Antiphospholipid antibodies, haemostatic variables and thrombosis--a survey of 144 patients

Several clotting abnormalities have been put forth to explain the thrombotic tendency of the antiphospholipid syndrome, but a possible role for fibrinogen and von Willebrand factor has been poorly investigated. The present cross-sectional retrospective study evaluated the relationship of IgG anticardiolipin antibodies, lupus anticoagulants, fibrinogen and von Willebrand factor with the occurrence of arterial and venous thromboses in patients with antiphospholipid antibodies. Among the clotting assays for the detection of lupus anticoagulant, dilute Russell's viper venom time correlated with a history of venous thrombosis more strongly than activated partial thromboplastin time (p < 0.0002 vs p < 0.009) and was the only test which correlated with a history of arterial thrombosis (p < 0.01), also at low levels of IgG anticardiolipin antibodies (p = 0.003). By regression analysis, and after correction for confounders, serum levels of IgG anticardiolipin antibodies were found to be positively associated with the number of venous events (p < 0.001). Plasma levels of fibrinogen and von Willebrand factor were associated with each other (p < 0.0001; r: 0.48) and with the occurrence of arterial and venous thromboses (p < 0.001). Moreover, plasma levels of fibrinogen and von Willebrand factor in thrombotic patients with antiphospholipid antibodies were significantly higher than those of a control group of thrombotic patients who suffered thrombosis for other reasons (p < 0.0001 and p = 0.0008 respectively). Titres of IgG anticardiolipin antibodies correlated with plasma levels of von Willebrand factor (p < 0.0001; r: 0.42).(ABSTRACT TRUNCATED AT 250 WORDS)     

The response of the antioxidant defense system in rat hepatocytes challenged with oxysterols is modified by Covi-ox

We studied positivity for anti-cardiolipin antibody, intraglomerular capillary thrombi on renal biopsy, and the progression of renal disease in 51 patients (10 male and 41 female), mean age 37 years (range 17-65 years), with a diagnosis of systemic lupus erythematosis and clinically evident nephritis confirmed by renal biopsy. Serum creatinine, serum indicators of disease activity and biopsies were analysed in subgroups according to thrombi and anticardiolipin status. End-points were death or chronic dialysis requirement and survival. Degree of sclerosis, crescent formation and necrosed glomeruli were all greater in those specimens positive for thrombi and in those specimens of patients who were serum ACA-positive, suggesting a relationship to disease activity/severity at presentation. The increase in serum anti-DNA antibodies and ANA and the reduction in C3 and C4 were significant in ACA-positive patients, with a strong relationship to disease activity when compared with changes in the ACA-negative patients (p < 0.05 in all cases). There was no significant difference when patients were separated according to the presence or absence of thrombi. Renal function at presentation was worse in patients with intracapillary thrombi and ACA positivity (p = 0.085 and p = 0.042, respectively). All patients progressed, but only those with intracapillary thrombi or anti-cardiolipin antibody positivity had a significant deterioration in renal function. Twenty-one thrombotic episodes occurred in 14 patients, of whom 13 were ACA-positive. Anticardiolipin antibody is a strong predictor of the presence of intraglomerular thrombi in SLE patients with renal involvement. The presence of thrombi and/or anticardiolipin antibodies indicate a worse long-term renal outcome. Anti-cardiolipin antibody positivity is a strong predictor of systemic vascular thrombotic complications.     

Anti-cardiolipin and anti-beta2-glycoprotein I antibodies in patients with inflammatory bowel disease

Patients with inflammatory bowel disease (IBD) frequently suffer from thromboembolic events. Anti-cardiolipin (aCL) antibodies have been shown to be associated with thrombosis. Recently, the antibodies against the anti-cardiolipin cofactor beta2-glycoprotein I (a(beta2)GPI) have been found with higher specificity for thrombosis. The presence of these antibodies was assessed in 128 patients with IBD [83 with ulcerative colitis (UC) and 45 with Crohn's disease (CD)] and 100 healthy controls (blood donors). Patients with UC and CD had a significantly higher prevalence of aCL (18.1% and 15.6%, respectively) than healthy controls (HC) (3%). Eleven IBD patients (8.6%) but no HC had a(beta2)GPI. None of the IBD patients with a history of thrombosis had aCL and only one of them (a UC patient with deep vein thrombosis of the right leg) had a high titer of IgG a(beta2)GPI. In conclusion, these data show that both aCL and a(beta2)GPI are significantly associated with IBD but further studies are needed to determine the significance of our findings.     

