Susanna Hilda Hutajulu
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Journal : Jurnal Acta Interna

JAK2 mutation and treatment of JAK2 inhibitors in Philadelphia chromosome-negative myeloproliferative neoplasms Hutajulu, Susanna Hilda; Kurnianda, Johan
Acta Interna The Journal of Internal Medicine Vol 3, No 2 (2013): Acta Interna The Journal of Internal Medicine
Publisher : Acta Interna The Journal of Internal Medicine

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Abstract

ABSTRACTThe Philadelphia chromosome-negative (Ph-negative) myeloproliferative neoplasms (MPNs) polycythaemia vera (PV), essential thombocythaemia (ET) and primary myelofi brosis (PMF) are clonal disorders of multipotent haematopoietic progenitors. The genetic cause of these disorders was not fully defi ned until a somatic activating mutation in the JAK2 non-receptor tyrosine kinase, JAK2V617F, was identifi ed in most patients with PV and a considerable proportion of patients with ET and PMF. The discovery of JAK2 mutation has changed the molecular reclassification of MPNs and served as a genomic target for therapeutic implication. A number of JAK2 inhibitors have been developed and tested for MPNs. Several JAK2 inhibitors have reached the phases of clinical trial and included patients with intermediate-risk or high-risk MF. This population of MF is the best candidate for trials because currently it has no effective therapy besides patients’ poor survival. Considering all clinical data on Ph negative MPNs, JAK2 inhibitors have shown a clinical benefi t and reduced symptoms in the vast majority of MF cases. The most developed among JAK2 inhibitors is Ruxolitinib, which has demonstrated clinical improvement with well tolerated toxicities. However, JAK2 inhibitor was equally active in patients with and without JAK2 mutation. Other JAK2 inhibitors are less developed, but showed a similar clinical benefi t. Furthermore, its effect on the natural course of MPNs in treating patients needs to be investigated.Keywords: myeloproliferative neoplasms – JAK2 mutation – JAK2 inhibitors.
JAK2 mutation and treatment of JAK2 inhibitors in Philadelphia chromosome-negative myeloproliferative neoplasms Hutajulu, Susanna Hilda; Kurnianda, Johan
Acta Interna The Journal of Internal Medicine Vol 3, No 2 (2013): Acta Interna The Journal of Internal Medicine
Publisher : Faculty of Medicine Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (8753.06 KB) | DOI: 10.22146/acta interna.5003

Abstract

ABSTRACTThe Philadelphia chromosome-negative (Ph-negative) myeloproliferative neoplasms (MPNs) polycythaemia vera (PV), essential thombocythaemia (ET) and primary myelofi brosis (PMF) are clonal disorders of multipotent haematopoietic progenitors. The genetic cause of these disorders was not fully defi ned until a somatic activating mutation in the JAK2 non-receptor tyrosine kinase, JAK2V617F, was identifi ed in most patients with PV and a considerable proportion of patients with ET and PMF. The discovery of JAK2 mutation has changed the molecular reclassification of MPNs and served as a genomic target for therapeutic implication. A number of JAK2 inhibitors have been developed and tested for MPNs. Several JAK2 inhibitors have reached the phases of clinical trial and included patients with intermediate-risk or high-risk MF. This population of MF is the best candidate for trials because currently it has no effective therapy besides patients’ poor survival. Considering all clinical data on Ph negative MPNs, JAK2 inhibitors have shown a clinical benefi t and reduced symptoms in the vast majority of MF cases. The most developed among JAK2 inhibitors is Ruxolitinib, which has demonstrated clinical improvement with well tolerated toxicities. However, JAK2 inhibitor was equally active in patients with and without JAK2 mutation. Other JAK2 inhibitors are less developed, but showed a similar clinical benefi t. Furthermore, its effect on the natural course of MPNs in treating patients needs to be investigated.Keywords: myeloproliferative neoplasms – JAK2 mutation – JAK2 inhibitors.
Cisplatin Desensitization in a Patient with Nasopharyngeal Carcinoma Experiencing Urticarial Allergic to Cisplatin Nugraha, Doddy Rizqi; Mulya, Deshinta Putri; Hutajulu, Susanna Hilda
Acta Interna The Journal of Internal Medicine Vol 9, No 1 (2019): Acta Interna The Journal of Internal Medicine
Publisher : Faculty of Medicine Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (137.833 KB) | DOI: 10.22146/actainterna.51362

Abstract

Background. Allergic reactions to cisplatin are not uncommon situations with an incidence of 5-20%. In general, allergic reactions to cisplatin is a type 1 hypersensitivity with manifestations of itching, redness, papules, urticaria, chest pain, and anaphylactic symptoms. Desensitization methods are needed for patients who have no alternative medication.Case Report. A 59-year-old woman with nasopharyngeal carcinoma experienced urticaria because of cisplatin in her first cycle of chemotherapy. In the second cycle, chemotherapy desensitization program was applied using a 12-step Castell protocol. We measured vital signs and symptoms every 15 minutes. Administration of cisplatin was completed in 2 hours and the patient tolerated the whole program very well.Discussion. Risk factors of hypersensitivity to cisplatin include age <70 years, previous allergy history, history of carboplatin use with dose >650 mg, mutation of BRACA1/2 gene, and administration of combined regimens with taxane groups or liposomal inhibitor. Desensitization uses 3 solutions with 12 steps. Solution is 100 times the dilution of the target dose. Solution 2 is 10 times the dilution of the target dose and solution 3 uses the appropriate target dose. Each solution is administered for 15 minutes using an infusion pump. Strict monitoring of vital signs and patient symptoms are done every 15 minutes during the program.Conclusion. Doctors should be aware of allergies to cisplatin. Currently, the allergic reaction to cisplatin can be overcome using the desensitization method when no alternative drug is not available.