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PubMed1980

[Computerized tomography in atrophy of the posterior fossa (author's transl)].

Cranial computerized tomography was carried out in 69 patients with cerebellar ataxia (45 with Friedreich's ataxia, 4 with Marie's spastic ataxia, 14 with cerebellar atrophy, and one patient with olivo-pontocerebellar atrophy). In CT scans cerebellar atrophy is found to be of various localisation and partially of characteristic distribution. CT, therefore, greatly helps to distinguish different types of cerebellar and spino-cerebellar atrophy and also distinguishes separate cerebellar atrophy of various origin from other diseases like multiple sclerosis.

Adult↗

PubMed1982

[Differential diagnosis of infratentorial atrophies by computed tomography (author's transl)].

Computed tomographical findings are documented for 140 patients with different cerebellar atrophic or heredodegenerative processes. There are idiopathic cerebellar atrophies, so called alcoholic and paraneoplastic cerebellar atrophies, cerebellar atrophies associated with nutritional deficiency diseases or intake of diphenylhydantoin. Further, there are patients suffering from Friedreich's ataxia. Nonne-Marie's spastic ataxia, olivo-ponto-cerebellar atrophy and various other diseases. With the aid of CT individual patterns of atrophy can be recognized. The method therefore, helps to distinguish the above mentioned diseases from each other and also distinguishes them from inflammatory, cerebrovascular or neoplastic processes.

Adolescent↗

PubMed1994

Alzheimer's disease with asymmetric atrophy of the cerebral hemispheres: morphometric analysis of four cases.

To examine the clinicopathological correlations in rare Alzheimer's disease patients with asymmetric cerebral atrophy and to compare their pattern of cortical involvement by senile lesions with that observed in other cases with atypical Alzheimer's disease, we performed an extensive neuropathological analysis of the cerebral cortex in four such cases. Three patients presented with severe language impairment but relatively good preservation of praxis and gnosis even after several years of clinical evolution. Cerebral autopsies of these cases revealed a predominant left hemisphere atrophy. Conversely, in one case with marked right hemisphere atrophy, all of the cognitive functions were involved early in the course of dementia. Neurofibrillary tangles and senile plaques were preferentially localized in the prefrontal, temporal and posterior parietal cortex in both hemispheres, whereas the hippocampal formation displayed lower lesion densities than neocortical areas. Significantly higher neurofibrillary tangle and senile plaque densities were found in the more atrophic side in most of the areas studied. The ratio of neurofibrillary tangle and senile plaque densities between the two hemispheres was not correlated with the number of these lesions in the cerebral cortex. These results indicate that the degenerative process in demented cases with interhemispheric asymmetric cerebral atrophy is characterized by a widespread involvement of the neocortex by senile lesions and lacks clear regional topography of neurofibrillary tangle and senile plaque distribution. Moreover, the relative sparing of the hippocampus, comparable to that found in cases with focal progressive dementia, suggests that the dementing process may involve different cortical structures in cases with asymmetric cerebral atrophy than in typical Alzheimer's disease cases.

Aged↗

PubMed1979

Cerebral atrophy in Parkinson's disease--represented in CT.

To clarify the importance of brain atrophy in relation to the symptoms of Parkinson's disease, 173 patients were examined by computed tomography (CT). In 51.4% of the CT findings, brain atrophy was considered to be pathological. Statistically significant relations of age and sex were found with regard to the extent and localization of brain atrophy. Cortical atrophy also showed a significant dependence on duration of disease. Linear measurements at the lateral ventricles and the third ventricle lead us to assume that brain atrophy in Parkinson's patients is more prevalent than in normal patients within the scope of age involution.

Adult↗

PubMed1987

Automated measurements of cerebral atrophy in multiple sclerosis.

An automated method of measuring cerebral atrophy is introduced. Using this method we studied patients with multiple sclerosis and a control group showing premature cerebral atrophy in multiple sclerosis (P = 1,32 x 10(-8) for male and P = 3,6 x 10(-14) for female). There was only a weak correlation between cerebral atrophy and psychological deficits. Multivariate analysis did not show any significant correlation between cerebral atrophy, duration of disease, clinical manifestations and progression of disease. We conclude that our method to measure cerebral atrophy is more accurate and less time-consuming than the use of linear indices. It might be appropriate for further investigations in evaluating atrophic processes in cerebro-vascular, degenerative and exogen-toxic disease of brain.

