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This case report concerns a 44-year-old woman with subacute myelomonocytic leukemia who developed an unusual bullous lesion on her leg. Initially treated as a bacterial ecthyma, this lesion proved to be a specific leukemic infiltrate. We will briefly review myelomonocytic leukemia and the skin findings of the myeloid leukemias.
We report a case, in a 74-year-old man, of chronic myelomonocytic leukemia (CMML) that showed cutaneous involvement in its terminal phase. The patient developed a nodular eruption with an irregular distribution over the entire skin surface. Histology showed an acute leukemic infiltration in the reticular dermis. We were able to demonstrate cells with intermediate myeloid and monocytic characteristics ("paramyeloid cells") in the skin biopsy and in bone marrow smears. There have been only four patients reported previously with similar clinical findings. In one of them the cutaneous eruption heralded an aggressive clinical shift of the disease, as in our case. The present case confirms the utility of skin biopsy in similar cases for predicting the evolution of the disease.
We present a patient with chronic lymphocytic leukemia who developed a painful penile ulcer that was initially diagnosed as leukemia cutis, as evidenced by an atypical leukemic infiltrate on biopsy. A Tzanck preparation was positive for multinucleated giant cells, and the diagnosis of herpes genitalis was confirmed by viral culture. In patients with hematologic malignancies, herpes simplex virus must be included in the differential diagnosis of ulcerative lesions. The histopathologic findings of inflammatory dermatoses in these patients may include an atypical infiltrate, because of the predominance of atypical inflammatory cells in the peripheral circulation.
The leukemic infiltrate in the liver in hairy cell leukemia may be easily overlooked in conventional histological slides and an exact classification may not always be possible. In order to facilitate the identification of tricholeukocytes , it is suggested to perform the tartrate-resistant acid phosphatase stain on routinely formalin fixed and paraffin-embedded liver biopsy specimens. Thereby it will be in most cases possible to demonstrate sufficiently enough enzyme activity to establish unequivocally the diagnosis of hairy cell leukemia.
In acute myeloid leukemia (AML-46 patients) and various entities of chronic myeloproliferative diseases (CMPD-58 patients) an evaluation and comparison of clinical and postmortem findings has been performed. This study included also aspirates and core biopsies of the bone marrow which were initially taken on admission of those patients. Classification of CMPD was done following the concept of Georgii et al. (1984) into CGL -24-, CMGM-6-, E-MS-13- and MS/OMS-15 cases. There was a significant increase in blastic crisis in CGL compared with the other entities and in the latter a prolongation of the total course of disease due to a long period between symptoms--clinical diagnosis. As revealed by the autopsies causes of death were mostly infections (pneumonia, septicemia-50%) and lethal hemorrhages (gastrointestinal and cerebral--about 30%) in both AML and CMGM patients. Rare causes comprised fatal pulmonary embolism due to a peripheral thrombocytosis in CMPD, acute rupture of the spleen and extensive leukemic infiltrates of the myocard in AML. In addition to the well known giant enlargement of the spleen in MS/OMS, the relatively high frequency of a meningeal involvement (meningeosis leukemica) in AML (about 35%) and during an acute transformation in CMPD (up to 30%) was conspicuous. The examination of the bone marrow at various sites became feasible during the postmortem procedure and thus provided the opportunity to investigate the development and extent of a myelosclerosis evolving in CMPD. In contrast to the a- or hypoplasia and regeneration of the hematopoiesis following chemotherapy, the evolution of myelosclerotic lesions showed a very uniform pattern throughout the skeleton and obviously no reversal of a manifest MS/OMS after cytotoxic treatment.
A 66-year-old woman was seen and treated for a chronic lymphocystic leukemic infiltrate of a proximal interphalangeal joint, which presented with clinical and radiologic signs consistent with a pyogenic arthritis.
Facial paralysis in children is most often idiopathic, and isolated facial nerve palsy resulting from leukemic infiltration is a rare occurrence. We report a 13-year-old male with acute lymphoblastic leukemia presenting with bilateral facial palsy, who was previously diagnosed with idiopathic facial palsy and treated with steroids. This rare presentation of acute lymphoblastic leukemia should be kept in mind as a diagnostic possibility in a patient with bilateral facial nerve paralysis.
The cause of eyelid pruritus (itching) may be difficult to determine, particularly in preverbal children. Tearing, photophobia, or eye rubbing may be the first manifestation of leukemic infiltration or graft-versus-host disease, necessitating early appropriate therapy. We report a child in whom persistent eye rubbing developed after bone marrow transplantation for leukemia. Morphine administration was found to be the cause of this symptom.
