Browsing by Author "Čolović, Nataša (6701607753)"

Introduction In patients with acute leukemias hemorrhage is the most frequent problem. Vein thrombotic events may appear rarely but arterial thromboses are exceptionally rare. We present a patient with acute leukemia and bilateral deep leg vein thrombosis who developed an acute myocardial infarction (AMI) during induction chemotherapy. The etiology and treatment of AMI in patients with acute leukemia, which is a rare occurrence, is discussed. Case Outline In April of 2012 a 37-year-old male presented with bilateral deep leg vein thrombosis and malaise. Laboratory data were as follows: Hb 118 g/L, WBC 354.109/L (with 91% blasts in differential leukocyte count), platelets 60.109/L. Bone marrow aspirate and immunophenotype revealed the presence of acute lymphoblastic leukemia. Cytogenetic analysis was as follows: 46,XY,t(4;11)(q21:q23) [2]/62-82,XY,t(4;11)[18]. Molecular analysis showed MLL-AF4 rearrangement. The patient was on low molecular weight heparin and combined chemotherapy according to protocol HyperCVAD. On day 10 after chemotherapy he got chest pain. Three days later AMI was diagnosed (creatine kinase 66 U/L, CK-MB 13U/L, troponin 1.19 μg/L). Electrocardiogram showed the ST elevation in leads D1, D2, aVL, V5 and V6 and “micro q” in D1. On echocardiography, hypokinesia of the left ventricle and ejection fraction of 39% was found. After recovering from AMI and restoring left ventricle ejection fraction to 59%, second course of HyperCVAD was given. The control bone marrow aspirate showed 88% of blasts but with monoblastic appearance. Flow cytometry confirmed a lineage switch from lymphoblasts to monoblasts. In further course of the disease he was treated with a variety of chemotherapeutic combinations without achieving remission. Eventually, palliative chemotherapy was administered to reduce the bulk of blasts. He died five months after the initial diagnosis. Conclusion AMI in young adults with acute leukemia is a very rare complication which may occur in patients with very high white blood cell count in addition with presence of a CD56 adhesion molecule and other concomitant thrombophilic factors. The treatment of AMI in patients with acute leukemias should include antiplatelet and anticoagulant therapy, even with more aggressive methods depending on patient’s age and clinical risk assessment. © 2015, Serbia Medical Society. All rights reserved.

[No abstract available]

Background. Littoral-cell angioma (LCA) is a recently described benign vascular tumor of the spleen, whose imaging and pathologic characteristics have been discussed only by a few authors. The tumor is characterized by a mixture of papillary and cystic areas lined by neoplastic cells deriving from normal splenic lining - littoral cells. The neoplastic LCA cells express both endothelial and histiocytic antigens associated with CD8 negativity, compared with the normal endothelium of the venous sinuses of the spleen red pulp that only expresses endothelial antigens and CD8 positivity. Therefore, the typical and characteristic immunohistochemical pattern of the LCA is as follows: CD31, CD68, CD163, CD21, FVIII antigen positive; CD34, CD8 negative. Case report. We reported a 60-year-old male with moderate nodular splenomegaly with one large hypoechogenic solid lesion and mild thrombocytopenia in whom the diagnosis of LCA was made after the elective splenectomy. Namely, histopathological and immunohistochemical data allowed a final diagnosis of classical LCA in spite of CD21 negativity. As far as we know this is the first reporeted CD21-negative LCA patient. Histological specimens were presented and differential diagnoses discussed. Conclusion. Littoral-cell angioma is a very rare benign splenic neoplasm that should be considered in the differential diagnosis of multinodular splenomegaly, particularly if the patient has the signs of hypersplenism.

The oldest records of developmental beginnings of patients’ healthcare relate to the first hospital founded by St. Sava at the monastery Studenica in 1199. The profile of the Kosovian girl became the hallmark of nursing profession in Serbia. The first school for midwives was founded in 1899 at the Department of Gynecology and Obstetrics of the General State Hospital in Belgrade. However, there were no other schools for nurses in Serbia until the foundation of the School for Midwives of the Red Cross Society in 1021. Until then the healthcare of patients and the injured was carried out by self-taught volunteer nurses with completed short courses of patients’ healthcare. The first course for male and female nurses was organized by the Serbian Red Cross at the beginning of the First Serbian-Turkish War in 1876. During wars with Serbian participation in 19th and 20th centuries with Serbian participation, nurses gave a remarkable contribution being exposed to extreme efforts and often sacrificing their own lives. In war times great merit belongs to the members of the humanitarian society the Circle of Serbian Sisters founded in Belgrade in 1903, which was the resource of a great number of nurses who became the pride of nursing profession. Generations of nurses were educated on their example. In 2004 the annual award “Dušica Spasić” was established which is awarded to the best medical nurse in Serbia. Dušica Spasić was a medical nurse that died at her workplace, when aged 23 years, nursing the sick from variola. © 2014, Serbia Medical Society. All rights reserved.