Adult↗

PubMed2003

Type 2 diabetes and atrophy of medial temporal lobe structures on brain MRI.

AIM/HYPOTHESIS: Type 2 diabetes increases the risk not only of vascular dementia but also of Alzheimer's disease. The question remains whether diabetes increases the risk of Alzheimer's disease by diabetic vasculopathy or whether diabetes influences directly the development of Alzheimer neuropathology. In vivo, hippocampal and amygdalar atrophy on brain MRI are good, early markers of the degree of Alzheimer neuropathology. We investigated the association between diabetes mellitus, insulin resistance and the degree of hippocampal and amygdalar atrophy on magnetic resonance imaging (MRI) accounting for vascular pathology. METHODS: Data was obtained in a population-based study of elderly subjects without dementia between 60 to 90 years of age. The presence of diabetes mellitus and, in non-diabetic subjects, insulin resistance was assessed for 506 participants in whom hippocampal and amygdalar volumes on MRI were measured. We assessed the degree of vascular morbidity by rating carotid atherosclerosis, and brain white matter lesions and infarcts on MRI. RESULTS: Subjects with diabetes mellitus had more hippocampal and amygdalar atrophy on MRI compared to subjects without diabetes mellitus. Furthermore, increasing insulin resistance was associated with more amygdalar atrophy on MRI. The associations were not due to vascular morbidity being more pronounced in persons with diabetes mellitus. CONCLUSIONS/INTERPRETATION: Type 2 diabetes is associated with hippocampal and amygdalar atrophy, regardless of vascular pathology. This could suggest that Type 2 diabetes directly influences the development of Alzheimer neuropathology.

Aged↗

PubMed2003

Normalized regional brain atrophy measurements in multiple sclerosis.

There is still a controversy regarding the best regional brain atrophy measurements in multiple sclerosis (MS) studies. The aim of this study was to establish whether, in a cross-sectional study, the normalized measurements of regional brain atrophy correlate better with the MRI-defined regional brain lesions than the absolute measurements of regional brain atrophy. We assessed 45 patients with clinically definite relapsing-remitting (RR) MS (median disease duration 12 years), and measured T1-lesion load (LL) and T2-LL of frontal lobes and pons, using a reproducible semi-automated technique. The regional brain parenchymal volume (RBPV) of frontal lobes and pons was obtained by use of a computerized interactive program, which incorporates semi-automated and automated segmentation processes. A normalized measurement, the regional brain parenchymal fraction (RBPF), was calculated as the ratio of RBPV to the total volume of the parenchyma and the cerebrospinal fluid (CSF) in the frontal lobes and in the region of the pons. The total regional brain volume fraction (TRBVF) was obtained after we had corrected for the total volume of the parenchyma and the CSF in the frontal lobes and in the region of the pons for the total intracranial volume. The mean coefficient of variation (CV) for RBPF of the pons was 1% for intra-observer reproducibility and 1.4% for inter-observer reproducibility. Generally, the normalized measurements of regional brain atrophy correlated with regional brain volumes and disability better than did the absolute measurements. RBPF and TRBVF correlated with T2-LL of the pons (r=-0.37, P=0.011, and r= -0.40, P=0.0005 respectively) and with T1-LL of the pons (r=-0.27, P=0.046, and r=-0.31, P=0.04, respectively), whereas RBPV did not (r=-0.18, P = NS). T1-LL of the frontal lobes was related to RBPF (r=-0.32, P=0.033) and TRBVF (r=-0.29, P=0.05), but not to RBPV (R=-0.27, P= NS). There was only a trend of correlation between T2-LL of the frontal lobes and RBPF (r=-0.27, P=0.06) and TRBVF (r=-0.28, P=0.057), and no correlation with RBPV (r=-0.23, P= NS). The magnitude of correlation between the expanded disability status scale (EDSS) and pontine and frontal lobe RBPF and TRBVF was more than twice as high as the correlation between EDSS and RBPV of the same regions. These data suggest that normalized regional brain atrophy measurements are preferable to absolute regional measurements in cross-sectional studies.

Adult↗

PubMed2000

Testicular focal atrophy--tubular blockade as partial degeneration of the tubule.

