SEARCH · PubMed Health

Results for “Atrophy”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed1998

Quantitative assessment of gastric atrophy using the syntactic structure analysis.

AIM: To assess the topographical relation between gastric glands, using the minimum spanning tree (MST), to derive both a model of neighbourhood and quantitative representation of the tissue's architecture, to assess the characteristic features of gastric atrophy, and to assess the grades of gastric atrophy. METHODS: Haematoxylin and eosin stained sections from corporal and antral biopsy specimens (n = 139) from normal patients and from patients with nonatrophic gastritis and atrophic gastritis of grades 1, 2, and 3 (Sydney system) were assessed by image analysis system (Prodit 5.2) and 11 syntactic structure features were derived. These included both line and connectivity features. RESULTS: Syntactic structure analysis was correlated with the semiquantitative grading system of gastric atrophy. The study showed significant reductions in the number of points and the length of MST in both body and antrum. The standard deviation of the length of MST was significantly increased in all grades of atrophy. The connectivity to two glands was the highest and most affected by the increased grade of atrophy. The reciprocal values of the Wiener, Randic, and Balaban indices showed significant changes in the volume of gland, abnormality in the shape of glands, and changes in irregularity and branching of the glands in both types of gastric mucosa. There was a complete separation in the MST, connectivity, and index values between low grade and high grade gastric atrophy. CONCLUSIONS: (1) Gastric atrophy was characterised by loss of the gland, variation in the volume, reduction in the neighbourhood, irregularity in spacing, and abnormality in the shape of the glands. (2) Syntactic structure analysis significantly differentiated minor changes in gastric gland (low grade atrophy) from high grade atrophy of clinical significance. (3) Syntactic structure analysis is a simple, fast, and highly reproducible technique and appears a promising method for quantitative assessment of atrophy.

Atrophy↗

PubMed2003

Infraspinatus muscle atrophy: implications?

PURPOSE: To evaluate associated findings in patients who exhibited atrophy of infraspinatus muscle at magnetic resonance (MR) examination of their shoulders to clarify implications of this abnormality. MATERIALS AND METHODS: With an electronic database search, cases of advanced infraspinatus muscle atrophy in patients who underwent MR imaging during a 1-year period for evaluation of shoulder pain or dysfunction were identified. The analysis was restricted to cases interpreted by one reader who applied a standardized method of reporting. Associated MR imaging findings in these cases were tabulated. RESULTS: Advanced infraspinatus muscle atrophy was encountered in 51 (4.3%) of 1,191 MR examinations of the shoulder. Tears of the infraspinatus tendon were present in only 27 (53%) of 51 cases. In 46 (90%) of 51 cases, a full-thickness tear was present in the anterior portion of the rotator cuff. In 10 (20%) of 51 cases with infraspinatus muscle atrophy, cuff muscle atrophy was confined to the infraspinatus muscle. Cuff muscle atrophy was isolated to the infraspinatus muscle in four (17%) of 24 cases in which atrophy of the infraspinatus muscle was present despite an intact tendon. In none of the 51 cases was there a mass in the suprascapular or sphenoglenoid notch. CONCLUSION: Infraspinatus muscle atrophy typically occurs with tendon tears in the anterior aspect of the rotator cuff. Concomitant atrophy in the supraspinatus muscle often is present, but infraspinatus muscle atrophy can occur in isolation, and this finding does not imply that the infraspinatus tendon is ruptured.

Adult↗

PubMed2004

Quantitative assessment of gastric antrum atrophy shows restitution to normal histology after Helicobacter pylori eradication.