We administered a "cocktail" of three model substrates for hepatic processes: antipyrine for oxidation, lorazepam for glucuronidation, and indocyanine green for hepatic blood flow, to children with acute lymphocytic leukemia (ALL). The plasma clearance of these substrates was determined before and after remission-induction therapy in 14 children with ALL. We found an improvement in clearance of antipyrine (0.65 to 0.95 ml/min/kg; P less than 0.01) and lorazepam (0.93 to 1.20 ml/min/kg; P less than 0.05) in 12 of 14 patients, with a mean increase of 67% and 52%, respectively, from before to after remission. There was no significant difference in mean indocyanine green clearance from before to after induction (14.8 vs. 14.4 ml/min/kg). There were no significant differences in liver function test results (SGOT, prothrombin time, or serum bilirubin) from before to after induction. Plasma concentrations of albumin, alpha 1-acid glycoprotein, and apolipoprotein A changed by a mean of +11.1%, -38.2%, and +68.6%, respectively, from before to after remission. However, these changes did not account for the changes in total plasma clearance of lorazepam, because lorazepam free fraction did not change and lorazepam free clearance increased by a mean of 83%. Our hypothesis is that eradication of hepatic leukemic infiltration by ALL remission therapy resulted in an improvement in microsomal metabolism of antipyrine and lorazepam.
In 49 children with acute lymphoblastic leukemia serial EEGs were performed during the course of treatment. Therapy in the first four weeks consisted of: Prednisone, vincristine, daunorubicine and L-asparaginase. In the second month 6-mercaptopurine, cytosin-arabinoside, cyclophosphamide, methotrexate-i. th. and cranial irradiation were administered. Maintenance-therapy consisted of 6-mercaptopurine, cyclophosphamide and methotrexate i.v. Before treatment only 24% of patients showed normal EEG-findings, whereas 57% presented sly induced by leukemic infiltrations and partly due to the impaired clinical state. At the end of the first phase of therapy, the combined toxicity of vincristine and L-asparaginase led to the finding of 23% severely and 37% moderately slowed EEGs. Slightly disturbed EEGs were found in 29% and normal ones in 11% of children. Regression occurred duirng the phase of CNS-prophylaxis. At its end 37% of recordings were normal and 57% slightly abnormal. After maintenance-therapy of 1/2 to 1 year duration, there were 65% normal findings. Moderate and severe disorders were no longer demonstrated. Paroxysmal activity developed twice, each during the first phase of therapy and accompnaying convulsions. In both cases we saw slowing of background-activity and signs of increased excitability still months after. In one of these patients, the probable cause was a vincristin-encephalopathy, the cause of the second case remained unknown. EEGs of two furtehr patients with rubella-encephalitis and subarachnoideal hemorrhage exhibited severe unspecific changes.
AIM: Oligo- or monarthritis is reported as an uncommon complication of both acute and chronic leukemia. Childhood leukemias are complicated more frequently by leukemic arthritis (LA) than adult cases. LA occurs rather in acute than in chronic leukemia and can present at any stage of the disease. Proposed pathogenic mechanisms of arthritis in leukemia are leukemic infiltration of synovial tissue and resulting periosteal and capsular inflammation. As the primary manifestation of chronic lymphocytic leukemia (CLL) and immunocytoma (IC), LA is extremely rare. In such cases osteoarthritis may then be misdiagnosed as the source of joint disease. METHOD: We report a case of glenohumeral arthritis with complete rotator cuff tear and humeral head migration in an 88-year-old patient. Surgery exposed joint effusion, synovitis and chondromalacia with glenohumeral joint destruction. RESULTS: Histopathological examination revealed an articular chondrocalcinosis and bone marrow infiltration by an immunocytoma (B-cell non-Hodgkin lymphoma of low malignancy). CONCLUSION: Although LA is an uncommon complication in CLL and IC, it may be considered in elderly patients with lymphocytosis and arthritis.
