2017-4

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Turk J Hematol 2017;34:291-299Öngören Ş, et al: First-Line Treatment in Patients with HCLFourth-Line TreatmentThere were only 2 patients who received a fourth-linetreatment. One of them was treated with INF-α and the otherwith rituximab. The patient who received INF-α died due torefractory disease, and the patient who was given rituximabachieved CR.InfectionsIn 47 patients, 76 infectious episodes were noted during theentire follow-up period (Table 3). Bacterial infections were theleading cause, and 64 bacterial infection episodes were observed.Of these 65 episodes, 14 were observed after diagnosis prior tothe initiation of any anti-HCL treatment, whereas 50 episodeswere noted during treatment (Table 3). The infections werediagnosed by means of cultures, radiological imaging techniques,and tissue biopsies as indicated. There were 18 patients whorequired hospitalization (mostly due to neutropenic fever), andin 17 cases infections occurred within 30 days after completionof treatment (all patients received 2-CdA).There were 7 infection episodes caused by Mycobacteriumtuberculosis in 6 patients (5 pulmonary cases, 2 disseminated).In 2 patients tuberculosis was diagnosed synchronously withHCL, and 5 episodes occurred during/after anti-HCL treatment.In patients for whom tuberculosis was diagnosed prior totreatment initiation, one had pulmonary tuberculosis and heexperienced disseminated disease 3 months after completing2-CdA. The other patient had disseminated tuberculosis atdiagnosis, which was diagnosed via splenectomy. That patientthen received INF-α due to relapse without any recurrenceof tuberculosis. None of the patients with tuberculosis haddrug-resistant disease, and none of them had any knowncomorbidities including diabetes. There were also 2 patientswith invasive pulmonary aspergillosis (IPA).Six of the 10 episodes of viral infections were related to flu. Oneof these patients had influenza A virus subtype H1N1 infection(swine flu) and had to be followed in the intensive care unit.Overall, 3 patients died due to infection, and one of them diedbecause of a febrile neutropenic episode prior to treatmentinitiation. In the remaining 2 cases, infections occurred during/after treatment; IPA was the reason for death in one patientreceiving first-line INF-α and the other patient died due tosepsis following frontline 2-CdA administration. The distributionof the infections and outcomes are shown in Table 3.SurvivalDuring the follow-up, 10 patients (12%) died (7 due to refractorydisease and/or infections, 3 due to AMI and sudden cardiacdeath) and 2 patients were lost to follow-up. PFS and OS ratesfor the entire cohort after a median follow-up of 57 monthswere 62% (Figure 3A) and 83% (Figure 3B), respectively. Withregard to the first-line treatment, the PFS rate was significantlyhigher for patients who received 2-CdA than those for patientswho were treated with INF-α and splenectomy (p=0.01 andp<0.0001, respectively). However, PFS did not statistically differbetween patients who were treated with INF-α and those whounderwent splenectomy (p=0.213) (Figure 4A). There was nostatistically significant OS difference between these 3 treatmentmodalities, although survival rates achieved with first-line2-CdA and INF-α seemed to be superior to those achieved withsplenectomy (Figure 4B).Figure 3. The progression-free survival (A) and overall survival (B) of the entire cohort.2-CdA: Cladribine, INF-α: interferon-alpha.295
Öngören Ş, et al: First-Line Treatment in Patients with HCLTurk J Hematol 2017;34:291-299Table 3. The distribution of infections among the patient cohort.Type of infectionViral (n=10)FluHerpes labialisHBVNumber ofevents, n621Timing of infection, n Type of treatment* Outcome ofinfection (resolved/death), nPrior totreatmentinitiation500During/aftertreatment1212-CdA (n=1)2-CdA (n=1)IFN (n=1)10/0HCV1012-CdA (n=1)IFN (n=1) [SPL, n=1]Bacterial (n=64)Pneumonia13762-CdA (n=4) [IFN, n=1]IFN (n=2) [SPL, n=2]13/0Tuberculosis725IFN (n=2) [SPL, n=1]2-CdA (n=2)RTX (n=1)7/0Febrile neutropenia213182-CdA (n=15) [IFN, n=3; RTX, n=1]IFN (n=2) [SPL, n=1]RTX (n=1)20/1Soft tissue infection6152-CdA (n=1) [RTX, n=1]IFN (n=4) [SPL, n=2]6/0Dental infection303IFN (n=1) [SPL, n=1]2-CdA (n=2) [IFN, n=1]3/0Paronychia202IFN (n=2) [SPL, n=1]2/0Sepsis4042-CdA (n=3) [IFN, n=1]IFN (n=1) [SPL, n=1]3/1 (2-CdA)Conjunctivitis2112-CdA (n=1)2/0Septic arthritis101IFN (n=1)1/0Meningitis101IFN (n=1)1/0Urinary tract infectionSplenic abscess3100312-CdA (n=2) [RTX, n=1]RTX (n=1)IFN (n=1)3/01/0Fungal (n=2)Invasive pulmonaryaspergillosis2 0 2 IFN (n=1)2-CdA (n=1)2/1 (IFN)*In this column, the number of patients who received the defined most recent therapies is shown in parentheses, whereas the number of patients with a previous anti-HCL therapy isdisplayed in square brackets.2-CdA: Cladribine, HBV: hepatitis B virus, HCV: hepatitis C virus, INF-α: interferon-alpha, SPL: splenectomy, HCL: hairy cell leukemia.DiscussionIn this study we retrospectively evaluated the demographicfeatures of patients with HCL and assessed the efficacy andtolerability of the main first-line treatments together with thesubsequent therapy options and outcomes. We also identifiedthe infections associated with the course of the disease. HCLoccurs more frequently in males, and the median age of diagnosisis 52 years [14]. Our patient cohort showed characteristics thatwere similar to the previously reported literature with a medianage of 49 years and a male/female ratio of approximately 7:1.In our cohort, we identified peripheral and/or viscerallymphadenopathy in 27 patients (38%). In the most recent296
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