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Number of infiltrating lymphocytes. Compared to phosphate-buffered saline PBS ; -treated controls n 4 ; , there was a significant decrease in the number of infiltrating lymphocytes in the conjunctiva of animals treated with topical cyclosporine A CsA ; 0.05% re 3 ; , CsA 0.2% n 5 ; , CsA 0.4% n 4 ; , or prednisolone acetate Pred ; n 4 ; . * 0.0033; * P 0.0091; * P 0.0192; * P 0.03. o Bars standard error. ' were counted to ensure an equal degranulating effect of compound 48 80 in each group Fig. 5 ; . In the first experiment, there was no difference in mast cells counted in the conjunctiva of animals treated with PBS, topical CsA, or pred Fig. 5A ; . These findings were confirmed in the second experiment; no statistically significant differences in mast cells were found in any group Fig. 5B ; . Immunohistochemical staining of the conjunctiva showed a statistically significant decrease in the number of infiltrating lymphocytes in animals treated with topical CsA or pred when compared to controls Fig. 6 ; . There also appeared to be a decrease in the number of infiltrating macrophages in animals treated with the higher doses of topical CsA 0.2% and 0.4% ; compared to pred-treated animals and PBS-treated controls Fig. 7 ; , although the differences were not statistically significant. DISCUSSION Our data show that the topical application of cyclosporine effectively inhibits a mast cell-mediated model of allergic conjunctivitis. Cyclosporine reduced the number of neutrophils, eosinophils, and lympho.
ICOS is a member of the CD28 CTLA-4 family and is expressed on activated T cells. Stimulation of the ICOS pathway promotes secretion of IFN , IL-4, and IL-10. Inhibition of the ICOS pathway with anti-ICOS antibody or the soluble form of ICOS ICOSIg ; prolongs cardiac allograft survival in a murine model, and combined treatment with anti-ICOS antibody and cyclosporine A97 or ICOSIg and CTLA-4Ig98 prolongs cardiac allograft survival indefinitely and prevents development of CAV. ICOS ligand, also known as B7-related protein 1 B7RP-1 ; , is expressed constitutively on B cells and in peripheral lymphoid tissues.65, 99 In vitro studies revealed that ICOS ligand expression is induced on fibroblasts treated with TNF- and that it is expressed constitutively on endothelial cells and is upregulated by treatment with IL-1 or TNF- .100 Although ICOS and CD28 signaling upregulate Th1 and Th2 cytokines, ICOS does not upregulate IL-2 production. Therefore, ICOS stimulates T cell effector function but not T cell clonal expansion.65 Treatment of cardiac allografts with ICOSIg with blockade of the CD40 ligand CD40 pathway attenuates development of CAV in mice.97 Our experiments revealed that ICOS ligand expression is induced on smooth muscle cells of thickened intima in CAV and treatment of recipient mice with either ICOSIg or anti-ICOS antibody suppresses development of CAV.101 Similar findings showing the importance of delayed blockade of this pathway have been reported by another laboratory.102 The authors speculate that delayed blockade of this pathway allows generation of regulatory mechanisms while inhibiting activation of effector memory T cells. Because ICOS and ICOS ligand are not expressed in normal tissues and expression is induced during immune activation, this pathway may be a suitable target for prevention of CAV and other arterial lesions.