Arterial tumour embolism causing acute limb ischaemia

Besides cytopenia related to treatment, several hematological disorders such as anemia, abnormal platelet activity, thrombosis, presence of anticardiolipin or anti-neutrophil antibodies, cyclic neutropenia, and myelodysplasia, have been reported in patients with Crohn's disease (CD). The case we report here is the first one documenting the association of idiopathic thrombocytopenic purpura (ITP) with CD.     

Lupus patients with peripheral vascular thrombosis: the significance of measuring anticardiolipin antibody

The purpose of this study was to determine the significance of measuring anticardiolipin (ACL) antibodies in Chinese lupus patients with peripheral vascular thrombosis. A total of 252 lupus patients were evaluated prospectively for the presence of peripheral vascular thrombosis in a 3-year period. Tests of ACL antibodies with three isotypes were done serially during follow-up. There were 10 lupus patients with five episodes of arterial thrombosis and seven episodes of venous thrombosis by the evidence of angiographical and/or pathological findings. The ACL antibody status was negative (< 2 standard deviation [SD]), low (2 to 5 SD) and high (> 5 SD) for 43.3%, 22.6%, and 34.1% patients, respectively. Patients with high levels (> 5 SD) of ACL antibodies had a high frequency of peripheral vascular thrombosis than patients with negative levels (> 2 SD) of ACL antibodies (P < .05). It is concluded that serial measurement of ACL antibodies in lupus patients is useful in predicting the occurrence of peripheral vascular thrombosis. Clinicians should be alert to the possibility of such complication in lupus patients with high ACL antibodies levels when visiting the emergency service.     

Anticardiolipin antibodies in serum and cerebrospinal fluid from patients with systemic lupus erythematosus

Anticardiolipin antibodies were studied in serum and cerebrospinal fluid from 32 consecutive patients with systemic lupus erythematosus, admitted for the assessment of neuropsychiatric disease. Ten of the 16 patients with active neuropsychiatric complaints showed positive anticardiolipin antibodies in cerebrospinal fluid, including eight with the simultaneous presence of antibodies in their sera. By contrast, only 2 of the 16 patients with headaches, lacking further data of neurological disease, revealed anticardiolipin antibodies in their cerebrospinal fluid. The assessment of Q-albumin index showed abnormal values in a subset of patients with active neuropsychiatric changes who showed positive cerebrospinal anticardiolipin antibodies, suggesting that an impairment of the blood brain barrier function may lead to a leakage of intrathecal antiphospholipid antibodies from systemic circulation. Additionally, few patients revealed normal Q-albumin values with high IgG-cerebrospinal fluid index suggesting increased intrathecal synthesis of autoantibodies. The study of anticardiolipin antibodies in cerebrospinal fluid was useful to detect active neuropsychiatric disease in systemic lupus erythematosus.     

Enhanced lipid peroxidation in patients positive for antiphospholipid antibodies

The mechanism leading to the formation of antiphospholipid antibodies (aPL) is still unknown. Because an in vitro study suggested that aPL may derive from pro-oxidant conditions, we sought a relationship between aPL and isoprostanes, indices of lipid peroxidation in vivo. Thirty patients with systemic lupus erythematosus have been studied. Seventeen (56.6%) were positive for aPL because they had lupus anticoagulant and/or high titer of anticardiolipin antibodies (aCL). Plasma levels of tumor necrosis factor (TNF ) and urinary excretion of two isoprostanes, 8-epi-PGF2alpha and IPF2alpha -I, free radical catalyzed oxidation products of arachidonic acid, were measured. Patients with systemic lupus erythematosus had higher urinary excretion of 8-epi-PGF2alpha and IPF2alpha -I than controls; urinary excretion of the two isoprostanes was highly correlated (Rho = 0.74, P < .0001). Urinary 8-epi-PGF2alpha was highly correlated with both aCL titer (Rho = 0. 70, P < .0001) and TNF (Rho = 0.84, P < .0001), a measure of disease severity. Excretion of this isoprostane was also higher in those patients who exhibited aPL (P < .0001). Comparable correlations were observed with the isoprostane IPF2alpha -I. No difference of 8-epi-PGF2alpha was observed between patients with and without previous history of thrombosis. This study, showing the existence of a close association between aPL and increased in vivo lipid peroxidation, supports the hypothesis that these antibodies may result from pro-oxidative conditions and suggests that inflammation may play an important role.     

