Devina Ravelia Tiffany Subroto
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Hubungan Keberadaan Jentik Nyamuk terhadap Kejadian Demam Berdarah Dengue (DBD) di Kecamatan Sawit, Kabupaten Boyolali Fandi Muhammad Nugroho; Gusti Fikrifauzi Alimmahiransyah; Hansel Deltino Bandaso; Ihsany Arafiasetyanto Prihadi; Devina Ravelia Tiffany Subroto; Yeni Maharani; Endang S. R; Sri Hayati; Sumardjo .
Nexus Kedokteran Komunitas Vol 7, No 1 (2018): Nexus Kedokteran Komunitas
Publisher : Fakultas Kedokteran Universitas Sebelas Maret Surakarta

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Abstract

Pendahuluan : Demam berdarah dengue (DBD) adalah penyakit yang disebabkan oleh virus Dengue yang ditularkan melalui gigitan nyamuk Aedes aegypti. Pada tahun 2019, dalam kurun waktu 3 tahun terakhir di Kecamatan Sawit, Kabupaten Boyolali ditemukan 16 kasus DBD dengan 3 diantaranya meninggal dunia. Tujuan dari penulisan ini adalah untuk mengetahui hubungan jentik nyamuk dengan kejadian demam berdarah dengue di Kecamatan Sawit, Kabupaten Boyolali.Metode : Penulis melakukan survei jentik untuk melihat Angka Bebas Jentik (ABJ) jumlah responden yang pada tempat penampungan air di rumahnya terdapat jentik nyamuk dan menderita DBD sebanyak 8 responden, ada jentik nyamuk tetapi tidak menderita DBD sebanyak 62 responden, tidak ada jentik nyamuk tapi menderita DBD sebanyak 0 responden, tidak ada jentik nyamuk dan tidak menderita DBD sebanyak 125 responden. Fisher Exact Test digunakan sebagai uji alternatifChi Square untuktabel silang (kontingensi) 2 x2 dengan ketentuan, sampel kurang atau sama dengan 40 dan terdapat sel yang nilai harapan (E) kurang dari 5. Uji Fisher Exact juga dapat digunakan untuk sampel kurang dari 20 dalam kondisiapapun (baik terdapat sel yang nilai E-nya kurang dari 5 ataupun tidak). Asumsidari uji iniadalah data yang akan diuji mempunyai skala pengukuran nominal.Hasil : Diperoleh hasil p < 0.0001 pada Fisher Exact Test.Kesimpulan : Berdasarkan hasil penelitian yang dilakukan, dapat disimpulkan bahwa keberadaan jentik memiliki hubungan yang bermakna dengan terjadinya penyakit DBD di Kecamatan Sawit, Boyolali.Kata Kunci: Dengue Hemorrhagic Fever, Aedes aegypti, Mosquito Larvae, Sawit Subdistrict
A Hematological Triad: Dissecting Synergistic Oxidative and Immune Hemolysis in Dapsone-Treated G6PD Deficiency Devina Ravelia Tiffany Subroto; I Putu Bayu Triguna
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.v5i6.817

Abstract

Dapsone, a key component of leprosy multidrug therapy (MDT), is a well-known precipitant of oxidative hemolytic anemia in individuals with Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency. Conversely, Dapsone-induced immune hemolytic anemia (DIIHA) is exceedingly rare. The concurrent presentation of both severe oxidative hemolysis and a positive Direct Antiglobulin Test (DAT) in a patient also receiving Rifampicin creates a profound diagnostic and mechanistic challenge. We present the case of a 42-year-old female with multibacillary leprosy who developed life-threatening, multifactorial hemolytic anemia (Hemoglobin 5.3 g/dL) three months after initiating MDT (Dapsone, Rifampicin, Clofazimine). A comprehensive diagnostic workup was performed, including detailed hematopathology and quantitative G6PD assay. The immunohematological evaluation was positive (DAT and IAT), but critical sub-testing, including monospecific DATs, was unavailable. The workup confirmed severe oxidative hemolysis (Heinz bodies, degmacytes) in the setting of G6PD deficiency (6.0 U/g Hb measured during 12.5% reticulocytosis). Concurrently, the polyspecific DAT and IAT were strongly positive with a pan-reactive antibody, confirming a simultaneous immune-mediated process. Due to polypharmacy (Dapsone, Rifampicin) and incomplete immunohematological data, the precise trigger for the DIIHA component—whether a rare Dapsone-induced autoantibody, a Rifampicin-induced immune-complex, or an oxidative-trigger mechanism—could not be definitively isolated. In conclusion, this case unmasks a complex, synergistic pathophysiology of concurrent oxidative and immune hemolysis. The inability to attribute the autoimmune component definitively to either Dapsone or Rifampicin highlights a critical diagnostic gap. This report underscores the necessity of a complete immunohematological workup (including monospecific DATs) in such cases and demonstrates that management must be multifaceted—addressing both the oxidative insult (drug cessation) and the severe immune-mediated destruction (immunosuppression), even in the face of etiological uncertainty.
Severe Hyponatremia with Normokalemia in Pembrolizumab-Lenvatinib Combination Therapy for Metastatic Renal Cell Carcinoma: A Case of Suspected Secondary Adrenal Insufficiency and Clinical Differentials Devina Ravelia Tiffany Subroto; Steven Jonathan; I Putu Bayu Triguna
Open Access Indonesian Journal of Medical Reviews Vol. 6 No. 1 (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.v6i1.826

Abstract

The combination of Pembrolizumab and Lenvatinib has become the standard first-line treatment for advanced renal cell carcinoma (RCC). However, the overlapping toxicity profiles of immune checkpoint inhibitors (ICIs) and tyrosine kinase inhibitors (TKIs) create significant diagnostic challenges, particularly regarding electrolyte disturbances. Differentiating ICI-induced secondary adrenal insufficiency from TKI-induced toxicity or syndrome of inappropriate antidiuretic hormone (SIADH) is critical, especially in resource-limited settings where rapid hormonal assays are unavailable. A 67-year-old male with metastatic clear cell RCC presented with confusion, fatigue, and nausea 14 days after initiating palliative Pembrolizumab and Lenvatinib. He had a history of partial nephrectomy and was on Candesartan. Evaluation revealed severe hypotonic hyponatremia (113 mmol/L), acute kidney injury (Creatinine 2.2 mg/dL), and a hypertensive crisis (BP 229/138 mmHg). Notably, despite renal impairment and angiotensin receptor blocker therapy, potassium levels were normal (4.2 mmol/L). The hyponatremia was refractory to 3% hypertonic saline. Suspecting secondary adrenal insufficiency, empiric high-dose corticosteroids were administered, resulting in rapid normalization of serum sodium and resolution of symptoms. In conclusion, in patients receiving ICI-TKI therapy, the specific profile of severe hyponatremia with normokalemia—particularly in the context of renal insufficiency and RAAS blockade—serves as a high-value clinical indicator of preserved mineralocorticoid function. This points toward secondary adrenal insufficiency rather than primary adrenal injury or TKI-induced renal tubular acidosis. This case underscores the utility of deductive physiology in oncology practice.