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PubMed1998

Increased familial history of arterial hypertension, coronary heart disease, and renal disease in Brazilian type 2 diabetic patients with diabetic nephropathy.

OBJECTIVE: To evaluate whether there is a familial association of arterial hypertension, coronary heart disease, renal disease, and stroke with diabetic nephropathy RESEARCH DESIGN AND METHODS: There were 115 outpatients and 34 patients with end-stage renal disease treated by hemodialysis (61 men, age range 41-81 years) and having at least one sibling with type 2 diabetes studied. The positive or negative history of siblings (n = 765) was assessed by a standard questionnaire. The urinary albumin excretion rate (UAER) was measured by radioimmunoassay in 24-h sterile urine (three samples). The subjects were grouped as normoalbuminuric (UAER <20 microg/min, n = 59), microalbuminuric (UAER 20-200 microg/min, n = 35), macroalbuminuric (UAER >200 microg/min, n = 21), and end-stage renal disease (n = 34). RESULTS: Patients with microalbuminuria, macroalbuminuria, or end-stage renal disease had an increased prevalence of sibling history of arterial hypertension (33.2, 37.3, and 33.8 vs. 23.4%, P < 0.001) and coronary heart disease (15.2, 17.0, and 19.4 vs. 10.2%, P = 0.044) compared with the normoalbuminuric group. The renal disease history was increased only in the siblings of patients with macroalbuminuria or end-stage renal disease (12.8 and 15.6 vs. 7.6 and 6.1%, P = 0.005). The presence of sibling arterial hypertension strongly increases the prevalence of sibling renal and coronary heart disease independent of patient renal status. CONCLUSIONS: There is an association of diabetic nephropathy and sibling history of arterial hypertension and renal and coronary heart disease in type 2 diabetic patients. These associations are not independent, and arterial hypertension may be their main determining factor.

Adult↗

PubMed2001

Autoimmunity in isolated Addison's disease and in polyglandular autoimmune diseases type 1, 2 and 4.

Sera from 300 Italian patients with Addison's disease were collected over a 30 year period. Among these patients, 82% had autoimmune disease, 13% had tuberculosis and 5% had another causal condition. In 59% of the cases, autoimmune disease was associated with the autoimmune manifestations contributing to the description of polyglandular autoimmune disease (PGAD). In PGAD type 1, the disease was associated with chronic candidiasis and/or chronic hypoparathyroidism. In PGAD type 2, the patients had autoimmune thyroid disease and/or diabetes mellitus type 1, and in PGAD type 4, they presented a combination with other autoimmune diseases excluding those previously mentioned. Finally, the autoimmune disease was apparently isolated in 41% of the cases. In addition, patients with these four forms of disease exhibited a different genetic pattern, sex distribution, and age at presentation in addition to minor frequency of autoimmune diseases. Adrenal cortex autoantibodies directed against 21-hydroxylase were common serological markers for these four main clinical forms, showing a very high frequency at clinical onset of adrenal insufficiency. In some patients, steroid-producing cell autoantibodies were also present and correlated with gonadal failure and they recognize of 17alpha-hydroxylase or P450 side chain cleavage enzymes as target antigens.

Addison Disease↗

PubMed2001

[Occurrence of celiac disease in siblings and offspring of patients with celiac disease].

BACKGROUND: Incidence of the coeliac disease in our population is 0.3 to 0.5%, however, in direct relatives of patients with coeliac disease incidence rises up to 5-15%. Though the disease in not always clinically manifested, it can be identified by serologic screening. METHODS AND RESULTS: 96 patients treated for active coeliac disease and their 130 siblings were examined. In four of 130 siblings the disease clinically manifested and was confirmed with finding of enteropathy of jejunal mucosa. In 14 out of 126 asymptomatic siblings endomysial antibodies were identified and in 11 of them enteropathy was diagnosed. Coeliac disease was diagnosed in 15 (11.5%) persons from 130 siblings. Also 74 offsprings of 43 parent patients were examined. In four of them the coeliac disease manifested clinically and was later confirmed with finding of enteropathy. Antiglidin antibodies were tested in 45 asymptomatic offsprings with 6 positive results. Endomysial antibodies were tested in 25 asymptomatic offsprings with one positive result. Villous atrophy of jejunal mucosa was found in four asymptomatic offsprings. Coeliac disease was diagnosed in 8 (11.5%) persons from 74 offsprings. CONCLUSIONS: Coeliac disease represent a major risk for the patient's direct relatives. Goal-directed examination and the early diagnosis of the disease in childhood may help to prevent impairments in the development of the child and possible complications later.

