The effect of cyclophosphamide on leukocyte kinetics and susceptibility to infection in patients with wegener's granulomatosis

Dale, David C.; Fauci, Anthony S.; Wolff, Sheldon M.

doi:10.1002/art.1780160510

Cited by 44 publications

(11 citation statements)

References 20 publications

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“…The lymphocytes in culture are capable of a normal blastogenic response as shown by the normal response to mitogens. Monocytopenia is a feature of cyclophosphamide therapy (27) and was seen in our patients (28). However the lymphocyte to monocyte ratios in the present cultures were the same for all groups studied.…”

Section: Discussionsupporting

confidence: 48%

“…In this setting granulocyte inflammatory responses as measured by the Rebuck skin window test were normal (28). Yet at this relatively low dose of cyclophosphamide, significant lymphocytopenia was maintained.…”

Section: Discussionmentioning

confidence: 88%

“…I n our patients particular care was taken in adjusting the dose of cyclophosphamide so that the peripheral white blood cell count remained above 3000/mm3. In this setting granulocyte inflammatory responses as measured by the Rebuck skin window test were normal (28). Yet at this relatively low dose of cyclophosphamide, significant lymphocytopenia was maintained.…”

Section: Reports Of the Effects Of Cyclophosphamide On Both In Vivo Amentioning

confidence: 88%

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Cyclophosphamide and lymphocyte subpopulations in Wegener's granulomatosis

Fauci

Dale

Wolff

1974

Arthritis & Rheumatism

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In 10 patients with Wegener's granulomatosis, low doses of cyclophosphamide produced: severe lymphocytopenia of long duration even after therapy ceased; a greater percentage decrease in nonrosette forming lymphocytes than in rosette forming 1-lymphocytes; normal in vitro lymphocyte responses to mitogens (PHA, ConA, and PWM) with suppressed responses to one of two antigens tested (SK-SD). This regimen did not cause severe granulocytopenia and was successful in inducing and maintaining long-term clinical remissions.Cyclophosphamide is an alkylating agent with well-established immunosuppressive effects in animals and man (1,2). It has been used with therapeutic success in a variety of diseases, such as systemic lupus erythematosus (54) rheumatoid arthritis (5,6) and other inflammatory connective tissue disorders (7). in which autoimmune or immunologic phenomena are thought to play a predominant role.Wegener's granulomatosis (WG) serves as an excellent model of a diffuse hypersensitivity disease in humans (8). It characteristically begins with an inflammatory process in the nasopharynx and paranasal sinuses and progresses to granulomatous vasculitis of the upper and lower respiratory

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Section: Discussionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 88%

Section: Reports Of the Effects Of Cyclophosphamide On Both In Vivo Amentioning

confidence: 88%

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Cyclophosphamide and lymphocyte subpopulations in Wegener's granulomatosis

Fauci

Dale

Wolff

1974

Arthritis & Rheumatism

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“…This severe course of pseudomonas pneumonia may be attributed to depression of the host's defence by the treatment with cortisone acetate. Following the use of immunosuppressive agents such as glucocorticoid and cyclophosphamide, animals become depleted of phagocytes, particularly PMNs, the primary effector cells against bacterial invasion (Bicker et al, 1978;Dale et al, 1973Dale et al, , 1974Peters et al, 1972). This PMN-inflammatory response was virtually absent or decreased in immunosuppressed guinea pigs (Pennington, 1977a) and patients (Sickles et al, 1975).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Non-specific Resistance to Pseudomonas Pneumonia by a Synthetic Derivative of Muramoyl Dipeptide in Immunosuppressed Guinea Pigs

et al. 1982

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A synthetic derivative of muramoyl dipeptide, 6-O-stearoyl-N-acetylmuramoyl-L-alanyl-D-isoglutamine [L18-MDP(A)], showed a protective effect against bacteraemic and non-bacteraemic pneumonia caused by Pseudomonas aeruginosa in immunosuppressed guinea pigs. In about half of the animals treated with the compound before infection, death from bacteraemic pneumonia produced by intratracheal inoculation of P. aeruginosa was delayed for 7 d, although all of the animals infected without prior treatment with the compound died within 4 d of infection. Multiplication of the organisms in the lung was also suppressed for at least 10 d by treatment with the compound when the animals inhaled an aerosol of P. aeruginosa. In contrast, in untreated animals the numbers of bacteria in the lung gradually increased from 10(6) to 10(9) c.f.u. g-1, and a few animals in which the organism increased to 10(9) c.f.u. g-1 had died by 6 and 10 d after infection. In both healthy and immunosuppressed animals, the accumulation of polymorphonuclear leukocytes (PMNs) in a subcutaneous air-pouch injected with heat-killed organisms was augmented by subcutaneous treatment with L18-MDP(A) 1 d before bacterial injection. The phagocytic activity of peritoneal PMNs was also increased by treatment with this compound. The augmentation of protective mechanisms against pseudomonas pneumonia by L18-MDP(A) may be attributed at least partly to the increased chemotactic and phagocytic activity of PMNs.

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“…aeyuginosa infection.Although P. acnes pretreatment has been shown to increase the resistance to some bacterial infection [1] as well as tumor growth [6], decreased resistance to infection can also be resulted when the time of P. acnes injection is altered as Collins and Scott [2] reported that growth of Salmonella enteritidis in mice was enhanced when killed P. acnes was given 24 hr after infection. Some workers showed that high dose Cy treatment resulted in severe neutropenia in man as well as in animals [3,5]. Therefore, decreased resistance due to killed P. acnes and neutropenia due to Cy might synergistically result in aggravation of Ps.…”

mentioning

confidence: 99%