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Bone marrow fibrosis leading to dry tap aspiration and often associated with blast crisis has previously been reported in both Chronic myeloid leukemia and Primary myelofibrosis. The similarities between these two conditions in terms of clinical presentation and morphology can really create a diagnostic dilemma. Here we present a case of Chronic myeloid leukemia in fibrosis and blast crisis in a 32 year old lady which closely resembled Primary myelofibrosis in transformation. All myeloproliferative neoplasms can undergo blast transformation. In this case, the detection of Philadelphia chromosome helped to distinguish Chronic myeloid leukemia from other myeloproliferative neoplasms.

Case report - Introduction We present a rare case of a patient with a culture-negative mono arthritis. Our patient had a history of Essential Thrombocythemia (ET), and his mono arthritis initially responded to antibiotics. He had a fluctuating clinical course, and a multi-disciplinary approach with rheumatology, orthopaedics, haematology and radiology was needed. After multiple MRIs and two bone biopsies, he was diagnosed with acute myeloid leukaemia (AML) with blast transformation of his myeloproliferative neoplasm, essential thrombocythemia. This case highlights the need to consider the differentials of mono arthritis despite initial response to treatment, and the value of a multi-disciplinary approach. Case report - Case description A 59-year-old male was referred to rheumatology with new right hip pain, and high inflammatory markers. He was negative for infection, trauma, seronegative or crystal arthritis. Past history of ET diagnosed in 2011 with high-risk genetics. At haematology review 3 months prior he had new pancytopenia with deranged LFTs. A bone marrow biopsy (BMBx) showed post-ET myelofibrosis with no circulating blasts. His hydroxycarbamide and aspirin were stopped and blood counts recovered without other intervention. He was afebrile and had a right hip effusion. The hip aspirate revealed no growth after 48 hours and negative crystals. Bloods: Hb 101 WCC 5.1 Neutrophils 3.8 Platelets 318 CRP 276 ESR 72 Urate normal. MRI showed a right hip joint effusion, with extensive soft tissue oedema likely secondary to infection. He was commenced on IV Flucloxacillin, clinically improved and was discharged to complete antibiotics. At review in 2 weeks he had worsening hip pain, night sweats, raised CRP, and was anaemic with normal WCC and platelets. A repeat MRI showed evolving abscess formation within the acetabular roof. After discussion with haematology and orthopaedics, the clinical impression was septic arthritis as he was responding to treatment, his blood film was normal and recent BMBx showed no transformation. The plan was to continue with antibiotics and to perform a bone biopsy. Bone biopsy showed necrotic debris secondary to the underlying osteomyelitis. Due to fluctuating course a repeat MRI was performed showing a larger hip effusion with appearances suspicious for malignancy. A repeat bone biopsy showed post ET fibrosis with blasts and large tumour cells. A blood film showed peripheral blasts circulating. The unifying diagnosis was AML with blast transformation of myeloproliferative neoplasm. Our patient was refractory to chemotherapy. He was treated with palliative radiotherapy and died with palliative care input. Case report - Discussion Septic arthritis typically affects one joint and mimics include abscess, AVN, cellulitis, crystal, malignancy, reactive and inflammatory arthritis, and transient synovitis. Synovial fluid analysis is the gold standard for the diagnosis and will demonstrate growth in approximately 80% of all cases of non-gonococcal septic arthritis. The remaining 20% are ‘culture negative’ and may demonstrate no growth for a variety of reasons. 14% of patients with ‘culture negative’ septic arthritis will have positive blood cultures and newer diagnostic tools such as PCR testing of synovial fluid increases the likelihood of correctly identifying an organism. Our patient initially responded to treatment for septic arthritis; however, the atypical clinical course and history of ET prompted further investigations for differentials of ‘seronegative arthritis.’ ET is a myeloproliferative neoplasm with a prevalence of 40/100000. It is usually indolent and recognised genes are JAK2, CALR and MPL. Complications include vascular events such as thrombosis and haemorrhage. More serious complications of transformation to myelodysplasia, AML or myelofibrosis are rare with an incidence of 1—5% and median time to transformation is between 84 and138 months. Rheumatic manifestations of leukaemia include leukaemia arthritis. This is uncommon and develops due to infiltration of synovial membrane by leukaemia cells. Synovial fluid or synovial biopsy can be analysed for blasts and flow cytometry. The reported incidence is 12% in children, and only case reports in adults. The blast infiltrative phase of leukaemia usually occurs in the bone marrow, or blood. Previous case reports describe extra medullary blasts present in lymphoid tissues, and here we report an extra medullary blast sarcoma. Transformation of ET to AML is typically very difficult to manage, with a poor prognosis. Treatment options include chemotherapy, stem cell transplants and the JAK inhibitor ruxolitinib. Case report - Key learning points Differentials for a mono arthritis are wide and this is a rare case of hip mono arthritis as the clinical presentation of transformation of an ET to AML. Septic arthritis is one of the most important diagnoses to rule out in a patient with a mono arthritis and high inflammatory markers. Up to 20% of septic arthritis can be ‘culture negative.’ Peripheral blood cultures and PCR testing of synovial fluid can be used to enhance the identification of organisms. Although our index of suspicion was high, our patient was not displaying typical manifestations of transformation to AML. The development of an acute leukaemia can be insidious, and case reports have described infiltration of bone marrow simultaneously or months following an extra medullary blast crisis. This case highlights the importance of further, and if necessary repeated, investigations in a patient with an atypical history or clinical course. Malignancy as a differential for mono arthritis is important to consider as mis diagnosis could delay treatment and prognosis is very different. Both bone biopsies yielded abnormal bone; however, it was the second biopsy that showed circulating blasts. In our case the bone biopsies were performed without radiological guidance, and studies have shown that CT guided biopsies have a higher yield. In future, consideration could be given to utilising radiologically guided biopsy. A multi-disciplinary approach between a number of specialities is often needed in complex cases. This case highlights the value of this with collaboration with our haematology, orthopaedic, radiology and pathology colleagues.