Treatment of refractory rapid cycling bipolar disorder with risperidone

BACKGROUND: There is evidence for a hypercoagulable state in inflammatory bowel disease (IBD), and small vessel thrombosis has been identified in the bowel of patients with Crohn's disease, suggesting thrombosis as a possible etiologic factor. Activated protein C (APC) resistance is the most common inherited disorder leading to thrombosis and accounts for 30% to 40% of episodes of idiopathic venous thrombosis. METHODS: The prevalence of APC resistance was studied in 23 patients with IBD (17 with Crohn's disease, 6 with ulcerative colitis) and in 11 control subjects with recurrent abdominal pain or celiac disease, using an APC resistance screening method. RESULTS: One patient with Crohn's disease had a positive screen result, two patients (one with Crohn's, one with ulcerative colitis) had borderline results, and results in all of the control subjects were normal. One patient with Crohn's disease had a history of a thromboembolic event but had a normal screen result. CONCLUSIONS: Activated protein C resistance does not seem to play a major role in the etiology of the hypercoagulable state in inflammatory bowel disease.     

Antiphospholipid antibodies other than lupus anticoagulant and anticardiolipin antibodies in women with recurrent pregnancy loss, fertile controls, and antiphospholipid syndrome

OBJECTIVE: To determine whether antiphospholipid antibodies other than lupus anticoagulant and anticardiolipin are associated with recurrent pregnancy loss. METHODS: Sera from three groups of women were studied: 1) 147 women with recurrent pregnancy loss but no clinical signs or symptoms of autoimmune disease who tested negative for lupus anticoagulant and medium-to-high levels of immunoglobulin G anticardiolipin antibodies; 2) 104 healthy, fertile controls of similar age and gravidity; and 3) 43 women with well-characterized antiphospholipid syndrome. Serum antibody binding against six phospholipids (cardiolipin, phosphatidic acid, phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol) was determined using enzyme-linked immunoassays, and results were normalized using an anticardiolipin standard. RESULTS: Twenty-six (18%) women with recurrent pregnancy loss and nine (9%) controls tested positive (above the 99th percentile) for antiphospholipid antibodies. Sera from five (3.4%) women with recurrent pregnancy loss and four (3.8%) controls demonstrated binding to phospholipid antigens other than cardiolipin. In contrast, binding to phospholipid antigens was demonstrated in sera from more than 90% of women with antiphospholipid syndrome. Among women testing positive for antiphospholipid antibodies, the median positive value for women in the antiphospholipid syndrome group was significantly higher than for those with recurrent pregnancy loss or normal fertile controls. CONCLUSIONS: Women with recurrent pregnancy loss are no more likely than fertile controls to have elevated levels of antiphospholipid antibodies once lupus anticoagulant, anticardiolipin, and an obvious clinical history of autoimmune disease have been excluded. Testing for antiphospholipid antibodies other than lupus anticoagulant and anticardiolipin is not clinically useful in the evaluation of recurrent pregnancy loss.     

Anticardiolipin antibody-associated cerebral infarction in cirrhosis: clearance of anticardiolipin antibody after liver transplantation

We report a 47-yr-old woman with a 30-yr history of cryptogenic cirrhosis who sustained a cerebral infarction shortly before undergoing liver transplantation. Anticardiolipin antibody titers were positive prior to transplantation (IgG = 24 GPL; IgM > 80 MPL; IgA < 10 APL). After liver transplantation, however, the titers dropped to normal (< 10 PL units). This report suggests that cirrhotic patients with high anticardiolipin antibody titers may be at risk for thrombotic events, and that this tendency may be reversed by liver transplantation or post-transplant immunosuppressive agents.     

Anticardiolipin antibodies and osteonecrosis of the femoral head

The current study evaluated the prevalence of anticardiolipin antibodies, which have been associated with thrombotic phenomena, in patients with nontraumatic osteonecrosis of the hip and assessed whether the presence of such antibodies is associated with an increased risk for the development of bone necrosis. Forty consecutive patients (25 men and 15 women) with nontraumatic osteonecrosis of the hip were studied. Their ages ranged from 19 to 56 years (average, 34.3 years). Anticardiolipin antibodies were present in 37.5% (15 of 40) of the tested patients, a significantly higher rate than is seen in healthy subjects, of whom only one of 100 had low titer anticardiolipin antibodies (1%). Six of 40 patients tested positive for immunoglobulin M alone, and six of 40 patients tested positive for immunoglobulin A alone. Three of 40 patients tested positive for immunoglobulin M and immunoglobulin A isotype. The results of the current study indicate an increased incidence of anticardiolipin antibodies in patients with nontraumatic osteonecrosis of the femoral head, which may reflect that anticardiolipin antibodies play a role in the pathogenesis of bone necrosis by predisposing to thrombotic phenomena.     