Introduction: Biliobronchial fistula is rare. Very rarely it may be congenital, more frequently it is acquired as a complication of the hydatide cyst of the liver, pyogenic abscess, serious trauma and resection of the liver as well as recurrent cholangitis due to benign bile duct stricture or cholangtolithiasis. The main causes of the biliobronchial fistula are billiary obstruction and infectious lesion (abscess) in the liver. Case Outline: We present a 56-year-old man with benign stricture of the hepaticojejunostomy performed after operative common bile duct injury, who developed biliobronchial fistula following repeated percutaneous drainage of the liver abscess and percutaneous dilatation of the strictured anastomosis. Over the years the patient developed atrophy/hypertrophy complex, portal hypertension, grade II esophageal varicosities, ascites and splenomegaly. Although biliobronchial fistula was solved by a successful surgical reconstruction (new wide hepaticojejunostomy), the operation had a limited value as it was performed late after permanent lesions of the liver and intrahepatic bile ducts had already developed. Conclusion: Surgical reconstruction of strictured biliodigestive anastomosis should be considered on time as a possibly better solution than percutaneous dilatation. According to the authors' knowledge, a similar case of biliobronchial fistula as a complication of percutaneous dilatation of the benign biliary stricture has not been reported before in the literature.

The hypocellular acute leukemia is very rare atypical leukemia with frequency of 5–7% among patients with acute leukemias. It mainly occurs in older patients and usually has a myeloid phenotype. It is still unclear whether the outcome of hypocellular acute myeloid leukemia is less favorable than adult acute myeloid leukemia with normal cellularity. We retrospectively analyzed all hypocellular acute myeloid leukemias which were treated in 16 years period, between January 1998 and December 2014. There were 33 patients, 21 male and 12 female. The median age of the patients was 58.9 years (ranging from 19 to 88 years) and median cellularity of bone marrow was 16%. All patients presented with cytopenias with median white blood cell count 1.9 × 109/l, platelets 47.2 × 109/l and hemoglobin 85.9 g/l. Nineteen patients were treated with standard 3 + 7 protocol (daunoblastin 45 mg/m2 1, 3, 5 days, cytosin-arabinozide 100 mg/m2/12 h for 7 days), 5 patients with HDAC protocol and, 3 (9%) with low dose cytosin-arabinoside and in 6 (18.1%) patients only supportive therapy was applied. One patient died on 34 day after treatment with HiDAC, 3 patients after treatment with 3 + 7 regimen in full doses on days 23, 35, and 58 days. Complete remission was achieved in 20/33 (60.60%) patients, with median duration of 14 months. Median overall survival (OS) of the entire cohort was 16 months, and for the treated group 21 months (range 5–67 months). Median OS of patients treated with low dose cytosine-arabinoside was 6 months. The advanced age (p = 0.009, KK = − 0.46, Log rank, p = 0.031) as well as therapy options (Log rank p < 0.0001) shows a significant correlation with OS. We report a cohort of patients with hypocellular acute myeloid leukemia who responded to standard induction chemotherapy as are in standard acute myeloid leukemia. © 2019, Indian Society of Hematology and Blood Transfusion.

Introduction Cystic dystrophy of the duodenal wall is a rare complication of the ectopic pancreas that is characterized by cyst/s formation within thickened duodenal wall. Case Outline A 61-year-old male with recurrent abdominal pain, weight loss (about 25 kg) who had been moderate alcohol abuser and heavy smoker was presented. On ultrasonography, very thickened duodenal wall (2.5 cm), an enlarged head of the pancreas with cyst of 3 cm in diameter as well as dilated pancreatic duct (<6 mm) were seen. Barium meal showed stenosis of the first and second part of the duodenum. CT and endoscopic ultrasound confirmed the ultrasonographic finding. The patient underwent surgery. The pathologic finding was established only on first two portions of the duodenum and limited part of the head of the pancreas along duodenum while the rest of the pancreas was normal. Due to poor general condition, gastrojejunostomy was performed. Although some improvement was evident, the patient did not become asymptomatic, and, therefore, four months later a cephalic duodenopancreatectomy was carried out which made him fully asymptomatic. A year later, the patient was symptom-free and in good health. Histologic examination showed a cystic dystrophy of the duodenal wall in the ectopic pancreas. Conclusion Unless there are strong contraindications, cephalic duodenopancreatectomy is best treatment of the disease.