BACKGROUND/AIMS: Grading gastric mucosal atrophy in antrum biopsy specimens remains a controversial subject because of limitations in interobserver agreement. We previously described a reliable, quantitative method for grading atrophy of the corpus mucosa with excellent reproducibility and good correlation with the Sydney scores. The aims of the present study were to evaluate the applicability of this method for the grading of antral atrophy and to study the effect of Helicobacter pylori eradication on the antral mucosa. METHODS: Antrum biopsy specimens were collected from 71 gastroesophageal reflux disease patients at baseline and after 3 and 12 months. After the first endoscopy, all subjects were treated with omeprazole 40 mg daily for 12 months. After randomization, 27 of the 48 H. pylori-positive patients additionally received eradication therapy. In 182 hematoxylin-eosin-stained specimens, which were of sufficient quality, the proportions (volume percentages) of glands (VPGL), stroma (VPS), infiltrate (VPI), and intestinal metaplasia in the glandular zone of the antrum mucosa were measured using a point-counting method. In these specimens, mucosal atrophy was assessed by two experienced gastrointestinal tract pathologists (E.B. and J.L.) according to the updated Sydney classification as either nonatrophic mucosa (n = 47) or as mild (n = 29), moderate (n = 50), or marked (n = 56) atrophy. In addition, a group of 23 cases with difficult-to-classify grades of atrophy were included. RESULTS: The mean VPGL decreased with increasing Sydney grades of atrophy (p < 0.001), while the mean VPS and VPI increased (both p < 0.001). After H. pylori eradication, even the cases with the lowest VPGL regressed to normal levels. CONCLUSIONS: Overall, a low VPGL correlates with increasing grades of antrum mucosal atrophy. The present data indicate that gastric mucosal atrophy is reversible, since almost all cases showed regression of VPGL after H. pylori eradication. The cases with difficult-to-classify grades of atrophy showed significantly lower VPGLs and higher VPIs than the reference cases.

Anti-Bacterial Agents↗

PubMed2006

Reduction of skeletal muscle atrophy by a proteasome inhibitor in a rat model of denervation.

The ubiquitin-proteasome system is the primary proteolytic pathway implicated in skeletal muscle atrophy under catabolic conditions. Although several studies showed that proteasome inhibitors reduced proteolysis under catabolic conditions, few studies have demonstrated the ability of these inhibitors to preserve skeletal muscle mass and architecture in vivo. To explore this, we studied the effect of the proteasome inhibitor Velcade (also known as PS-341 and bortezomib) in denervated skeletal muscle in rats. Rats were given vehicle or Velcade (3 mg/kg po) daily for 7 days beginning immediately after induction of muscle atrophy by crushing the sciatic nerve. At the end of the study, the rats were euthanized and the soleus and extensor digitorum longus (EDL) muscles were harvested. In vehicle-treated rats, denervation caused a 33.5 +/- 2.8% and 16.2 +/- 2.7% decrease in the soleus and EDL muscle wet weights (% atrophy), respectively, compared to muscles from the contralateral (innervated) limb. Velcade significantly reduced denervation-induced atrophy to 17.1 +/- 3.3% in the soleus (P < 0.01), a 51.6% reduction in atrophy associated with denervation, with little effect on the EDL (9.8 +/- 3.2% atrophy). Histology showed a preservation of muscle mass and preservation of normal cellular architecture after Velcade treatment. Ubiquitin mRNA levels in denervated soleus muscle at the end of the study were significantly elevated 120 +/- 25% above sham control levels and were reduced to control levels by Velcade. In contrast, testosterone proprionate (3 mg/kg sc) did not alleviate denervation-induced skeletal muscle atrophy but did prevent castration-induced levator ani atrophy, while Velcade was without effect. These results show that proteasome inhibition attenuates denervation-induced muscle atrophy in vivo in soleus muscles. However, this mechanism may not be operative in all types of atrophy.

Animals↗

PubMed1981

Cerebellar atrophy demonstrated by computed tomography.

We studied 55 cases of cerebellar atrophy identified by computerized tomography. Atrophy was determined by subjective assessment and objective measurements (superior cerebellar cistern, fourth ventricle, and brainstem). Different patterns of cerebellar atrophy were related to clinical diagnoses. A high incidence of vermal atrophy was observed in primary cerebellar degeneration and chronic alcoholism. More than half the patients with alcoholism had hemispheral atrophy. Vermal atrophy and enlargement of superior cerebellar cisterns (but not hemispheral atrophy) were associated with carcinomatous cerebellar degeneration. Atrophy caused by chronic phenytoin usage showed a specific pattern of enlargement of the cisterna magna, cerebellopontine angle, and superior cerebellar cisterns. Supratentorial atrophy was increased significantly only in the alcoholics. In general, limb ataxia, dysarthria, and nystagmus were related to hemispheral but not to vermal atrophy.

Adult↗

PubMed2000

Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease.

BACKGROUND: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. OBJECTIVES: To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD. METHODS: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i. e., hippocampal, cortical gray matter, and CSF volumes). RESULTS: Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy. Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group. CONCLUSIONS: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.

Aged↗

PubMedDate not supplied

Association between anti-endomysial antibody and total intestinal villous atrophy in children with coeliac disease.