Chronic Myelogenous Leukemia (CML) is a chronic myeloproliferative neoplasm characterised by uncontrolled proliferation of mature and maturating granulocytes. In our case 42 year male over a period of 13 months showed blastic transformation with severe thrombocytopenia, disseminated intravascular coagulation and bleeding. Herewith we present this case for its clinical behaviour, hematological findings and disease course. Keyword: Myeloproliferative Neoplasms, Blast crisis, Leukemia.

Among 274 patients with chronic myelomonocytic leukemia (CMML) and followed for a median of 17.1 months, blast transformation (BT) occurred in 36 (13%). On multivariable analysis, risk factors for BT were presence of circulating blasts (HR 5.7; 95% CI 2.8–11.9) and female gender (HR 2.6; 95% CI 1.3–5.1); the results remained unchanged when analysis was restricted to CMML-1. ASXL1/SRSF2/SF3B1/U2AF1/SETBP1 mutational frequencies were not significantly different between time of CMML diagnosis and BT. Median survival post-BT was 4.7 months (5-year survival 6%) and better with allogeneic stem cell transplant (SCT) (14.3 months vs. 4.3 months for chemotherapy vs. 0.9 months for supportive care; P = 0.03). Neither karyotype nor mutational status was independently associated with risk of BT or post-BT survival. We conclude that female patients with CMML and those with circulating blasts are at a higher risk of BT. Post-BT survival is dismal and our observations suggest consideration of allogeneic SCT prior to BT.Am. J. Hematol. 90:411–416, 2015. © 2015 Wiley Periodicals, Inc.

