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PubMed1993

Waldenström macroglobulinemia: MR imaging of the spine and CT of the abdomen and pelvis.

Twenty-three consecutive patients with Waldenström macroglobulinemia were studied with magnetic resonance (MR) imaging of the spine and computed tomography (CT) of the abdomen and pelvis. MR imaging studies included sagittal T1-weighted and gradient-recalled-echo sequences performed with and without contrast material enhancement. Marrow involvement was identified with MR imaging in 21 of 23 (91%) patients. Diffuse involvement was noted in 13 patients (56%), and a variegated pattern in eight (35%). CT demonstrated enlarged nodes in 10 of 23 (43%) patients. Correlation of MR imaging patterns and presence of adenopathy at CT with standard laboratory values for Waldenström macroglobulinemia revealed an association of the diffuse MR imaging pattern of marrow involvement and the presence of enlarged nodes at CT with more advanced disease. MR imaging of the spine and CT are reliable means of evaluation of disease status in Waldenström macroglobulinemia. They may be employed as additional means in the staging of Waldenström macroglobulinemia and may be helpful in the follow-up of patients with this rare hematologic malignancy.

Abdomen↗

PubMedDate not supplied

Positional nystagmus in association with macroglobulinemia.

Summary--Waldenstrom's macroglobulinemia is a malignant lymphoproliferative disease associated with a monoclonal macroglobulinemia. Most explanations of the cochlear and vestibular symptoms in this disease have dealt with vascular thrombotic or hemorrhagic phenomena. Five patients currently being treated for macroglobulinemia have been reviewed. Three patients gave a history of periodic dizziness and underwent extensive neuro-otologic examination. The results suggestsed an alternate mechanism for the pathophysiology of the vestibular disturbance in macroglobulinemia. Vestibular examination by use of electronystagmography provided information which suggest that the cupulae may be altered by the macroglobulins to act as gravity receptors.

Adult↗

PubMedDate not supplied

Hepatocellular carcinoma followed by Waldenström's macroglobulinemia: a case report.

A case of hepatocellular carcinoma associated with Waldenström's macroglobulinemia is reported. During treatment and follow-up of hepatocellular carcinoma, a 54-year-old man was found to have a progressive monoclonal increase in serum IgM level and subsequently was diagnosed as having Waldenström's macroglobulinemia. Chemotherapy was carried out to prevent hyperviscosity syndrome due to Waldenström's macroglobulinemia without any surgical management for hepatocellular carcinoma. The association of these diseases is quite rare; only 6 cases have been reported in the literature, and this is the first case in which hepatocellular carcinoma preceded Waldenström's macroglobulinemia.

Blood Viscosity↗

PubMed1993

Incidence of Waldenström's macroglobulinemia.

This study sought to determine the incidence and pattern of occurrence of Waldenström's macroglobulinemia, a plasmacytoid lymphocyte malignancy that involves monoclonal production of the IgM M-component type. Cases with Waldenström's macroglobulinemia have been reported since 1978 to the population-based cancer registry that serves western Washington state, and since 1988 to the eight other cancer registries that participate in the National Cancer Institute's Surveillance, Epidemiology, and End-Results program. Persons less than 85 years old newly diagnosed with Waldenström's macroglobulinemia were identified through 1989. The age-standardized annual incidence rate was 6.1 per million in white men and 2.5 per million in white women (1980 US standard). Only five cases were reported in black women, among whom the age-standardized annual incidence rate was 3.6 per million. No cases were reported among black men (5.8 cases expected, based on the rates in white men); this finding may be due to chance, underdiagnosis of Waldenström's macroglobulinemia in this group, or may reflect a truly low rate. Further investigation of a large, racially diverse population is required to better characterize the epidemiology of this rare disease.

Adult↗

PubMed1997

[Waldenstrom's macroglobulinemia with antibasement membrane activity of monoclonal immunoglobulin].

INTRODUCTION: Waldenström macroglobulinemia is a rare hematologic disorder with characteristic malignant plasma cell proliferation associated with the secretion of a IgM monoclonal immunoglobulin which is the cause of most of the clinical manifestations. Skin involvement is exceptional. We report a new case of Waldenström macroglobulinemia discovered in a patient who developed specific skin lesions with monoclonal immunoglobulin deposits. CASE REPORT: A 50-year-old woman developed spontaneously painful infiltrated erythematopapular plaques over the extension aspects of the limbs. There were no other clinical manifestations. The patient had a kappa IgM monoclonal gammapathy. The diagnosis of Waldenström macroglobulinemia was proposed after the discovery of voluminous intra-abdominal adenopathies and was confirmed by immunohistochemistry of the biopsies, indirect immunofluorescence evidenced reactivity against the epidermal basal membrane. Chemotherapy led to successful regression of the skin lesions, the tumoral mass and circulating IgM. DISCUSSION: This is the second reported case of Waldenström macroglobulinemia with anti-basal membrane monoclonal immunoglobulin. This IgM would recognize an 82 kD antigen on the dermal side of the dermo-epidermal junction situated in the anchoring fibres of the lamina densa, a zone classically involved in acquired bullous epidermolysis.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1977

Monoclonal macroglobulinemia with osteolytic lesions: a case report and review of the literature.

