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From Patches to Plaques: A Diagnostic Challenge in a Case of Erythroderma Secondary to Pityriasis Rubra Pilaris Kamilah, Lian; Rahmat Firdaus Dwi Utama; Shelly Lavenia Sambodo; Muhammad Eko Irawanto
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 6 (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.v9i6.1297

Background: Erythroderma, a dramatic and potentially life-threatening condition characterized by fiery redness engulfing over 90% of the skin's surface, presents a formidable diagnostic challenge due to its myriad underlying causes. Among these, pityriasis rubra pilaris (PRP), a rare inflammatory skin disorder, stands out with its distinctive features and often perplexing presentation. This case unveils the intricate diagnostic journey of a young man whose erythroderma masked an underlying PRP, further complicated by the subtle interplay of stress. Case presentation: An 18-year-old male presented with a one-month history of alarming erythroderma accompanied by distressing itching, fever, and sleep disturbances. Adding to the complexity, he exhibited characteristic 'nappes claires' – islands of normal skin amidst the erythrodermic sea – a hallmark of PRP. Palmoplantar keratoderma, alopecia areata, and ectropion further painted an intriguing clinical picture. Histopathological examination revealed the telltale 'checkboard' pattern, confirming PRP as the culprit. Notably, the patient's history revealed a compelling link between stress and disease exacerbation, adding a psychosomatic dimension to the case. Systemic corticosteroids and methotrexate, alongside topical emollients, brought about significant clinical improvement, underscoring the importance of early diagnosis and targeted treatment. Conclusion: This case underscores the critical need to consider PRP in the labyrinth of erythroderma diagnoses, particularly when 'nappes claires' and a history of stress are intertwined. By shining a light on the diagnostic subtleties and therapeutic nuances of PRP-associated erythroderma, this report empowers clinicians to navigate the complexities of this rare and challenging condition, ultimately improving patient outcomes and quality of life.

From Patches to Plaques: A Diagnostic Challenge in a Case of Erythroderma Secondary to Pityriasis Rubra Pilaris Kamilah, Lian; Rahmat Firdaus Dwi Utama; Shelly Lavenia Sambodo; Muhammad Eko Irawanto
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 6 (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.v9i6.1297

Background: Erythroderma, a dramatic and potentially life-threatening condition characterized by fiery redness engulfing over 90% of the skin's surface, presents a formidable diagnostic challenge due to its myriad underlying causes. Among these, pityriasis rubra pilaris (PRP), a rare inflammatory skin disorder, stands out with its distinctive features and often perplexing presentation. This case unveils the intricate diagnostic journey of a young man whose erythroderma masked an underlying PRP, further complicated by the subtle interplay of stress. Case presentation: An 18-year-old male presented with a one-month history of alarming erythroderma accompanied by distressing itching, fever, and sleep disturbances. Adding to the complexity, he exhibited characteristic 'nappes claires' – islands of normal skin amidst the erythrodermic sea – a hallmark of PRP. Palmoplantar keratoderma, alopecia areata, and ectropion further painted an intriguing clinical picture. Histopathological examination revealed the telltale 'checkboard' pattern, confirming PRP as the culprit. Notably, the patient's history revealed a compelling link between stress and disease exacerbation, adding a psychosomatic dimension to the case. Systemic corticosteroids and methotrexate, alongside topical emollients, brought about significant clinical improvement, underscoring the importance of early diagnosis and targeted treatment. Conclusion: This case underscores the critical need to consider PRP in the labyrinth of erythroderma diagnoses, particularly when 'nappes claires' and a history of stress are intertwined. By shining a light on the diagnostic subtleties and therapeutic nuances of PRP-associated erythroderma, this report empowers clinicians to navigate the complexities of this rare and challenging condition, ultimately improving patient outcomes and quality of life.

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.

Fulminant Perianal Donovanosis Manifesting as Septic Shock in a Treatment-Naïve AIDS Patient: A Clinico-Pathological Case Report Rahmat Firdaus Dwi Utama; Muhammad Eko Irawanto; Ayu Kusuma Dewi; Shelly Lavenia Sambodo; Stella Gracia Octarica; Sugih Primas Adjie
Open Access Indonesian Journal of Medical Reviews Vol. 5 No. 6 (2025): Open Access Indonesian Journal of Medical Reviews
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/oaijmr.v5i6.799

Donovanosis (Granuloma Inguinale), caused by Klebsiella granulomatis, is a rare sexually transmitted infection that can follow a devastating course in severely immunocompromised individuals. Its clinical progression in the context of advanced acquired immunodeficiency syndrome (AIDS) is not extensively documented. We present a case of fulminant donovanosis to illustrate its potential for rapid systemic deterioration and mortality. A 20-year-old Indonesian man, with a recent diagnosis of human immunodeficiency virus (HIV) for which he was treatment-naïve, presented with a two-month history of extensive, painful perianal ulcerations. Clinical examination revealed large, coalescing, "beefy-red" ulcers in the perianal and gluteal regions. Laboratory investigations confirmed profound immunosuppression (CD4+ T-cell count: 3 cells/µL; HIV viral load: >750,000 copies/mL). The diagnosis of donovanosis was definitively established by the microscopic identification of pathognomonic intracellular Donovan bodies on a Giemsa-stained tissue smear, with findings corroborated by histopathological analysis of a skin biopsy. Despite the initiation of appropriate antibiotic and supportive therapy, the patient's condition rapidly progressed to septic shock and multi-organ dysfunction syndrome, leading to his death within six days of hospital admission. In conclusion, this case highlights the aggressive, life-threatening nature of donovanosis in the setting of advanced AIDS. The profound collapse of cell-mediated immunity likely facilitated uncontrolled bacterial replication and systemic dissemination, rendering standard antibiotic therapy ineffective. This report serves as a critical clinical reminder to maintain a high index of suspicion for donovanosis in immunocompromised patients presenting with atypical anogenital ulcers, as early diagnosis and aggressive multimodal management are paramount.