Zusammenfassung: Es wird ein 20jahriger Patient aus Mozambique mit einer nordamerikanischen Blastomykose n. Bl. vorgestellt. Die Verabreichung von Ketoconazol fuhrtezu einer Besserung des klinischen Bildes, jedoch nicht zur Abheilung. Als Mittel der Wahl erwies sich nach chirugischer Exstirpation beteiligter Rippenanteile eine Kombinationstherapie von Amphotericn B i.v. + 5-Flucytosin. Immunologische Parameter wurden vor und am Ende der Therapie gepruft: Der Intrakutantest mit Varidase, PPD, Tkichosan, Histoplasmin und Blastomycin war positiv. Dysreguiationen unspezifiscber Abwehrmechanismen und zellvermittelter Immunreaktionen konnten nachgewiesen werden. Die Leukozytenadharenz war sehr stark herabgesetzt, die Zahl E+ -T-Zellen erniedrigt. Im LTT fehlte die T-Zellmitogenreaktivitat vollstandig; monozytare Suppressionseffekte”kurzlebige Suppressorellen“konnten nicht registriert werden. Im Leukozytenmigrationstest war mit Trichophytin, Candidin und Histoplasmin eine Hemmung der Migration gegen diese Antigene nachweisbar LMT 1, 2. Mit Blastomycin war keine Sensibilisierung erkennbar. Nach der Behandlung regiderten wir weiterhin eine Abnahme der Phagozytoserate weit unter den Normbereich beigegenlaunfiger Tendenz des Phagozytoseindex. - Im LTT waren jetzt T-Zellmitogeneffekte erkennbar, der Normbereich de nicht erreicht. PPD und Candida-Antigen fuhrten zu einer erheblichen Stimulierung der Blasttransformation; die Histoplasmin-Stimulierbarkeit nahm unter der Therapie ab. Monozytare Suppressoreffekte konnten jetzt verstarkt nachgewiesen werden SZI 4.0. Die immunologischen Befunde werden als kombinierter T-Zell- und Monozytendefekt gewertet und diskutiert. Summary: A 20-year-old patient from Mozambique with a North American Blastomycosis n. BL was admitted for treatment. The administration of ketoconazole brought a clinical improvement, but did not heal the patient. Combined therapy with amphotericin B+5-flucytosine following surgical exstirpation proved successful. Immunological parameters were tested before and after therapy: The intracutaneous tests with varidase, PPD, tricbosan, histoplasmin and blastomycin were positive. Dysregulation of nonspecific and specific immune responses was detected. The leucocyte adherence LA was substantially, and the number of T-cells slightly, reduced. In the LTT the T cell mitogen reactivity was absent. No monocytic suppression effects (shortlived suppressor cells) could be detected. The leucocytes migration test LMT with trichophytin, candidin and histoplasmin revealed a specifrc sensitization LMT l, 2. This sensitization could not be detected with blastomycin. After therapy we also observed a reduction in the phagocytosis rate far below the normal range, the phagocytosis index showing the opposite tendency. T-cell mitogenic effets now also appeared in the LTT, but the normal range was not reached. PPD and Candida-antigen continued to induce substantial stimulation of blast transformation. Monocytic suppressor effects were more pronounced SZI 4.0. - The immunological results were discussed as a combined T cell and monocyte defect.

We report a patient with granulomatous mycosis fungoides whose disease transformed into a high grade blast lymphoma with angiocentric features within 12 months of the initial diagnosis. This repudiates previous claims that granulomatous inflammation is protective in cutaneous T-cell lymphoma.

In the majority of the patients with myeloproliferative neoplasm-associated myelofibrosis (MPN-MF), the disease interferes with the quality of life and social activities. A great proportion of patients suffer of general symptoms, such as fatigue, constitutional symptoms, or pruritus, that reflect the biological activity of the underlying disease. The greatest impact on the patients’ well-being is offered by severe anemia and progressive splenomegaly, and the therapy of these manifestations represents a major medical needs. Some of the disease complications, such as hemorrhagic or thrombotic events and infections, need treatments that are not specific for MPN-MF. On the contrary, treatment of extramedullary nonhepatosplenic hematopoiesis, treatment of pulmonary or portal hypertension, and therapy for the accelerated phase and of blast transformation of the disease are MPN-MF-specific medical needs.

Diabetes insipidus (DI) is a rare complication of leukaemia. An association between monosomy 7 and DI in leukaemias has been proposed. We present a case of Ph1-positive CML who developed polyuria at the time of lymphoid blast transformation associated with loss of chromosome 7. Biochemical results were not diagnostic of DI and a therapeutic trial of DDAVP was unsuccessful. Post-mortem showed a peripituitary and renal leukaemic infiltrate and although DI is a possibility, the cause of his polyuria remains unresolved.