In vitro glucocorticoid receptor binding and transcriptional activation by topically active glucocorticoids

BACKGROUND: To study body composition at the whole-body level in patients with Crohn's disease and a history of intestinal resection compared with healthy controls, we performed a cross-sectional study using dual-energy X-ray absorptiometry (DXA). METHODS: Thirty-one patients, 13 men and 18 women, were included. They had a history of Crohn's disease for a mean period of 20 years (range, 4-45 years). All patients had undergone intestinal resections. The colon had been resected in 24 patients, and the mean length of the resected small intestine was 97 cm (range, 0-305 cm). At the time of investigation the Crohn's disease had been in remission for at least 24 months. Patients presented with significantly increased faecal volume and faecal fat excretion. A group of 69 women and 19 men were investigated with DXA and used as reference group. The fat-free mass (FFM), fat mass (FM), percentage fat mass (FM%), and total body mineral content (TBMC) were measured by DXA, and the results were expressed as a z-score. RESULTS: The mean z-score of the body mass index (BMI) was significantly reduced to -0.35 (P=0.036). The FFM was significantly reduced with a mean z-score of -1.74 (P=0.0001). The FM was unchanged (z-score, 0.12; P=0.42). However, FM expressed as percentage of body weight was significantly increased, with a z-score of 0.88 (P=0.001). The TBMC was significantly decreased, with a mean z-score of -1.42 (P=0.0001). There was positive direct correlation between the BMI and TBMC z-scores. There was no correlation between malabsorption and body composition variables. CONCLUSION: Patients with clinically quiescent Crohn's disease showed significant changes in body composition, with low BMI, significant loss of FFM, and unchanged FM. However, when expressed as percentage of body weight, FM was significantly increased. The TBMC was significantly reduced.     

Medullary metastasis causing impairment of respiratory pressure output with intact respiratory rhythm

BACKGROUND: Vascular access failure is an important cause of morbidity in end-stage renal failure patients on hemodialysis. Currently, little is known about risk factors that predispose certain hemodialysis patients to recurrent access thrombosis. Hyperhomocysteinemia (common in patients with renal failure) predisposes people with normal renal function to recurrent and early-onset venous thrombosis, although the effect on vascular access thrombosis is currently unknown. Previous studies have suggested that high titers of IgG anticardiolipin antibody (IgG-ACA) predispose hemodialysis patients to access thrombosis. This cross sectional study was designed to assess for an association between two predictive variables, hyperhomocysteinemia and elevated titers of IgG-ACA, and vascular access thrombosis in patients undergoing chronic hemodialysis. METHODS: Risk factors for vascular access thrombosis were documented, and the number of episodes of access thrombosis was recorded for the previous three years in patients undergoing hemodialysis. Midweek predialysis total homocysteine and IgG-ACA levels were measured in all subjects. RESULTS: Of the 118 patients who were enrolled, 75.4% had a native arteriovenous fistula. Episodes of vascular access thrombosis were recorded for the previous three years; 34 (28.8%, 95% CI 20.9 to 37.9%) patients had 72 episodes of access thrombosis over the period of risk. Mean homocysteine levels were not significantly different between these 34 patients (28.6 micromol/liter, 95% CI 24.5 to 32.7) and the patients who had no episodes of graft thrombosis (29.8 micromol/liter, 95% CI 26.7 to 32.9). Sixty-seven unselected patients had IgG-ACA levels drawn for analysis, and all assays were negative. The only variable that was associated with a higher risk for graft thrombosis was the type of vascular access placed (odds ratio 4.0, 95% CI 1.6 to 9.6 for patients with a synthetic graft compared with those with an arteriovenous fistula). CONCLUSIONS: No association was found between homocysteine levels or anticardiolipin antibody and vascular access thrombosis in our patient population.     

pH-sensitive liposomes for receptor-mediated delivery to chicken hepatoma (LMH) cells