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HGV HGBV-C in patients on chronic dialysis and a large discrepancy, ranging from 3.1 [ 3] to 20% [48] has been reported. We studied HGV HGBV-C presence in sera from 110 patients on maintenance haemodialysis 70 men, 40 women; mean age 5514.9 years; dialysis age 102.693.5 months, range 1336 ; . Patients were grouped on the basis of markers for HCV HBV HIV infection into three groups as follows: 42 patients positive for antibodies anti-HCV, of whom 29 were HCV-RNA + with dierent detectable genotypes, 13 HCV-RNA- and 68 anti-HCV-. Four patients were coinfected with HBSAg, while the only HIV + patient was in the anti-HCV-group. HGV HGBV-C-RNA was also tested in a study group of 36 patients with chronic HCV hepatitis. Viral RNA was extracted from serum that was stored at -80C by absorption to silica and spin chromatography QUIAmp, HCV kit, Quiagen, Hilden, Germany ; , then subjected to reverse transcription polymerase chain reaction PCR ; with primers from the helicase non-structural region NS3 of HGV HGBV-C 85.5% nucleotide identity between the two viruses ; [9 ]. The amplified products were identified by hybridization to an HGV HGBV-C probe and detected by DNA enzyme immunoassay DEIA, Sorin, Italy ; . Fifteen samples from dialysis patients were also tested by RT-PCR with primers from the 5 untranslated region of HGV HGBC. They were all negative for HGV HGB-C-RNA. The prevalence of HGV HGBV-C RNA was zero in both anti-HCV + and anti-HCV- dialysis patients, whereas three of 36 8% ; patients with HCV + chronic hepatitis showed HGV HGBV-C RNA in serum. We cannot exclude that the prevalence we report underestimates the actual epidemiological relevance of the HGV HGBV-C infection in patients undergoing haemodialysis, because of genetic variability among strains. However, as in the other Italian study [4] HGV was the predominant genotype in 73.6% of infection; it is unlikely that this reason can account by itself for the dierence in the prevalence data. We conclude that, as the geographic distribution of HGV HGBV-C is not yet known, our data at least are against a genuinely increased risk of infection with this viral agent among Italian patients on haemodialysis. Furthermore, taking into consideration other data reported for dialysis patients [ 3, 4, 8, it is evident that HGV viraemia is low in comparison to hepatitis C infection, which should share common pathways of transmission and diusion. As a similar observation has been made among Italian [11] as well as Australian [12] haemophilia patients, it is possible to speculate.
Monitoring concentrations of cyclosporine CsA ; in body fluids has been used as a guide for the appropriate adjustment of dosage to reduce the frequency of side effects and yet maintain the immunosuppressive potential 1-4 ; . Routine monitoring of the drug in whole blood has been recommended with a selective assay that specifically measures the parent CsA and not its metabolites 1-3 ; . At present, this can be done by either HPLC or RIA 4 ; . The former procedure is laborious and not well suited for routine use in clinical laboratories. Currently two RIAs that involve a selective monoclonal antibody, which exhibits minima! cross-reactivity with CsA metabolites, are commercially available 5-8 ; . As requests for CsA analysis increase, the need for commercially available, reliable automated assays for selectively measuring CsA in whole blood increases. A few.
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That we started a preventive programme based on universal precautions to minimize the risk of exposure to hepatitis C virus HCV ; , with good results [2]. Actually, from 1990 to March 1997 we had no cases of seroconversion to HCV antibodies among new patients starting haemodialysis treatment. Surprisingly, from March 1997 to January 1998 we had five new cases, as reported in Table 1. We were seriously considering the possibility of a new cluster of HCV infection which might have been favoured by our lowering attention for universal precautions of blood-borne infections. In all our patients who had positive HCV antibodies Abbott HCV EIA 3.0, Abbott Labs, USA ; we analysed HCV genotype with inverse hybridization Amplicor extraction, Roche, immunoblotted Innolipa, Nuclear Laser ; and classified them as suggested by Simmonds et al. [3]. In January 1997 we had 36 143 haemodialysis patients with HCV antibodies. We found genotype 1B in 16 44.4% ; , genotypes 2 in 15 41.6% ; , and undetermined genotype in 5 36 haemodialysis patients 13.9% ; . In our geographical area the presence of HCV antibodies is 36%, depending on age. We therefore controlled the distribution of different genotypes in a non-selected, successively enrolled group of 453 patients with community acquired HCV infection. We found genotype 1A in 41 453 haemodialysis patients 9.1% ; , genotype 1B in 204 453 34.9% ; , genotypes 2 in 158 453 24.9% ; , genotype 3A in 33 453 7.3% ; , genotype 4 in 5 453 1.1% ; and undetermined genotype in 12 453 2.6% ; . We then controlled the day and turn of dialysis of all five patients from June 1996 to January 1998. We found that only patients No. 4 and 5 were regularly dialysed in the same room and turn. Moreover, the genotyping of our five new cases revealed different HCV subtypes. We conclude that this apparent cluster of HCV infection was not an epidemic but corresponded to independent infections, possibly related to surgical procedures patients Nos 1, 3 and 4 ; or community acquired infection patient No. 2 ; . Only one out of the five cases was potentially acquired in the dialysis unit. After January 1998 we followed the usual procedure to avoid exposure to HCV and until January 1999 no other cases have occurred. This observation led to a debate with dialysis staff as to the importance of respecting universal precaution measures in the unit. We think that it is useful to maintain permanent alertness on blood-borne infections. 1Department of Nephrology and Dialysis 2Department of Infectious Diseases 3Department of Immunohematology Ospedali Riuniti di Bergamo Bergamo, Italy D. Marchesi1 E. Minola2 O. Vicari3.