BACKGROUND: There is growing evidence to suggest that detection of anti-gliadin antibody (AGA) and anti-endomysial antibody (EmA) can serve as sensitive markers of the degree of histological abnormalities in patients with coeliac disease. AIM: To evaluate the association between the presence of AGA and EmA and villous atrophy in intestinal biopsies of children with suspected coeliac disease. SETTINGS AND DESIGN: Intestinal samples of 46 children with failure to thrive, chronic diarrhoea, malabsorption and short stature with either AGA and/or EmA positivity were evaluated, retrospectively. The diagnosis of coeliac disease was based on ESPGHAN criteria. METHODS AND MATERIAL: Patients with total villous atrophy who fulfilled the ESPGHAN criteria for the diagnosis of coeliac disease were diagnosed to have coeliac disease. Nine patients without villous atrophy were taken as negative controls for this study. AGA-IgA was measured both by immunoflourescence (IF) and ELISA and EmA-IgA by IF while patients were on normal diet. Relationship between autoantibody positivity and intestinal total villous atrophy was evaluated. RESULTS: Overall positivity for AGA IgA was 85% (39/46) by IF+ELISA and EmA positivity was 85% (39/46) by IF within the study group. Histological examination revealed total villous atrophy with lymphocyte infiltration and crypt hyperplasia in 37 (80%) patients. AGA IgA was positive in 14 (38%) and 31 (84%) of these children by ELISA and IF, respectively. EmA positivity was detected in 35/37 (95%) cases with atrophy and 4/9 (44%) without atrophy (p=0.002). Thirty out of 37 (81%) patients with villous atrophy had both AGA IgA (IF) and EmA positivity (p=0.186). All of the sixteen patients that had both positive AGA IgA (ELISA+IF) and EmA had total villous atrophy (p=0.037). CONCLUSION: A significant association between total villous atrophy and EmA positivity has been documented in this study.

Adolescent↗

PubMed1999

Early onset cerebellar ataxia with retained tendon reflexes (EOCA) and olivopontocerebellar atrophy (OPCA): a computed tomographic study.

Computed tomographic (CT) studies in olivopontocerebellar atrophies (OPCA) and 'early onset cerebellar ataxia with retained tendon reflexes (EOCA)' are few and vary widely in methodology and criteria for cerebellar and brainstem atrophy. In this prospective study, CT scan observations on 26 patients (EOCA-11, OPCA-15) were compared with 31 controls using qualitative and quantitative assessment of cisterns, ventricles and atrophy of brain. Vermian and/or cerebellar hemispheric (predominantly anterior) atrophy was present in 80.8% and both were equally common. Cerebral cortical atrophy (26.9%) and leukoariosis (15.4%) were less frequently seen. Statistically significant atrophy of pons, brachium pontis, cerebellum and midbrain was noted in patient group. No significant differences were observed between EOCA and OPCA groups. Evidence of atrophy did not correlate with either the duration of illness or the severity of cerebellar ataxia in both the groups. The severity of brainstem atrophy in 14 patients with and 12 patients without abnormal brainstem auditory evoked response did not differ significantly. This study highlights the methodology of CT evaluation for brainstem and cerebellar atrophy, draws attention to cerebral atrophy and emphasizes the lack of significant differences in CT morphology between OPCA and EOCA patients.

Adolescent↗

PubMed2001

Patterns of temporal lobe atrophy in semantic dementia and Alzheimer's disease.

Volumetric magnetic resonance imaging analyses of 30 subjects were undertaken to quantify the global and temporal lobe atrophy in semantic dementia and Alzheimer's disease. Three groups of 10 subjects were studied: semantic dementia patients, Alzheimer's disease patients, and control subjects. The temporal lobe structures measured were the amygdala, hippocampus, entorhinal cortex, parahippocampal gyrus, fusiform gyrus, and superior, middle, and inferior temporal gyri. Semantic dementia and Alzheimer's disease groups did not differ significantly on global atrophy measures. In semantic dementia, there was asymmetrical temporal lobe atrophy, with greater left-sided damage. There was an anteroposterior gradient in the distribution of temporal lobe atrophy, with more marked atrophy anteriorly. All left anterior temporal lobe structures were affected in semantic dementia, with the entorhinal cortex, amygdala, middle and inferior temporal gyri, and fusiform gyrus the most severely damaged. Asymmetrical, predominantly anterior hippocampal atrophy was also present. In Alzheimer's disease, there was symmetrical atrophy of the entorhinal cortex, hippocampus, and amygdala, with no evidence of an anteroposterior gradient in the distribution of temporal lobe or hippocampal atrophy. These data demonstrate that there is a marked difference in the distribution of temporal lobe atrophy in semantic dementia and Alzheimer's disease. In addition, the pattern of atrophy in semantic dementia suggests that semantic memory is subserved by anterior temporal lobe structures, within which the middle and inferior temporal gyri may play a key role.

