agustia sukri ekadamayanti
Unknown Affiliation

Published : 3 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 3 Documents
Search

Successful Management of Antithyroid Drug-Induced Agranulocytosis Using Granulocyte Colony-Stimulating Factor: A Case Report Nur Arfah Rizki; Hendra Zufry; Krishna W Sucipto; Agustia Sukri Ekadamayanti
‎ InaJEMD - Indonesian Journal of Endocrinology Metabolic and Diabetes Vol. 2 No. 1 (2025): InaJEMD Vol. 2, No. 1
Publisher : PP PERKENI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.66266/inajemd.v2i1.43

Abstract

Agranulocytosis is a rare condition and occurs in all age groups. Incidence ranges from 6 to 8 cases per million population per year. About 70% of the cases are found to be involved with medication usage. The use of granulocyte colony-stimulating factor (G-CSF) is effective for ATD-induced agranulocytosis, though some patients do not respond. A 22-year-old female was diagnosed with Grave's disease (GD) three months ago and began using Methimazole (MMI) at an initial dose of 20 mg/day. She was taken to the emergency room after complaining of a fever and stomachache for a week. Laboratories: The patient had leucopenia (white blood cell count 2040/mm3) and severe neutropenia, with an absolute neutrophil count (ANC) of 122.4/μL, thyroid stimulating hormone (TSH) of 0.005 IU/mL, and free thyroxine (FT4) of 46.81 pmol/L. The patient received G-CSF, which normalized her neutrophil counts after the first injection and resolved her fever. She was recommended to quit methimazole therapy. MMI is thionamide used as a first-line treatment for GD. The most severe side effect is agranulocytosis. Agranulocytosis can have various presentations; it most frequently occurs between 2 weeks and 3 months after the initiation of treatment. If the patient recovers, granulocytes begin to reappear in the periphery within a few days to 3 weeks. This drug-induced agranulocytosis is a lethal condition but reversible if recognized early and treated accordingly. G-CSF may shorten the recovery period.
Varicella Zoster-Induced Severe Diabetic Ketoacidosis Asri Mukti Nanta; Agustia Sukri Ekadamayanti; Krishna Wardhana Sucipto; Hendra Zufry
‎ InaJEMD - Indonesian Journal of Endocrinology Metabolic and Diabetes Vol. 2 No. 1 (2025): InaJEMD Vol. 2, No. 1
Publisher : PP PERKENI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.66266/inajemd.v2i1.47

Abstract

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes. There are not many cases reported relate to this case. This case report aims to present a case of DKA which is a common and potentially life-threatening complication in T1DM and can be the first sign of undiagnosed diabetes. A 36-year-old female presented with altered mental status and breathing difficulty. The patient's three children had recently contracted varicella (chickenpox). The patient was diagnosed with type 1 diabetes mellitus 8 months ago, with irregular adherence to treatment. Vital signs included a blood pressure of 84/60 mmHg on norepinephrine at 12 mcg/min, heart rate of 135 bpm, respiratory rate of 33 breaths/min, and temperature of 38.9°C. Physical examination revealed multiple lenticular, circumscribed vesicles with an erythematous base across the entire body. Laboratory results showed leukocytosis (leukocytes: 16,000 x 103/μL), hyperglycemia (random blood glucose: 273 mg/dL), severe metabolic acidosis (pH: 7.002, HCO3: 5.7 mEq/L, BE: -23.6 mEq/L), hypoxemia (pO2: 38 mmHg, SaO2: 52.8%), hypoalbuminemia (albumin: 3.48 g/dL), and stage I acute kidney injury (creatinine: 1.36 mg/dL). Urinalysis revealed the presence of ketone bodies. The patient was subsequently diagnosed with severe diabetic ketoacidosis, varicella zoster infection, septic shock with multiorgan failure, and type 1 diabetes mellitus. Despite initial treatment efforts, the patient’s condition continued to deteriorate, with no signs of clinical improvement. After 3 days, the patient deceased. In conclusion, although varicella zoster infection is an uncommon precipitant of DKA, the present case report highlights the critical role of varicella zoster vaccination and optimal glycemic control in DMT1 to prevent infection-related DKA progression.
Mixed Hyperglycemic Crisis in a Young Obese DiabeticTriggered by Hypertriglyceridemia-Induced Pancreatitis:A Case Report and Review of Pathophysiolo Teuku Mirzal Safari; Agustia Sukri Ekadamayanti; Krishna W. Sucipto; Hendra Zufry
‎ InaJEMD - Indonesian Journal of Endocrinology Metabolic and Diabetes Vol. 2 No. 2 (2025): InaJEMD Vol. 2, No. 2
Publisher : PP PERKENI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.66266/inajemd.v2i2.60

Abstract

Mixed diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS), accompanied by hypertriglyceridemia-induced pancreatitis, represent a rare but life-threatening complication of type 2 diabetes mellitus (T2DM). This case report aimed to illustrate a young adult in whom these three critical conditions converged, highlighting the complexity of such presentations—a 28-year-old male presented with altered consciousness and Kussmaul respiration. The patient was diagnosed with T2DM two weeks earlier but had not yet initiated treatment. Physical examination revealed obesity (BMI: 31 kg/m²) and acanthosis nigricans on the neck and in the axillary regions. Laboratory results showed hyperglycemia (798 mg/dL), metabolic acidosis (pH: 7.08; anion gap: 24), ketonuria, hyperosmolarity (336 mOsm/kg), severe hypertriglyceridemia (965 mg/dL), and elevated lipase (892 U/L). A diagnosis of mixed DKA-HHS secondary to hypertriglyceridemic pancreatitis was established. Treatment included aggressive intravenous (IV) fluid resuscitation of 0.9% sodium chloride (6 L in the first 12 hours) and insulin infusion (0.1 units/kg/hour). During hospitalization, the patient developed acute kidney injury, necessitating continuous renal replacement therapy (CRRT). The patient gradually recovered and was discharged after 20 days. In obese T2DM patients, insulin resistance drives severe hyperglycemia typical of HHS. However, metabolic stress caused by acute pancreatitis induces relative insulin deficiency, triggering lipolysis, ketogenesis, and hypertriglyceridemia, leading to overlapping DKA. Severe hypertriglyceridemia exacerbates systemic inflammation, insulin resistance, and ketosis, creating a vicious cycle that worsens mixed DKA-HHS. This case report highlights the importance of recognizing that T2DM can occasionally present with atypical, life-threatening metabolic complications, necessitatingprompt diagnosis and multidisciplinary management.