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The thalassaemias are a group of genetic disorders of haemoglobin which are endemic in the tropics but are now found worldwide due to migration. Basic standard of care therapy includes regular transfusions to maintain a haemoglobin level of around 10 g/dL, together with iron chelation therapy to prevent iron overload. Novel therapies, bone marrow transplantation, and gene therapy are treatment options that are unavailable in many countries with stressed economies. This Wider Perspectives article presents the strategies for management of an adolescent refugee patient with beta thalassaemia, as it would be performed by expert haematologists in six countries: Italy, Lebanon, Oman, the Sudan, Thailand and the United States. The experienced clinicians in each country have adapted their practice according to the resources available, which vary greatly. Even in the current modern era, providing adequate transfusions and chelation is problematic in many countries. On the other hand, ensuring adherence to therapy, particularly during adolescence, is a similar challenge seen in all countries. The concluding section highlights the disparities in available therapies and puts the role of novel therapies into a societal context.

In the not so distant past, pregnancy in thalassaemia patients was considered a very high risk and often not recommended. The results regarding alpha-thalassaemia and in particular haemoglobin H disease by Srimeuniwai and colleagues are very encouraging. Nowadays thalassaemic women not only become pregnant, but maternal outcome is not decreased compared to controls. Commentary on: Ake-sittipaisarn, et al. Outcomes of pregnancies complicated by haemoglobin H-Constant Spring and deletional haemoglobin H disease: A retrospective cohort study. Br J Haematol 2022;199:122-129.

Introduction Major thalassemia (TM) and sickle cell disease (SCD), two common genetic hemoglobinopathies, were often fatal 50 years ago. Novel therapeutic and diagnostic methods are increasing lifespan and quality of life. Recent advances in iron chelation for transfusion-dependent hemoglobinopathies have significant improved patient prognosis. Young adult TM and SCD patients often ask about the possibility of conception and pregnancy. The increase in the worldwide movement of carriers and subjects has lead to new cultural, ethical and psychosocial aspects that must be taken into consideration. The present study investigated the fertility rate, maternity/paternity status, need for assisted reproductive techniques (ART), abortion rate, pregnancy/newborn complications in patients with hemoglobinopathies. Methods We followed 130 female (FPs) and male (MPs) patients (F:M=93:37); 75 with TM, 32 with thalassemia intermedia (TI), 13 with SCD and 10 with microdrepanocytosis (MDC). Median age is 55 yo (15-90) for TM+TI and 45 yo (18-79) for SCD+MDC. Pregnancy was reported in 37/52 FP of childbearing age (15-49 yo), and conception in 15 MP with fertility rates of 71% and 70%, respectively. Results We reviewed 66 conceptions from 1999 to 2020. Mother age at pregnancy was between 32-39 yo. Forty-seven pregnancies were spontaneous and 19 medically assisted. There were 3 ovodonations and 2 ICSI; 64% of pregnancies were planned. Pregnancy outcomes of 22 TM, 16 TI, 8 SCD and 3 MDC patients are described. There were 7 miscarriages in the first 12 weeks: 3 in TI, 1 in SCD FP; 1 in TM and 2 in SCD MP. Abortion rate was 9%, comparable to the general population. Intrauterine death at 24w occurred in a SCD FP for placental thrombosis and eclampsia. Sixty live healthy newborns were delivered;4 twin pregnancies occurred (1 TM MP, 3 TM FP). Only 1 malformation was observed, in an infant born after ovodonation in a TM FP who had minor gastroenteric and urinary malformations that were surgically corrected. Obstetric complications were eclampsia, disseminated intravascular coagulation, cardiac failure, and acute chest syndrome in SCD patients. One ovarian hyperstimulation syndrome in the 1st month of pregnancy with ascites and admission to the ER was reported. There were 30 (94%) caesarians (CD) and 3 vaginal deliveries (VG) in FP, with 7 preterm babies (22%). In partners of MPs there were 15 CD (56%), and 11 VG with 5 preterm babies (Table I). Births from MPs occurred between 34-40w with a median birth weight of 3 kg (2.17-4) and 30-41w in FPs with a median birth weight of 2,5 kg (1,1-3,4) . FPs were able to breast fed in 56% of cases for a medium time of 66 days (20-120), while female partners of MPs breastfed for 193 days (20-540). Newborn events includes 14 jaundices; 9 babies were placed in intensive care and required incubator use due to cerebral hemorrhage or infections requiring antibiotic therapy. Discussion Spontaneous pregnancies occur in well chelated and transfused patients but a relevant part of those patients are infertile due to hypogonadism due to transfusional hemosiderosis and may need ART. These patients present a base-line pro-coagulant state which can worsen during pregnancy, needing antithrombotic prophylaxis and require regular consultations, since pregnancies are considered high risk for both mother and baby. As osteopenia-osteoporosis are the common endocrine complications in hemoglobinopathies (67% of FPs), both cesarean delivery and breast feeding are strongly suggested. Even though chelating therapy during lactation does not alter iron excretion, our patients didn't receive chelating therapy when breastfeeding. Multidisciplinary programs including transfusions, cardiac and clinical evaluations should be monthly performed. Our Institution has a team of hematologists and other dedicated specialists that work together during the planning, conception, pregnancy, delivery and immediate post-delivery processes to assure best care to mother and child. Conclusions Survival of hemoglobinopathic patients in developed countries is improving and patients aspire to reproductive aims of their healthy peers. TM and SCD patients often request fertility and pregnancy information, including screening of partners. We provide insights regarding reproductive health experience of hemoglobinopathies in both genders. Detailed results, mothers and child follow up and practical management will be presented. Figure Disclosures Abruzzese: Incyte:Consultancy, Membership on an entity's Board of Directors or advisory committees;Pfizer:Consultancy, Membership on an entity's Board of Directors or advisory committees;Novartis:Consultancy, Membership on an entity's Board of Directors or advisory committees;Bms:Honoraria.