Aged↗

PubMed1958

Nerve lesions in industry; atrophy of disuse as a confusing element in diagnosis; the value of electromyogrphy.

Traumatic peripheral nerve lesions characteristically result in denervation muscular atrophy. Atrophy of disuse may take place concomitantly, either proximal, adjacent to or distal to the denervation muscular atrophy. The degree of atrophy of disuse depends upon the severity of the nerve lesion. Clinically, it is difficult to determine where true denervation muscular atrophy ends and accompanying atrophy of disuse begins. In such circumstances a clinician may be misled into belief that the cause of so apparently extensive a lesion is elsewhere. The patient then is often submitted to other complex diagnostic procedures and treatments. This difficulty can usually be dissipated by the use of electromyography, for each specific type of muscular atrophy produces its own characteristic electromyographic changes. Disuse atrophy produces no changes in electrical activity, whereas denervation atrophy manifests itself by typical denervation activity. Moreover it is possible to determine what part of muscular atrophy in a given area is owing to damage to a nerve and what part is owing only to disuse without denervation.

Accidents↗

PubMed1995

The relation of spike foci and of clinical seizure characteristics to different patterns of mesial temporal atrophy.

We reviewed clinical data and scalp electroencephalograms in 61 consecutive patients with temporal lobe epilepsy and mesial temporal atrophy assessed with volumetric magnetic resonance imaging: 39 patients had unilateral and 22 patients had bilateral atrophy. We attempted to determine whether any aspects of seizure symptoms and any electrographic features could be correlated to degree and anatomic pattern of mesial temporal atrophy. Spikes were always confined to temporal regions and were frequently bilateral without a statistically significant difference between patients with unilateral atrophy (33%) and those with bilateral atrophy (50%). Twenty-five of 40 foci associated with amygdala atrophy had maximum field over the anterior temporal regions. In contrast, 19 of 19 foci with isolated hippocampal formation atrophy were never maximum anteriorly. Secondarily generalized seizures and temporal lobe syncopes were correlated with anatomically extensive, particularly amygdala, atrophy. Prolonged postictal confusion was always associated with bitemporal abnormalities in the form of atrophy or spiking. These results explain some of the variability in the clinical and electrographic manifestations of temporal epilepsy and outline the specific role of amygdala involvement in addition to the commonly reported hippocampal atrophy.

Action Potentials↗

PubMed2000

Is ictal recording mandatory in temporal lobe epilepsy? Not when the interictal electroencephalogram and hippocampal atrophy coincide.

OBJECTIVE: To investigate the concordance between scalp electroencephalogram (EEG) lateralization and side of hippocampal atrophy in patients with temporal lobe epilepsy (TLE). METHODS: We studied 184 consecutive patients with TLE without lesions other than those compatible with mesial temporal sclerosis. In this study, we studied specifically hippocampal atrophy and the results of scalp EEG investigation. Patients were classified according to the localization of interictal epileptiform discharges as unilateral, bilateral asymmetric, and bilateral symmetric. The EEG seizure onsets were also classified separately as unilateral, bilateral asymmetric, and bilateral symmetric. The hippocampal atrophy was determined by volumetric measurements using high-resolution magnetic resonance imaging (MRIVol). RESULTS: Only 3% of patients had discordance between the ictal and interictal EEG lateralizations; however, none of these had unilateral interictal EEG abnormalities. Interictal EEGs were considered unilateral in 62.0% of patients, bilateral asymmetric in 31.5%, and bilateral symmetric in 6.5%. Ictal EEGs were considered unilateral in 63.5% of patients, bilateral asymmetric in 30.0%, and bilateral symmetric in 6.5%. The MRIVol showed unilateral hippocampal atrophy in 60.9% of patients, bilateral asymmetric hippocampal atrophy in 19.0%, symmetric hippocampal atrophy in 3.8%, and normal volumes in 16.3%. There was a significant concordance between MRIVol lateralization and both interictal and ictal EEG lateralization (P<.001). All patients with unilateral hippocampal atrophy had concordant interictal and ictal EEG lateralization. Six (18.2%) of the 33 patients with bilateral asymmetric hippocampal atrophy had MRI lateralization discordant with EEG lateralization. CONCLUSIONS: We found a strong concordance between EEG and MRIVol lateralization in patients with TLE. Unilateral hippocampal atrophy predicted ipsilateral interictal epileptiform abnormalities and ipsilateral seizure onsets with no false lateralization. Previous studies in addition to the present series support that a concordant outpatient EEG evaluation in patients with TLE and unilateral hippocampal atrophy would obviate the need for inpatient EEG monitoring.