A patient with monoclonal macroglobulinemia and osteolytic lesions was studied and 24 previously reported closely related cases were reviewed. Cases studied by ultracentrifugation without an immunoelectrophoresis were not considered. Patients presenting with a primary increase in monoclonal IgM molecules may be divided into three groups: typical Waldenstrom's macroglobulinemia, macroglobulinemia with osteolytic lesions resembling multiple myeloma, and a group displaying features of both diseases. At present, cell morphology is not helpful in separating these groups, and a bone survey is recommended. The authors underscore the clinical importance of the early recognition of these entities since procedures such as plasmapheresis for the management of hyperviscosity syndrome, mobilization and local radiotherapy to symptomatic lytic lesions may be necessary for optimal management.

Adult↗

PubMed1979

Depressed PHA transformation and acute leukemia in macroglobulinemia.

Two out of fifty-three patients with macroglobulinemia developed acute leukemia following chemotherapy. The Phytohemagglutinin (PHA) Transformation Index performed prior to the appearance of acute leukemia was found to be markedly depressed in these two patients in comparison with ten other patients with macroglobulinemia. In addition, a clone with monosomy 7 was detected in one of the currently reported patients when the leukemic process became apparent. The cytogenetic analysis was normal in the same patient 48 months earlier, when macroglobulinemia was diagnosed. The low PHA Transformation Index and the chromosomal hypodiploidy are of interest and their clinical significance merits further investigation.

Adolescent↗

PubMed1982

Peripheral nerve damage during multiple myeloma and Waldenstrom's macroglobulinemia: an ultrastructural and immunopathologic study.

Peripheral nerve biopsies of 22 patients who were seen with a peripheral neuropathy were studied. On each occasion an ultrastructural study was performed and on 12 occasions an immunopathologic study was done. Ten patients had Waldenström's macroglobulinemia and 12 had multiple myeloma. Cellular infiltrates were observed in three cases of Waldenström's macroglobulinemia by light microscopy. A widening of the myelin sheath, corresponding to an accumulation of macroglobulin, was found in three cases of Waldenström's macroglobulinemia. The presence of abundant deposits of amyloid was noted in one case of multiple myeloma. These diverse features show the various possible mechanisms that can produce peripheral nerve damage during the course of malignant dysglobulinemias. The segmental demyelination is probably of immunologic origin. The axonal lesions cannot be explained satisfactorily except in those rare cases where amyloid deposits are present in the endoneurium.

Adult↗

PubMed2002

Occurrence of acute monocytic leukemia in a case of untreated Waldenström's macroglobulinemia.

Acute myeloid leukemia is a rare complication of untreated Waldenström's macroglobulinemia. Although two such cases have been reported, occurrence of acute monocytic leukemia, FAB M5b subtype, in a patient with untreated Waldenström's macroglobulinemia has not been reported. The patient had distinct foci with clear demarcation of lymphoid infiltrates and myeloid infiltrates in the bone marrow, representing Waldenström's macroglobulinemia and acute monocytic leukemia, indicating the concurrence of two primary malignancies.

Aged↗

PubMed1994

Peripheral neuropathy in IgM monoclonal gammopathy and Wäldenstrom's macroglobulinemia: a frequent complication in elderly males with low MAG-reactive serum monoclonal component.

Peripheral neuropathy (PN) is a frequent complication during primary macroglobulinemia (PM), whose immunological genesis has been suggested by various authors. This study involved 65 PM patients (44 men and 21 women aged 35-78), diagnostically divided into MGUS (31 cases), and indolent (IWM, 24 cases) or symptomatic (WM, 10 cases) Waldenstrom macroglobulinemia groups. All patients underwent neurological examination, including electrodiagnostic evaluation and the determination of the serum titre of antimyelin-associated glycoprotein (MAG). An evaluation was made of the prevalence of PN and its correlation with a series of hematological variables. The prevalence of PN was 31.6%: of those with PN, 73.1% manifested both clinical and electrophysiological signs of PN, primarily of the demyelinating type. Significant correlations emerged between the presence of PN and sex (M vs. F P = 0.0001), advanced age (P = 0.049), low MC levels (P = 0.025), high anti-MAG titres (P = 0.001) and high Hb levels (P = 0.001). No significant correlation with the diagnostic definition of PM was found, although the majority of cases with (particularly demyelinating) PN were MGUS or IWM. At multivariate analysis, the presence of PN significantly correlated with sex (P = 0.0001), age (P = 0.019), and anti-MAG titre (P = 0.001). Ten of the 26 PN cases showed no MAG reactivity. Significant correlations between PN and low serum MC levels/high MAG reactivity support the hypothesis of the antibody-mediated origin of many PN, and that the presence of PN depends on the characteristics of the proliferating pathological B clone, rather than on the tumor burden of the form of macroglobulinemia. Clinically, our data reconfirm the frequency of PN during PM and indicate simple clinicohematological variables useful for identifying patients at high neuropathic risk.