Of the Odontoid Process in Rheumatoid Arthritis. RanaNAetal * Autograft Reconstruction, Post-Traumatic Lesions of the Brachial Plexus, Treatment by Transclavicular Exploration and Neurolysis or. Lusskin R, Catispbell iB and Thompson WAL `Axillary Artery as a Complication of Shoulder Dislocation, Complete Avulsion of the. Jardon OM, Hood LT and Lynch RD and cytarabine.
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From spontaneous mutations in the mdr1 P-glycoprotein ; gene. Cell 1988; 53: 519-529. Schinkel AH, Smit JJ, van Tellingen O et al. Disruption of the mouse mdr1a P-glycoprotein gene leads to a deficiency in the blood-brain barrier and to increased sensitivity to drugs. Cell 1994; 77: 491-502. Tsuruo T, Iida H, Tsukagoshi S et al. Overcoming of vincristine resistance in P388 leukemia in vivo and in vitro through enhancing cytotoxicity of vincristine and vinblastine by verapamil. Cancer Res 1981; 41: 1967-1972. Sonneveld P, Durie BG, Lokhorst HM et al. Modulation of multidrug-resistant multiple myeloma by cyclosporin. The Leukaemia Group of the EORTC and the HOVON. Lancet 1992; 340: 255-259. Sonneveld P, Schoester M, de Leeuw K. Clinical modulation of multidrug resistance in multiple myeloma: effect of cyclosporine on resistant tumor cells. J Clin Oncol 1994; 12: 1584-1591. Sonneveld P, Suciu S, Weijermans P et al. Cyclosporin A combined with vincristine, doxorubicin and dexamethasone VAD ; compared with VAD alone in patients with advanced refractory multiple myeloma: an EORTC-HOVON randomized phase III study 06914 ; . Br J Haematol 2001; 115: 895-902. Dalton WS, Crowley JJ, Salmon SS et al. A phase III randomized study of oral verapamil as a chemosensitizer to reverse drug resistance in patients with refractory myeloma. A Southwest Oncology Group Study. Cancer 1995; 75: 815-820. Twentyman PR. Cyclosporins as drug resistance modifiers. Biochem Pharmacol 1992; 43: 109-117. Bates SE. Solving the problems of multidrug resistance: ABC transporters in clinical oncology. In: Holland IB, Cole SP, Kuchler K et al., eds. ABC Proteins: From Bacteria to Man. London: Elsevier Science, 2002: 359-391. 60 Toppmeyer D, Seidman AD, Pollak M et al. Safety and efficacy of the multidrug resistance inhibitor Incel biricodar; VX710 ; in combination with paclitaxel for advanced breast cancer refractory to paclitaxel. Clin Cancer Res 2002; 8: 670-678. Bramwell VH, Morris D, Ernst DS et al. Safety and efficacy of the multidrug-resistance inhibitor biricodar VX-710 ; with concurrent doxorubicin in patients with anthracyclineresistant advanced soft tissue sarcoma. Clin Cancer Res 2002; 8: 383-393. Bates SE, Chen C, Robey R et al. Reversal of multidrug resistance: lessons from clinical oncology. 2002 Mechanisms of Drug Resistance in Epilepsy: Lessons from Oncology. Novartis Foundation Symposium 243. Chichester: Wiley, 2002: 83-102. 63 Fracasso PM, Westervelt P, Fears CL et al. Phase I study of paclitaxel in combination with a multidrug resistance modulator, PSC 833 Valspodar ; , in refractory malignancies. J Clin Oncol 2000; 18: 1124-1134. Stewart A, Steiner J, Mellows G et al. Phase I trial of XR9576 in healthy volunteers demonstrates modulation of P-glycoprotein in CD56 + lymphocytes after oral and intravenous administration. Clin Cancer Res 2000; 6: 4186-4191. Robey R, Bakke S, Stein W et al. Efflux of rhodamine from CD56 + cells as a surrogate marker for reversal of P-glycoprotein-mediated drug efflux by PSC 833. Blood 1999; 93: 306-314.