Adult↗

PubMed1999

Three dimensional MRI estimates of brain and spinal cord atrophy in multiple sclerosis.

OBJECTIVE: The association between brain atrophy and permanent functional deficits in multiple sclerosis and the temporal relation between atrophy and the clinical disease course have seldom been investigated. This study aims to determine the amount of infratentorial and supratentorial atrophy in patients by comparison with healthy controls, to establish the relation between atrophy and disability, and to derive the rates of volume loss in individual patients from their estimated disease durations. METHODS: Three dimensional acquired MRI was performed on 20 relapsing-remitting and 20 secondary progressive multiple sclerosis patients and 10 control subjects. Volume data on infratentorial and supratentorial structures were obtained using the Cavalieri method of modern design stereology in combination with point counting. Corpus callosal sectional area and "T2 lesion load" were also determined. RESULTS: Significantly reduced infratentorial and cerebral white matter volumes and corpus callosal sectional areas occurred in all patients compared with controls (p=0.0001-0.004). Mean estimates of volume loss in the cohort were -21%, -19%, -46%, and -12% for the brain stem, cerebellum, upper cervical cord and white matter, respectively, and -21% for the corpus callosal sectional area. Analysis of the amount of atrophy (volume differences between patients and controls) showed that upper cervical cord and cerebral white matter atrophy correlated with the expanded disability status scale (r=-0.37 and -0.37, p=0.018-0.023) and the Scripps neurologic rating scale scores (r=+0.49 and +0.43, p=0.002-0.007). There was no relation between estimated volume loss in the supratentorial and infratentorial compartments. The "T2 lesion load" was associated with ventricular enlargement and corpus callosal atrophy (r=+0.50 and -0.55, p=0.0003-0.0012). Infratentorial atrophy rates correlated with baseline exacerbation rates (r=-0.50 to -0.48, p=0.0016-0.0021) and were higher in relapsing-remitting than secondary progressive patients (p=0.009-0.02). CONCLUSIONS: Significant cerebral and spinal cord volume reductions occurred in both patient subgroups compared with controls. Functional correlates were found with estimated volume loss in the upper cervical cord and cerebral white matter. Particularly for infratentorial structures, estimated rates of atrophy were higher in relapsing-remitting than secondary progressive patients, suggesting that atrophy, perhaps mainly due to tract degeneration, begins early in multiple sclerosis and may relate predominantly to acute inflammatory events, with or without other gradual non-inflammatory processes later in the disease course.

Adult↗

PubMed2004

The relation of Helicobacter pylori with intestinal metaplasia, gastric atrophy and BCL-2.