Transformation of myelodysplastic syndrome to hematologic malignancies is not uncommon, but involvement of three committed progenitor cell lines at one time is seldom seen. We present a case of myelodysplastic syndrome with blast transformation, neoplastic cells that were difficult to classify morphologically, and basophilia found in marrow and peripheral blood. Differential diagnosis included myeloblastic leukemia, erythroblastic leukemia, megakaryoblastic leukemia, basophiloblastic leukemia, and systemic mast cell disease (SMCD). By using a battery of cytochemical techniques niques and irnrnuno~tochemicalm ethods, we were able to demonstrate the presence of myeloblasts, erythroblasts, and megakaryoblasts, thus excluding the possibility of SMCD and basophiloblastic leukemia. (The J Histotechnol 13:67, 1990)

Blast transformation of peripheral blood lymphocytes (PBL) in dilated cardiomyopathy (DCM) patients and normal controls was examined to assess the cell mediated immune response of these patients. Uptake of3H-thymidine by PBL of DCM patients incubated for 72 hrs with phytohaemagglutinin (PHA) was 17787±9513 CPM and without PHA was 1475±529 CPM showing a stimulation index (SI) by PHA of 12.95±6.35. The corresponding values in healthy controls were 55078±12282 and 1868±792 respectively with a SI of 38.0±26.0. Blast transformation of PBL by PHA was significantly suppressed in DCM patients as compared to normal controls. This suppression was found to be highly significant and possibly indicates the defective cell medicated immune response in DCM patients.

We report a case of chronic myelogenous leukemia (CML) with a Philadelphia (Ph) chromosome. During the transformation phase of the disease, a del(7)(p11p15) and a +Ph were identified as additional chromosomal anomalies. We believe that loss of the segment 7p11→p15 may play an important role in the progression of the disease.

A 66-year-old man was diagnosed 10 years ago with thrombocytosis and treated with hydroxyurea. Recently, his condition deteriorated and he was found to have 68% blasts in the blood and AML-M5a. Conventional cytogenetic analysis and fluorescence in situ hybridization studies using 11-painting and MLL probes showed that chromosome 11 had duplications or triplications; the markers were also derived from the chromosome 11-MLL region. Therefore, we have demonstrated segmental rearrangement of chromosome 11 involving the MLL region resulting in multiple copies of the MLL gene.

Translocation (2;8)(p12;q24) in blastic transformation of atypical chronic myeloid leukemia

We report the occurrence of the same translocation, t(1;7)(p36;q32), in bone marrow cells from two patients with de novo myelodysplastic syndrome (MDS), each of whom displayed the morphologic signs of refractory anemia with excess of blasts (RAEB) and a poor response to treatment.

A 40-year-old male was diagnosed with refractory anemia with excess blast in transformation; 11 months later, with the same hematologic situation, a cytogenetic study was carried out on bone marrow and a translocation between chromosomes 6 and 9 with breakpoints at p23 and q34, respectively, was found.

We report a case of chronic myelomonocytic leukemia (CMMoL) with unusual features and an isochromosome 14q as the sole abnormality. A review of the literature suggests that isochromosome 14q (or trisomy 14) is a marker of leukemia with dysplastic features.

We report a patient with Ph+ chronic myelogenous leukemia (CML) whose recurrent blast crises were associated with marrow eosinophilia and inv(16). After intensive chemotherapy, for each blast crisis, the patient reentered chronic phase with disappearance of both the inv(16) and the eosinophilia.

A balanced reciprocal t(6;8)(q22;q12) was detected in a female with Philadelphia chromosome (Ph)-positive chronic myelocytic leukemia (CML) after blastic transformation.

We present a case of an 18-year-old patient with refractory anemia with excess blasts in transformation (RAEB-t). Trisomy 14 was the only abnormality found in bone marrow cells on five occasions in 15 months.

A 27-year-old male developed massive generalized lymphadenopathy with chronic myelomonocytic leukemia (CMML) presenting as extramedullary blast crisis mimicking a lymphocytic lymphoma. On presentation, a consistent chromosomal abnormality involving chromosomes 8 and 13, i.e. 46,XY,t(8;13) (q11;p11), was present in lymph node tissue, bone marrow and unstimulated peripheral blood. The appearance of trisomy 21 in addition to the presence of the original cytogenetic abnormality is simply regarded as clonal evolution, i.e. 47,XY,t(8;13)(q11;p11),+21. The importance of the cytogenetics lies in finding the same abnormality in bone marrow and lymph node, adding evidence that the immunologically similar cells in the two sites have arisen from a common progenitor cell. To our knowledge, this novel chromosomal abnormality has not been reported in association with a unique case.