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Introduction Multiple Myeloma (MM) is a hematologic malignancy characterized by proliferation of clonal plasmacells in the bone marrow and sometimes extramedullary sites which inevitably tend to relapse. Patients with relapsed/refractory MM (R/R MM) who are treated with conventional drugs as immunomodulating agents (IMiDs) and proteasoma inhibitors (PIs) have a poor survival. Based on the results of MM 003 phase III randomised trial, pomalidomide in association with dexamethasone has shown to improve R/R MM outcome. We conducted a single-center real life-based observational and pharmacological analysis to investigate the efficacy and tolerability of pomalidomide in a group of patients with R/R MM previously exposed to IMiDs and PIs. Method and Materials We included 34 patients (females 21) treated with pomalidomide (POMA) from January 2015 to May 2018 at the Hematology Department of "Santo Spirito" Hospital in Pescara, Italy. All patients were diagnosed by R/R MM according to IMWG guidelines and were classificated using ISS criteria. Prognostic cytogenetic value was identified by FISH analysis. POMA was administred at the oral daily dose of 3-4 mg (days 1-21) in combination with oral dexamethasone (days 1,8,15,22) at the dosage of 20 mg/day. Adverse events were evaluated according to the common terminology criteria for adverse reactions (CTCAE version 4.0). Overall survival (OS) and progression free survival (PFS) were designed according to Kaplan-Myer method. The adherence to therapy was determined using 'received daily dose/prescribed daily dose' method (RDD/PDD). Statistic analysis were conducted with GraphPad Prism 7.0; p values ≤ 0.05 were considered statistically significant. Results The clinical and biological characteristics of 34 patients are described in Tab.1. The median follow up after POMA therapy was 5 months (range, 1-32); at the end of this period 12 patients had completed at least 6 cycles of therapy (range, 1-21). Overall response rate (ORR) was 24%: 4 complete remission (CR), 3 very good partial response (VGPR), 1 partial response (PR); moreover 6 patients (18%) achieved a minimal response (MR). Clinical benefit rate (CBR) was 74%: ORR plus 6 MR and 11 stable disease (SD). At time of this report 12 patients (35%) are living. Among living patients, 4 are now receiving other treatments and 8 are still under POMA treatment: 4 are in CR, 1 is in PR, 1 in MR and 2 in SD. Median OS of all patients was 10 months, whereas median PFS was 6 months (Fig.1,A-B). Median PFS was notably lower in high cytogenetic risk patients (4 months) as compared to the PFS of standard cytogenetic risk patients (16 months) (p= 0.02) (Fig.1,D). Patients treated with at least 4 previous lines of therapy had a median PFS of 5 months, while those receiving until 3 previous lines of therapy had a median PFS of 24 months (p= 0.01) (Fig.1,C). Patients receiving a drug regimen lenalidomide-based as last treatment before starting POMA didn't show significant difference in PFS from those receiving other treatments (4 months vs 6 months) (p=NS). During treatment with POMA, 22 patients (65%) showed adverse drug reactions (ADRs) for a total of 77. Seventy-four ADRs were ≥ 2 grade. Forty nine ADRs (63%) were hematological and 43 ADRs (56%) occurred in the first 3 months of therapy. In particular Twenty-two of them occurred within the first month of therapy. Thirty two cases of ADRs (41%) were successfully managed with simple delay of treatment. As consequence, the adherence to therapy was not optimal (78%). However only 9 (12%) of the total ADRs were cause of end of treatment. Conclusions Despite the low sample size and short follow-up, our real life analysis contributes to show that pomalidomide therapy is a favorable option for patients with R/R MM, leading to good responses in terms of OS and PFS. The best results were obtained when POMA treatment was utilized at first relapses and in particular in patients with favorable genetic profile. About the safety, despite the frequent hematological toxicity, ADRs can be quite easily managed to allow few interruptions of the treatment and improve the adherence. Disclosures No relevant conflicts of interest to declare.

