Yulistiani

ANALYSIS OF CORTISOL LEVEL AFTER HIGH-DOSE AND LONG-TERM PREDNISONE EXPOSURE IN CHILDREN WITH STEROID-SENSITIVE NEPHROTIC SYNDROME

Objective: The objective of this study is to analyze the cortisol levels in induction and alternate phases associated with the clinical manifestation in the developing of adrenal suppression.Methods: An observational, longitudinal study which had been approved by the ethical committee of Dr. Soetomo Teaching Hospital Surabaya was conducted from June to October 2016. The cortisol levels were measured before induction phase (t=0), after induction phase (t=1), and after alternate phase (t=2). The venous blood samples were obtained in the morning at 08.00–09.00 am. The data were analyzed using student’s t-test.Results: A total of 15 patients were included, but 6 patients were excluded because of cross-reactivity with prednisone when using ADVIA Centaur Cortisol Assay. 9 patients (55.56% boys) had a mean age 6–< 12 years old and 33.33% were initial attack and dependent steroid nephrotic syndrome. 8 of 9 patients had a normal cortisol level at baseline (t=0). The cortisol level decrement in the induction phase was 72.92% (11.79±10.66 mcg/dL–1.75±1.08 mcg/dL) (*p=0.024). After alternate phase, the cortisol levels increased 417.60% (1.75±1.08 mcg/dL to 5.95±3.33 mcg/dL (*p=0.007). The clinical manifestation as nausea/vomiting and abdominal distension only appeared in 11.11% of patients in the induction phase but not in the alternate phase.Conclusions: Hypothalamus-pituitary-adrenal (HPA) axis suppression could develop after induction phase which was indicated by low cortisol levels. High-dose and long-term prednisone exposure decreased the cortisol levels reversibly. The clinical manifestation of adrenal suppression as weakness, nausea/vomiting, acute dehydration, and abdominal distension almost did not manifest in all patients.

ANALYSIS OF INDUCTION PHASE GLUCOCORTICOID USE ON ADRENAL SUPPRESSION IN PEDIATRIC PATIENTS WITH ACUTE LYMPHOBLASTIC LEUKEMIA

Glucocorticoids play an important role in the treatment of acute lymphoblastic leukemia (ALL). However, supraphysiological doses may cause suppression of the adrenal. Adrenal suppression resulting in reduced cortisol response may cause an inadequate host defence against infections, which remains a cause of morbidity and mortality in children with ALL. The occurrence of adrenal suppression before and after glucocorticoid therapy for childhood ALL is unclear. The aim of this study is to analysis the effect of glucocorticoid on cortisol levels during induction phase chemotherapy in children with acute lymphoblastic leukemia. A cross-sectional, observational prospective study was conducted to determine the effect of glucocorticoid on cortisol levels in children with acute lymphoblastic leukemia. Patients who met inclusion criteria were given dexamethasone or prednisone therapy for 49 days according to the 2013 Indonesian Chemotherapy ALL Protocol. Cortisol levels were measured on days 0, 14, 28, 42 and 56 of induction phase chemotherapy. There were 24 children, among 31 children recruited, who suffered from acute lymphoblastic leukemia. Before treatment, the means of cortisol levels were 228.95 ng/ml in standard risk group (prednisone) and 199.67 ng/ml in high risk group (dexamethasone). In standard risk group, the adrenal suppression occurs at about day 56. There was a significant decrement of cortisol levels in high risk group in days 14, 28, 42 against days 0 of induction phase (p=0.001). Both groups displayed different peak cortisol levels after 6 week of induction phase (p=0.028). Dexamethasone resulted in lower cortisol levels than prednisone during induction phase chemotherapy in children with acute lymphoblastic leukemia.

ANALYSIS OF NACL-MANNITOL HYDRATION ON RENAL FUNCTION OF HEAD AND NECK CANCER PATIENTS RECEIVING HIGH-DOSE CISPLATIN CHEMOTHERAPY COMBINATION

Cisplatin is one of platinum cytostatic drug for the medication of solid cancers, one of which is head and neck cancer. Adverse event that resulted during drug treatment was acute or chronic nephrotoxicity. Cisplatin concentration in proximal tubular epithelial cells is about 5 times the serum concentration. Platinum exposure on renal tubular cells bonding covalent complex which stimulate production of inflammatory factors that lead to apoptosis and necrosis cell. Cisplatin nephrotoxicity can be prevented by aggressive hydration or alternate method of administration. The aim of this study was to analyze the effectiveness of NaCl-Mannitol hydration on renal function of head and neck cancer patients receiving cisplatin 100 mg/m2 chemotherapy combination with 5FU or paclitaxel. This was a cohort, prospective, and observational study to analyze renal function of head and neck cancer patients receiving cisplatin 100 mg/m2 chemotherapy combination with 5FU or paclitaxel. Inclusion criteria were BUN 7-18 mg/dl and serum creatinine < 2 mg/dl of any cycle. All patients received infuse NaCl-Mannitol hydration with term that provided in Surgeon Departement of Dr. Soetomo General Hospital. Data obtained were BUN, SCr, and eClCr Cockroft-Gault, each was measured pre- and post-hydration. In cisplatin and 5FU chemotherapy combination value BUN pre-hydration (11,99 + 4,62) mg/dl, value BUN post-hydration (12,14 + 4,74) mg/dl and value serum creatinine pre-hydration (0,97 + 0,34) mg/dl, value serum creatinine post-hydration (1,02 + 0,37) mg/dl. Meanwhile to the combination of cisplatin and paclitaxel chemotherapy, value BUN pre-hydration (10,19 + 2,58) mg/dl, value of BUN post-hydration (10,43 + 2,31) mg/dl and value of serum creatinine post- hydration (0,98 + 0,26) mg/dl. In conclusion, NaCl-Mannitol hydration administration is adequate which is shown by BUN and serum creatinine in pre- and post-hydration data within normal limits.