This study investigated whether focal atrophy is a degenerative process of a whole tubule or tubular blockade as partial intratesticular degeneration. Serial section analyses of testicular tissue from 19 men with different andrologic diseases were examined. From every fifth section of any series, defined areas were viewed under a light microscope, and tubule sections were drawn. Three-dimensional reconstructions were made from these materials. Reconstructions of the seminiferous tubules showed tubular blockade as partial degeneration of the tubules. Transition from an intact portion to a blockade was accompanied by an increase in the thickness of the lamina propria. The blockade was a cell cord that contained Sertoli cells and, at most, spermatogonia, or it was a completely atrophied tubule, a so-called tubular scar. In a given tubule, defined areas of atrophy and areas of spermatogenic activity were both found. Occurrence of tubular blockade increased with age. Serial section analyses of testicular tissue showed tubular blockade as the partial degeneration of seminiferous tubules. In focal atrophy, a given tubule can have defined areas of atrophy and areas of spermatogenic activity.

Adult↗

PubMedDate not supplied

CT of agenesis and atrophy of the right hepatic lobe.

BACKGROUND: To identify and differentiate agenesis and severe atrophy of the right hepatic lobe on computed tomography (CT). METHODS: The CT examinations of three cases of agenesis and 11 cases of severe atrophy of the right hepatic lobe were reviewed. We evaluated visibility of the three hepatic veins, the two main portal veins (including their branches if necessary), the dilated intrahepatic ducts, enlargement of the medial and lateral segments of the left lobe and caudate lobe of the liver, presence of a retrohepatic gallbladder, hyperattenuation of the atrophic liver parenchyma, posterolateral interposition of the hepatic flexure of the colon, and upward migration of the right kidney. RESULTS: In the three cases of agenesis, no structure can be recognized as the right hepatic vein, right portal vein, or dilated right intrahepatic ducts. In the 11 cases of severe lobar atrophy, the right portal vein (or its branches) was recognized in eight cases, the right hepatic vein in four cases, and the dilated right intrahepatic ducts in 11 cases. The degree of enlargement of the lateral segment does not necessarily change inversely with the size of the medial segment and the caudate lobe. The retrohepatic gallbladder is present in eight cases (two in agenesis and six in atrophy). The phenomenon of hyperattenuation of the atrophic liver parenchyma was noted in six cases. CONCLUSION: Even though a retrohepatic gallbladder and a severely distorted hepatic morphology due to compensatory hypertrophy of the left and caudate lobes may raise a suspicion of agenesis of the right lobe of the liver, absence of visualization of all of the right hepatic vein, right portal vein and its branches, and dilated right intrahepatic ducts is a prerequisite of the diagnosis of agenesis of the right hepatic lobe on CT. In severe lobar atrophy, at least one of these structures is recognizable.

Adult↗

PubMed1998

Dominant optic atrophy: exclusion and fine genetic mapping of the candidate gene, HRY.

Autosomal dominant optic atrophy (OPA1) maps to Chromosome (Chr) 3q28, and the disease interval has been refined to within 1.4 cM, flanked by the markers D3S3669 and D3S3562. HRY, the human homolog of the Drosophila segmentation gene, hairy, maps by in situ hybridization to the chromosomal region 3q28-q29. We screened for mutations in HRY in 36 patients from 18 pedigrees with dominant optic atrophy and a group of normal control individuals. Heteroduplex mutation analysis and direct sequencing of all four coding exons and one upstream putative untranslated exon were performed. No disease-associated sequence alterations were identified. A polymorphism in the untranslated region of exon 2 was found, with four alleles. PCR amplification of this part of exon 2 in four of the pedigrees affected by autosomal dominant optic atrophy mapping to chromosome 3q, followed by haplotype analysis, showed recombination between HRY and OPA1 in one pedigree. This allows us to genetically position HRY in relation to known microsatellite markers in the region, placing HRY telomeric to marker D3S3562 and centromeric to D3S1305. This is outside the published critical disease interval for dominant optic atrophy. We have, therefore, excluded HRY as the gene for dominant optic atrophy by sequence analysis, mapped it genetically, and identified a polymorphism in our population.

Animals↗

PubMed2005

The ultrastructure of peripheral nerve, motor end-plate and skeletal muscle in patients suffering from spinal muscular atrophy with respiratory distress type 1 (SMARD1).

Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is genetically and clinically distinct from classic spinal muscular atrophy (SMA1). It results from mutations in the gene encoding immunoglobulin mu-binding protein 2 (IGHMBP2) on chromosome 11q13. Patients develop distally pronounced muscular weakness and early involvement of the diaphragm, resulting in respiratory failure. Sensory and autonomic nerves are also affected at later stages of the disease. We investigated peripheral nerves, skeletal muscles and neuromuscular junctions (NMJ) ultrastructurally in five unrelated patients and three siblings with genetically confirmed SMARD1. In mixed motor and sensory nerves we detected Wallerian degeneration and axonal atrophy similar to the ultrastructural findings described in SMA1. Isolated axonal atrophy was evident in purely sensory nerves. All investigated NMJ of patients with SMARD1 were dysmorphic and lacked a terminal axon. Moreover, we also observed characteristics of neuropathies, such as abnormalities in myelination, that have not been described in spinal muscular atrophies so far. Based on these findings we conclude that impairment of IGHMBP2 function leads to axonal degeneration, abnormal myelin formation, and motor end-plate degeneration.

Axons↗

PubMed2002

MR correlates of cerebral atrophy in patients with multiple sclerosis.

OBJECTIVE: To investigate the in-vivo correlates of brain atrophy in patients with multiple sclerosis (MS) by assessing the relationship between normalized measures of brain volume (NBV) and other magnetic resonance (MR) measures of tissue damage. BACKGROUND: Brain atrophy diffusely occurs and progressively increases in patients with MS. Nevertheless, the mechanisms leading to brain atrophy in this disease are not fully understood. METHODS: MR examinations were performed in 20 patients with relapsing-remitting MS. Conventional MRI was used to assess NBV and total brain T2-hyperintense and T1-hypointense lesion volumes. Proton MR spectroscopic imaging and diffusion tensor MR imaging were also performed for large portions of brain containing mainly normal-appearing tissue to provide indices of tissue damage, including N-acetylaspartate to creatine ratio (NAA/Cr) and mean diffusivity (D). RESULTS: Values of NBV correlated significantly with those of average brain (r = -0.58, p = 0.007) and NAA/Cr (r = 0.67, p < 0.001). The relationship of these markers of tissue damage to NBV was also found when NAA/Cr and were computed together in a composite MR score (r = 0.70, p < 0.001). In contrast, NBV values did not correlate with measurements of average lesion, T(2) and T(1) weighted total brain MRI lesion volumes. CONCLUSIONS: This study suggests that brain atrophy in MS is not simply due to axonal loss, but rather reflects a more generalized process that involves various brain tissue components. Damage to the normal-appearing tissue rather than the extent and intrinsic pathology of macroscopic lesions seems to be important in the destructive process leading to MS-related irreversible cerebral atrophy.

Adult↗

PubMed2004

Different mechanisms of corpus callosum atrophy in Alzheimer's disease and vascular dementia.

Previous neuroimaging studies have indicated that corpus callosum atrophy in Alzheimer's disease (AD) and large vessel occlusive disease (LVOD) is caused by interhemispheric disconnection, namely Wallerian degeneration of interhemispheric commissural nerve fibers originating from pyramidal neurons in the cerebral cortex. However, this hypothesis has not been tested from a neuropathological viewpoint. In the present study, 22 brains with AD (presenile onset, 9; senile onset, 13), 6 brains with Binswanger's disease (BD), a form of vascular dementia and 3 brains with LVOD were compared with 6 non-neurological control brains. White matter lesions in the deep white matter and corpus callosum were quantified as a fiber density score by image analysis of myelin-stained sections. Axonal damage and astrogliosis were assessed by immunohistochemistry for amyloid precursor protein and glial fibrillary acidic protein, respectively.The corpus callosum thickness at the anterior part of the body was decreased in AD and LVOD,but not in BD significantly, as compared with the controls. The corpus callosum thickness correlated roughly with brain weight in AD (R=0.50),and with the severity of deep white matter lesions in BD (R=0.81). Atrophy of the brain and corpus callosum was more marked in presenile onset AD than in senile onset AD. With immunohistochemistry, the corpus callosum showed axonal damage and gliosis with a decreased fiber density score in BD and LVOD, but not in AD. Thus, corpus callosum atrophy was correlated with brain atrophy in AD, which is relevant to the mechanism of interhemispheric disconnection,whereas corpus callosum lesions in BD were secondary to deep white matter lesions. Corpus callosum atrophy in LVOD may indicate interhemispheric disconnection, but focal ischemic injuries may also be involved.