The purpose of this study was to evaluate pediatric patients with systemic lupus erythematosus (SLE) to determine 1) the incidence of thrombosis, 2) the incidence of antiphospholipid antibodies, and 3) whether there is an association between the presence of antiphospholipid antibodies and thrombosis. We performed a cross-sectional cohort study in 59 consecutive SLE patients who had been managed at rheumatology clinics in two pediatric hospitals. A history, questionnaire, and chart review were completed by the study nurse blinded to laboratory results. Only the thrombotic events that could be substantiated by review of radiographic tests were accepted. The presence of antiphospholipid antibodies was determined by prospective analysis for a lupus anticoagulant and anticardiolipin antibodies on two separate occasions at least 3 mo apart. Patients were considered to be positive if one or more tests were positive on both occasions. Thirteen thrombotic events occurred in 10 of the 59 patients (17%). Fourteen patients (24%) were classified as positive for lupus anticoagulant, and 19 patients (27%) were classified as positive for anticardiolipin antibodies. A significant relationship between the presence of a lupus anticoagulant and a thrombotic event was shown: odds ratio 28.7 (95% confidence interval 4.03-138.2, p < 0.001). A nonsignificant trend was seen for the presence of an anticardiolipin antibody and a thrombotic event: odds ratio 2.12 (95% confidence interval 0.71-22.8, p=0.08). We conclude that in pediatric patients with SLE: 1) a significant proportion of patients have thrombotic events, 2) a significant proportion of patients have antiphospholipid antibodies, and 3) there is a significant relationship between the presence of a lupus anticoagulant and thrombotic events.     

Prothrombin fragment 1 + 2 and thrombin-antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases

OBJECTIVES AND METHODS: The aims of the present work were to assess the presence of thrombin generation in Crohn's disease and in ulcerative colitis by using the prothrombin fragment 1 + 2 and the thrombin-antithrombin III complex assays and to study the possible relationships between these markers and disease activity. RESULTS: Prothrombin fragment 1 + 2 and thrombin-antithrombin III complex were significantly raised in patients with Crohn's disease (n = 69) and with ulcerative colitis (n = 25) as compared with healthy controls (n = 50). In Crohn's disease these two markers of thrombin generation were correlated with the Van Hees index (P < 0.05 and P < 0.001, respectively); values were significantly different from controls even in the patient group displaying the lowest disease activity (P < 0.001). No correlation was found with tumour necrosis factor alpha and C-reactive protein; nevertheless patients with C-reactive protein less than or equal to 10 mg/l had significant lower values of prothrombin fragment 1 + 2 (P < 0.03). In ulcerative colitis prothrombin fragment 1 + 2 and thrombin-antithrombin III complex were significantly increased by comparison with controls, were higher in patients with pancolitis and correlated with C-reactive protein (P < 0.002 and P < 0.009, respectively). CONCLUSION: These data show that prothrombin fragment 1 + 2 and thrombin-antithrombin III complex are increased in inflammatory bowel diseases and suggest that thrombin generation might be an early event in their pathogenesis.     

Axonal regeneration through muscle autografts submitted to local anaesthetic pretreatment

Over a 3 year period the R506Q mutation in the factor V (FV) FV:Q506 gene, FV, factor XII (FXII), prothrombin, protein C, protein S, antithrombin, heparin cofactor II, anticardiolipin antibodies and lipoprotein (a) (Lp(a)) were measured in 32 infants and children with sinus thrombosis. Heterozygous FV:Q506 (n=5), homozygous FV:Q506 (n=2), homozygous FXII deficiency (n=1), protein C deficiency type I (n=5), protein C deficiency type II (n=1), antithrombin deficiency type I (n=1) increased Lp (a) (n=5), activated protein C-resistance without mutation in the FV gene (n=2), and increased anticardiolipin IgG antibodies (n=2) were diagnosed in the children investigated. In a further two patients we found combinations of increased Lp(a) with moderate hyperhomocystinaemia and heterozygous plasminogen deficiency with heterozygous FXII deficiency. In addition, increased anticardiolipin IgG antibodies were found in combination with heterozygous FV:Q506 (n=1) and protein C type I deficiency (n=2) respectively. Out of 32 patients with venous sinus thrombosis, 3 showed additional peripheral venous vascular occlusion. Contributing factors were present in 31 out of 32 patients investigated. Family members of 10 affected children had suffered from venous thrombo-embolism prior to the study. CONCLUSION: Our data suggest that additional contributing factors may promote manifestation of cerebral venous sinus thrombosis in infants and children with an inherited prothrombotic state. Further prospective studies are required to evaluate their potential role as "triggering" agents.     

