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Clinical Profile of Scabies in Children in the Outpatient Installation of Dr. Moewardi General Hospital Surakarta, the Period of January 2015- December 2019 Eka Devinta Novi Diana; Alfina Rahma; Frieda; Indah Julianto; Moerbono Mochtar; Suci Widhiati
Indian Journal of Forensic Medicine & Toxicology Vol. 15 No. 4 (2021): Indian Journal of Forensic Medicine & Toxicology
Publisher : Institute of Medico-legal Publications Pvt Ltd

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37506/ijfmt.v15i4.16841

Background: Scabies is caused by parasite, called Sarcoptes scabiei, infestation into the skin. Scabies isgenerally found in children who live in crowded environments and poor hygiene.Methods: This is a retrospective descriptive study with secondary data collection from medical record datain the Outpatient Installation of RSDM for the period January 2015-December 2019. The subjects wereinfants to children aged 14 years with a diagnosis of scabies. Data variables used included age, gender,family history of scabies, diagnosis, comorbidities, supporting examinations and, therapy in scabies patients.Results: There were 88 pediatric patients with scabies. The most age group that experienced child scabieswas 11-14 years (33%) with the most sex being male (55%). The largest source of scabies transmission wasfrom the family (39%). The most common lesion morphology was papules and excoriations (49%). Thelesion location was found mostly between the fingers (24%). Examination of skin scrapings using NaCl0.9% was positive only in 5 patients (6%) with the most diagnosis was scabies (77%)Conclusion: This study shows that most of pediatric patients with scabies in the 11-14 years range aredominated by males. The most common sources of infection were families with papule morphology andexcoriation, whereas the most lesions were found between the fingers. Skin scrapings are only positive 6%of cases. The most commonly used topical therapies are 5% permethrin and 2% ointment mupirocin whilethe systemic therapies are cetirizine and cefadroxil.

GAMBARAN DEPOSISI KOLAGEN TIPE I TERHADAP USIA TIKUS GALUR WISTAR: PENELITIAN IN VIVO Frieda Yanuar; Indah Julianto; Nugrohoaji Dharmawan; Arie Kusumawardani; Novan Adi; Endra Yustin Ellistasari
Medika Kartika : Jurnal Kedokteran dan Kesehatan Vol 5 No 2 (2022): Medika Kartika : Jurnal Kedokteran dan Kesehatan
Publisher : Fakultas Kedokteran Universitas Jenderal Achmad Yani

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (379.183 KB)

Penuaan kulit merupakan akumulasi berbagai perubahan progresif yang terjadi pada sel dan jaringan kulit. Kulit manusia terdiri matriks ekstraseluler (MES) dermal dengan protein penyusunnya adalah kolagen. Selama penuaan, kolagen tipe I mengalami perubahan organisasi dan struktural, penurunan sintesis protein MES, dan terjadi peningkatan degradasi metaloproteinase mengakibatkan hilangnya kekuatan mekanik. Studi menunjukkan peran penurunan fungsi penghalang kulit terkait usia dalam penuaan pada tikus. Tujuan penelitian ini untuk mengetahui deposisi kolagen tipe I berdasarkan usia pada jaringan kulit tikus Wistar. Desain penelitian merupakan observasional analitik cross-sectional. Penelitian menggunakan tikus Wistar yang telah memenuhi kriteria inklusi dan eksklusi. Tikus dikelompokkan menjadi kelompok usia 3 bulan, 6 bulan, 12 bulan, dan 18 bulan. Pengambilan jaringan kulit dengan biopsi plong dilanjutkan pembuatan preparat dengan pewarnaan Trichome masson. Perhitungan deposisi kolagen dilakukan pada area berwarna biru dan diinterpretasikan (%) menggunakan software ImageJ. Rerata persentase deposisi kolagen terbesar pada kelompok usia 3 bulan dengan nilai 57,6±0,17% dan 57,5±0,43% pada pembesaran 40x dan 100x. Persentase deposisi kolagen terendah terdapat pada kelompok usia 18 bulan dengan nilai 12,1±1,6% dan 6,9±0,52% pada pembesaran 40x dan 100x. Pada penelitian ini dapat disimpulkan bahwa terdapat penurunan deposisi kolagen jaringan kulit tikus Wistar seiring dengan pertambahan usia akibat proses penuaan, dengan deposisi kolagen jaringan kulit tikus Wistar kelompok usia muda lebih besar dibandingkan kelompok usia yang lebih tua. DOI : 10.35990/mk.v5n2.p183-194