Aged↗

PubMed2004

The relationship between inflammation and atrophy in clinically isolated syndromes suggestive of multiple sclerosis: a monthly MRI study after triple-dose gadolinium-DTPA.

OBJECTIVE: To examine the relationship between inflammation and brain atrophy in patients with a clinically isolated syndrome (CIS) suggestive of multiple sclerosis (MS). METHODS: Monthly triple-dose gadolinium (Gd/DTPA)-enhanced MRI scans over 6 months were obtained in 62 consecutive CIS patients with an abnormal baseline MRI scan. Subsequently MRI was performed at months 12 and 18. Patients who developed a clinically definite MS (i. e., a second clinical episode) ended the study at the time of the relapse. For each scan, the number and volume of newly active lesions (Gd-enhancement/new or newly enlarging T2 lesion that did not enhance), and the number and volume of T2 hyperintense lesions (T2-LL) and T1-black holes (T1-LL) were calculated. The percentage of brain volume changes (PBVC) was assessed using a fully automated technique (SIENA; Structural Image Evaluation using Normalization of Atrophy). RESULTS: Twenty-four (39%) developed clinically definite MS by month 18. Thirty-eight (61%) were relapsefree and completed the MRI follow-up. Relapse-free patients showed a progressive median increase between baseline and month 18 in T1-LL (25%, p<0.001), but not in T2-LL (8.5%, p=ns). PBVC decreased by 1.1% (p<0.001) in a time-dependent pattern (Kendall coefficient of concordance=0.85). Exploratory subgroup analyses showed a trend towards progressive decreases in brain volume in active patients (i. e., those with at least one newly active lesion during monthly MRI scanning; Spearman's R=-0.61; p<0.001), but not among inactive patients (Spearman's R=-0.10; p=0.53). Significant differences in median brain volume changes between the active and inactive patient groups were found at months 12 and 18; the difference detected at month 6 was not significant. The cumulative number and volume of new Gd-enhancing lesions developed during the 6 months of frequent MRI scanning were highly correlated with PBVC over the 18-month period (Spearman R values were 0.73 and 0.85, respectively). The strongest predictor of PBVC at 18 months was the cumulative volume of newly active lesions during frequent MRI scanning [ss=-0. 83, standard error (SE)=0.07, p<0.001]. CONCLUSIONS: This study shows that visible inflammation as detected by monthly, triple-dose Gd-enhanced MRI is an important factor in the pathogenesis of brain tissue loss in CIS patients. However, inflammation and brain atrophy do not proceed in parallel: atrophy appeared only after a delay of months following acute inflammation. Frequent MRI scanning allows for the detection of CIS patients who will develop brain atrophy in the short-term.

Adolescent↗

PubMed2006

Profound midbrain atrophy in patients with Wilson's disease and neurological symptoms?

Wilson's disease (WD) is characterized by impaired hepatic copper secretion and subsequent copper accumulation in many organs predominantly liver and brain, secondary to loss of function mutations in the copper transport protein ATP7B. If the disease is recognized too late or treatment is not adequate, brain copper accumulation leads to progressive neurodegeneration with a variety of clinical symptoms. The nigrostriatal dopaminergic system seems rather vulnerable. Midbrain atrophy, however, has not been recognized as one of the prime features of patients with WD. Here we report quantification of midbrain diameter in 41 patients with WD. Data were correlated to the severity of neurological symptoms and the integrity of dopaminergic neurons measured via dopamine transporter binding. For control, we measured midbrain diameter in 18 patients with no evidence for brainstem dysfunction and 5 patients with progressive supranuclear palsy (PSP). Patients with WD had a reduced midbrain diameter (15.5 +/- 0.4 mm) compared to controls (18.5 +/- 0.2 mm). WD patients without neurological symptoms had midbrain diameter that were not different from controls (18.0 +/- 0.3 mm), while patients with neurological symptoms showed midbrain atrophy similar to patients with PSP (14.4 +/- 0.3 mm versus 14.1 +/- 0.3). There was a strong and significant correlation between midbrain atrophy and the severity of neurological symptoms (r= -0.68, p < 0.001) while midbrain atrophy and dopamine transporter binding correlated significantly but was less pronounced (r=0.46, p < 0.001). In summary, we were able to show, that midbrain diameter is an easy to perform quantification of neurodegeneration induced by brain copper accumulation and that other structures than substantia nigra dopaminergic neurons seem to contribute to midbrain atrophy in WD.