Adult↗

PubMed1994

Preferential expression of human lambda-light-chain variable-region subgroups in multiple myeloma, AL amyloidosis, and Waldenström's macroglobulinemia.

We have compared the distribution of lambda-light-chain variable-region (V lambda) subgroups among Ig lambda molecules found in the serum of normal individuals with that of monoclonal Ig lambda components obtained from patients with plasma cell and related immunoproliferative disorders. A panel of monoclonal antibodies specific for each of the major human V lambda subgroups--V lambda I, V lambda II, V lambda III, V lambda IV, V lambda VI, and V lambda VIII--was used in a highly sensitive enzyme-linked immunosorbent assay (ELISA) to quantitate each of these populations. The mean distribution of Ig lambda I, Ig lambda II, Ig lambda III, Ig lambda IV, Ig lambda VI, and Ig lambda VIII molecules in serum specimens collected from 20 normal adults was approximately 40, 3, 43, 5, 5, and 3% of the total Ig lambda population, respectively. In contrast, that of monoclonal IgG, IgA, and IgD proteins and Bence Jones proteins obtained from patients with multiple myeloma and related gammopathies (n = 196) was approximately 27, 28, 39, 5, 0, and 1%, respectively. The percentage of monoclonal Ig lambda II components found in individuals with AL lambda amyloidosis (n = 41) was comparably increased to that seen in multiple myeloma and was even higher in patients with Waldenström's macroglobulinemia (n = 16), in whom 63% of the IgM lambda proteins were of the V lambda II subgroup. Also evidenced were differences in the distribution of other V lambda subgroups in the disease states: Most striking was the predominance (41%) of the V lambda VI subgroup among monoclonal lambda chains obtained from patients with AL amyloidosis and that this subgroup was found exclusively on amyloidosis-associated proteins. No Ig lambda VI-type myeloma- or macroglobulinemia-related proteins were identified. The observed alterations in V lambda subgroup distribution among "pathologic" monoclonal Igs were attributed to the particular disease and not related to the heavy-chain class. Our finding that certain V lambda subgroups are nonstochastically expressed in lambda-type multiple myeloma, AL amyloidosis, and Waldenström's macroglobulinemia provides evidence for abnormal VL gene usage in these disorders and, thus, furnishes new insight into their pathogenesis.

Amyloid↗

PubMed1993

Fludarabine therapy in Waldenström's macroglobulinemia.

PURPOSE: To assess the response rate, remission duration, and survival of patients with Waldenström's macroglobulinemia treated with the adenine nucleoside analogue fludarabine. PATIENTS AND METHODS: Twenty-eight patients with Waldenström's macroglobulinemia, of whom only 2 were previously untreated, received fludarabine at a dose of 20 to 30 mg/m2 intravenously daily for 5 days (20 patients) or 30 mg/m2 intravenously daily for 3 days (8 patients). Treatment was continued until maximum response was achieved. Responding patients were followed with no further treatment until relapse. RESULTS: Ten patients responded (36%), including the 2 previously untreated patients and 8 of 26 patients (31%) who were resistant to prior therapies. Unmaintained remissions lasted for a median of 38 months. There were no fatalities associated with this treatment. Previously untreated patients and those with a primary resistant disease of relatively short duration were more likely to benefit from this treatment. CONCLUSION: Fludarabine is an effective salvage agent for the treatment of patients with resistant Waldenström's macroglobulinemia. Further investigations of fludarabine in untreated patients and in combination with other active agents are warranted.

Adult↗

PubMed2004

Waldenström's macroglobulinemia-associated retinopathy.