BACKGROUND/AIMS: It is assumed that the sequence of events in gastric cancer is as follows: chronic gastritis, atrophy, intestinal metaplasia (IM), dysplasia, and carcinoma. It is also known that Helicobacter pylori (Hp) can be involved in the chain of these chronic phenomena. Therefore, we studied the relation of Hp with chronic inflammation, atrophy, activity level, IM and bcl-2. METHODS: The number of patients included in this study was 52; 35 (67.3%) were female and 17 (32.7%) were male. The average ages of women and men were determined as 44.5 and 41.5 years, respectively. Hp was determined in 53.8% of all cases and chronic inflammation was found in all cases. No dysplasia or gastric cancer was found in our cases. A statistically significant positive correlation was found between the Hp intensity and the degrees of chronic inflammation, atrophy and activity. RESULTS: Bcl-2 was found positive in 7.1% of the patients with Hp, and in 4.1% of the Hp-negative patients. However, bcl-2 was positive in 2 (8.7%) of 23 Hp-positive patients with chronic atrophic gastritis and in 1 (11.1%) of 9 Hp-negative patients with chronic atrophic gastritis. In other words, bcl-2 was found more in Hp-negative chronic atrophic gastritis than in Hp-positive chronic atrophic gastritis. Also, atrophy and IM were present together in 2 bcl-2-positive patients in whom Hp was positive. Bcl-2 was found positive more in IM than atrophy, proportionally. According to these data, although bcl-2 was found positive more often in Hp (+) cases proportionally, it was not statistically significant. Nevertheless, no significant difference was found between bcl-2 positivity and atrophy according to the statistical data. The data regarding the relation between IM and bcl-2 were statistically significant, and a positive correlation was found between them. CONCLUSIONS: We concluded that Hp infections result in chronic gastritis, have a role in the development of atrophy and IM, and that Hp infection has a significant relation with neutrophile activation. The more Hp intensity increases, the greater the degrees of chronic gastritis, activity and atrophy. We also found that Hp, which is known to increase apoptosis, increases the expression of bcl-2, an anti-apoptotic gene, not directly but rather by causing atrophy development. We observed more bcl-2 positivity in IM than in atrophy. Further studies with an extensive series of cases, including patients with dysplasia and gastric cancer, are needed to clarify statistical rates and to support the suggestion that bcl-2 expression increases with the progression to gastric cancer.

Adult↗

PubMed2026

Associations Between Antiparietal Cell Antibody Values and Atrophy in a South and Southeast Asian General Population.

GOALS: To investigate the association between atrophy severity and antiparietal cell antibody (APCA) levels in South and Southeast Asia. BACKGROUND: APCA is an autoantibody that damages gastric parietal cells; autoimmune gastritis (AIG) is a chronic gastric inflammatory disease related to APCA and severe predominant corpus atrophy. Although a positive APCA result is a key clinical diagnostic tool for AIG, its rates vary widely among ethnic groups, and its exact relationship with AIG and predominant corpus atrophy remains unclear. STUDY: Associations between histopathology-assessed and endoscopy-assessed atrophy, APCA positivity rates, Helicobacter pylori status, and pepsinogen levels were investigated in 1982 symptomatic patients from Vietnam, Thailand, Myanmar, Bangladesh, and Nepal. RESULTS: Overall, 38.5% of participants were negative for Helicobacter pylori infection, while 57.6% had a current infection. A positive APCA result, defined as a titer >10, was present in 44.0% of participants (95% confidence interval: 41.8%-46.3%, 873/1982). Pathologic atrophy, corpus atrophy, and predominant corpus atrophy were found in 8.7% (169/1982), 5.1% (101/1982), and 4.1% (81/1982) of participants, respectively. Positive APCA rates significantly differed among countries (10.6% to 63.8%, P <0.001). No significant correlation was found between APCA results and the presence or severity of atrophy. CONCLUSIONS: Although APCA positivity was high among symptomatic patients from South and Southeast Asian countries, few had severe predominant corpus atrophy or positive pepsinogen tests, which suggests a low rate of AIG in this population. Long-term surveillance of APCA-positive individuals is necessary to determine the clinical significance of a positive APCA result without AIG.

Humans↗

PubMed2002

Bicaudate ratio as a magnetic resonance imaging marker of brain atrophy in multiple sclerosis.

CONTEXT: Brain atrophy has emerged as a useful surrogate marker of disease involvement in multiple sclerosis (MS). The relationship between whole-brain or regional atrophy and cognitive dysfunction is poorly understood. OBJECTIVES: To determine whether the bicaudate ratio (BCR)-the minimum intercaudate distance divided by brain width along the same line-is increased in MS and to compare the ability of the BCR, whole-brain atrophy, and other magnetic resonance imaging markers to predict cognitive dysfunction. DESIGN: Case-control study. SETTING: University-affiliated clinic. PARTICIPANTS: Sixty patients with MS and 50 age- and sex-matched control subjects. MAIN OUTCOME MEASURES: Bicaudate ratio, whole-brain atrophy, T2 lesion load, T1 ("black hole") lesion load, and caudate volume were measured quantitatively using fluid-attenuated inversion recovery, T1-weighted, and gradient-echo magnetic resonance imaging scans. Symbol Digit Modalities Test was used to assess cognitive function. RESULTS: The BCR (mean [SD]) was higher in patients with MS (0.11 [0.03]) than in controls (0.09 [0.02]) (P<.001), suggesting subcortical atrophy in MS. The BCR was related to total T2 (r = 0.56, P<.001) and T1 (r = 0.40, P<.002) lesion volumes, but not caudate volume in patients with MS. Regression modeling selected BCR (P<.05), but not whole-brain atrophy, T1 or T2 lesion volume, or caudate volume as predictive of Symbol Digit Modalities Test score in patients with MS. CONCLUSIONS: The BCR is increased in MS and is more closely associated with cognitive dysfunction than are other magnetic resonance imaging surrogate markers including whole-brain atrophy. Increased BCR is best explained by frontal horn ventricular enlargement due to atrophy of deep frontal subcortical white matter. This highlights the close relationship between subcortical atrophy and cognitive impairment in patients with MS.