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Murine primary cells are poorly permissive to human immunodeficiency virus type 1 HIV-1 ; vector infection. Retroviral infectivity is influenced by dominant inhibitors such as TRIM5 . Sensitivity to TRIM5 is altered by interactions between cyclophilin A and the HIV-1 capsid. Here we demonstrate that competitive inhibitors of cyclophilins, cyclosporine or the related Debio-025, stimulate HIV-1 vector transduction of primary murine cells, including bone marrow and macrophages, up to 20-fold. Unexpectedly, the infectivity of an HIV-1 mutant or a simian lentivirus that does not recruit cyclophilin A is also stimulated by these drugs. We propose that cyclosporine and related compounds will be useful tools for experimental infection of murine primary cells. It is possible that HIV-1 infection of murine cells is inhibited by dominant factors related to immunophilins.
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Metabolism occurs through hydrolytic deamidation, S-oxidation, aromatic ring hydroxylation, and glucuronide conjugation. Less than 10% of an administered dose is excreted as the parent compound. In a clinical study using radiolabeled modafinil, a total of 81% of the administered radioactivity was recovered in 11 days post-dose, predominantly in the urine 80% vs. 1.0% in the feces ; . The largest fraction of the drug in urine was modafinil acid, but at least six other metabolites were present in lower concentrations. Only two metabolites reach appreciable concentrations in plasma, i.e., modafinil acid and modafinil sulfone. In preclinical models, modafinil acid, modafinil sulfone, 2-[ diphenylmethyl ; sulfonyl]acetic acid and 4-hydroxy modafinil, were inactive or did not appear to mediate the arousal effects of modafinil. In humans, modafinil shows a possible induction effect on its own metabolism after chronic administration of doses 400 mg day. Induction of hepatic metabolizing enzymes, most importantly cytochrome P-450 CYP ; 3A4, has also been observed in vitro after incubation of primary cultures of human hepatocytes with modafinil. For further discussion of the effects of modafinil on CYP enzyme activities see PRECAUTIONS, Drug Interactions ; . Drug-Drug Interactions: Because modafinil is a reversible inhibitor of the drug-metabolizing enzyme CYP2C19, co-administration of modafinil with drugs such as diazepam, phenytoin and propranolol, which are largely eliminated via that pathway, may increase the circulating levels of those compounds. In addition, in individuals deficient in the enzyme CYP2D6 i.e., 7-10% of the Caucasian population; similar or lower in other populations ; , the levels of CYP2D6 substrates such as tricyclic antidepressants and selective serotonin reuptake inhibitors, which have ancillary routes of elimination through CYP2C19, may be increased by co -administration of modafinil. Dose adjustments may be necessary for patients being treated with these and similar medications See PRECAUTIONS, Drug Interactions ; . Chronic administration of modafinil may also cause modest induction of the metabolizing enzyme CYP3A4, thus reducing the levels of co-administered substrates for that enzyme system, such as steroidal contraceptives, cyclosporine and, to a lesser degree, theophylline. Dose adjustments may be necessary for patients being treated with these and similar medications See PRECAUTIONS, Drug Interactions ; . An apparent concentration-related suppression of CYP2C9 activity was observed in human hepatocytes after exposure to modafinil in vitro. Although no other indication of CYP2C9 suppression has been observed, the in vitro results suggest that there is potential for metabolic interaction between PROVIGIL and CYP2C9 substrates, such as warfarin or phenytoin See PRECAUTIONS, Drug Interactions ; . Special Populations Gender Effect: The pharmacokinetics of modafinil are not affected