Adolescent↗

PubMedDate not supplied

[Polycystic liver disease without autosomal dominant polycystic kidney disease].

Polycystic liver disease is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. The natural history and clinical manifestations of polycystic liver disease are based on the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD). The occurrence of polycystic liver disease independently from polycystic kidney disease has been known for a long time. More recently, a gene for autosomal dominant polycystic liver disease has been identified on chromosome 19p 13.2-13.1. Isolated polycystic liver disease is underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with similar pathogenesis and clinical manifestations. We report here two men with polycystic liver disease no associated with ADPKD. Ultrasound and computed tomography imaging were effective in documenting the underlying lesions non-invasively.

Adult↗

PubMed2004

A moral emergency and a medical problem: negotiating the control of venereal disease--the Saskatchewan Venereal Disease Protection Act, 1946.

The author examines Saskatchewan legislation that regulated venereal disease. Although venereal disease legislation was introduced in Saskatchewan in 1919, the centrepiece of this article is The Venereal Disease Prevention Act, 1946. In an attempt to understand the nuances of and underlying rationale for these laws, the author situates the legislation within its social context. The author demonstrates that the trends and contradictions apparent in society's approach to the regulation of venereal disease were reflected in the legislation. The concept of a continuum is used to illustrate the coexistence of two approaches to the control of venereal disease. On one side of the continuum, venereal disease was a moral problem and a taboo subject. Force was the key to controlling venereal disease; involuntary examinations and intrusions into people's personal lives were the solution. On the other side of the continuum, venereal disease was a medical problem. If approached rationally and openly, control of venereal disease was possible; through education and social acceptance of venereal disease as just another illness, people would voluntarily come forward for treatment. The approaches represented at the extreme ends of the continuum did not exist in isolation; these views existed simultaneously, producing contradictory and colourful rhetoric.

Coercion↗

PubMed1991

[Serum acute phase proteins for determining disease activity of ulcerative colitis and Crohn disease].

We studied the activity assessment of ulcerative colitis and Crohn's disease by 5 acute phase reactants: C-reactive protein (CRP), alpha 1-acid glycoprotein, alpha 1 antitrypsin, haptoglobin and fibrinogen. From a large register of patients with inflammatory bowel disease (IBD) we chose randomly 91 patients: 61 with ulcerative colitis and 30 with Crohn's disease. As a reference point in the disease activity assessment we used standard clinical indices. Statistical analysis was performed by non-parametric methods: the Kruskal-Wallis and Fisher's exact test. The disease activity assessment in patients with ulcerative colitis by the index according to Powell-Tuck indicated that the patients with active disease (N = 19) had significantly higher levels of all acute phase proteins mentioned above except fibrinogen (alpha less than 0.05 to 0.001) than patients in remission (N = 42). Analysis of the same data by Fisher's exact test indicated that there had been a probability for all the proteins measured to be higher than the normal values, particullary CRP (p less than 10(-8) and the other somewhat less. In patients with Crohn's disease, the disease activity assessment was performed by 2 indices. According to "The Crohn's Disease Activity Index" (CDAI), only alpha-1 acid glycoprotein and haptoglobin (alpha less than 0.05) were higher in patients with active disease (N = 4) than in patients with remission (N = 26).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗

PubMed1983

Quantitative fecal indium 111-labeled leukocyte excretion in the assessment of disease in Crohn's disease.

The assessment of disease activity in Crohn's disease involves determination of either clinical indexes (e.g., Crohn's disease activity index) or laboratory measurements (e.g., C-reactive protein and erythrocyte sedimentation rate). These have the disadvantage of being indirect and nonspecific correlates of gut inflammation. We have assessed disease activity in Crohn's disease by measurement of fecal leukocyte excretion after intravenous administration of either 111In-labeled mixed leukocyte or pure granulocyte preparations. With mixed leukocyte preparations, fecal excretion of radioactivity correlated with Crohn's disease activity index (r = 0.78, p less than 0.001) and C-reactive protein (r = 0.74, p less than 0.01). Using pure granulocytes, fecal 111In excretion (range 1.5%-52%) was much higher than with mixed leukocytes (range 0.1%-11.0%), showing significant correlations with Crohn's disease activity index (r = 0.731, p less than 0.001), C-reactive protein (r = 0.716, p less than 0.001), and erythrocyte sedimentation rate (r = 0.676, p less than 0.001). Quantitative fecal excretion of 111In-leukocytes is a new method of assessing disease activity in Crohn's disease, specific for bowel inflammation and suitable for objective assessment of disease activity in therapeutic trials.