BACKGROUND: Cochleovestibular lesions in patients with acute myeloid leukemia or the blastic phase of chronic myeloid leukemia are usually due to leukemic infiltration, infection or hemorrhage. In contrast, the most likely cause of cochleovestibular lesions in the chronic phase of the chronic myeloid leukemia seems to be disturbed microvascular perfusion and vascular occlusion. CASE REPORT: A 45-year old patient with a chronic myeloid leukemia presented with the sudden onset of profound deafness in his right ear combined with a total loss of vestibular function on the same side. The hemoglobin count was 10.5 g/dl; the white blood cell count 448 x 10(9)/I; the platelet count 71 x 10(9)/I. All of the plasmatic coagulation factors were in the normal range. The patient was treated with cytostatic drugs and responded well (rapid cytoreduction), but the deafness persisted. DISCUSSION: Cochleovestibular lesions in the chronic phase of the chronic myeloid leukemia are very rare. The most likely cause in the case described above seems to be increased blood viscosity due to the high white cell count and alterations in the leukocyte rheology (leukostasis syndrome). CONCLUSION: In patients with leukemia and acute cochleovestibular lesions in contrast to other patients with sudden deafness and/or sudden loss of peripheral vestibular function, a combination of chemotherapy and leukopheresis capable of rapid cytoreduction is necessary, whereas a conventional hemorrheologic therapy seems to be insufficient.
The article presents the case of a 37-year-old patient with acute leukemia. Four days before the appearance of acute symptoms, the patient manifested unspecific prodromes, with headache, coughing, and tiredness. Within 18 hours, he then presented the complete picture of acute leukemia, with multiple brain hemorrhages, diffused leukemic infiltration of all organs, and the typical alterations in blood picture. Eighteen hours after the first specific symptoms, the patient died of therapy-resistant cerebral pressure.
Findings in a total of 200 children suffering from leukemia were evaluated. Ocular symptoms were found in 26% of the cases. Typically, fundus hemorrhages were found in the initial stage, leukemic infiltrates in the final stage and papilledema in the meningosis leucaemica stage. In patients with ophthalmologic changes the survival time was shorter than in patients with no ocular involvement. Ophthalmological "dispensaire" treatment is generally recommended.
We investigated the surface markers on lymphoblasts from 37 patients with acute lymphoblastic leukemia. Spontaneous rosette formation with sheep erythrocytes (E rosettes) identified T cells and the presence of surface immunoglobulin identified B cells. Eight patients had T-marker lymphoblasts; 28 had no markers (null lymphoblasts), and one patient had B-marker lymphoblasts. The eight patients with T-marker acute lymphoblastic leukemia had massive leukemic infiltration, frequently a mediastinal mass, and a poor prognosis. The T-marker lymphoblasts had a weak or negative periodic acid-Schiff reaction and a very low antigenic stimulation to allogeneic lymphocytes. The association of T-marker lymphoblasts and some of the conventional poor-risk factors appears to be reliable in predicting a poor prognosis.
Leukemia cutis may clinically mimic many inflammatory dermatoses. A patient with myelodysplastic syndrome presented with an acute eruption of bilateral, lower-extremity, tender, indurated, brown plaques that clinically resembled chronic stasis dermatitis. Histologic study revealed a dermal myeloblastic leukemic infiltrate.
A patient with relapsed acute myelomonocytic leukemia (AML, FAB M4) developed skin infiltration by leukemic blasts. On immunochemistry, the blasts showed "bot" positive cytoplasmic staining for cytokeratins AE1/AE3 and CAM 5.2, resembling the pattern seen in Merkel cell carcinoma of skin. However, the blasts were positive for myeloid markers and negative for cytokeratin 19 and chromogranin. Aberrant immunochemical staining can lead to misdiagnosis unless a panel of antibodies of known specificity is used in tumor diagnosis, and the clinical context is taken into account. The possible role of cytokeratin 19 as a more specific marker for epithelia than keratin cocktails is discussed.
A 29-year-old male was admitted because of thrombocytopenia. A diagnosis of acute lymphoblastic leukaemia was made on the basis of a 61.6% infiltration of leukemic cells in his bone marrow. Standard G-binding chromosome analysis of bone marrow cells revealed a normal karyotype. He received combination chemotherapy, and achieved hematological complete remission. However, chromosomal analysis of bone marrow cells after 2 courses of consolidation therapy showed the Philadelphia (Ph) chromosome in two cells out of 20 analysed. We retrospectively examined the sample of bone marrow cells before chemotherapy; It showed minor BCR/ABL positivity with FISH and RT-PCR methods. The Ph chromosome disappeared after consolidation chemotherapy and allogeneic bone marrow transplantation, but the Ph chromosome reappeared at relapse. We postulated that there were two clones, both a Ph-positive clone and Ph-negative clone. At the initial diagnosis, Ph chromosome was not detected because the G-banding method analyzed only metaphase cells, which contained few Ph-positive clones. In order to offer effective therapy with molecular targeting agents, in this poor prognostic disease, it is necessary to detect Ph chromosome before the first chemotherapy and BCR/ABL detection with FISH or RT-PCR methods appears more useful than G-banding chromosome analysis.