by gender. Age Effect: A slight decrease ~20% ; in the oral clearance CL F ; of modafinil was observed in a single dose study at 200 mg in 12 subjects with a mean age of 63 years range 53 72 years ; , but the change was considered unlikely to be clinically significant. In a multiple dose study 300 mg day ; in 12 patients with a mean age of 82 years range 67 87 years ; , the mean levels of modafinil in plasma were approximately two times those historically obtained in matched younger subjects. Due to potential effects from the multiple concomitant medications with which most of the patients were being treated, the apparent difference in modafinil pharmacokinetics may not be attributable solely to the effects of aging. However, the results suggest that the clearance of modafinil may be reduced in the elderly See DOSAGE AND ADMINISTRATION ; . Race Effect: The influence of race on the pharmacokinetics of modafinil has not been studied. Renal Impairment: In a single dose 200 mg modafinil study, severe chronic renal failure creatinine clearance 20 mL min ; did not significantly influence the pharmacokinetics of modafinil, but exposure to modafinil acid an inactive metabolite ; was increased 9 fold See PRECAUTIONS ; . Hepatic Impairment: Pharmacokinetics and metabolism were examined in patients with cirrhosis of the liver 6 M and 3 F ; . Three patients had stage B or B cirrhosis per the Child criteria ; and 6 patients had stage C or C cirrhosis. Clinically 8 of 9 patients were icteric and all had ascites. In these patients, the oral clearance of modafinil was decreased by about 60% and the steady state concentration was doubled compared to normal patients. The dose of PROVIGIL should be reduced in patients with severe hepatic impairment See PRECAUTIONS and DOSAGE AND ADMINISTRATION ; . CLINICAL TRIALS The effectiveness of PROVIGIL in reducing the excessive daytime sleepiness EDS ; associated with narcolepsy was established in two US 9 -week, multicenter, placebo-controlled, two-dose 200 mg per day and 400 mg per day ; parallel-group, double -blind studies of outpatients who met the ICD-9 and American Sleep Disorders Association criteria for narcolepsy which are also consistent with the American Psychiatric Association DSM-IV criteria ; . These criteria include either 1 ; recurrent daytime naps or lapses into sleep that occur almost daily for at least three months, plus sudden bilateral loss of postural muscle tone in association with intense emotion cataplexy ; or 2 ; a complaint of excessive sleepiness or sudden muscle weakness with associated features: sleep paralysis, hypnagogic hallucinations, automatic behaviors, disrupted major sleep episode; and polysomnography demonstrating one of the following: sleep latency less than 10 minutes or rapid eye movement REM ; sleep latency less than 20 minutes. In addition, for entry into these studies, all patients were required to have objectively documented excessive daytime sleepiness, a Multiple Sleep Latency Test MSLT ; with two or more sleep onset REM periods, and the absence of any other clinically significant active medical or psychiatric disorder. The MSLT, an objective daytime polysomnographic assessment of the patient's ability to fall asleep in an unstimulating environment, measures latency in minutes ; to sleep onset averaged over 4 test sessions at 2-hour intervals following nocturnal polysomnography. For each test session, the subject was told to lie quietly and attempt to sleep. Each test session was terminated after 20 minutes if no sleep occurred or 15 minutes after sleep onset. In both studies, the primary measures of effectiveness were 1 ; sleep latency, as assessed by the Maintenance of Wakefulness Test MWT ; and 2 ; the change in the patient's overall disease status, as measured by the Clinical Global Impression of Change CGI-C ; . For a successful trial, both measures had to show significant improvement.