Blood Sedimentation↗

PubMed1995

Wilson's disease: a new gene and an animal model for an old disease.

Wilson's disease is an autosomal recessive, inherited disorder of copper metabolism. In normal individuals, copper homeostasis is controlled by the balance between intestinal absorption of dietary copper and hepatic excretion of excess copper in bile. In Wilson's disease, hepatic copper is neither excreted in bile nor incorporated into ceruloplasmin and copper accumulates to toxic levels. The Wilson's disease gene (WND) encodes a putative copper-transporting protein that is expressed almost exclusively in the liver. The predicted structure of the protein product is that of a P-type ATPase with striking homology to bacterial copper transporters and the gene product of another inherited disorder of copper metabolism, Menkes' disease. A rat model of Wilson's disease has recently been identified. The Long-Evans Cinnamon (LEC) rat manifests elevated hepatic copper, defective incorporation of copper into ceruloplasmin, and reduced biliary excretion of copper. The rat homologue of the WND is abnormal in LEC rats. Clinical manifestations of Wilson's disease arise directly from copper-induced damage to hepatocytes (hepatic presentation) or indirectly after the release of copper from the liver with subsequent damage to the brain (neuropsychiatric presentation) and other organs. Genetic heterogeneity (different mutations in a single gene) may account for some of the variability in Wilsonian presentations. The diagnosis of Wilson's disease depends on the demonstration of disordered copper metabolism, manifested as elevated urinary and hepatic copper and low ceruloplasmin levels. However, none of the abnormal findings in Wilson's disease is pathognomonic. Genetic diagnosis, in the absence of family studies, is likely to be difficult since many different mutations result in the disease. Management of Wilson's disease involves decreasing excess levels of copper accumulated in the liver, brain, and other organs. Copper chelation therapy, to increase urinary excretion of copper, is the mainstay of treatment. In addition, oral zinc therapy may be useful at decreasing absorption of dietary copper and rendering tissue copper nontoxic, by increasing the formation of complexes with copper-binding proteins. Liver transplantation can be necessary for individuals with acute hepatic failure or complications of cirrhosis. Gene therapy may evolve in the future; however, medical management is effective in most patients.

Amino Acid Sequence↗

PubMed1994

[A new index of disease activity in Crohn's disease].

A comprehensive assessment including subjective and objective parameters seems to be essential for evaluation of disease activity in Crohn's disease. The aim of the present study was to develop an activity index (AI) of Crohn's disease, composed of both subjective and objective variables. Data composed of a total 132 clinical examinations in 100 patients with Crohn's disease were used to determine the AI. Three physicians independently evaluated disease severity in each patient. Stepwise multiple regression analysis was carried out with the overall evaluation as a dependent variable, and with 18 parameters as independent variables. Analysis showed that the following seven variables had a significant correlation with physician's overall evaluation: abdominal pain, abdominal tenderness, complications, C-reactive protein (CRP), body temperature, diarrhea, and body mass index (BMI). AI was expressed as follows: AI = 3.5 x abdominal pain + 3 x abdominal tenderness + 3 x complications + CRP + 3 x body temperature + 4 x diarrhea - 0.4 x BMI. AI values below 15 corresponded to inactive disease, values between 15 and 25 to mild disease, values between 25 and 35 to moderate disease, and values above 35 to severe disease. This study suggests that the activity index is useful for evaluation of the effect of medical treatment in Crohn's disease.

Adult↗

PubMed1996

The incidence of pediatric rheumatic diseases: results from the Canadian Pediatric Rheumatology Association Disease Registry.

