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PubMed1975

[Sarcomatous and leukemic forms of Waldenström's macroglobulinemia].

Four cases of sarcomatous or leukaemic types of Waldenström's macroglobulinemia are presented. They are characterized by tumoral and compressive localizations of lymph node or spleen, or by a hyper-leukocytosis with many circulating abnormal cells. These cells are different from the lympho-plasma cells regularly observed in Waldenström's macroglobulinemia, and can be assimilated to malignant immunoblasts. They have a proliferative aspect and seem to produce less macroglobulin and to recover some beta-glucuronidase activity. The sarcomatous and leukemic types of Waldenström's macroglobullinemia have a poor prognosis and may appear as terminal transformation of the disease.

Aged↗

PubMed1975

[Waldenström's macroglobulinemia with preserved antierythrocyte and antilipoprotein antibody activity].

One case of Waldenström's macroglobulinemia is reported, in which the monoclonal IgM has an antibody activity against stored red cells, beta-lipoproteins and mammalian glomeruli. The antibody activity is observed with the purified IgM molecule, which cross reacts with the three antigens, and with the Fab piece. The study of the cross reactions shows that the antibody recognizes similar rather than identical antigens. This observation is to be added to the few cases already published of antibody against stored red cells, and of Waldenström's macroglobulinemia with antibody activity. The physiopathology of the occurrence of a M component with such an activity is discussed.

Blood Preservation↗

PubMed1991

Idiotypic cross-reactivity of immunoglobulins expressed in Waldenström's macroglobulinemia, chronic lymphocytic leukemia, and mantle zone lymphocytes of secondary B-cell follicles.

Monoclonal antibodies (MoAbs) specific for autoantibody-associated cross-reactive idiotypes (CRIs) of Waldenström's IgM react frequently with the surface Ig (slg) expressed by leukemia cells of patients with chronic lymphocytic leukemia (CLL). Evaluation of the molecular basis for this cross-reactivity indicates that such CRIs are encoded by conserved antibody variable region genes (V genes) that have undergone little or no somatic hypermutation. We find that such anti-CRI MoAbs stain a subpopulation of cells within the mantle zones surrounding the germinal centers of normal human tonsil. In contrast, MoAbs specific for variable region subgroup determinants react with cells in both the mantle zones and germinal centers of secondary B-cell follicles. To test whether mantle zone B cells not reactive with existing anti-CRI MoAbs may express slg bearing as-yet-unrecognized CRIs present on Igs produced by neoplastic cells of some patients with Waldenström's macroglobulinemia or CLL, we immunized mice with purified Waldenström's IgM that have been characterized for their variable region subgroups using subgroup-specific antisera raised against synthetic peptides. The supernatants of hybridomas generated from the splenocytes of immunized mice were screened for their ability to stain a subpopulation of mantle zone lymphocytes in human tonsil. With this approach, two new anti-CRI MoAbs were identified, designated OAK1 and VOH3. OAK1 binds to a CRI present on a subset of kappa light chains of the VK1 subgroup. VOH3 recognizes a CRI determinant(s) present on a subset of antibody heavy chains of the VH3 subgroup. Flow cytometric analyses demonstrated that OAK1 specifically binds leukemia cells from 5 to 20 patients (25%) with kappa light chain expressing CLL. In addition, VOH3 reacted with the leukemia cells from 1 of 17 (6%) patients tested. The success of these methods demonstrates that the variable regions of the Igs produced by mantle zone B cells share idiotypic determinants with Igs expressed in B-cell CLL (B-CLL) and Waldenström's macroglobulinemia.

Antibodies, Monoclonal↗

PubMed1991

Chronic calcific pancreatitis in a patient with Waldenstrom's macroglobulinemia.

We report on a patient with chronic calcific pancreatitis associated with Waldenstrom's macroglobulinemia, and we have hypothesized a possible relationship between these two entities. The hyperviscosity of serum in Waldenstrom's macroglobulinemia may be associated with a viscous pancreatic juice that leads to stone formation.

Aged↗

PubMed1990

[Waldenström's macroglobulinemia and arthritis].