Pengaruh Astaxantine Oral terhadap Kadar Serum Tumor Necrosis Factor Alpha pada Pasien Akne Vulgaris-lores Reti Anggraeni; Niluh Widjayanti; Harijono Kariosentono; Indah Julianto; Endra Yustin; Muhammad Eko Irawanto; Prasetyadi Mawardi
MEDICINUS Vol. 33 No. 3 (2020): MEDICINUS
Publisher : PT Dexa Medica

Background: Acne vulgaris (AV) is chronic inflammatory disease affecting the pilosebaceous unit manifested as closed and open comedones, papules, pustules, and nodules. Treatment of AV generally involves more than one drug due to multifactorial pathogenesis. Objective: This study aims to determine the efficacy of 4 mg oral astaxanthin as an adjuvant AV therapy in decreasing serum level of inflammatory marker tumor necrosis factor alpha (TNF-α). Method: This is a double-blind randomized controlled trial. Subjects were 34 patients with mild and moderate AV (Global Acne Grading System/GAGS 1-30) that were treated with combination of tretinoin 0.025% and clindamycin phosphate 1.2%. Astaxanthin was added to the treatment group and lactulose as placebo was added to the control groups, given for 4 weeks. The pretest and posttest results in both groups were analyzed statistically using nonparametric test. Results: Decrease in TNF-α serum levels occurred in both groups but significant difference compared to baseline were only found in treatment group (p=0.015). There was no significant difference in the reduction of TNF-α levels between both groups (p=0.459). Conclusion: Although the results did not show a significant difference overall, but in the treatment group, astaxanthin can significantly lower TNF-α serum levels compared to baseline.

Modalitas Terapi Vitiligo pada Anak Nathania Amelinda; Endra Yustin Ellistasari; Indah Julianto
MEDICINUS Vol. 35 No. 3 (2022): MEDICINUS
Publisher : PT Dexa Medica

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.56951/medicinus.v35i3.106

itiligo is a pigmentation disorder characterized by depigmented patches on skin and hair due to functional loss of melanocytes. Vitiligo in children is generally associated with other autoimmune diseases and has serious cosmetic and psychosocial impact. Treatment modalities for vitiligo in children consist of topical therapy, phototherapy, systemic therapy, and surgery. Vitiligo in children has a relatively good prognosis compared to adult cases. Repigmentation in childhood vitiligo usually happen spontaneously and relapses are rare.

Modalitas Terapi Striae Ambar Aliwardani; Putti Fatiharani Dewi; Fiska Rosita; Indah Julianto
MEDICINUS Vol. 36 No. 2 (2023): MEDICINUS
Publisher : PT Dexa Medica

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.56951/medicinus.v36i2.124

Striae or strechmark is a form of benign skin lesion manifested as inflammatory streaks perpendicular to the direction of skin tension which has cosmetic morbidity and possesses risk of secondary infection in severe case. Various therapeutic modalities have been introduced, such as topical therapy, physical therapy using devices, lasers, and the latest is celullar therapy using platelet-rich plasma. Such varied treatment modalities are reported to have varied results.

UVB-Induced Oxidative Collapse and Melanogenic Activation in a Rat Model of Cutaneous Hyperpigmentation: A Multi-Parametric Analysis Sesia Pradestine; Endra Yustin Ellistasari; Nurrachmat Mulianto; Indah Julianto; Muhammad Eko Irawanto; Nugrohoaji Dharmawan
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 11 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i11.1442

