3.7 (1.0-9.5)

RR relative risk; CI: 95% confidence interval; NHL: non-Hodgkin's lymphoma.

RR relative risk; CI: 95% confidence interval; NHL: non-Hodgkin's lymphoma.

No cases of Hodgkin's lymphoma were found in the major cohorts studying the association between SLE and malignancies [12-16], However, Bhalla et al. [4] reviewed 14 cases of Hodgkin's lymphoma in patients with SLE. Similar to Hodgkin's lymphoma in the general population, the disease occurred in patients aged between 15-35 years and above the age of 50. In 8 cases, Hodgkin's lymphoma occurred subsequently to the diagnosis of SLE, and in 6 cases it was diagnosed concurrently with SLE.

No specific clinical feature was associated with SLE patients who developed Hodgkin's lymphoma. However, a significant reduction in the amount of y -globulins was observed in some SLE patients who developed Hodgkin's lymphoma [4].

Nonmalignant forms of lymph nodes enlargement in patients with SLE include the Kikushi syndrome [27]: A disease that affect usually young women and manifested as generalized or cervical lymphadenopa-

thy, symptoms of systemic illness and histological features of histiocytic necrotizing lymphadenitis. Kikushi syndrome may precede the development of SLE. Out of 8 patients with primary Kikushi syndrome, 2 developed SLE years after the onset of the Kikushi syndrome [27].

The association between SLE and plasma cells dyscresia is unclear. Monoclonal (M) proteins occur in 2% of patients with SLE [28-29]. This frequency is higher than the expected rate of M proteins in the general population [28]. In a review of 9 cases of SLE patients and M gammopathies followed at a single center, the isotypes of the M protein were IgG in 6 patients, IgA in 2 patients and IgM in 1 patient. No clinical features suggesting multiple myeloma were seen in this group of SLE patients [28], On the other hand, high percentages of the sera of patients with M gammopathies were found to bind various autoantibodies including, DNA, RNA, Sm, RNP, histones, phospholipids and others. Taken together, the data may suggest a common etiologic agent for SLE and M proliferation of B cells [30-33].

Few studies have described SLE patients who developed Waldenstrom's macroglobulenimea and/or multiple myeloma [12, 34], The myeloma developed in SLE patients with long-standing disease and usually when the SLE is quiescent.

Two cohort have shown a trend of increased risk of leukemia among patients with SLE [12, 16]. A 2- and 3-fold increased risk of leukemia was found in these studies. However, these increased risks of leukemia were not statistically significant. Patients with SLE were found to develop chronic lymphocytic leukemia (CLL), chronic granulocytic leukemia (CGL) acute nonlymphoblastic leukemia (ANLL) and acute lymphoblastic leukemia (ALL) [7, 35-43], However, in the majority of cases, SLE patients developed either CLL or ANLL. None of the SLE patients included in the major cohorts developed CGL or ALL [1116].

In most cases of SLE patients with leukemia, the development of leukemia, and particularly ANLL, was associated with cytotoxic and immunosuppressive therapy, including cyclophosphamide, azathioprine, and methotremate [7, 35-37, 43]. Six case of acute nonlymphocytic leukemia were reported in SLE patients treated with these agents [7, 35-37, 43], One case was associated with inversion of chromosome-16 and reported in a patient with SLE treated with cyclophosphamide and azathioprine [35]. In an another case, acute leukemia occurred in a patient after receiving 4 g of cyclophosphamide for lupus nephritis [7].

However, none of the 2 SLE patients with leukemia included in the Toronto cohort received cyclophosphamide and/or other cytotoxic agents before the diagnosis of the leukemia [12]. Similarly, Colovic et al. [40] described a 72-year-old SLE patient who developed acute megacaryocytic (M7) leukemia. Cytotoxic drugs were not given to this patient prior to the diagnosis of leukemia.

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