Adult↗

PubMed2003

Atrophy is detectable within a 3-month period in untreated patients with active relapsing remitting multiple sclerosis.

BACKGROUND: Atrophy is recognized as a measure of destructive changes in multiple sclerosis (MS). The time course and pathologic mechanisms of atrophy development are not well understood. Significant atrophy was reported to occur within 9 to 12 months in relapsing remitting MS. OBJECTIVES: To test whether atrophy can be detected over short time intervals, and to evaluate its relationship to inflammation. DESIGN AND METHODS: Prior to randomization to a treatment trial, 138 untreated patients with relapsing remitting MS had 3 magnetic resonance imaging scans within a mean +/- SD follow-up of 76 +/- 20.2 days. Brain parenchymal fraction (BPF), a normalized measure of whole brain volume, the proportion of active (gadolinium-enhancing) scans, and the volume of T1-weighted gadolinium-enhancing and T2-weighted hyperintense lesions were determined at all time points. An annualized atrophy rate was estimated by calculating a regression slope. RESULTS: The median Expanded Disability Status Scale score was 3.5, the mean disease duration was 7.6, and the mean age was 38.5 years. The BPF decreased significantly by -0.229% from scan 1 to scan 3, while the proportion of active scans remained high (65%, 63%, and 67%). The BPF change was only weakly correlated to the volume of T1-weighted gadolinium-enhancing lesions in scan 1 (r = -0.185). The estimated annualized atrophy rate was -1.06% (95% confidence interval, -1.50% to -0.62%). CONCLUSIONS: The annualized atrophy rate found in this study is comparable with rates reported previously. Measurements of BPF allow detection of atrophy over short time intervals in active disease. The short-term relationship of inflammation to atrophy development was weak. Brain parenchymal fraction might be a promising measure in future phase 2 studies of agents, with an expected effect on tissue-destructive pathologic mechanisms of MS.

Adult↗

PubMed2006

Patterns of brain atrophy that differentiate corticobasal degeneration syndrome from progressive supranuclear palsy.

BACKGROUND: Progressive brain atrophy is associated with the corticobasal degeneration syndrome (CBDS) and progressive supranuclear palsy (PSP). Regional differences in brain atrophy may reflect the clinical features of disease. OBJECTIVE: To quantify the structural neuroanatomical differences between CBDS and PSP. DESIGN: A survey of neurologic deficits was conducted in all patients. Voxel-based morphometry was used to quantify structural neuroanatomical differences on magnetic resonance images in each subject group. SETTING: University hospital dementia clinic. PARTICIPANTS: Fourteen patients who met clinical research criteria for CBD and 15 patients who met clinical research criteria for PSP, who were matched for severity of disease, age, and functional status, and 80 age-matched control subjects. MAIN OUTCOME MEASURES: Statistically significant differences in regional gray and white matter volume, after multiple comparisons correction, between groups of subjects. RESULTS: The patients with CBDS displayed an asymmetric (left > right) pattern of brain atrophy that involved the bilateral premotor cortex, superior parietal lobules, and striatum. Progressive supranuclear palsy was associated with atrophy of the midbrain, pons, thalamus, and striatum, with minimal involvement of the frontal cortex. Midbrain structures were more atrophied in PSP than in CBD, whereas dorsal frontal and parietal cortices were more atrophied in CBD than in PSP. The degree of atrophy of the midbrain and pontine tegmentum and the left frontal eye field differentiated the 2 patient groups with 93% accuracy. CONCLUSIONS: Distinct patterns of brain atrophy exist in CBDS and PSP that can be used to differentiate the 2 diseases. Assessments of brain atrophy in these disorders should be focused on cortical and brainstem ocular motor control areas.

Aged↗