We report the case of a female aged 67 years suffering a Waldenström's macroglobulinemia which began with arthritis at the knee and pleural effusion. In both locations the anatomopathological examination showed infiltration by typical lympho-plasmatic cells. Other possible etiologies such as amyloid, infection or arthritis produced by microcrystals were ruled out. The relevant finding in this case was the presence of infiltrative reaction at the synovial tissue which has been rarely reported in the literature. We review the incidence of articular manifestations in cases of Waldenström's macroglobulinemia and the possible pathogenetic mechanisms involved.

Aged↗

PubMed1990

[Acute myeloblastic leukemia and hepatocellular carcinoma following Waldenström's macroglobulinemia].

A 54-year-old man was admitted to our hospital for precise examination of pancytopenia in October 1988. He had been cut off his left femur and irradiated because of osteosarcoma in 1954. After 30 years, he was diagnosed as Waldenström's macroglobulinemia. Melphalan had been given 2 mg daily for 19 months until August 1988, when it was discontinued due to pancytopenia. Peripheral blood showed Hb 6.6 g/dl, platelet 40 x 10(3)/microliters, and WBC 2000/microliters with 33% blasts. Bone marrow showed normocellularity with 36% blasts. Although blasts were negative for peroxidase staining, surface marker analysis revealed myeloid (CD 13, CD 33) phenotypes. Chromosome analysis showed 45, XY, -7, inv (3). A CT scan of the liver showed a mass, 10 by 10 cm, compatible with hepatocellular carcinoma. He was treated with very low dose Ara-C without noticeable effect. Hepatic tumor gradually enlarged, and he died of hepatic failure. This is a rare case of quadruplicate malignancies. The chromosomal abnormality suggests that AML was secondary leukemia which might be associated with immunosuppression due to macroglobulinemia and/or melphalan therapy.

Carcinoma, Hepatocellular↗

PubMed1989

[Primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock].

A 88-year-old man was admitted because of the left chest pain due to herpes zoster for 1 week. Blood analyses and immunoelectrophoresis revealed anemia, severe neutropenia, rouleaux formation and IgM, lambda-type monoclonal gammopathy. The HE staining and peroxidase-anti-peroxidase staining of biopsy specimens of the cervical lymph node swelling appeared from the fifth hospital day, revealed an increase in atypical lymphocytes bearing IgM, lambda-type immunoglobulin. Then a diagnosis of primary macroglobulinemia was made. Although the patient's clinical findings transiently improved after chemotherapy with prednisolone and vindesine, he died of a septic shock which appeared after klebsiella pneumonia and sepsis. We reported an unusual case of primary macroglobulinemia with severe neutropenia, leading to a rapid development of septic shock after the chemotherapy.

Aged↗

PubMed1986

Secretory piece and IgA deficiency in a patient with Waldenstrom's macroglobulinemia.

A case of a patient suffering from Waldenstrom's macroglobulinemia who developed diarrhea and mild steatorrhea is described. Laboratory studies revealed low serum IgA, intestinal secretory IgA deficiency, and small intestine bacterial overgrowth as demonstrated by the C14-cholylglycine breath test. These findings suggest that selective IgA deficiency and secretory component deficiency may be contributing factors in the development of diarrhea in Waldenstrom's macroglobulinemia.

Aged↗

PubMed1986

[Alleviation of ocular complications of the hyperviscosity syndrome in Waldenström's macroglobulinemia using plasma exchange].

Two patients presenting ocular complications of hyperviscosity syndrome in Waldenström's macroglobulinemia have been treated by plasmapheresis after inefficiency of immunosuppressive therapy. Plasma exchange seems an useful treatment as shown by clinic and angiographic improvement. In each case improvement of retinopathy was correlated with decrease of serum IgM level and blood viscosity measured by isotopic method. Fluorescein angiography, easily repeated, seems a very good method for following hyperviscosity syndrome in Waldenström's macroglobulinemia.

Aged↗

PubMed1985

Acute renal failure in primary macroglobulinemia with small-molecule IgM.