Background: Ultraviolet B (UVB) radiation is a primary driver of cutaneous hyperpigmentation disorders, with oxidative stress recognized as a key pathogenic mechanism. However, a comprehensive, multi-level characterization of the causal link between chronic UVB exposure and the resulting oxidative, histological, and melanogenic responses is needed. This study aimed to quantitatively validate a preclinical model of UVB-induced hyperpigmentation by characterizing the reciprocal regulation of key oxidative stress biomarkers and correlating these changes with objective histological evidence of hyperpigmentation. Methods: This controlled in vivo experimental study used 14 male Sprague Dawley rats, divided into a control group (KN; n=7) and a UVB-exposed group (KP; n=7). The KP group received chronic UVB radiation (300 mJ/cm² daily, 5 days/week for 4 weeks). Dorsal skin tissue was harvested for analysis. Oxidative stress was assessed by quantifying malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels via ELISA. Hyperpigmentation was objectively validated and quantified using Fontana-Masson staining for melanin deposition and immunohistochemistry for microphthalmia-associated transcription factor (MITF). Results: Chronic UVB exposure induced significant hyperpigmentation, confirmed by a 5.8-fold increase in epidermal melanin content (p < 0.001) and a 4.1-fold increase in the number of MITF-positive melanocytes (p < 0.001) in the KP group. This was accompanied by a profound oxidative imbalance: MDA levels increased by 7.5-fold (p < 0.001), while the activities of SOD, CAT, and GPx decreased by 80.5%, 65.2%, and 71.4%, respectively (all p < 0.001). A strong negative correlation was observed between MDA and all antioxidant enzymes, particularly SOD (r = -0.985, p < 0.001). Conclusion: Chronic UVB exposure directly triggers a collapse of the cutaneous antioxidant network, leading to severe lipid peroxidation. This state of profound oxidative stress is causally linked to melanocyte activation and excessive melanin synthesis, driving the hyperpigmentation phenotype. This robustly validated preclinical model provides a powerful platform for investigating the molecular pathophysiology of UVB-induced pigmentary disorders and for evaluating novel therapeutic interventions.

UVB-Induced Oxidative Collapse and Melanogenic Activation in a Rat Model of Cutaneous Hyperpigmentation: A Multi-Parametric Analysis Sesia Pradestine; Endra Yustin Ellistasari; Nurrachmat Mulianto; Indah Julianto; Muhammad Eko Irawanto; Nugrohoaji Dharmawan
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 11 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i11.1442

Background: Ultraviolet B (UVB) radiation is a primary driver of cutaneous hyperpigmentation disorders, with oxidative stress recognized as a key pathogenic mechanism. However, a comprehensive, multi-level characterization of the causal link between chronic UVB exposure and the resulting oxidative, histological, and melanogenic responses is needed. This study aimed to quantitatively validate a preclinical model of UVB-induced hyperpigmentation by characterizing the reciprocal regulation of key oxidative stress biomarkers and correlating these changes with objective histological evidence of hyperpigmentation. Methods: This controlled in vivo experimental study used 14 male Sprague Dawley rats, divided into a control group (KN; n=7) and a UVB-exposed group (KP; n=7). The KP group received chronic UVB radiation (300 mJ/cm² daily, 5 days/week for 4 weeks). Dorsal skin tissue was harvested for analysis. Oxidative stress was assessed by quantifying malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels via ELISA. Hyperpigmentation was objectively validated and quantified using Fontana-Masson staining for melanin deposition and immunohistochemistry for microphthalmia-associated transcription factor (MITF). Results: Chronic UVB exposure induced significant hyperpigmentation, confirmed by a 5.8-fold increase in epidermal melanin content (p < 0.001) and a 4.1-fold increase in the number of MITF-positive melanocytes (p < 0.001) in the KP group. This was accompanied by a profound oxidative imbalance: MDA levels increased by 7.5-fold (p < 0.001), while the activities of SOD, CAT, and GPx decreased by 80.5%, 65.2%, and 71.4%, respectively (all p < 0.001). A strong negative correlation was observed between MDA and all antioxidant enzymes, particularly SOD (r = -0.985, p < 0.001). Conclusion: Chronic UVB exposure directly triggers a collapse of the cutaneous antioxidant network, leading to severe lipid peroxidation. This state of profound oxidative stress is causally linked to melanocyte activation and excessive melanin synthesis, driving the hyperpigmentation phenotype. This robustly validated preclinical model provides a powerful platform for investigating the molecular pathophysiology of UVB-induced pigmentary disorders and for evaluating novel therapeutic interventions.

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