Objective: Human immunodeficiency virus (HIV)-infected people exhibit a high incidence of vascular diseases. Since in the general population the high cardiovascular risk has been associated with an impaired endothelial cell function, we investigated circulating endothelial progenitor cells in HIV-positive patients. Design: We evaluated circulating colony-forming unit–endothelial cell (CFU-EC) and endothelial colony-forming cell (ECFC) progenitors in 14 antiviral therapy-naive HIV-positive patients, in comparison with 15 normal controls. Methods: CFU-EC and ECFC derived from peripheral blood mononuclear cells from HIV-infected and HIV-uninfected individuals were recovered and evaluated for HIV genome presence by PCR. Vascular endothelial growth factor (VEGF) and apolipoprotein B mRNA-editing enzyme catalytic polypeptide like (APOBEC) subunits expression were evaluated in infected colonies by real-time PCR. Results: We found that circulating CFU-EC but not ECFC were significantly reduced in HIV-positive patients and that proviral HIV DNA was detectable only in CFU-EC but not in ECFC. Furthermore, the expression of APOBEC subunits was significantly lower in CFU-EC than in circulating monocytes. Accordingly, the CFU-EC displayed a high content of proviral DNA copies, suggesting that these cells have a high sensitivity to the HIV infection. Conclusions: Although HIV does not affect the ‘true endothelial progenitor’ compartment, it infects and strongly depletes circulating endothelial progenitors with hematopoietic signature. We unravel a novel pathogenetic mechanism by which HIV infection might cause vascular diseases.

In order to analyze the clinical relevance of the pharmacokinetic interactions between vinblastine and antiretrovirals described in literature, we evaluated all HIV-infected patients with Hodgkin's lymphoma treated with vinblastine-containing regimens and combination antiretroviral therapy, in a single clinical center. The use of protease inhibitors was independently associated with WHO grade III-IV neutropenia. Moreover, an inverse correlation between dosage of ritonavir and mean nadir neutrophil count was found. The concomitant administration of vinblastine-containing chemotherapy regimens with protease inhibitors can lead to higher levels of neutropenia than those of different classes of drugs such as nonnucleoside reverse transcriptase inhibitors or integrase inhibitors.

Background The MPLSer505Asn mutation has been reported to be a cause of hereditary thrombocythemia. Recently, we detected this mutation in a large proportion of children with familial thrombocythemia, suggesting that in Italy the incidence of MPLSer505Asn mutation could be underestimated.Design and Methods We extended the search for this mutation to all patients with essential thrombocythemia who had a positive family history for thrombocytosis or essential thrombocythemia. We identified eight Italian families positive for the MPLSer505Asn mutation. Clinical and hematologic data were available for members of seven families, including 21 patients with a proven mutation and 20 relatives with thrombocytosis.Results Fifteen major thrombotic episodes, nine of which were fatal, were recorded among 41 patients. The thrombotic manifestation was stroke in four cases, myocardial infarction in seven cases, fetal loss in two cases, deep vein thrombosis of the leg in one case and Budd Chiari syndrome in one case. Almost all patients over 20 years old had splenomegaly and bone marrow fibrosis, while these were rarely observed in patients under 20 years old, suggesting that these manifestations are associated with aging. Finally, the life expectancy of family members with thrombocytosis was significantly shorter than that of members without thrombocytosis (P=0.003).Conclusions Patients with familial thrombocytosis caused by a MPLSer505Asn mutation have a high risk of thrombosis and, with aging, develop splenomegaly and bone marrow fibrosis, significantly affecting their life expectancy.