Primary macroglobulinemia with acute renal failure developed in a 46-year-old man after administration of contrast medium (containing diatrizoate sodium and meglumine [Urografin]) for intravenous pyelography. On admission, the monoclonal protein peak could not be detected in serum by cellulose acetate electrophoresis, but the serial electrophoresis revealed a gradual increase in monoclonal protein peak, which later became two peaks. The serum of the patient contained the monoclonal small-molecule IgM kappa-chain protein with 13 to 14 Svedberg units in sedimentation constants, which is antigenetically the same as native IgM heavy chain. Although acute renal failure is extremely rare in primary macroglobulinemia, the small-molecule IgM seems to be one factor that induces acute renal failure.

Acute Kidney Injury↗

PubMed1985

[Myelopathy manifesting as macroglobulinemia].

Slowly progressive cervical cord symptoms over a 2 year period led to the diagnosis of Waldenström macroglobulinemia in a 32 year old man. Diagnosis was made on the finding of circulating monoclonal IgM and lymphocyte infiltration of the bone marrow. Perimedullary infiltration of cervico-dorsal cord was visualized by CT scan. No other tumor tissue was found. Intrathecal secretion of IgM in the CSF was demonstrated. Cervico-dorsal cord radiotherapy followed by systemic chemotherapy led to a rapid improvement in the neurological signs. Reports of spinal cord lesions in Waldenström macroglobulinemia are rare and the relationship of this condition with respect to so-called secreting neurolymphomatosis is discussed.

Adult↗

PubMed1985

[Peritoneal amyloidosis in Waldenström's macroglobulinemia. X-ray computed tomographic aspects].

A 74 years old man, know to have Waldenström's macroglobulinemia was hospitalized for intestinal obstruction. Upper gastrointestinal barium study revealed an extrinsic stenosis of duodenum. Ultrasonography and abdominal computed tomography revealed a diffuse mesenteric infiltration with medium level echoes and encasing of mesenteric vessels. Histologic examination of biopsies taken at exploratory laparotomy disclosed amyloidosis of the epiploon and mesentery. The review of amyloidosis in macroglobulinemia shows peritoneal amyloidosis to be a very rare event. Sonographic, computed tomographic and pathologic findings of this unusual case are discussed.

Aged↗

PubMed1977

[Waldenström's macroglobulinemia with immunocytoma of the lung].

A case of Waldenström's macroglobulinemia in a 63-year-old man is presented. The clinical course was complicated by pulmonary infiltration classified by biopsy as immunocytoma. The clinical findings and therapeutic possibilities in this rare case of Waldenström's macroglobulinemia with with pulmonary complications are discussed in the light of the literature.

Chlorambucil↗

PubMed1977

Monomyelocytic leukemia in an untreated case of Waldenström macroglobulinemia.

The development of acute leukemia occurring in the presence of Waldenström macroglobulinemia has been reported only twice, occurring once after many years of treatment, and on the second occasion, simultaneously. The intention of this report is to record a case of spontaneous onset of acute monomyelocytic leukemia occurring in an untreated patient with Waldenström macroglobulinemia after four years of observation without intervening chemotherapy or radioactive therapy, and without the influence of any known carcinogens.

Aged↗

PubMedDate not supplied

Cytologic diagnosis of multiple myeloma and macroglobulinemia in effusions.

The presence of effusion in association with multiple myeloma or macroglobulinemia is an unusual finding which generally occurs late in the course of the disease. Occasionally, cytoligic detection is a diagnostic problem. In both conditions, the fluid is characrerized by a high specific gravity and high protein content. In myeloma, plasma cells at varying stages of differentiation are present, while in macroglobulinemia atypical lymphocytes and plasma cells resembling those found in the blood and bone marrow are seen. Generally, the diagnosis can be readily made on the basis of clinical features, characteristics of the fluid and cytologic findings. In difficult cases, additional procedures helpful in establishing a definite diagnosis include methyl green pyronine stain, fluid electrophoresis and electron microscopy.