Introduction Waldenström's macroglobulinaemia is a rare B cell lymphoproliferative disorder characterized by lymphoplasmocyte bone marrow infiltration and monoclonal IgM gammopathy. In the majority of cases, Waldenström's macroglobulinaemia is a chronic disease with variable course. Therapy consists of alkylating agents, purine analogs and antiCD20 monoclonal antibody. In the literature, there have been descriptions of rare cases of progression of Waldenström's macroglobulinaemia to aggressive lymphoma, as well as secondary carcinoma in the patients after treatment of macroglobulinaemia. Case Outline A 63-year-old patient was diagnosed with serum monoclonal IgM kappa gammopathy (Waldenström's macroglobulinaemia). Chemotherapy was applied and a good clinical and haematological response had been achieved. Ten years later, the patient was diagnosed with colon adenocarcinoma as a secondary malignancy, and operated on. Within one month, the patient rapidly developed a large neck tumour mass. Tumour biopsy revealed the diagnosis of diffuse large B cell lymphoma with the expression of monoclonal lambda chain, which more likely pointed out to coexistence of two different B cell lympho proliferative disorders, rather than the transformation of Waldenström's macroglobulinaemia to aggressive lymphoma. The patient was treated with chemotherapy following R-CHOP protocol, and clinical remission was achieved. Seven months later, despite the successful treatment of lymphoproliferative disorder, dissemination of adenocarcinoma led to the lethal outcome. Conclusion The patient was diagnosed with a rare occurrence of three neoplastic diseases: Waldenström's macroglobulinaemia, colon adenocarcinoma and diffuse large B cell lymphoma. The possible mechanisms of the combined appearance of lymphoproliferative and other malignant diseases include the previous treatment with alkylating agents, genetic, immunomodulatory and environmental factors.

Introduction Acute leukemias treatment requires strong chemotherapy. Patients that develop bone marrow aplasia become immunocompromised, thus becoming liable to bacterial and fungal infections. Fungal infections caused by Candida are frequent. Hepatosplenic candidiasis (HSC) is a frequent consequence of invasive candidiasis which is clinically presented with prolonged febrility unresponsive to antibiotics. Case Outline A 53-year-old patient with acute myeloid leukemia was submitted to standard chemotherapy “3+7” regimen (daunoblastine 80 mg i.v. on days 1 to 3, cytarabine 2×170 mg i.v. during 7 days) and achieved complete remission. However, during remission he developed febrility unresponsive to antibiotics. Computerised tomography (CT) of the abdomen showed multiple hypodense lesions within the liver and spleen. Haemocultures on fungi were negative. However, seroconversion of biomarkers for invasive fungal infection (IFI) (Candida and Aspergillus antigen/Ag and antibody/Ab) indicated possible HSC. Only high positivity of anti-Candida IgG antibodies, positivity of mannan and CT finding we regarded sufficient for the diagnosis and antimycotic therapy. Three months of treatment with different antimycotics were necessary for complete disappearance of both clinical symptoms and CT findings. Conclusion In patients with prolonged febrile neutropenia IFI has to be strongly suspected. If imaging techniques show multiple hypodense lesions within liver and spleen, HSC has to be taken seriously into consideration. We believe that, along with CT finding, positive laboratory Candida biomarkers (mannan and IgG antibodies) should be considered sufficient for “probable HSC” and commencement of antifungal therapy, which must be long enough, i.e. until complete disappearance of clinical symptoms and CT findings are achieved. © 2015, Serbia Medical Society.

Introduction Acute lymphoblastic leukemia (ALL) is very rarely presented with diffuse osteolytic lesions and hypercalcemia. Case Outline We report a 28-year-old male with the B-cell ALL who presented with extensive osteolytic lesions, bone pain, hepatosplenomegaly, and pancytopenia without circulating blasts in peripheral blood. An increased serum level of tumor necrosis factor (TNF-α) was registered while the levels of IL-1α and IL-1β were normal. The patient failed to achieve remission on two induction regimens but achieved one after the successful allogeneic stem cell transplantation, which lasted for six months, after which he developed a relapse and died. Conclusion The presented case may serve as a clinical demonstration of possible involvement of TNF-α as a pathogenic factor in the evolution of osteolytic lesions that are occasionally observed in patients with ALL. This might have relevance in the management of such patients as chemotherapy alone may not represent the beneficial option in this clinical context. © 2016, Serbia Medical Society. All rights reserved.