OBJECTIVE: To determine the incidence of rheumatic diseases in children, and the frequency of musculoskeletal disorders seen by pediatric rheumatology specialists in Canada. METHODS: Applying standardized disease definitions and disease codes modified from ICD-9, members of the Canadian Pediatric Rheumatology Association from 13 centers in all 10 provinces of Canada registered all new patients seen between May 1, 1991 and April 30, 1993. Patient data included age, sex, ethnicity, date of birth, date of disease onset, date of diagnosis, and diagnostic codes (more than one diagnosis could be entered). To minimize the bias of right censoring, only data from patients with disease onset between May 1, 1991 and October 31, 1992 were used to estimate disease incidence. RESULTS: 3362 records totalling 3683 diagnoses (92 separate diagnoses) were registered. Median referral rate per year to a pediatric rheumatology center was 26 per 100,000 children at risk. The frequency of diseases seen was 23.3% for all forms of chronic arthritis, 6.5% for connective tissue diseases, and 6.1% for all forms of vasculitis. The minimum incidence rates per 100,000 children at risk per year calculated from the whole registry were: all forms of chronic arthritis 4.08 (95% CI: 3.62, 4.60), systemic lupus erythematosus 0.28 (0.18, 0.45), and dermatomyositis 0.15 (0.09, 0.29). Substantially higher figures were obtained if the figures were calculated excluding the 2 provinces (Alberta and Quebec) that had disproportionately low referral rates. CONCLUSION: Pediatric rheumatologists see children with a wide variety of diseases. It is important that pediatric rheumatology training reflects this and does not focus exclusively on the classical inflammatory arthropathies. The minimum incidence data show there are substantial numbers of children developing potentially lifelong chronic rheumatic diseases each year in Canada. These data should be helpful in planning the delivery of pediatric rheumatology services not only in Canada, but also in other developed countries.

Adolescent↗

PubMed2001

Alpha-synuclein in familial Alzheimer disease: epitope mapping parallels dementia with Lewy bodies and Parkinson disease.

BACKGROUND: Alpha-synuclein is a major component of Lewy bodies (LBs) in Parkinson disease and dementia with LBs and of glial cytoplasmic inclusions in multiple system atrophy. However, epitope mapping for alpha-synuclein is distinctive in different neurodegenerative diseases. The reasons for this are poorly understood but may reflect fundamental differences in disease mechanisms. OBJECTIVE: To investigate the alpha-synuclein epitope mapping properties of LBs in familial Alzheimer disease. DESIGN AND SETTING: We compared LBs in familial Alzheimer disease with those in synucleinopathies by probing 6 brains of persons with familial Alzheimer disease using a panel of antibodies to epitopes spanning the alpha-synuclein protein. Results were compared with data from brains of persons with Parkinson disease, dementia with LBs, and multiple system atrophy. RESULTS: The brains of persons with familial Alzheimer disease showed consistent staining of LBs with all antibodies, similar to Parkinson disease and dementia with LBs but different from alpha-synuclein aggregates that occurred in multiple system atrophy. CONCLUSIONS: These data suggest that the epitope profiles of alpha-synuclein in LBs are similar, regardless of whether the biological trigger is related to synuclein or a different genetic pathway. These findings support the hypothesis that the mechanism of alpha-synuclein aggregation is the same within cell types but distinctive between cell types.

Aged↗

PubMed1980

Specificity of biophysical and biochemical alterations in erythrocyte membranes in neurological disorders--Huntington's disease, Friedreich's ataxia, Alzheimer's disease, amyotrophic lateral sclerosis, and myotonic and duchenne muscular dystrophy.

Previous studies in our laboratory had demonstrated alterations in the physical state of membrane proteins in erythrocytes in Huntington's disease. In order to assess the specificity of our findings, the results of electron spin resonance studies of protein and lipid components, scanning electron-microscopic studies, enzymatic analyses of membrane-bound sodium plus potassium stimulated, magnesium-dependent adenosine triphosphatase and protein kinase, and cell deformability studies of erythrocyte membranes have been performed in the neurological disorders, Huntington's disease, Friedreich's ataxia, Alzheimer's disease, amyotrophic lateral sclerosis, and myotonic and Duchenne muscular dystrophy. Comparison of the results revealed that alterations in the biophysical and biochemical states of erythrocyte membranes in each disorder are specific to the particular disease state with the exception of those in Friedreich's ataxia and Alzheimer's disease. In the latter instance, the clinical and pathological alterations suggest that these two diseases have different primary defects. Our studies suggest that the molecular basis of each disease is different. In addition, the results suggest that biophysical and biochemical investigations of extraneural tissue in Huntington's disease and other neurological disordes have the potential of clarifying the molecular mechanisms by which these diseases arise.