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| Cyclosporine wikiTransplant immunosuppression was administered. Fourteen patients were reconstituted with mobilized peripheral blood stem cells and one with bone marrow cells. Donors of the peripheral blood stem cells were injected subcutaneously with granulocytecolony stimulating factor G-CSF; Neupogen 5 mg kg twice daily for 5 days ; and the mobilized peripheral blood stem cells were collected on days 5 and 6. Bone marrow collection was done under epidural anesthesia. Prior to transplantation, all patients received trimethoprim sulfamethoxazole 10 mg kg day trimethoprin ; on days -8 to -2, acyclovir 500 mg m23 day ; from day 8 until day + 100, and allopurinol 300 mg day ; on days -8 to -1. Administration of trimethoprim sulfamethoxazole twice weekly ; was reinstituted after recovery from neutropenia as a preventive measure against Pneumocystis carinii infection. Neutropenic patients with culture-negative fever received a combination of gentamicin, cefazolin and mezlocillin, as a first-line antibiotic protocol. Persisting fever was treated with amikacin and tazocin as a second-line protocol, while meropenem and vancomycin were used as the third-line protocol. In cases of persistent fever not responding to antibiotic therapy within 5 days, amphotericin B 1 mg kg every other day ; was added until the neutropenia resolved. Starting on day -8, a DNA-polymerase chain reacton PCR ; test and, later during the follow-up period assay of pp65 antigenemia, was done weekly to detect cytomegalovirus. Two consecutive positive PCR results or one antigenemia assay with more then one cell positive for pp65 served as an indication for replacing acyclovir with ganciclovir 10 mg kg day ; , until a minimum of two negative tests were obtained. Patients were treated with reverse isolation in rooms equipped with HEPA filters, and received a regular diet. Additional supportive measures, such as blood components were administered as necessary. Acute and chronic GVHD were graded according to Glucksberg's criteria.17 Upon the appearance of signs and symptoms of acute GVHD grade I, treatment was immediately started with methylprednisolone 2 mg kg day i.v. and cyclosporine 3 mg kg day i.v. in two divided doses for patients in the hospital and 6 mg kg twice daily orally for outpatients. In order to assess engraftment, degree of chimerism, minimal residual disease and early relapse, patients were monitored at regular intervals by cytogenetic analysis, and by donor and host-specific DNA markers as previously described, including male and female amelogenine gene PCR bands, 18 and by variable number of tandem repeats-PCR assay in patients with no sex mismatch.19 and dacarbazine.
Vol 23, No 4 April 1992 athy, and cerebral ischemia has only rarely been appreciated, 1-2 and IHSS has never been considered a high-risk disease for stroke. Russell et al3 have recently reported in Stroke an extremely high incidence of cerebral ischemic events 22% ; in a large series of patients with IHSS followed for 6.5 years. In five patients, stroke was the presenting manifestation of IHSS. The authors conclude that patients with IHSS are at high risk for ischemic cerebrovascular complications. These new, interesting data are apparently in contrast with current cardiological opinion. Who is right? In dealing with patients with cardiac disease and stroke, it is crucial to establish a cause-and-effect relationship between cardiac disease and cerebral ischemia. Besides presumptive clinical neurological criteria, the absence of atherosclerotic vascular disease based on cerebral angiography or carotid echotomography is an essential requisite for the diagnosis of cardiogenic cerebral embolism.4 It is likely that, following these criteria, a presumably cardioembolic etiology of cerebral ischemia was consequently established in only nine patients in the series of Russell et al.3 Considering only these