Introduction Biliary cystadenomas of the liver are rare benign tumors prone to malignant alteration so that a total excision is recommended. Objective The aim of the paper is to present our experience in treatment and to evaluate whether a simple ablation represents the appropriate treatment. Methods Over a 10-year period 25 patients (24 women) of the average age of 58 years suffering from cystadenomas of the liver, 18 in the right, 4 in the left and 3 in both lobes of the liver were operated. Twenty-three patients had a single lesion, while two patients had 3 and 6 lesions, respectively. Pain was present in 20, occasional vomiting in 4, discomfort in 2 and a sense of fullness in 2 patients. Three patients were jaundiced, 1 due to cystadenoma of the liver, 2 due to concomitant tumors of the head of the pancreas, while 5 patients had concomitant diseases. Results A total ablation was performed in 22 patients, left lateral bisegmentectomy in 1 and partial excision in 2 patients. Six additional procedures were performed. Five cystadenomas of the liver had "ovarian like" stroma, all in women. A focal malignant alteration was found in 2 patients aged 66 and 79 years, respectively. Recurrence was registered in 1 female patient in whom a partial excision had been done. Two patients with concomitant malignancy and 1 patient who developed malignant histiocytosis six months after surgery, died after 1, 2 and 3 years, respectively. Conclusion Biliary cystadenomas of the liver may be misdiagnosed as simple liver cysts, so that "frozen section" histology is highly recommended. In most cases the tumor may be successfully treated by ablation up to the healthy liver tissue. Major liver resections are rarely necessary.

Introduction Invasive fungal infection is among the leading causes of morbidity, mortality, and economic burden for patients with acute leukemia after induction of chemotherapy. In the past few decades, the incidence of invasive fungal infection has increased dramatically. Its management has been further complicated by the increasing frequency of infection by non-Aspergillus molds (e.g. Mucorales). Neutropenic patients are at a high risk of developing an invasive mucormycosis with fulminant course and high mortality rate (35–100%). Case Outline We are presenting the case of a 72-year-old male with an acute monoblastic leukemia. The patient was treated during five days with hydroxycarbamide 2 × 500 mg/day, followed by cytarabine 2 × 20 mg/sc over the next 10 days. He developed febrile neutropenia, headache, and edema of the right orbital region of the face. Computed tomography of the sinuses revealed shadow in sinuses with thickening of mucosa of the right paranasal sinuses. Lavage and aspirate from the sinuses revealed Rhizopus oryzae. Mucormycosis was successfully treated with amphotericin B (5 mg/kg/day) followed by ketoconazole (400 mg/day). Two months later the patient died from primary disease. Conclusion In patients with acute leukemia who developed aplasia, febrile neutropenia, and pain in paranasal sinuses, fungal infection should be taken into consideration. New and non-invasive methods for taking samples from sinuses should be standardized in order to establish an early and accurate diagnosis of mucormycosis with the source in paranasal sinuses, and to start early treatment by a proper antifungal drug. Clear communication between physician and mycologist is critical to ensure proper and timely sampling of lavage and aspirate from sinuses and correct specimen processing when mucormycosis is suspected clinically. ©2016, Serbia Medical Society. All rights reserved.

Two patients with lymphoplasmacytic lymphoma, and monoclonal proteins of IgM in one, and IgG and lambda light chains in the second patient, nephrotic syndrome and acute renal failure are reported. A 58-year-old man previously treated for pre-B acute lymphoblastic leukemia, developed 3 years later nephrotic syndrome as a complication of lymphoplasmacytic lymphoma and high-paraprotein IgM kappa type. Immunofluorescent analysis of kidney biopsy showed extensive IgM and light kappa chain deposits, which caused membranoproliferative glomerulonephritis. Treatment with cyclophosphamide was ineffective and patient died 2 months later. The second patient is a 42-year-old female diagnosed with lymphoplasmacytic lymphoma and paraprotein IgG lambda type. The course of the disease was fulminant with developing nephrotic syndrome and fatal acute renal failure. Immunofluorescent and light microscopic studies of kidney biopsy showed signs of immunotactoid glomerulonephritis with deposits of IgG and C3. Hemodyalises and cytostatic therapy were without response and she died after 45 days. © 2008 Humana Press Inc.