Adult↗

PubMed2004

Immunological and morphogenic basis of gastric mucosa atrophy and metaplasia.

Chronic gastritis with gastric mucosa atrophy, intestinal metaplasia and endocrine cell hyperplasia are alterations with an increased risk for the development of gastric neoplasias. Immunological studies in autoimmune gastritis, in atrophic Helicobacter pylori gastritis and in studies with transgenic mice point to a central role of the parietal cell in the development of gastric mucosa atrophy. Destruction of gastric epithelial cells alone might not be sufficient for the loss of complete gastric glands. Gastric atrophy, endocrine cell hyperplasia and intestinal and pancreatic metaplasia can be regarded as the result of altered morphogenesis within the gastric mucosa. Impaired expression of the gastric morphogenic factor Sonic Hedgehog by parietal cells and increased expression of the transcriptional activators of intestinal and pancreatic differentiation, namely CDX2 and PDX1, seem to be crucial for the development of gastric atrophy and for intestinal, endocrine and pancreatic transdifferentiation processes. Altered expression of these morphogenic factors is partly caused by changes in the gastric milieu. Further studies concerning the normal and pathological morphogenesis of the gastric mucosa and related tissues might give new insight into the pathogenesis of gastric atrophy and metaplasia.

Animals↗

PubMed2005

Age-related quadriceps-dominant muscle atrophy and incident radiographic knee osteoarthritis.

Muscle atrophy is common in the elderly. However, the etiologic role of muscle atrophy associated with osteoarthritis of the knee has not been studied in detail. We assessed the association between age-related muscle atrophy around the knee joint and incident radiographic osteoarthritis of the knee. Twenty-one women in their thirties and 17 women in their sixties participated. They had no history, symptoms, or objective findings of any knee problems, and none of the participants was limited in performing daily activities. Radiographs of the knee joint were graded for the presence of osteoarthritis, and the cross-sectional imaging around the knee joint was carried out using computed tomography. Incident radiographic osteoarthritis was observed in 6 of the 17 women in their sixties. Quadriceps-dominant muscle atrophy was marked in the elderly women with radiographic osteoarthritis. In a multivariate analysis, the risk of incident radiographic osteoarthritis of the knee was significantly increased among women with a higher hamstrings/quadriceps cross-sectional area ratio. The results suggest the possibility that age-related quadriceps-dominant muscle atrophy may play a role in the pathogenesis of osteoarthritis of the knee.

Adult↗

PubMed2003

Atrophy and neoplastic transformation of the ileal pouch mucosa in patients with ulcerative colitis and primary sclerosing cholangitis: a case control study.

INTRODUCTION: Patients with ulcerative colitis and primary sclerosing cholangitis have an increased risk of developing carcinoma both in the bile ducts and in the colon. PURPOSE: To investigate whether this patient group also has an increased risk of developing atrophy and neoplasia in the ileal pouch mucosa after construction of a pelvic pouch with an ileoanal anastomosis or a continent Kock ileostomy. METHODS: Flexible video endoscopic examinations of the ileal pouch were performed in 16 patients with ulcerative colitis and primary sclerosing cholangitis and in 16 matched patients with ulcerative colitis without sclerosing cholangitis. Biopsies were sampled from different locations in the pouch for histologic assessment of mucosal atrophy and dysplasia and for flow cytometric DNA analysis assessing chromosomal aberrations. RESULTS: The patients with sclerosing cholangitis developed moderate or severe atrophy in the pouch significantly more often (P < 0.01). Persistent severe mucosal atrophy was revealed in eight patients with sclerosing cholangitis and only in two controls. One patient with sclerosing cholangitis had high-grade dysplasia in multiple locations. Low-grade dysplasia was assessed in three patients with sclerosing cholangitis and in two of the controls. DNA aneuploidy was displayed in three patients, all with sclerosing cholangitis and dysplasia. All patients with neoplastic transformation had a pouch with ileoanal anastomosis and a long pouch duration (> 8 years). CONCLUSION: Patients with ulcerative colitis and primary sclerosing cholangitis with an ileal reservoir are more prone to developing mucosal atrophy in the pouch and seem to have a higher risk of neoplastic transformation in the pouch mucosa than patients with ulcerative colitis without sclerosing cholangitis.

Adult↗