In polycythemia vera (PV) and essential thrombocythemia (ET) specific JAK2 mutations constitutively activate the JAK-STAT pathway, explaining biologic findings such as endogenous erythroid colony (EECs) growth or PRV-1 RNA overexpression. Since these markers are detected also in JAK2 wild type patients, we hypothesized that, in these cases, the activation of the JAK-STAT pathway could be produced by a deregulation of the suppressor of cytokine signaling (SOCS) protein system. Eighty-one patients with PV and ET (53 adults and 28 children) were investigated for the methylation status of the SOCS-1, SOCS-2 and SOCS-3 CpG islands and for several myeloproliferative markers (including JAK2 and MPL mutations and clonality of hematopoiesis). SOCS-1 or SOCS-3 hypermethylation was identified in 23 patients and was associated with a significant decrease of SOCS-1 or SOCS-3 RNA and protein levels. The gene expression was restored by exposing cells to the demethylating agent 2-deoxyazacytidin. Interestingly, SOCS-1 or SOCS-3 hypermethylation was detected in 6 female patients, proved negative for JAK2 or MPL mutations and exhibiting monoclonal hematopoiesis. In conclusion, SOCS-1 or SOCS-3 hypermethylation can activate the JAK-STAT signaling pathway in alternative or together with JAK2 mutations. These alterations might represent a potential therapeutic target.

The V617F JAK2 mutation reported in Ph-negative myeloproliferative diseases (MPDs) induces the constitutive activation of JAK2, which produces an increased phosphorylation of signal transducer activator of transcription (STAT). In this study, we have analyzed a series of 114 patients (54 with polycythemia vera [PV], 44 with essential thrombocythemia [ET], 12 with idiopathic myelofibrosis [IM], and 4 with myelofibrosis secondary to MPD) for the expression pattern of phosphorylated STAT-3 and STAT-5 (pSTAT-3 and pSTAT-5, respectively) by immunostaining bone marrow biopsies. We found 3 specific patterns of pSTAT-3 and pSTAT-5 expression, significantly different from the normal staining pattern: uniformly increased pSTAT-3 and pSTAT-5 expression in PV, increased pSTAT-3 and reduced pSTAT-5 expression in ET, and uniformly reduced pSTAT-3 and pSTAT-5 expression in IM. A moderate increase of pSTAT-3 and pSTAT-5 expression was observed in secondary forms of erythrocytosis and thrombocytosis. In all evaluated MPDs, the pSTAT-5 and pSTAT-3 expression pattern was not influenced by the presence of V617F JAK2 mutation. These findings underline the importance of bone marrow histology in the differential diagnosis of Ph-negative MPD and support the hypothesis that V617F mutation simply contributes with other molecular defects in allowing the PV, ET, or IM phenotype to emerge.

