Immune Complexes in Myelofibrosis: a Possible Guide to Management

Lewis, C. M.; Pegrum, G. D.

doi:10.1111/j.1365-2141.1978.tb01093.x

Cited by 49 publications

(22 citation statements)

References 7 publications

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“…Thus, in the early phase of IMF the myeloproliferation may be accompanied by immune activity in the bone marrow with a marked increase of lymphoid nodules [54]. Furthermore, the favourable outcome of immunosuppressive therapy in MF-patients with biochemical evidence of autoimmune activity supports the involvement of autoimmune bone marrow damage in the development of myelofibrosis in a subgroup of patients [52,55].…”

Section: Discussionmentioning

confidence: 90%

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Idiopathic myelofibrosis: A clinical study of 80 patients

Hasselbalch

1990

American J Hematol

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A series of 122 consecutive patients with bone marrow fibrosis initially referred or categorized as idiopathic myelofibrosis is described. After a clinical and pathological review 14 patients were classified as postpolycythaemic myelofibrosis and 7 patients as a transitional myeloproliferative disorder. In 13 patients a diagnosis of hairy cell leukaemia was made, 3 patients had malignant lymphoma, 2 had malignant histiocytosis, and 1 patient had systemic lupus erythematosus with myelofibrosis. Two patients were excluded for further analysis owing to insufficient data. In the remaining 80 patients a diagnosis of idiopathic myelofibrosis was made. The clinical and laboratory findings in this series of patients are presented and compared to those in previous series. Infectious, cardiovascular, thromboembolic, and haemorrhagic complications were frequent, being recorded in 63%, 50%, 40%, and 33% of the patients, respectively. Various autoimmune phenomena were found in a proportion of the patients, but none had clinical evidence of connective tissue disease. Fifteen patients (19%) had a syndrome of acute myelofibrosis. The diagnostic criteria for this disease entity and its place within the spectrum of myeloproliferative disorders are discussed. In the present series acute myelofibrosis was found to encompass various transitional stages toward the evolution of acute leukaemia. It is proposed that acute or malignant myelofibrosis is considered as an acute variant of idiopathic myelofibrosis. Within this syndrome the acute variant seems to be far more common than previously recognized, which may also explain the marked clinical heterogeneity of the myelofibrosis/osteomyelosclerosis syndrome in this and most previous series.

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Section: Discussionmentioning

confidence: 90%

“…Circulating immune complexes (CIC) and complement activation have been demonstrated [44,52,53], but the pathogenetic significance of these findings is uncertain, since the occurrence of CIC may solely reflect impaired clearance in the reticu-lymphocytic cells with ensuing impairment of both cellular and humoral immune reponses [60].…”

Section: Discussionmentioning

confidence: 99%

Idiopathic myelofibrosis: A clinical study of 80 patients

Hasselbalch

1990

American J Hematol

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“…Since the severe refrac tory anemia of the patients responded to the treat ment, and immune complexes of our first patient dis appeared as in the study of Lewis and Pegrum [23], we believe that bolus treatment of méthylprednisolone was effective through its immunosuppressor effect, which should be shown by the study of other cases. More recently, Manoharan and Pitney [24] have shown that chemotherapy resolves symptoms and re verses marrow fibrosis in myelofibrosis, which could also be explained by the immunosuppressive effect of busulfan or6-thioguanine.…”

Section: Discussionmentioning

confidence: 95%

“…Various immunologic abnormalities such as in creased serum antinuclear and antismooth muscle au toantibodies, rheumatoid factor and polyclonal ele vation of immunoglobulin levels have been reported in patients with IMF [21][22][23]. Since the severe refrac tory anemia of the patients responded to the treat ment, and immune complexes of our first patient dis appeared as in the study of Lewis and Pegrum [23], we believe that bolus treatment of méthylprednisolone was effective through its immunosuppressor effect, which should be shown by the study of other cases.…”

Section: Discussionmentioning

confidence: 99%

High-Dose Intravenous Corticosteroid Treatment in Childhood Idiopathic Myelofibrosis

Özsoylu

Ruacan²

1986

Acta Haematol

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“…In PNH, in addition to a depressed cellu lar immunity, there is an increase in the im munoglobulin level [10]; antierythrocyte isoantibodies (anti-D, anti-C + D, antiCw), and antileukocyte antibodies [5], In myelofibrosis [14] and leukemia [24] there is experimental evidence of the existence of circulating immune complexes. Our findings provide evidence for the presence of circu lating immune complexes in PNH.…”

Section: Discussionmentioning

confidence: 99%

Circulating Immune Complexes in Paroxysmal Nocturnal Hemoglobinuria

Villaescusa¹,

Santos²,

García³

et al. 1982

Acta Haematol

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Circulating immune complexes were investigated in sera of 13 patients with paroxysmal nocturnal hemoglobinuria. A significant inhibition was observed in the complement-dependent rosette formation (EAC) in 6 cases; 2 patients presented an increased anti-complementary activity; antilymphocyte antibodies were demonstrated in 2 patients. The levels of C₃d and immunoconglutinins were also increased; there were no differences in the total hemolytic complement between patients and normal controls. There was a significant correlation between C₃d and immunoconglutinins with the inhibition of the EAC rosette formation test. These results provide evidence for the presence of circulating immune complexes in paroxysmal nocturnal hemoglobinuria.

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Immune Complexes in Myelofibrosis: a Possible Guide to Management

Cited by 49 publications

References 7 publications

Idiopathic myelofibrosis: A clinical study of 80 patients

Idiopathic myelofibrosis: A clinical study of 80 patients

High-Dose Intravenous Corticosteroid Treatment in Childhood Idiopathic Myelofibrosis

Circulating Immune Complexes in Paroxysmal Nocturnal Hemoglobinuria

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