Alzheimer Disease↗

PubMed2004

Frequency of NOD2/CARD15 variants in both sporadic and familial cases of Crohn's disease across Italy. An Italian Group for Inflammatory Bowel Disease Study.

BACKGROUND: Three variants of the NOD2/CARD15 gene are strongly associated with susceptibility to Crohn's disease; however, striking racial and geographic differences of their frequency have been described. AIMS: We have compared the allele frequencies of familial cases of Crohn's disease recruited in a multicentre study across Italy, in order to disclose possible geographic heterogeneity. Moreover, we also compared the allele frequencies in sporadic cases of Crohn's disease and healthy controls from Southern Italy with those reported in other two populations from Central and Northern Italy. SUBJECTS AND METHODS: A total of 731 subjects were genotyped for the polymorphism of three main variants (R702W, G908R and 1007 fs): 152 patients were familial cases of Crohn's disease, 183 were healthy first-degree relatives, 180 were sporadic cases of Crohn's disease, and 216 were unrelated healthy subjects. RESULTS: The frequency of the frameshift mutation (1007 fs) was significantly higher in both familial and sporadic cases of Crohn's disease (P = 0.000001), and healthy first-degree relatives (P = 0.0001) compared to controls. At least one risk allele was found in 44% of familial Crohn's disease patients, compared to 7% of healthy controls (OR = 4; CI = 2-6.5). Two risk alleles were found in 14% of familial Crohn's disease, compared to less than 1% of controls (OR = 26: CI = 4-129). CONCLUSIONS: Our data confirm the strong correlation between the 1007 fs variant and Crohn's disease, in both familial and sporadic cases. Moreover, no significant difference of allele frequencies was detected in familial cases, sporadic cases and healthy controls among different geographic areas of Italy.

Adult↗

PubMed2001

Clinical and subclinical autoimmune thyroid disease in adult celiac disease.

Our aim was to investigate the occurrence of clinical and subclinical autoimmune thyroid disease in 79 patients with celiac disease as reflected in thyroid function, antibodies, and ultrasound. Since subclinical thyroid diseases are common in the population, 184 nonceliac controls were also studied. Normal thyroid function combined with positive antibodies and marked hypoechogenicity was considered subclinical disease. Autoimmune thyroid disease was observed in 13.9% of celiac patients and in 2.1% of controls (P = 0.0005); and subclinical disease in 10.1% and 3.3%, respectively (P = 0.048). The mean thyroid gland volume was 8.3 ml in celiac patients and 10.4 ml in controls (P = 0.007). Hypoechogenicity was found in 73% of celiac patients and in 42% of controls (P < 0.0001). Positive thyroid antibodies were associated with hypoechogenicity in celiac patients but not in controls. In conclusion, the occurrence of both clinical and subclinical autoimmune thyroid disease was increased in celiac disease; subclinical thyroid disease indicates regular surveillance.

Autoimmune Diseases↗

PubMed2005

Work-related infectious disease reported to the Occupational Disease Intelligence Network and The Health and Occupation Reporting network in the UK (2000-2003).

BACKGROUND: Infectious diseases remain an important cause of self-reported work-related illness, with socio-economic consequences, including sickness absence. Reporting of infectious disease by occupational and specialist physicians is an important tool in the investigation of occupationally related infections and is relevant in their management. AIMS: To examine the reporting of cases of infectious disease by occupational and specialist physicians to schemes collecting data on occupational ill-health. METHODS: Cases of infectious disease reported by occupational and specialist physicians to the UK based schemes, Occupational Disease Intelligence Network (ODIN) and The Health and Occupation Reporting network (THOR), from 2000 to 2003 were analysed by reporting patterns, diagnosis, single case or outbreak reporting and industry. RESULTS: The total number of estimated cases of infectious disease reported to ODIN and THOR from 2000 to 2003 was 5606; 74.9% cases were diarrhoeal disease, and 11.1% scabies. The majority (81.4%) of cases were reported in SIDAW, where the participation rate for reporters was 55%. Reporting rates were much higher in OPRA, SWORD and EPIDERM (ranging from 86 to 96%). The most frequently reported industrial sectors were social care (39.5%) and health (29.4%); while the manufacture of chemical products contributed 4.3% overall, but 33.8% to estimated cases in OPRA. CONCLUSIONS: Despite limitations related to under reporting, the occupational and specialist physician schemes in ODIN and THOR provide data that may be used to look at patterns of case reporting for occupational ill-health, including infectious disease. The reporting schemes also provide an important means of alerting peers about potential novel causes, precipitating factors, or industrial sectors associated with occupational disease.