Antibodies binding to anionic phospholipids but not to oxidized low-density lipoprotein are associated with thrombosis in patients with systemic lupus erythematosus

OBJECTIVE: Elevated levels of antibodies against oxidized low-density lipoprotein (LDL) frequently occur in patients with systemic lupus erythematosus (SLE) and these antibodies crossreact in many sera with anticardiolipin antibodies, known to be associated with thrombosis. Therefore, a study was carried out to assess the mutual relationship between antibodies against oxidized LDL and thrombosis. METHODS: The occurrence of IgG class antibodies against oxidized LDL, cardiolipin and phosphatidyl serine were determined by enzyme-linked immunosorbent assay in a series of 146 patients with SLE. Twenty-one patients had had thromboembolic complications. At least one of three tests used to detect lupus anticoagulant was positive in 34 out of 133 patients. RESULTS: The level of antibodies against oxidized LDL correlated significantly with that of antibodies against cardiolipin (r = 0.52) but only marginally with antibodies against phosphatidyl serine (r = 0.18). Antibodies against cardiolipin and phosphatidyl serine, but not those against oxidized LDL, were significantly associated with the presence of lupus anticoagulant (odds ratios of the risk in the highest tertile relative to the lower tertiles of the antibody were 5.3, 6.9 and 1.1, respectively) and with thrombosis (odds ratios 2.5, 4.0 and 1.0, respectively). CONCLUSION: The observations suggest that only those antibodies reacting specifically with cardiolipin and phosphatidyl serine are associated with thrombosis and with the presence of lupus anticoagulant in patients with SLE, whereas antibodies crossreacting with oxidized LDL and those reacting specifically with oxidized LDL are not associated.     

Prevalence and significance of anticardiolipin, anti-beta2 glycoprotein I and anti-prothrombin antibodies in chronic hepatitis C

Antiphospholipid antibodies have been demonstrated in chronic hepatitis C, but their clinical and pathogenetic significance remains elusive. We prospectively studied 115 patients (85 men, mean age 36.9 years) with chronic hepatitis C without cirrhosis and treated by alpha-interferon (alpha-IFN). Antiphospholipid determinations comprised anticardiolipin (ACA), anti-beta2-glycoprotein I and anti-prothrombin antibodies of the IgG and IgM classes. At entry, 24 patients (21%) were found to possess low to moderate ACA levels (18 IgG, two IgM and four both isotypes) compared with only 4/115 age- and sex-matched control subjects (3.5% P=0.001). ACA positivity rate increased to 31% (P=0.01) after a 6-month course of alpha-IFN treatment. In contrast, the prevalence of anti-beta2-glycoprotein I and anti-prothrombin antibodies was not significantly different from controls at either time point. The presence of ACA correlated with that of antinuclear antibodies (P=0.0002), but was not associated with parameters such as histological activity, viral burden and response to alpha-IFN, nor with a history of thrombosis or pregnancy loss. However, a non-significant trend of higher incidence of mild thrombocytopenia among ACA-positive patients was observed. We conclude that low-titre ACA positivity is a common finding in patients with chronic hepatitis C, especially following alpha-IFN treatment, but does not select a category with different clinical features. These data are in keeping with the absence of associated anti-beta2GPI and anti-prothrombin antibodies, and do not support a role for HCV infection in the pathogenesis of the antiphospholipid syndrome.     

Characterization of the cadmium-binding capacity of Chlorella vulgaris

BACKGROUND & AIMS: Remission of several autoimmune diseases has been described after allogeneic marrow transplantation. The aim of this study was to determine if the natural history of Crohn's disease was altered by hematopoietic cell transplants from healthy allogeneic donors. METHODS: Between 1982 and 1992, 6 patients with Crohn's disease and leukemia underwent allogeneic marrow transplantation and were followed up clinically. RESULTS: Five patients had active Crohn's disease before transplantation, and 3 had clinical evidence of sclerosing cholangitis. Four marrow donors were HLA-identical siblings, 1 related donor was mismatched at the DR locus, and 1 unrelated donor was HLA-matched. One patient died of septicemia 97 days after transplantation; 5 patients were observed for 4.5, 5.8, 8.4, 9.9, and 15.3 years after transplantation. Four of 5 patients evaluated had no signs or symptoms of Crohn's disease after transplantation. One patient with mixed donor-host hematopoietic chimerism had a relapse of Crohn's disease 1.5 years after transplantation. CONCLUSIONS: Four of 5 patients followed up for 4.5 to 15.3 years after allogeneic hematopoietic cell transplantation remained free of Crohn's disease. These observations suggest that host immune dysregulation plays a role in the perpetuation of Crohn's disease that can be corrected by allogeneic hematopoietic cell transplantation.