Newly significant advances have been made in diagnosis and treatment of multiple-myeloma (MM).Until recently,MM was defined by presence of end-organ-damage,specifically hypercalcemia, renal-failure, anemia and bone-lesions(CRAB-features). International-Myeloma-Working-Group(IMWG)revised diagnostic-criteria adding three specific-markers:clonal-bone-marrow-plasma-cells greater than 60%, serum-free-light-chain-ratio (FLC)more than 100 and at least two focal-lesions on magnetic-resonance-imaging(MRI). After this update,it's now time to change therapeutic-paradigm: new-IMWG-guidelines allow earlier intervention without waiting end-organ-damage to treat . Nevertheless there is much to learn and share about these new standards that change treatment. When is the right-time to start therapy?We have tried to answer to this dilemma in our work comparing traditional-CRAB-features with recent-myeloma-diagnostic-criteria in a group of 220 newly-diagnosed-MM followed in our Department from 1999 to 2015. The aim of our retrospective-study was to analyze development of new-IMWG-biomarkers during disease-course before CRAB-events and beginning-treatment,discussing their strengths and weaknesses as well as lights and shadows. We evaluated 110 young-patients elegible for high-dose-chemotherapy and autologous-stem-cell-transplant(ASCT)and 110 old(more than 65-year-old)treated with different-kind of therapies. We highlighted presence of IMWG-new-criteria as myeloma-defining-events(MDEs) before CRAB-markers in 44 MM-patients (20% of all): 33 of them are old (median-age of 72 years,range 53-91)and 11 are young (median-age 57,range 41-65) and treated with transplant-procedure. In details most of them presented FLC ratio >100 (30 patients as 68% of this subgroup), following by MRI-lesions(10 patients as 23%) and lastly plasma-cells-bone-marrow-involvement greater of 60%(4 patients as 9%). The majority of these patients (39 as 89%) developed CRAB-characteristics after six months (median value, range 3-15) and have evolved in myeloma-requesting-treatment in less than a year. 27 of them have IgG, 12 IgA and 5 micromolecular-MM. The largest-part (40 patients)has an antecedent MGUS and smouldering-MM.Moreover five young-patients of the whole-population analysed with MDEs and good-clinical-status weren't treated based-on our clinical-judgement and continued close-observation,saving them from both early-therapeutic-toxicity and clonal-selection. Only two patients of 220 started treatment based-on new-IMWG-biomarkers,presenting with clinical-deterioration and increase in monoclonal-component. In conclusion our paper proved that movement from symptoms to biomarkers is a huge-step-forward expecially for elderly-patients,considering both clinical-signs and biological-features. However we need more pratical-implementation of new markers that are changing philosophy of treatment: these patients should be offered appropriate clinical-trial. More caution is needed in high-risk-group expecially young to avoid an overtreating-policy,considering also counter-arguments. Physicians should continue monitoring patients using tools- now-available,while waiting for results from future-prospective-studies. Increase of monoclonal-componenent was analysed not as CRAB-classic-criterion but like disease-marker. The time-difference between new -IMWG-criteria and CRAB-events is less than one year (mean-value 6 months). Figure 1 New-IMWG-criteria-versus-traditional-CRAB. We have studied in our 44-patients with new-diagnostic-markers,time-course of hemoglobin, monoclonal-protein and creatinine-values. Figure 1. New-IMWG-criteria-versus-traditional-CRAB. We have studied in our 44-patients with new-diagnostic-markers,time-course of hemoglobin, monoclonal-protein and creatinine-values. Disclosures No relevant conflicts of interest to declare.

In the proposed revised World Health Organization (WHO) criteria for the diagnosis of BCR-ABL− myeloproliferative diseases (MPDs), exclusion criteria have been replaced by the presence of JAK2 mutations. We applied these criteria to 45 children with MPDs: 13 with polycythemia vera (PV) and 32 with essential thrombocythemia (ET). Among these 45 patients, 12 with ET and 5 with PV had a familial history of MPD, and had been investigated for hereditary mutations of the erythropoietin receptor, thrombopoietin, or MPL genes. We found that the JAK2V617F mutation in children occurs less frequently than in adults, and that exon 12 JAK2 mutations are absent. On the basis of the revised WHO criteria, a significant proportion of childhood PVs were misdiagnosed. Furthermore, all familial ET, including patients carrying the hereditary MPLSer505Asn activating mutation, were erroneously diagnosed as MPDs. Our observations suggest that childhood MPDs require a set of specific diagnostic criteria.

Frequent blood loss induces progressive depletion of iron stores, leading to iron deficiency and, ultimately, to overt iron-deficient anaemia. The erythropoietin-mediated bone marrow response to anaemia is under the control of hypoxia-inducible factors (HIF), the master regulators of oxygen and iron homeostasis. Since the HIF-1α(Pro-582-Ser) variant is associated with elevated trans-activation capacity of hypoxia responsive elements of target genes, we investigated whether the HIF-1α(Pro-582-Ser) polymorphism might influence the response to repeated blood withdrawals.Using polymerase chain reaction analysis and DNA sequencing, we retrospectively investigated the presence of HIF-1α(Pro-582-Ser) in a series of 163 blood donors. Haematological findings, serum ferritin levels and frequency of donations were compared according to the mutational status of the HIF-1α gene.We found that male carriers of the HIF-1α(Pro-582-Ser) polymorphism had higher haemoglobin and ferritin levels than individuals homozygous for the wild-type allele. Moreover, the HIF-1α(Pro-582-Ser) polymorphism protected regular blood donors from developing iron deficiency and anaemia and predicted uninterrupted donation activity.These findings show for the first time that the HIF-1α(Pro-582-Ser) polymorphism significantly affects red blood cell and iron homeostasis after blood loss, conferring to male carriers a resistance to anaemia. Regarding the female gender, large series of individuals should be investigated to establish whether there is an effect of the HIF-1α(Pro-582-Ser) polymorphism in this population. Although these data need to be confirmed in prospective studies, they could have important implications in blood donor selection and donation procedures.