Two patients with lymphoplasmacytic lymphoma, and monoclonal proteins of IgM in one, and IgG and lambda light chains in the second patient, nephrotic syndrome and acute renal failure are reported. A 58-year-old man previously treated for pre-B acute lymphoblastic leukemia, developed 3 years later nephrotic syndrome as a complication of lymphoplasmacytic lymphoma and high-paraprotein IgM kappa type. Immunofluorescent analysis of kidney biopsy showed extensive IgM and light kappa chain deposits, which caused membranoproliferative glomerulonephritis. Treatment with cyclophosphamide was ineffective and patient died 2 months later. The second patient is a 42-year-old female diagnosed with lymphoplasmacytic lymphoma and paraprotein IgG lambda type. The course of the disease was fulminant with developing nephrotic syndrome and fatal acute renal failure. Immunofluorescent and light microscopic studies of kidney biopsy showed signs of immunotactoid glomerulonephritis with deposits of IgG and C3. Hemodyalises and cytostatic therapy were without response and she died after 45 days. © 2008 Humana Press Inc.

Introduction Peripartum cardiomyopathy usually presents with systolic heart failure during the last months of pregnancy and up to five months postpartum. The disease is rare and can be fatal. Case Outline We report a 30-year-old female who was diagnosed with acute myeloid leukemia, with maturation and cytogenetic finding of t(8;21)(q22;q22),del(9)(q22) in January 2004. She was treated with chemotherapy and achieved complete remission that lasts to date. She became pregnant and delivered a healthy newborn with caesarean section in 2009. Seven months later, she again became pregnant and delivered the second child with caesarean section in January 2011. Seven days after delivery she developed symptoms and signs of heart failure. Electrocardiogram showed sinus rhythm, low voltage and negative T-waves in inferior and lateral leads. Echocardiography revealed global left ventricular dysfunction with ejection fraction of 15%, with mobile thrombotic mass of 12 mm attached to the left ventricle wall. She was treated with both unfractionated and low-molecular heparin, diuretics, cardiotonics, and beta-blockers. Within six following weeks left ventricle systolic function improved up to 25–30%. The full clinical recovery was achieved in September 2013, resulting in absence of heart failure and left ventricular ejection fraction of 54%. Conclusion Peripartum cardiomyopathy is a rare condition. The cause of cardiomyopathy is unknown, but it is believed that it could be triggered by various conditions and risk factors. Although the patient was treated with cardiotoxic drugs (doxorubicin and mitoxantrone) in permitted doses, they could have been contributory factors of myocardial damage. Close monitoring of cardiac function in the peripartal period might be beneficial in patients treated with cardiotoxic drugs. © 2016, Serbia Medical Society. All rights reserved.

[No abstract available]

Introduction Sjógren's syndrome is a chronic autoimmune disorder carrying the risk of the development of non-Hodgkin's lymphoma, most frequently marginal zone lymphoma. Case Outline A 66-year-old male patient with Sjógren's syndrome, after a year of the disease, developed a nodal marginal zone lymphoma with lymphoma cells in peripheral blood which had the following immunophenotype: CD19, CD20, CD22, CD19/kappa, CD79b+. After six cycles of chemotherapy according to CHOP protocol (cyclophosphamide, doxorubicin, vincristine and prednisone) disease remission was achieved lasting four months, followed by enlargement of lymph nodes in all areas (generalized lymphadenopathy), splenomegaly and enlargement of the right parotid gland. Bone marrow biopsy and histology confirmed lymphoma of the same morphologic and immunohistochemic profile. Biopsy of a very enlarged hard right parotid gland, by using histology and immunohistochemistry, showed lymphoid tumour tissue with blast appearance and a number of nucleoli corresponding to centroblasts and less to immunoblasts. Immunophenotypes of these cells were as follows: CD79alfa+, CD20+, CD3-, bcl-2-; proliferative activity measured with KI-67 was high rating 60%. Histology and immunohistochemistry showed the co-existence of a diffuse large B cell lymphoma with marginal zone lymphoma. In spite of aggressive chemotherapy treatment according to protocol ESHAP (Vepesid 200 mg i.v. on 1st and 2nd day and 100 mg on 3rd, 4th and 5th day; Cisplatin 20-20-10 mg on 1st to 4th day) the disease showed a progressive course. Conclusion In patients with Sjógren's syndrome, the possibility of lymphoma should be kept in mind and in suspected cases timely diagnostic and therapeutic measures should be undertaken.