Adult↗

PubMed1984

Plasmapheresis and cold sensitivity of immunoglobulin molecules. II. A study of macroglobulinemia polyclonalis spuria and immune complex disease.

The indications for plasmapheresis in the different hyperviscosity syndromes are discussed on the basis of data on relative serum viscosity at 13 and 37 degrees C. Beside monoclonal macroglobulinemia there are conditions with a high content of polyclonal IgM and also of IgG and IgA where hyperviscosity is a dominant symptom. The importance of what may be called macroglobulinemia polyclonalis spuria is stated and a number of patients belonging to this type are discussed. Polyclonal increase in IgG, even at high levels, usually does not cause severe hyperviscosity. Case histories of patients with rheumatoid disease and marked hyperviscosity constitute one group. Another is formed by diseases leading to the development of immune complexes. Such complexes are usually caused by binding of polyclonal IgG to monoclonal IgM, but other combinations are also known. A number of clinical examples of these different disease conditions, some probably indicating intense plasmapheresis, are analyzed. The limited value of plasmapheresis alone without cytostatic treatment is stressed as regards hyperviscosity. Another indication is removal of noxious protein components.

Aged↗

PubMed1983

Waldenström's macroglobulinemia and peripheral neuropathy: a clinical and immunologic study of 25 patients.

We investigated, by indirect immunofluorescence, the binding of monoclonal IgM to human peripheral nerve in 25 patients with Waldenström's macroglobulinemia and peripheral neuropathy. In 10 cases (40%), an antibody activity against the myelin sheaths was demonstrated. The reactivity was mediated by the F(ab')2 fragments of the IgM. Prior delipidation of nervous tissue was needed to allow full expression of the target antigen(s). In nine cases, the IgM reacted with both peripheral and central myelin of primates, but not mouse or rabbit nervous tissue. In one case, the IgM reacted only with human peripheral nerve. The patients, whose IgM had an antibody activity to myelin antigen(s), had some distinct hematologic and neurologic features. The peripheral neuropathy always antedated the hematologic symptoms by several years. The serum level of the monoclonal IgM was low in all cases, and overt lymphoid malignancy was frequently absent. In other patients with neuropathy, the monoclonal IgM, which lacked antimyelin antibody activity, displayed either cross-idiotypic antigenic determinants or anti-intermediate filament antibody activity. These results taken together emphasize the heterogeneity of antibody activity of the monoclonal IgM from patients with Waldenström's macroglobulinemia and peripheral neuropathy.

Antibodies, Monoclonal↗

PubMed1983

Cytogenetic studies and clinical aspects of patients with plasma cell leukemia and leukemic macroglobulinemia.

Chromosomes of six patients with plasma cell leukemia and one patient with leukemic macroglobulinemia were examined from peripheral blood, bone marrow, and/or pleural fluid. All the patients had a clonal chromosomal abnormality. The modal chromosome number was near tetraploid in two, pseudodiploid in two, and hypodiploid in three patients. Rearrangements of chromosome 1 were found in all the patients. The most consistent abnormality was a large marker involving the long arm of No. 1, found in six patients, including the patient with macroglobulinemia. Each patient had one to four large markers which resulted in partial trisomy to hexasomy for the long arm of No. 1. The translocations occurred with No. 9 in two, with No. 16 in two, and Nos. 8, 17, and 18 each in one patient. The survival time from the diagnosis was less than 1 year in five of them and over 2 years in one. The only patient whose cells lacked an extra 1q lived for over 3 years. Five 14q+ marker chromosomes were detected in three patients. The donor chromosome was No. 11 in one of these and was undetermined in the others; the size of each 14q+ marker seemed quite different which suggested different donor chromosomes. Loss of a sex chromosome was found in five patients. Loss of No. 13 and gain of No. 7 or 7q were each found in two patients. Rearrangement or deletion of the short arm of No. 8 was found in five patients. A rearrangement of 9p was found in three patients. The myeloma cells had a different morphology in the peripheral blood, bone marrow, and/or pleural fluid before and after the leukemic phase of one patient; however, chromosome analysis revealed the same clone despite the altered morphology.

Adult↗