OBJECTIVE: To report the clinical, electrophysiologic, and immunopathologic findings in a patient with progressive retinal degeneration associated with Waldenström's macroglobulinemia. DESIGN: Case report with immunohistochemical studies. METHODS: A 46-year-old female with elevated serum immunoglobulin M (IgM) levels complained of photophobia and photopsias. Complete ophthalmic examinations including electrophysiologic testing and hematologic evaluations were performed over a 3-year period. Immunohistochemical studies to determine the presence of serum antiretinal antibodies were evaluated using confocal microscopy. RESULTS: Examination of the patient's fundus remained normal, although there was deterioration in her visual acuity, visual field, and electroretinogram over the follow-up period. Waldenström's macroglobulinemia was diagnosed by bone marrow biopsy. Indirect immunohistochemistry revealed reactivity of the patient's serum against the photoreceptor-connecting cilium. CONCLUSION: The paraneoplastic retinopathy associated with Waldenström's macroglobulinemia in this patient is presumed to result from antibodies of the IgM subtype reacting to proteins in the retinal photoreceptors.

Autoantibodies↗

PubMed1998

Vitreitis and Waldenström's macroglobulinemia.

PURPOSE: To describe vitreitis in a patient with Waldenström's macroglobulinemia. METHODS: Case report and review of pertinent literature. RESULTS: A 90-year-old man developed vitreitis 10 years after a systemic diagnosis of a lymphoproliferative disorder. Numerous small, normal-appearing lymphocytes were seen on pathologic examination of the vitreous. He developed worsening lymphadenopathy and was diagnosed with Waldenström's macroglobulinemia after systemic review. CONCLUSION: Chronic lymphoproliferative diseases such as Waldenstrom's macroglobulinemia may cause vitreitis.

Aged↗

PubMed1998

Ptosis in Waldenström's macroglobulinemia.

PURPOSE: To report a case of chronic, progressive unilateral blepharoptosis in a 73-year-old woman with Waldenström's macroglobulinemia. METHOD: Case report. A biopsy was performed on a thickened and indurated tarsal plate that we believed had resulted in mechanical blepharoptosis. RESULTS: Histologic and immunohistochemistry studies of the biopsy specimen demonstrated a lymphoplasmacytoid cell infiltrate with monoclonal antibodies consistent with Waldenström's macroglobulinemia. CONCLUSION: Involvement of the tarsal conjunctiva and tarsus in Waldenstrom's macroglobulinemia is a newly recognized cause of eyelid thickening and ptosis.

Aged↗

PubMed2000

Rearrangement of immunoglobulin gene in metastatic Waldenström macroglobulinemia to the vitreous.

PURPOSE: To report metastatic Waldenström macroglobulinemia cells with immunoglobulin heavy chain gene rearrangement in the vitreous and the blood. METHODS: A 58-year-old man with Waldenström macroglobulinemia developed bilateral vitreitis. Diagnostic vitrectomy was performed on the left eye. The vitreous cells and the peripheral blood lymphocytes were analyzed using microdissection and polymerase chain reaction amplification. RESULTS: Vitrectomy specimen of the left eye contained a few degenerated cells. Molecular analysis showed immunoglobulin heavy chain gene rearrangement at the third complementary determining region of the vitreal infiltrating cells and peripheral blood lymphocytes. CONCLUSIONS: Waldenström macroglobulinemia rarely metastasizes to the vitreous. Molecular detection of the immunoglobulin heavy chain gene third complementary determining region rearrangement is helpful in the diagnosis of the malignancy. Microdissection combined with polymerase chain reaction is a useful and innovative tool for molecular pathological investigation.

B-Lymphocytes↗

PubMed2001

High-dose chemotherapy followed by stem cell transplantation in patients with resistant Waldenstrom's macroglobulinemia.

Preliminary evidence suggests that high-dose chemotherapy followed by autologous or allogeneic stem cell transplantation may be effective in some patients with resistant Waldenstrom's macroglobulinemia. During the last 10 years, seven patients with Waldenstrom's macroglobulinemia have received transplants at the MD Anderson Cancer Center, four with autologous and three with allogeneic stem cells. Four patients achieved partial remission, and three patients have remained alive for at least 2 years. Our data confirm the feasibility of high-dose therapy in patients with macroglobulinemia and support the need for prospective studies of this modality in patients with chemosensitive disease.

Adult↗

PubMed1999

A case of anaplastic large cell (Ki-1) lymphoma of B-cell phenotype, occurring in Waldenström's macroglobulinemia.

A case of anaplastic large cell (Ki-1) lymphoma of B-cell lineage occurred in a 59-year-old male with Waldenström's macroglobulinemia. Immunostaining of the lymphoma cells showed sporadic positivity for IgM and occasional positivity for kappa chain. This immunoglobulin specificity is the same as that of plasmacytoid lymphocytes in the bone marrow; therefore anaplastic transformation of Waldenström's macroglobulinemia was strongly suggested. This seems to be the first reported case of anaplastic large cell lymphoma, confirmed by CD30 expression, arising in Waldenström's macroglobulinemia.

Antigens, CD20↗