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Presumed Polymyositis in Chronic Hepatitis C: Navigating Diagnostic Uncertainty and Therapeutic Imperatives in Recurrent Myopathy I Ketut Wardika; Pande Ketut Kurniari
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (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.v9i12.1446

Abstract

Background: Polymyositis (PM) is a cell-mediated inflammatory myopathy for which viral triggers, particularly the Hepatitis C virus (HCV), are increasingly recognized. The convergence of these conditions creates a formidable clinical scenario, often compelling urgent therapeutic intervention despite incomplete diagnostic data. This report explores the management of such a case, highlighting the pragmatic decision-making required when definitive investigations are deferred. Case presentation: A 48-year-old male with untreated chronic HCV infection (Genotype 1b, viral load 2.8 x 10⁶ IU/mL) presented with a debilitating relapse of severe, symmetric proximal muscle weakness, three years after a similar episode. He exhibited profound weakness (Medical Research Council grade 2/5 in hip flexors) and marked myonecrosis (Creatine Kinase 8,572 U/L). Although comprehensive myositis-specific autoantibodies were negative, a strong clinical and biochemical profile led to a presumptive diagnosis of an acute PM exacerbation. Definitive diagnostics, including muscle biopsy, were deferred by the patient. Empirical treatment with high-dose corticosteroids and azathioprine was initiated, predicated on a careful risk-benefit analysis concerning immunosuppression in active viral infection. This strategy resulted in rapid and significant clinical and biochemical improvement. The patient was subsequently scheduled for direct-acting antiviral therapy to address the underlying viral trigger. Conclusion: This case underscores the critical challenge of managing severe, presumed autoimmune disease in the face of diagnostic ambiguity. It demonstrates that a therapeutic strategy guided by strong clinical evidence can be effective for controlling acute, disabling flares. Furthermore, it champions a necessary dual-paradigm approach: acute immunomodulation to preserve function, followed by targeted antiviral therapy to eradicate the probable etiological trigger, thereby aiming to prevent future recurrence and achieve durable remission.
Presumed Polymyositis in Chronic Hepatitis C: Navigating Diagnostic Uncertainty and Therapeutic Imperatives in Recurrent Myopathy I Ketut Wardika; Pande Ketut Kurniari
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (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.v9i12.1446

Abstract

Background: Polymyositis (PM) is a cell-mediated inflammatory myopathy for which viral triggers, particularly the Hepatitis C virus (HCV), are increasingly recognized. The convergence of these conditions creates a formidable clinical scenario, often compelling urgent therapeutic intervention despite incomplete diagnostic data. This report explores the management of such a case, highlighting the pragmatic decision-making required when definitive investigations are deferred. Case presentation: A 48-year-old male with untreated chronic HCV infection (Genotype 1b, viral load 2.8 x 10⁶ IU/mL) presented with a debilitating relapse of severe, symmetric proximal muscle weakness, three years after a similar episode. He exhibited profound weakness (Medical Research Council grade 2/5 in hip flexors) and marked myonecrosis (Creatine Kinase 8,572 U/L). Although comprehensive myositis-specific autoantibodies were negative, a strong clinical and biochemical profile led to a presumptive diagnosis of an acute PM exacerbation. Definitive diagnostics, including muscle biopsy, were deferred by the patient. Empirical treatment with high-dose corticosteroids and azathioprine was initiated, predicated on a careful risk-benefit analysis concerning immunosuppression in active viral infection. This strategy resulted in rapid and significant clinical and biochemical improvement. The patient was subsequently scheduled for direct-acting antiviral therapy to address the underlying viral trigger. Conclusion: This case underscores the critical challenge of managing severe, presumed autoimmune disease in the face of diagnostic ambiguity. It demonstrates that a therapeutic strategy guided by strong clinical evidence can be effective for controlling acute, disabling flares. Furthermore, it champions a necessary dual-paradigm approach: acute immunomodulation to preserve function, followed by targeted antiviral therapy to eradicate the probable etiological trigger, thereby aiming to prevent future recurrence and achieve durable remission.
Faktor yang Berhubungan dengan Penyebab Admisi dan Kematian Pasien Systemic Lupus Erythematosus (SLE) di RSUP Prof. dr. I.G.N.G. Ngoerah, Denpasar Ni Kadek Ariesta Dwijayanthi; Pande Ketut Kurniari
MEDICINUS Vol. 39 No. 5 (2026): MEDICINUS
Publisher : PT Dexa Medica

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.56951/6553mv58

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with high mortality. Epidemiological data on SLE related mortality in Indonesia remain limited, therefore, this study was conducted to identify the characteristics of patients with SLE who died. This study used a cross-sectional design with total sampling based on medical record data of SLE patients who died during hospitalization at RSUP Prof. dr. I.G.N.G Ngoerah, Denpasar from August 2022 to October 2024. Data were analyzed using SPSS version 22.The mortality of SLE patients at RSUP Prof. dr. I.G.N.G Ngoerah, Denpasar during this study period were 45 patients. The female-to-male patient ratio was 10:1, with a mean age of 34.96 (±11.50) years, history of hospitalizations of 2,27 (±1.09) times in the last 3 months, and the length of hospitalization of 6.40 (±3.48) days. Approximately 55% of patients died within less than 3 months after the diagnosis of SLE was established. Most patients (73.33%) experienced infections, and40% patients had cardiovascular and 55.55% had renal comorbidities. Vasculitis and neuropsychiatric SLE (NPSLE) were associated with severe disease activity. While worsening SLE activity was a major factor in patient admission, deaths were primarily attributed to infections (19 cases; 42.22%) and comorbid complications (17 cases; 37.78%).Cardiovascular disease was associated with hospital admissions due to comorbid complications (p=0.05) and with increased SLE disease activity at admission (p=0.02). Infection remains the leading cause of mortality in SLE and also a contributing factor to delays in initiating high-dose corticosteroid administration. Cardiovascular disease appears to be a comorbidity that progresses and worsens earlier in SLE patients. Multidisciplinary management of infectious andcardiovascular comorbidities may reduce mortality and morbidity in SLE.