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1/11. Apparent cyclophosphamide (cytoxan) embryopathy: a distinct phenotype?

    cyclophosphamide (CP) is an alkylating agent widely used in treating cancer and autoimmune disease. CP is classified as a pregnancy risk factor D drug and is teratogenic in animals, but population studies have not conclusively demonstrated teratogenicity in humans. Six isolated reports of prenatally exposed infants with various congenital anomalies exist, but to date no specific phenotype has been delineated. The purpose of this report is to document a new case of in utero CP exposure with multiple congenital anomalies and to establish an apparent CP embryopathy phenotype. The mother had systemic lupus erythematosus and cyclophosphamide exposure in the first trimester. She also took nifedipine, atenolol, clonidine, prednisone, aspirin, and potassium chloride throughout pregnancy. The infant had growth retardation and multiple anomalies including microbrachycephaly, coronal craniosynostosis, hypotelorism, shallow orbits, proptosis, blepharophimosis, small, abnormal ears, unilateral preauricular pit, broad, flat nasal bridge, microstomia, high-arched palate, micrognathia, preaxial upper limb and postaxial lower limb defects consisting of hypoplastic thumbs, and bilateral absence of the 4th and 5th toes. chromosomes were apparently normal. The reported cases of in utero exposure to cyclosposphamide shared the following manifestations with our patient: growth deficiency, developmental delay, craniosynostosis, blepharophimosis, flat nasal bridge, abnormal ears, and distal limb defects including hypoplastic thumbs and oligodactyly. We conclude that (a) cyclophosphamide is a human teratogen, (b) a distinct phenotype exists, and (c) the safety of CP in pregnancy is in serious question.
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2/11. Cyclosporin A in a pregnant patient affected with systemic lupus erythematosus.

    Few data regarding the use of cyclosporin A (CyA) in pregnancy are available and those available refer mainly to transplant recipients and not to patients with connective tissue diseases. We report the case of a patient with systemic lupus erythematosus (SLE), taking CyA before, during and after her pregnancy at a dose of 4 mg/kg per day. CyA was effective in controlling SLE activity and no side effects were observed in mother or baby. The lack of teratogenicity in this case was in keeping with previous reports in experimental systems, animals and human transplant recipients. If our observation is confirmed by further studies, CyA might become useful in the treatment of pregnant patients with SLE.
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3/11. IL-1RA in refractory systemic lupus erythematosus.

    There is evidence from animal and human studies that IL-1 might play an important role in the development and maintainence of inflammation in systemic lupus erythemathosus (SLE). We hypothesized that, in SLE, there might be a relative deficiency in the physiologic antagonist of IL-1, IL-1 receptor antagonist (IL-1RA). We therefore treated three patients with active SLE in whom conventional therapy has failed with the human IL-1RA, Anakinra. In two of the three patients there was a transient effect on muscle pain and/or polyarthritis. In one patient with lupus myositis there was no effect at all. The therapy was well tolerated and the only significant side effect was a transient drop in complement levels (C3 and C4) without clinical or laboratory signs of increased SLE activity in all three patients.
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4/11. Conditioning as an adjunct in the pharmacotherapy of lupus erythematosus.

    Several studies have provided evidence suggesting that "placebo effects" represent conditioning phenomena and that learning processes influence the response to placebo medication. This case report describes an adolescent with severe lupus erythematosus who received cyclophosphamide (CY) paired with taste (cod liver oil) and smell (rose perfume) as conditioned stimuli. The regimen was based on conditioning experiments with animals who had lupuslike autoimmune disease. After the initial pairings, the taste alone was offered between CY treatments. Over 12 months, the patient received six rather than 12 CY treatments, half the cumulative dose that might have been administered. The patient improved clinically, and 5 years later continues to do well.
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5/11. q fever with clinical features resembling systemic lupus erythematosus.

    A 23-year-old woman with prolonged fever, rash, and pericarditis associated with high titers of antinuclear, anti-Sm, and anti-RNP antibodies was suspected of having systemic lupus erythematosus (SLE). However, we also considered infectious diseases, particularly q fever, as the c-reactive protein level was elevated and the patient reported contact with zoo animals around two weeks before the onset. The condition responded rapidly to administration of minocycline; symptoms resolved without using steroids. Thereafter, no recurrence of the illness was observed. Titer of coxiella burnetii antibody was high and the illness was accordingly diagnosed as acute q fever rather than SLE.
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6/11. Reversal of the vasospastic component of lupus vasculopathy by infusion of prostaglandin E1.