We describe here a patient with a low-grade follicular lymphoma evolving to a Burkitt-like lymphoma which at the time of blastic conversion showed multiple chromosome aberrations, including a t(8;22) (q24;q11) typical Burckitt variant translocation associated with a translocation between chromosome 2p11 and chromosome 18q21 which may be an undescribed variant of the t(14;18) follicular lymphoma chromosomal rearrangement

Clinically chronic myeloid leukemia is a biphasic or triphasic disease that is usually diagnosed in the initial 'chronic', 'indolent' or 'stable' phase and then spontaneously evolves after some years into an advanced phase. This advanced phase can sometimes be subdivided into an earlier accelerated phase and a later blast phase or blast transformation--in about one-half of patients the chronic phase transforms unpredictably and abruptly to a blast phase, while in the other half of patients, the disease evolves somewhat more gradually, through an accelerated phase, which may last for months or years, before a blast phase ensues; this may have myeloblastic or lymphoblastic features. Although much is now known about the molecular biology of the disease, the molecular basis of disease progression is still obscure. The popular thinking has been that one or more probably a sequence of additional genetic events occurs in the BCR-ABL positive clone. When the critical combination of additional events is achieved, clinically definable transformation occurs. Here we review what is known of the mechanisms underlying the evolution of chronic myeloid leukemia from a chronic phase to a blast transformation.

Microsatellites are highly polymorphic, short-tandem repeat sequences dispersed throughout the genome. To test the occurrence of genetic instability in the progression of chronic myelocytic leukemia (CML), we studied microsatellite instability (MSI) in 17 patients with CML. The DNAs from both chronic phase and blast crisis were analyzed at 10 loci. No MSI was observed in any of the 17 cases of blast crisis. These results indicate that MSI is rare and is not associated with progression to blast crisis in most cases of CML.

We attempted treatment with low-dose aclarubicin (ACR), a new anthracycline, in a 66-year-old man with blastic transformation of essential thrombocythemia (ET). Two courses of ACR (20 mg/day x 7 days) were given intravenously. He showed a good response to this therapy without severe side effects. He has since maintained a state of prolonged remission. These observations indicate that low-dose ACR may be beneficial for management of the blastic transformation of ET.

A case of successful pregnancy in a 47-year-old Omani grand-multipara who had Myelodysplastic Syndrome (MDS) is described for the first time in Oman. A review of the literature suggests that in Japan the problem may be more common than elsewhere. The unusual features in the case reported here include, improvement in haematological parameters during the pregnancy contrary to expectation, and in addition, the religious and cultural factors that intruded into the clinical decision making process. Suggestions to combat the latter factors are made.

Fifteen cases of chronic lymphadenitis with massive hemophagocytic sinus histiocytosis were analyzed. Fourteen patients were whites, 13 were Europeans, and 11 were males; 10 patients were under 10, 4 were over 20, and 2 over 60 years old. The oldest patient died; all other either healed without therapy or are in excellent condition. We studied the cytologic features of lymph node imprints. A 5-year-old girl was examined more thoroughly. High antibody titers to Klebsiella antigens were found repeatedly. The patient also had a constant lymphocytopenia. Phytohemagglutinin-induced blast transformation and lymphotoxin production were within normal limits. No serum Epstein-Barr virus-antibodies could be detected.

Two case of acute blast cell transformation in myeloproliferative disorders associated with a dicentric 17q isochromosome are reported. In both cases, the karyotypes also also included a Philadelphia 9q;22q translocation, and in one case, an additional chromosome 8 (trisomy 8).

This report describes the acquisition of tuberculin skin-test sensitivity by six of eight sarcoid patients after a single injection of dialyzable transfer factor (TFd) from tuberculin-positive healthy subjects. The acquisition of cellular immunity to purified protein derivative (PPD) by the recipient was also demonstrated in vitro by PPD-induced blast transformation. TFd did not cause PPD-induced blast transformation when added directly to cultures of lymphocytes from sarcoid patients.

Using morphological criteria, patients with Crohn's disease have higher in vitro spontaneous peripheral blood lymphocyte blast transformation than control subjects (P < 0.01). The rate of spontaneous thymidine uptake did not differ between the two groups. The immune mechanism responsible for this phenomenon is unknown.