Communicable Diseases↗

PubMed1986

Bowen's disease, Paget's disease, and malignant melanoma in situ.

The histologic differential diagnosis of skin lesions characterized by large, atypical, clear cells in the epidermis includes Bowen's disease, Paget's disease (mammary and extramammary), malignant melanoma in situ (pagetoid precancerous melanosis), mycosis fungoides, Spitz nevus, and artifact. Our experience with these lesions indicates that these diseases can be differentiated immunohistologically by the standard peroxidase-antiperoxidase technique, using antibodies directed against keratin (KER), carcinoembryonic antigen (CEA), and S-100 protein (S-100). Based on a study of 11 cases of Bowen's disease, eight cases of Paget's disease, and nine cases of malignant melanoma in situ, we conclude that the atypical clear cells of Bowen's disease stain only with antibodies to KER; those of Paget's disease, exclusively with antibodies to CEA; and those of malignant melanoma in situ, with antibodies to S-100. Additionally, we report a case in which clinical and histologic findings suggested Bowen's disease, but immunohistologic findings supported the diagnosis of Paget's disease.

Adult↗

PubMedDate not supplied

Chronic obstructive pulmonary disease and chronic heart failure: two muscle diseases?

Chronic obstructive pulmonary disease and congestive heart failure are two increasingly prevalent chronic diseases. Although care for these patients often is provided by different clinical teams, both disease conditions have much in common. In recent decades, more knowledge about the systemic impact of both diseases has become available, highlighting remarkable similarities in terms of prognostic factors and disease management. Rehabilitation programs deal with the systemic consequences of both diseases. Although clinical research also is conducted by various researchers investigating chronic obstructive pulmonary disease and chronic heart failure, it is worthwhile to compare the progress in relation to these two diseases over recent decades. Such comparison, the purpose of the current review, may help clinicians and scientists to learn about progress made in different, yet related, fields. The current review focuses on the similarities observed in the clinical impact of muscle weakness, the mechanisms of muscle dysfunction, the strategies to improve muscle function, and the effects of exercise training on chronic obstructive pulmonary disease and chronic heart failure.

Aged↗

PubMed1996

Neutrophil antibodies (pANCA) in chronic liver disease and inflammatory bowel disease: do they react with different antigens?

OBJECTIVE: A high frequency of perinuclear neutrophil antibodies (pANCA) has been described in patients with ulcerative colitis (UC) and primary sclerosing cholangitis (PSC). We evaluated the presence of pANCA in chronic liver disease and compared the immunoglobulin G (IgG) subclasses of pANCA in inflammatory bowel disease with chronic liver disease. Since the antigen reacting with pANCA could not be determined, the antigenic role of various neutrophil antigens was evaluated. SUBJECTS AND METHODS: Detection of pANCA and their IgG subclass was performed by immunofluorescence. One hundred and forty patients with chronic liver disease, 96 patients with inflammatory bowel disease and 40 healthy controls were tested for pANCA. pANCA positive and negative sera were evaluated for their reactivity with different neutrophil antigens in an enzyme-linked immunosorbent assay (ELISA) system. RESULTS: pANCA were found in 8 of 23 patients (35%) with autoimmune hepatitis, in 6 of 21 patients (28%) with primary biliary cirrhosis (PBC), in 18 of 25 patients (72%) with PSC, in 3 of 48 patients (6%) with viral hepatitis, in 30 of 48 patients (62%) with UC, and in 2 of 48 patients (4%) with Crohn's disease. All 20 patients with alcoholic liver disease and 40 healthy controls were negative for pANCA. In contrast to the patients with UC who had 83% IgG1 and only 13% IgG3 antibodies, patients with PSC and PBC had an overexpression of IgG3 antibodies (PSC: 50% IgG3; PBC: 67% IgG3). A proportion of pANCA positive sera recognized lactoferrin, myeloperoxidase, cathepsin G, laminarase and alpha 1-antitrypsin. CONCLUSION: pANCA is not present only in patients with UC but in autoimmune liver diseases such as PSC, autoimmune hepatitis and PBC. Considering the IgG subclass of pANCA, the antibody response of patients with UC is different from patients with liver disease. No unique pANCA specific antigen could be detected, so heterogeneity of pANCA has to be considered.

Adolescent↗