cases, the incidence of cerebral ischemic events approximates the figures reported in the literature15"11 Table 1 ; . In the remaining patients with atheroembolic, atherothrombotic, or lacunar stroke, IHSS can represent only a coincidental finding. An advanced age at stroke and an extremely high prevalence of hypertension may represent the major risk factors for cerebral ischemia rather than IHSS itself. Moreover, in the presence of long-standing hypertension, whose prevalence in the series of Russell et al was as high as 69%, the diagnosis of IHSS may be complicated by a differential diagnosis of hypertensive heart disease. But even considering only those nine patients with cardioembolic stroke or transient ischemic attack, the data reported by Russell et al3 are noteworthy, confirming our previous observations derived by a different approach to the problem. In a series of 380 consecutive patients mean age 53.6 years ; with cerebral ischemia who were referred to the Neurosurgical Department, embologenic cardiac lesions were documented by two-dimensional echocardiography in 27 patients 7% among these cases, six patients with IHSS were identified. Infivecases, associated factors responsible for embolism were identified: paroxysmal atrial fibrillation in three patients, infective endocarditis with mitral valve vegetations in one, and evolution of IHSS into a dilatative form with intraventricular thrombus in one. In all cases, cerebral angiography or carotid echotomography excluded the presence of atherosclerotic vascular lesions.12 A careful analysis of larger series of IHSS reported in the literature demonstrates that the risk of cerebral embolism in IHSS is not negligible, occurring in 2-15% of patients, with an estimated incidence of embolism of 0.4-2.4% yearly. Nevertheless, the stratification of the embolic risk has not received much attention up to the present time. Russell et al3 deserve credit for stressing this aspect. Idiopathic hypertrophic subaortic stenosis per se is not an embolic cardiac condition; the rapid flow and lack of opportunity for stasis do not predispose the patient to the formation of left ventricular thrombi. The risk of embolism is almost always related to the occurrence of atrial fibrillation, which occurs in 5-10% of patients with IHSS, usually late in the course of the disease.7-913 Similarfindingsresulted from the series of Russell et al seven of nine patients ; . Infective endocarditis or evolution toward dilation with systolic dysfunction and congestive heart failure, which develops in about 10% of patients with IHSS, represent other major events predisposing patients to embolism. Left atrial enlargement, mitral annulus calcification, and low cardiac output can be invoked as contributing mechanisms. In Table 1 the incidence of atrial fibrillation, infective endocarditis, and embolism in larger series of IHSS is reported. The risk factors for embolism are specified in the last column.
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REFERENCES 1. Anaissie, E., D. P. Kontoyiannis, C. Huls, S. Vartivarian, C. Karl, R. A. Prince, J. Bosso, and G. P. Bodey. 1995. Safety, plasma concentrations, and efficacy of high-dose fluconazole in invasive mold infections. J. Infect. Dis. 172: 599602. 2. Beck-Sague, C. M., W. R. Jarvis, and the National Nosocomial Infection Surveillance System. 1993. Secular trends in the epidemiology of nosocomial fungal infections in the United States, 19801990. J. Infect. Dis 167: 1247 1251. Brammer, K. W., P. R. Farrow, and J. K. Faulkner. 1990. Pharmacokinetics and tissue penetration of fluconazole in humans. Rev. Infect. Dis. 12 Suppl. 3 ; : 318326. 4. Calderone, R. A., M. F. Rotondo, and M. A. Sande. 1978. Candida albicans endocarditis: ultrastructural studies of vegetation formation. Infect. Immun. 20: 279289. 5. Chemlal, K., L. Saint-Julien, V. Joly, R. Farinotti, N. Seta, P. Yeni, and C. Carbon. 