FADS2 terhadap substrat dan produk LCPUFA dan efeknya terhadap timbulnya DA, mengetahui pengaruh peningkatan rasio AA terhadap DHA di awal kehidupan terhadap timbulnya DA, mengetahui peran protektif ASI eksklusif untuk pencegahan DA. Digunakan dua desain penelitian 1) potong lintang untuk mengetahui peran polimorfisme gen FADS1 dan FADS2 terhadap perubahan komposisi LCPUFA saat lahir, 2) analisis kesintasan untuk melihat pengaruh mutasi gen Filaggrin dan polimorfisme gen FADS1 dan FADS2 terhadap timbulnya DA, mengetahui peran peningkatan rasio AA/DHA serta mengetahui efek protektif ASI eksklusif terhadap timbulnya DA pada usia satu tahun. Insidens DA dalam penelitian ini sebesar 15,4%. Tidak ditemukan 5 mutasi gen Filaggrin sesuai dengan data NCBI. Frekuensi alel minor pada polimorfisme gen FADS1 22−27%, sedangkan untuk FADS2 berkisar 15−48%. Dalam penelitian ini terlihat pengaruh polimorfisme gen FADS1 dan FADS2 terhadap perubahan komposisi LCPUFA, khususnya peningkatan asam arakidonat pada kelompok alel minor. Dalam penelitian ini tidak ditemukan hubungan antara komposisi LCPUFA dan polimorfisme gen FADS terhadap timbulnya DA. Pemberian ASI eksklusif selama 3−6 bulan tampaknya memberi efek proteksi terhadap DA PeneIitian ini diharapkan dapat menjadi landasan untuk tindakan pencegahan DA. Penelitian ini tidak berhasil menemukan common mutation yang dilaporkan NCBI. Mutasi gen Filaggrin tergantung perbedaan ras, maka untuk menemukan mutasi yang baru lebih baik digunakan sekuensing gen secara penuh. Adanya perbedaan frekuensi alel minor antara anak Indonesia dan Eropa dan aktivitas enzim yang bekerja dengan arah yang berlawanan dengan alel minor populasi Eropa, mengakibatkan peningkatan kadar AA dan DGLA pada populasi alel minor dalam penelitian ini.

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ABSTRACT
Pathomechanism of atopic dermatiis is linked to the gene-environment interactions. One genetic locus consistently linked with AD is mutations of filaggrin gene that can induce disruption in epidermal cytoskeleton aggregation. Some protective measures for the prevention of AD are breastfeeding and the provision of LCPUFA, but clinical studies and meta-analysis have shown inconsistent results, which maybe due variation in the activity of desaturating enzymes modulating PUFA metabolism, which are encoded by the FADS1 and FADS2 gene cluster and the age at which LCPUFA interventions are provided. The general objective is to characterize the impact of genetic variation in the FLG and FADS1, FADS2 genes cluster on LC-PUFA concentration in Indonesian infants. Specific objectives including the characterization of the frequency of FLG and FADS1, FADS2 gene single nucleotide polymorphisms (SNPs), the influence of FADS gene polymorphisms on fatty acid composition and on the occurence of AD, the impact of increasing ratio of arachidonic acid to docosahexaenoic acid on the progression of AD, and to see the protective effect of exclusive breastfeeding for the prevention of AD in the first year of life in Indonesian infants. Designs were 1) cross-sectional study to see the role of FADS1 and FADS2 gene polymorphism on the composition of LCPUFA at birth, 2) survival analysis to see the role of FLG mutation and FADS1 and FADS2 gene polymorphism on the progression of AD, the role of increasing ratio of AA/DHA and the protective effect of exclusively breastfeeding on the occurence of AD in the first year of life. The incidence of AD in this study is 15.4%, No Filaggrin gene mutations based on 5 reported pathogenic SNP was found. The minor allele frequency of FADS1 gene polymorphism were 22−27%, whereas for FADS2 were 15−48%. We found a strong correlation between FADS gene polymorphisms with the changes of LCPUFA composition, especially for the increment of arachidonic acid. No association was found between the composition of LCPUFA and between FADS genes polymorphisms with AD. Exclusive breastfeeding until 3 months was found to be protective against AD. In this study we did not find Filaggrin mutation that reported as pathogenic from NCBI. The frequency of FADS1 polymorphism were 22−27%, whereas FADS2 polymorphism were 15−48%. Strong correlation was seen between genetic variations of FADS genes with the alteration of LCPUFA. Arachidonic acid as the product of LCPUFA was higher in the minor allele compared with the major allele. No association were found between genetic variation of FADS genes and the increased ratio of AA/DHA with the occurence of AD. Exclusive breastfeeding for 3−6 months seems to give protective effect