    The responses of 3 patients with systemic lupus erythematosus (SLE) and progressive digital ischemia to intravenous prostaglandin E1 (PGE1) were studied prospectively in an open 3-day trial. All patients were unresponsive to corticosteroids, one had vasculitis proven by biopsy. Digital ischemia diminished in all 3 patients. In one patient, angiograms documented reappearance of a previously obstructed deep palmar arch. Vasospasm plays a role in the outcome of SLE vasculitis even in the absence of Raynaud's phenomenon. As suggested by animal models of necrotizing and leukocytoclastic vasculitis, and by case reports, intravenous PGE1 may be a relatively nontoxic, adjunctive treatment for vasculitis.
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7/11. interferon-gamma induced exacerbation of systemic lupus erythematosus.

    A patient with presumed rheumatoid arthritis based on clinical and serological evidence was subjected by her physician to interferon-gamma (IFN-gamma) therapy and developed a life threatening multiorgan flare of systemic lupus erythematosus (SLE). pulse cyclophosphamide therapy in conjunction with plasmapheresis led to complete remission. Retrospective analysis of serum drawn before IFN-gamma was started revealed high dna binding capacity. Thus, similar to observations in lupus-prone animals, IFN-gamma may have induced an exacerbation of preexisting SLE.
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8/11. Phytohemagglutinin (PHA) skin test. Characterization of immunological properties and clinical application.

    Immunological properties of phytohemagglutinin (PHA) skin reaction were investigated by animal and clinical experiments. In the guinea pigs an intradermal dose of PHA-P produced erythema and induration with a maximal response at 24 hours after the injection. Histologically it was characterized by perivascular infiltration of lymphoid cells in the dermis and subcutis, being similar to that of tuberculin (PPD) skin reaction. PHA skin reaction, however, showed some difference from that of PPD in the initial cellular response in that the former was composed of small mononuclear cells and granulocytes with rapid development and the latter was composed of large mononuclear cells (macrophages) and granulocytes with slow development. Intradermal injection of 1:1000 dilution of PHA-P produced a similar erythema in man. In 39 of 59 patients with connective tissue diseases, the results of the in vivo (skin test) and in vitro (lymphocyte transformation) response to PHA correlated well. In the 59 patients, the incidence of the positive rate of the PHA tests (55.9%) was significantly higher than that of the DNCB test (33.9%) and of the PPD test (23.7%). These observations suggest that the PHA skin test has properties of delayed hypersensitivity and is highly sensitive and that it may be a useful measure of cell-mediated immunity.
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9/11. Immune complex deposition and coronary vasculitis in systemic lupus erythematosus. Report of two cases.

    Extramural coronary arteries were examined in two patients with systemic lupus erythematosus (SLE). Coronary vasculitis was found in both patients. One patient with clinically and serologically inactive SLE had died suddenly and was found to have a myocardial infarction secondary to the coronary vasculitis. Immunopathologic studies demonstrated immune reactants in the walls of inflamed and noninflamed arterial segments in a pattern consistent with immune complex aggregates. Immunologic injury secondary to immune complex deposition may be responsible for the development of coronary disease in patients with SLE. This has been demonstrated in experimental animals but not in humans. Although this is an uncommon complication of SLE, it represents a cause of sudden death and a potentially treatable lesion in this patient population. Its occurrence may be related to the deposition of immune aggregates in the walls of coronary vessels.
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10/11. Systemic lupus erythematosus complicated by disseminated sarcoidosis. Report of a case associated with circulating immune complexes.

    The association of SLE with sarcoidosis has been reported infrequently. The case of a 47-year-old white woman who had the diagnosis of SLE made at our institution in October of 1979 is presented. In February 1980, the onset of bilateral hilar adenopathy prompted an investigation leading to the diagnosis of sarcoidosis. Circulating immune complexes were markedly elevated. The association of these two diseases has only recently been recognized and may be more widespread than previously suspected. Some animal and clinical data, in concert with our observations, suggest that humoral autoimmunity may give rise to both processes in the same patient.
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