1996. Comparison of fluconazole and amphotericin B for treatment of experimental Candida albicans endocarditis in rabbits. Antimicrob. Agents Chemother. 40: 263266. 6. Collier, S. J., R. Y. Calne, D. J. White, S. Winters, and S. Thiru. 1986. Blood levels and nephrotoxicity of cyclosporin A and G in rats. Lancet i: 216. 7. De Pauw, B. E., and E. Anaissie. 1997. Controversies in the management of candidiasis in neutropenic patients treated for malignant diseases: new versus old or better versus worse. Int. J. Infect. Dis. 1 Suppl. 1 ; : 3236. 8. Del Poeta, M., M. C. Cruz, M. E. Cardenas, J. Perfect, and J. Heitman. 2000. Synergistic antifungal activities of bafilomycin A1, fluconazole, and the pneumocandin MK-0991 caspofungin acetate L-743, 873 ; with calcineurin inhibitors FK 506 and L-685, 818 against Cryptococcus neoformans. Antimicrob. Agents Chemother. 44: 739746. 9. Egner, R., F. E. Rosenthal, A. Kralli, D. Sanglard, and K. Kuchler. 1998. Genetic separation of FK 506 susceptibility and drug transport in the yeast Pdr5 ATP-binding cassette multidrug resistance transporter. Mol. Biol. Cell 9: 523543. 10. Fields, B. T., J. H. Bates, and R. S. Abernathy. 1970. Amphotericin B serum concentrations during therapy. Appl. Microbiol. 19: 955959. 11. Fonzi, W. A, and M. Y. Irwin. 1993. Isogenic strain construction and gene mapping in Candida albicans. Genetics 134: 717728. 12. Fruma, D. A., C. B. Klee, B. E. Bierer, and S. J. Burakoff. 1992. Calcineurin phosphatase activity in T lymphocytes is inhibited by FK 506 and cyclosporin A. Proc. Natl. Acad. Sci. USA 89: 36863690. 13. Gallis, H. A., R. H. Drew, and W. W. Pickard. 1990. Amphotericin B: 30 years of clinical experience. Rev. Infect. Dis. 12: 308329. 14. Garcha, B. K., E. Brummer, and D. A. Stevens. 1995. Synergy of fluconazole with human monocytes or monocyte-derived macrophages for killing of Candida species. J. Infect. Dis. 172: 16201623. 15. Haynes, M., L. Fuller, D. H. Haynes, and J. Miller. 1985. Cyclosporin partitions into phospholipid vesicles and disrupts membrane architecture. Immunol. Lett. 11: 343349. 16. Heraief, E., M. P. Glauser, and L. R. Freedman. 1982. Natural history of aortic valve endocarditis in rats. Infect. Immun. 37: 127131. 17. Higgins, C. F. 1992. ABC transporters: from microorganisms to man. Annu. Rev. Cell Biol. 8: 67113. 18. Ho, S., N. Clipstone, L. Timmermann, J. Northrp, I. Graef, D. Fiorentino, J. Nourse, and G. R. Crabtree. 1996. The mechanism of action of cyclosporin A and FK 506. Clin. Immunol. Immunopathol. 80 Suppl. 3 ; : 4045. 19. Kirkland, T. N., and J. Fierer. 1983. Cyclosporin A inhibits Coccidioides immitis in vitro and in vivo. Antimicrob. Agents Chemother. 24: 921924. 20. Krause, M. W., and A. Schaffner. 1989. Comparison of immunosuppressive effects of cyclosporine A in a murine model of systemic candidiasis and of localized trushlike lesions. Infect. Immun. 57: 34723478. 21. List, A. F. 1996. Role of multidrug resistance and its pharmacological modulation in acute myeloid leukemia. Leukemia 10: 937942. 22. Liu, J., J. D. Farmer, W. S. Lane, J. Friedman, I. Weissman, and S. L. Schreiber. 1991. Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes. Cell 66: 807815. 23. Louie, A., Q. F. Liu, G. L. Drusano, W. Liu, M. Mayers, E. Anaissie, and M. H. Miller. 1998. Pharmacokinetic studies of fluconazole in rabbits characterizing doses which achieve peak levels in serum and area under the concentration-time curve values which mimic those of high-dose fluconazole in humans. Antimicrob. Agents Chemother. 42: 15121514. 24. Marchetti, O., P. Moreillon, M. P. Glauser, J. Bille, and D. Sanglard. 2000. Potent synergism of the combination of fluconazole and cyclosporine in Candida albicans. Antimicrob. Agents Chemother. 44: 23732381. 25. McGinnis, M. R., and M. G. Rinaldi. 1996. Antifungal drugs: mechanisms of action, drug resistance, susceptibility testing, and assays of activity in biologic and daclizumab.
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