A series of 55 patients with B-cell chronic lymphocytic leukaemia (CLL) and prolymphocytic leukaemia (PLL) was studied in order to investigate the evolution of prolymphocytoid transformation of CLL. Peripheral blood films were assessed for the percentages of prolymphocytes (%PROL) during a followup period of 2 months to 24 years. The majority of patients with typical CLL (less than or equal to 10% PROL) had minor variations or transient increases in %PROL throughout the course of the disease, but in one third of them a steady rise in the proportion of these cells was documented. Patients presenting with 11-55% PROL, referred to as CLL/PL, exhibited three patterns of evolution: half of them showed stability of the PROL counts, one third had unsustained increases in the %PROL and 18% showed definite progression to a PLL-like blood picture. Patients diagnosed as PLL (greater than 55% PROL) had maintained a high %PROL during the period of observation. Serial marker studies in some CLL and CLL/PL cases showed that the percentage of M-rosettes and the intensity of SmIg remained at the same initial levels in all but two cases. These two cases in the CLL/PL group showed a significant decrease in the percentage of M-rosettes and stronger SmIg staining associated with progressive prolymphocytoid transformation. Patients with CLL and CLL/PL who had a sustained rise in the %PROL responded poorly to treatment compared with those with stable disease.

When mycoplasmas infect lymphocytes they behave as multivalent ligands and cap on the lymphoid cell surface in the absence of added specific antibody. There is an apparent high correlation between mycoplasma capping and blast transformation of the infected lymphocytes. Mycoplasma caps are shed from the surface of cells as an aggregate containing host membrane vesicles. This novel interaction may suggest a physiological role for the phenomenon of capping and may play a part in mycoplasma pathogenesis.

We studied the multimeric composition of plasma von Willebrand factor (vWf) in 26 patients with chronic myelocytic leukaemia (CML); 13 in chronic phase, 8 in blast crisis, 5 in both chronic phase and blast crisis. The relative amount of large (multimer band greater than or equal to 11) multimers calculated by densitometer scan following SDS-agarose gel electrophoresis was 14.6 +/- 2.9% (mean +/- SD) in normal controls, 8.7 +/- 4.7% in chronic phase and 15.0 +/- 5.2% in blast crisis. CML patients in chronic phase (but not in blast crisis) had a significantly lower percentage of large multimers than normal controls (p less than 0.001). The relative amount of large multimers was positively correlated with a ratio of ristocetin cofactor/vWf antigen (p less than 0.005), and was negatively correlated with platelet count (p less than 0.001), WBC count (p less than 0.05) and granulocyte count (p less than 0.05). We conclude that some patients with CML, especially in chronic phase, lack large multimers. The negative correlation of the relative amount of large multimers with platelet and granulocyte count suggests that large multimers may be consumed in high platelet count states or degraded by protease(s) from increased blood cells.

Tetanus toxoid induced-blast transformation of peripheral blood lymphocytes of 15 immunized healthy subjects was studied. According to the magnitude of the [3H]thymidine incorporation, the subjects were classified into two groups: high and low blast specific responses. The high or low blast response induced by tetanus toxoid did not correlate with the stimulation induced by PHA and PPD nor with the antitetanus-antibody titer of these subjects. T cells were shown to be involved in this specific blast response. The differences in the magnitude of the blast response could be easily explained by the existence of B cells with suppressor activity on T cells functions rather than by inhibition of the tetanus toxoid induced stimulation by an antigen-antibody complex. Relationship with HL-A system will be investigated.

Therapy with vincristine and prednisone (VP) has produced remissions in 30% of patients with chronic myelogenous leukemia in blast transformation (CML-BT). The possibility that therapy with VP can adversely affect the production of mature granulocytes in this setting has not been appreciated, as these drugs are generally considered free of myelotoxicity. In this report we review eight courses of VP administered to three patients with CML-BT. Granulocytopenia developed following all five courses in which granulocyte counts were normal prior to therapy; granulocytopenia worsened in two of three courses in patients who were granulocytopenic prior to therapy. Progressive leukemia in the marrow was excluded as a cause of granulocytopenia. It is important to recognize that VP therapy rather than disease progression may be a cause of granulocytopenia in CML-BT.

The authors describe a case of Sweet's syndrome in a woman affected with chronic myeloid leukemia. They emphasize the association of the syndrome with a progression of the disease and the complete disappearance of it for 3 years until the present time after allogeneic bone marrow transplantation.

Human seminal plasma from normal or patients with abnormal parameters of the ejaculates contains an inhibitory material that expresses potent in vitro inhibitory activity on PHA-M-induced blast transf