Introduction Patients with COVID-19 infection are vulnerable to a variety of serious complications, including invasive fungal infections such as aspergillosis. Because pulmonary aspergillosis is difficult to confirm with perfect confidence, it has been classified as “proven,”“probable,” and “possible.”We present a patient with COVID-19 infection in whom a “probable” pulmonary aspergillosis was complicated by hematogenous spread into brain with formation of multiple abscesses. Case outline A 67-year-old female was diagnosed with COVID-19 infection using polymerase chain reaction (PCR) from a nasopharyngeal swab. The patient had never been vaccinated before. Despite standard therapy and noninvasive oxygen support, the patient’s health deteriorated one month following the onset of the disease, with chest discomfort, cough, and hemoptysis. Thoracic computed tomography (CT) revealed bilateral infiltrative lesions with varying diameters of cavities, primarily in the left lung, as well as modest effusions in both pleural spaces. Aspergillus hyphae were isolated from tracheobronchial aspirates. Despite therapy with Amphotericin B, which was only available antifungal medication at the time, the patient fell into a coma. A CT scan of the skull revealed several infiltrative lesions inside the brain, some with cavities suggestive to metastatic abscesses, most likely of fungal etiology (Aspergillus) as a result of hematogenous spread of pulmonary aspergillosis. Despite therapy and all other precautions, the patient died. The autopsy was not carried out. Conclusion In addition to other complications, COVID-19 patients may develop pulmonary aspergillosis, which can be fatal because of the possibility of hematogenous spread to the brain. © 2022, Serbia Medical Society. All rights reserved.

Introduction Chromosomal numerical aberrations are very common in hematological malignancies, but near-tetraploidy (80–104 chromosomes) is rare in myeloid lineage malignancies, with only a few cases reported in myelodysplastic syndrome (MDS). Due to a small number of cases with this rare cytogenetic abnormality, clinicopathological significance of near-tetraploidy in MDS is still unknown. In this case report we present a case of de novo MDS patient with near-tetraploidy in association with TP53 mutation, and we aimed to elucidate the prognostic significance of this rare genetic feature. Case outline In August of 2018, a 71-year-old male presented with severe anemia, thrombocytopenia, leu-copenia, and enlarged spleen. Laboratory data were as follows: hemoglobin (Hb) 93 g/L, white blood cells 2.8 × 109/L and platelets 23 × 109/L. The bone marrow aspirate was hypercellular, megakaryocytes were not found, 15% of granulocytic cells were with signs of dysplasia, and 16% of blast cells without Auer rods. The finding was in correlation with diagnosis of MDS, type refractory anemia with excess blasts 2 which was also confirmed by immunophenotyping. Cytogenetic finding was near-tetraploidy (48,XY+mar[10]/92,XXYY[10]), and TP53 mutational analysis showed the presence of mutation in exon 8 (p.D281A; c.842 A > C). The patient received from time to time packed red blood cells and platelets, and died four months after initial diagnosis. Conclusion Near-tetraploidy associated with TP53 mutation has been described in only a few MDS cases. Results of these reports including ours suggest that the association of TP53 mutation and near-tetra polyploidy is a poor prognostic factor. © 2023, Serbia Medical Society. All rights reserved.

Introduction. Systemic mastocytosis is a heterogeneous group of hematological disorders characterized by accumulation of mast cells in different organs. Case report. A 41-year-old woman presented with a three-year history of fatigue, occasional diarrhea, mild fever, skin rash and splenomegaly. Laboratory results showed severe anemia and thrombocytopenia. Cytological and histological investigation of bone marrow showed a marked increase of mast cells infiltration with following immunophenotype: CD117+, CD68+, CD34-, MPO-, CD15-. She was treated with cladribine 0.15 mg/kg body weight from day 1 to day 5, a total of six cycles, and achieved a good partial response, transfusion independency and normalization of spleen size. Although the patient responded to the treatment, the relapse with splenomegaly and bicytopenia was observed after 10 months. Conclusion. Cladribine therapy was efficient in the patient' with systemic mastocytosis but the response was transient, so there is the need to search for new therapeutic options and more effective strategies in the treatment of patients with aggressive mast cell disorders.