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Thus,romiplostim administration mimics the increased stimulation byTpo, while chronic eltrombopag administration reminds the consti-tutive activation of MPL. Given that these drugs have to be lifelongadministered, concern emerged when it was noticed that some pa-tients with immune thrombocytopenia (ITP) receiving romiplostindeveloped bone marrow fibrosis.

HIF2A transcription factor plays a central role in the regulation of the hypoxia responding pathway in mammalian cells, by modulating erythropoiesis and angiogenesis. Molecular alterations of oxygen sensing pathway constituents are implicated in hereditary erythrocytosis. Here we show that 2 members of a family with idiopathic erythrocytosis exhibited a new heterozygous G to A mutation at base 1605 of the exon 12 of hypoxia-inducible factor-2A (HIF2A) gene. This mutation determines the replacement of methionine by isoleucine at the position 535, very close to the position 531, where the hydroxyl acceptor prolyne is located. In addition, we found that mRNA expression of erythropoietin receptor, vascular endothelial growth factor, transferrin receptor, adrenomedullin and N-myc downstream regulated gene 1, up-regulated by HIF2A or hypoxia, were significantly higher in patients carrying the mutation than in normal controls. These results suggest that the HIF2A(M535I) gene mutation could induce hereditary erythrocytosis at a young age.

Purpose Polycythemia vera (PV) and essential thrombocythemia (ET) can present in pediatric age as sporadic or familial diseases. To define the biologic profile of childhood PV and ET, we evaluated specific markers in a cohort of pediatric patients affected by PV and ET, including cases with familial occurrence. Patients and Methods Thirty-eight children with PV and ET were investigated. The control group included 58 adults with PV and ET. Endogenous erythroid colonies, qualitative reverse transcriptase polymerase chain reaction for polycythemia rubra vera-1 (PRV-1) RNA expression, human androgen receptor assay and allele specific polymerase chain reaction for JAK2 V617F mutation were undertaken in all patients. Thrombopoietin, thrombopoietin receptor (c-mpl), and erythropoietin receptor mutation analysis was performed by direct sequencing in familial cases. Results The JAK2 V617F mutation in children with PV was significantly less frequent than in adult PV. The most common myeloproliferative marker found in these patients was PRV-1 RNA overexpression. Children and adults with sporadic ET showed a similar proportion of patients with PRV-1 RNA overexpression, JAK2 V617F mutation, and clonality, while none of the familial ET showed JAK2 V617F mutation and clonality. Also, PRV-1 RNA overexpression was significantly less common. Furthermore, most patients with familial ET exhibited the dominant-positive activating mutation of c-mpl. Finally, children with PV and ET had a significant lower incidence of thrombosis than adults. Conclusion This study demonstrates that familial and sporadic ET recognize different pathogenetic mechanisms. Myeloproliferative markers are specific tests for the diagnosis of ET in children with sporadic forms, while a significant proportion of children with PV can prove negative.

Background: Pharmacokinetic interaction between Vinca alkaloids and antiretrovirals has been widely demonstrated, even though its clinical relevance is still debated. The incidence of Hodgkin's lymphoma appears to be rising in HIV-infected people, and vinblastine - containing chemotherapy regimens are widely recommended in these pts. Supplement: Abstracts of the Tenth International Congress on Drug Therapy in HIV Infection http://www.biomedcentral.com/content/pdf/1758-2652-13-S4-info.pdf Conference: Tenth International Congress on Drug Therapy in HIV Infection 7-11 November 2010 Glasgow, UK (Published: 8 November 2010) doi:10.1186/1758-2652-13-S4-P215 Cite this article as: Cingolani et al.: Detrimental clinical interaction between ritonavir-boosted protease inhibitors and vinblastin in HIVinfected patients with Hodgkin lymphoma. Journal of the International AIDS Society 2010 13(Suppl 4):P215. Full text: PubMed Central: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3113000/