Muhammad Saiful Rahman
Department of Clinical Pathology, Faculty of Medicine, Airlangga University/Dr. Soetomo Hospital, Surabaya

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Clinical Gitelman Syndrome with Periodic Paralysis and Anemia Muhammad Saiful Rahman; Leonita Anniwati
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 27, No 1 (2020)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v27i1.1576

Abstract

Gitelman syndrome is a rare, autosomal recessive, renal tubular salt-wasting disorder characterized by hypokalemia andmetabolic alkalosis combined with hypomagnesemia and hypocalciuria. A 13-year-old male patient came with acute flaccidparalysis, pain, and weakness in limb muscles. Laboratory results showed hypokalemia, hypocalcemia, hypomagnesemia,and metabolic alkalosis accompanied by anemia and elevated serum transaminases. An electrocardiogram test showed aprolonged QT wave. Physical examination showed blood pressure 118/68 mmHg; heart rate 95x/minute; respiration rate 262 x/minute; temperature 37.6⁰C, weight 80 kg, height 160 cm, and BMI 31.25 kg/M . Neurological examination weakness inthe lower limb, negative pathological reflex. Hematology examination showed Hb 9.8 g/dL, MCV 82.3 fL, MCH 26.8 pg,MCHC 32.5 g/dl, WBC 16.87x10³/μL, platelets 320 x10 /μL, serum iron 47 mg/dL, TIBC 229 mg/dL, ferritin 38.45 ng/mL.Peripheral blood smear showed hypochromic microcytic anemia. Blood gas pH 7.47; pCO2 39 mmHg; pO2 44 mmHg;HCO3- 28.4 mmol/l; Beecf 4.7 mmol/l; SO2 83%; AaDO2 114; thus supporting metabolic alkalosis. Cortisol level was 11.39ug/dL, ANA test result was positive at 17.2 IU/mL, the complement level was normal, dsDNA antigen was negative. Due tohypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis, this patient was diagnosed with Gitelmansyndrome with anemia. The diagnosis should be confirmed by molecular DNA diagnostic studies to identify mutations ofthe gene encoding the thiazide-sensitive Na-Cl-cotransporter.
Difference Expressions CD34 in Acute Myeloid Leukemia Cell Culture in the Administration of Cytarabine-Daunorubicine Dose Standards Muhammad Saiful Rahman; Paulus Budiono Notopuro; Suprapto Ma'at; Made Putra Sedana; Arifoel Hajat
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol 27, No 2 (2021)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v27i2.1623

Abstract

The cure rate for patients with Acute Myeloid Leukemia (AML) is 20-75%. Standard-dose cytarabine + (SDAC)-daunorubicine gives a remission rate of ± 60%, and the case of relapse is frequently found. In-vivo CD34 expression is a reliable and straightforward test that must evaluate AML patients' response to predict the response of chemotherapy + induction phase accurately. Differences in in-vitro CD34 expression are expected to be able to predict chemosensitivity in AML patients. An experimental post-test-only control group study was conducted from May to December 2019, and 8 AML subjects were found. Peripheral Blood Mononuclear Cells (PBMC) were isolated from peripheral blood samples of patients with AML collected in EDTA tubes. The PBMC isolated from peripheral blood were divided into two groups, and each group contained 106 PBMC cells in culture media. The control group (without treatment) and the SDAC-daunorubicine group were 0 + incubated for 4 hours at 37 C with a 5% CO2 atmosphere. The expression of CD34 was measured using FACSCalibur™, while + CD34+ percentage was calculated with CellQuest™ software. The percentage of CD34 in the control, SDAC + DNR, showed a significant difference with p < 0.001. This study showed a significant difference between the control group and the group + administered with the standard dose of cytarabine-daunorubicine with p < 0.001. The average CD34 expression in the + SDAC-DNR treatment group was higher than in the control group. CD34 markers cannot be used as predictors of chemosensitivity in the administration of chemotherapy.
Clinical Gitelman Syndrome with Periodic Paralysis and Anemia Muhammad Saiful Rahman; Leonita Anniwati
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol. 27 No. 1 (2020)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v27i1.1576

Abstract

Gitelman syndrome is a rare, autosomal recessive, renal tubular salt-wasting disorder characterized by hypokalemia and metabolic alkalosis combined with hypomagnesemia and hypocalciuria. A 13-year-old male patient came with acute flaccid paralysis, pain, and weakness in limb muscles. Laboratory results showed hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis accompanied by anemia and elevated serum transaminases. An electrocardiogram test showed a prolonged QT wave. Physical examination showed blood pressure 118/68 mmHg; heart rate 95x/minute; respiration rate 26 2 x/minute; temperature 37.6⁰C, weight 80 kg, height 160 cm, and BMI 31.25 kg/M. Neurological examination weakness in the lower limb, negative pathological reflex. Hematology examination showed Hb 9.8 g/dL, MCV 82.3 fL, MCH 26.8 pg, MCHC 32.5 g/dl, WBC 16.87x10³/μL, platelets 320 x10 / μL, serum iron 47 mg/dL, TIBC 229 mg/dL, ferritin 38.45 ng/mL. Peripheral blood smear showed hypochromic microcytic anemia. Blood gas pH 7.47; pCO2 39 mmHg; pO2 44 mmHg; HCO3- 28.4 mmol/l; Beecf 4.7 mmol/l; SO2 83%; AaDO2 114; thus supporting metabolic alkalosis. Cortisol level was 11.39 ug/dL, ANA test result was positive at 17.2 IU/mL, the complement level was normal, dsDNA antigen was negative. Due to hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis, this patient was diagnosed with Gitelman syndrome with anemia. The diagnosis should be confirmed by molecular DNA diagnostic studies to identify mutations of the gene encoding the thiazide-sensitive Na-Cl-cotransporter.
Difference Expressions CD34 in Acute Myeloid Leukemia Cell Culture in the Administration of Cytarabine-Daunorubicine Dose Standards Muhammad Saiful Rahman; Paulus Budiono Notopuro; Suprapto Ma'at; Made Putra Sedana; Arifoel Hajat
INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY Vol. 27 No. 2 (2021)
Publisher : Indonesian Association of Clinical Pathologist and Medical laboratory

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24293/ijcpml.v27i2.1623

Abstract

The cure rate for patients with Acute Myeloid Leukemia (AML) is 20-75%. Standard-dose cytarabine + (SDAC)-daunorubicine gives a remission rate of ± 60%, and the case of relapse is frequently found. In-vivo CD34 expression is a reliable and straightforward test that must evaluate AML patients' response to predict the response of chemotherapy + induction phase accurately. Differences in in-vitro CD34 expression are expected to be able to predict chemosensitivity in AML patients. An experimental post-test-only control group study was conducted from May to December 2019, and 8 AML subjects were found. Peripheral Blood Mononuclear Cells (PBMC) were isolated from peripheral blood samples of patients with AML collected in EDTA tubes. The PBMC isolated from peripheral blood were divided into two groups, and each group contained 106 PBMC cells in culture media. The control group (without treatment) and the SDAC-daunorubicine group were 0 + incubated for 4 hours at 37 C with a 5% CO2 atmosphere. The expression of CD34 was measured using FACSCaliburâ„¢, while + CD34+ percentage was calculated with CellQuestâ„¢ software. The percentage of CD34 in the control, SDAC + DNR, showed a significant difference with p < 0.001. This study showed a significant difference between the control group and the group + administered with the standard dose of cytarabine-daunorubicine with p < 0.001. The average CD34 expression in the + SDAC-DNR treatment group was higher than in the control group. CD34 markers cannot be used as predictors of chemosensitivity in the administration of chemotherapy.