The Differential Biopsychosocial Burden of Psoriasis and Vitiligo: A Comparative Analysis of Participation Restriction and its Clinical and Psychiatric Correlates Nurrachmat Mulianto; Shelly Lavenia Sambodo; Muhammad Eko Irawanto; Arie Kusumawardani
Open Access Indonesian Journal of Medical Reviews Vol. 5 No. 6 (2025): Open Access Indonesian Journal of Medical Reviews
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/oaijmr.v5i6.805

Visible skin diseases like psoriasis vulgaris and vitiligo impose a significant psychosocial burden. However, the comparative impact on real-world functioning and the interplay of clinical, social, and psychiatric factors remain poorly understood, particularly in non-Western populations. This study aimed to quantitatively compare participation restriction between these two conditions and to identify its key biopsychosocial predictors. This comparative cross-sectional study, conducted in a tertiary Indonesian hospital, enrolled 50 patients (25 with psoriasis vulgaris, 25 with non-segmental vitiligo). The primary outcome was participation restriction, measured by the 18-item Participation Scale (P-Scale). Clinical severity was assessed using the Psoriasis Area and Severity Index (PASI) and Vitiligo Area Scoring Index (VASI). Crucially, depressive and anxiety symptoms were screened using the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) scale, respectively. A hierarchical multiple linear regression analysis was performed to identify predictors of participation restriction. Patients with psoriasis reported profoundly higher mean P-Scale scores (43.16 ± 5.01) compared to those with vitiligo (25.72 ± 4.21; p < 0.001), indicating more severe restrictions. Psoriasis patients also exhibited significantly higher scores for depressive symptoms (PHQ-9: 11.52 ± 3.18 vs. 5.68 ± 2.29; p < 0.001) and anxiety symptoms (GAD-7: 10.24 ± 2.95 vs. 5.12 ± 2.15; p < 0.001). The hierarchical regression model was highly significant (F(7, 42) = 28.14, p < 0.001), explaining 82.4% of the variance in P-Scale scores. After controlling for demographic and clinical factors, a diagnosis of psoriasis (β = 0.45, p < 0.001), higher clinical severity (β = 0.28, p = 0.002), and higher depressive symptom severity (PHQ-9 score; β = 0.39, p < 0.001) were significant independent predictors of greater participation restriction. In conclusion, psoriasis vulgaris is associated with a dramatically greater burden of participation restriction than vitiligo. This burden is driven by a complex interplay of the disease's clinical severity, its inherent diagnosis-specific factors, and, critically, comorbid depressive symptoms. These findings underscore the necessity of a biopsychosocial approach in dermatology, advocating for routine mental health screening and integrated care models to address the multifaceted drivers of disability in patients with chronic inflammatory skin disease.

Dose- and Time-Dependent Efficacy of Topical Hydroquinone in Establishing a C57BL/6 Mouse Model of Vitiligo Benedikta Lauda; Nurrachmat Mulianto; Endra Yustin Ellistasari; Muhammad Eko Irawanto
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 10 No. 1 (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.v10i1.1481

Background: Vitiligo is a complex autoimmune depigmenting disorder driven by melanocyte-specific CD8+ T cells, oxidative stress, and genetic susceptibility. The lack of standardized, accessible animal models that recapitulate these pathways hinders therapeutic development. This study aimed to systematically optimize and validate a chemically-induced vitiligo model in C57BL/6 mice. Methods: Eighty (80) male C57BL/6 mice were randomized into ten groups (n=8/group). Experimental groups received once-daily topical applications of hydroquinone (HQ) at 2.5%, 5%, or 10%, or monobenzone (MBZ) at 40% for 8 or 16 days. Vehicle-treated mice served as controls. Efficacy was assessed via quantitative histopathology (Masson-Fontana staining for melanin area), biomolecular assays for oxidative stress (Malondialdehyde [MDA] and Superoxide Dismutase [SOD]), and RT-qPCR for melanogenesis-related (Tyr) and inflammation-related (Tnf) gene expression. Results: A clear dose- and time-dependent depigmentation was observed. The 10% HQ 16-day protocol was maximally effective, inducing a profound reduction in epidermal melanin area (0.06 ± 0.02) compared to 16-day controls (0.40 ± 0.04; p < 0.001). This histopathological finding was significantly correlated with severe cutaneous oxidative stress, evidenced by a 3.75-fold increase in MDA (p < 0.001) and a 50% reduction in SOD activity (p < 0.001) versus controls. Furthermore, this regimen caused a potent suppression of Tyr expression (0.15-fold change; p < 0.001) and a significant upregulation of the pro-inflammatory cytokine Tnf (3.8-fold change; p < 0.001). Conclusion: The 16-day topical application of 10% hydroquinone is a reliable, rapid, and highly reproducible protocol for inducing vitiligo-like depigmentation in C57BL/6 mice. This model successfully recapitulates key pathophysiological pillars of human vitiligo, including melanocytotoxicity, profound oxidative stress, and a pro-inflammatory cutaneous environment, establishing it as a valuable platform for preclinical therapeutic screening.

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