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 1,459 records · Page 81Linked to original sources

PubMed1994

Root resorptions in a patient with hemifacial atrophy.

Hemifacial atrophy (Parry-Romberg syndrome) is a rare but well-recognized condition. The developmental effects on facial and oral structures have been well documented in the literature. However, the etiology of hemifacial atrophy remains unknown. Previous reported alterations in tooth growth and development include delayed tooth eruption, abnormal root morphology, and malocclusion but not root resorption. This report presents the orofacial changes from hemifacial atrophy in a 22-yr-old woman and describes the occurrence of root resorptions in two regions affected by this condition. The concurrent presence of root resorptions in both the maxilla and mandible in the regions showing the most severe dental malformations points to root resorption as an additional complication of hemifacial atrophy.

Adult↗

PubMedDate not supplied

Dementia following posterior cortical atrophy--a descriptive clinical case report.

Whether posterior cortical atrophy is a distinct entity or a variant of one of the other degenerative processes continues to be debated. We describe five patients four of whom had bilateral changes of posterior cortical atrophy on the CT scan. These four had a cluster of symptoms consistent with parieto-occiptial dysfunction together with a spectrum of dementia. The fifth patient with unilateral changes had optic ataxia, apraxia of gait and dementia. Three of the five patients were heavy drinkers of alcohol but any direct causal link between alcohol and posterior cortical atrophy is tenuous but alcohol could be a consideration in lowering the threshold for dementia in conjunction with other determinants. The study revealed there is little or no difficulty in recognizing posterior cortical atrophy in the early stages and the end stages are sufficiently uniform to reduce the diagnostic uncertainty.

Journal Article↗

PubMed1989

Topical all-trans-retinoic acid prevents corticosteroid-induced skin atrophy without abrogating the anti-inflammatory effect.

We tested the ability of all-trans-retinoic acid to prevent corticosteroid-induced skin atrophy without lessening the anti-inflammatory effect of the steroids. Histologic study and skin-fold thickness in hairless mice treated topically with various steroids, followed by topical all-trans-retinoic acid, were used to measure prevention of atrophy. By both assessments, all-trans-retinoic acid prevented atrophy. Noninterference with the anti-inflammatory property of steroids was tested in a phorbol ester-induced mouse ear edema model and by histologic assessment of croton oil-induced inflammation of mouse dermis. We found that all-trans-retinoic acid did not interfere with steroid suppression of either edema or dermal inflammation. Thus all-trans-retinoic acid was effective in preventing steroid-induced atrophy without affecting the steroid's anti-inflammatory property.

Administration, Topical↗

PubMed2002

Age-related atrophy of rat soleus muscle is accompanied by changes in fibre type composition, bioenergy decline and mtDNA rearrangements.

A variety of techniques have been applied to investigate the interrelationship between age-related atrophy of rat soleus muscle and other signs of muscle aging, such as changes in muscle fibre type composition, decrease in bioenergy capacity and accumulation of mitochondrial DNA (mtDNA) arrangements. Age-related atrophy of rat soleus muscle was shown to start at the age of about 28 months. It was accompanied by a decrease in the number of slow twitch muscle fibres (type I) and an increase in the proportion of muscle fibres co-expressing slow and fast myosins (type Ic and IIc fibres). Bioenergy capacity of the soleus muscle, assessed by the level of measurable cytochrome c oxidase (COX) activity, was found to be decreased both in the middle age and old rats compared to the young animals. Muscle atrophy was also accompanied by a decrease in the amount of full-length mitochondrial DNA (FL-mtDNA) amplifiable by the extra-long PCR (XL-PCR) and the increase in the number of mtDNA deletions. The results of the study show that the decline in the bioenergy capacity of the rat soleus occurs by the middle age. It is followed by the onset of the age-related muscle atrophy that is accompanied by both fibre type changes and functional mtDNA degradation.

Aging↗

PubMed1999

Repeated restraint stress facilitates fear conditioning independently of causing hippocampal CA3 dendritic atrophy.

This study investigated whether 21 days of restraint stress (6 hr/day) and the subsequent hippocampal dendritic atrophy would affect fear conditioning, a memory task with hippocampal-dependent and hippocampal-independent components. Restraint-stressed rats were injected daily (21 days) with tianeptine (10 mg/kg; to prevent hippocampal atrophy) or vehicle then tested on fear conditioning (Days 23-25, with 2 tone-shock pairings) and open field (Day 25). Restraint stress enhanced freezing to context (hippocampal-dependent behavior) and tone (hippocampal-independent) and decreased open-field exploration, irrespective of whether tianeptine was given. Results confirmed that stress produced CA3 dendritic atrophy and tianeptine prevented it. Moreover, CA3 dendritic atrophy was not permanent but reversed to control levels by 10 days after the cessation of restraint stress. These data argue that different neural substrates underlie spatial recognition memory and fear conditioning.

Animals↗

PubMed1993

Fuchs' heterochromic cyclitis and retinal vascular abnormalities in progressive hemifacial atrophy.

We report a case of progressive hemifacial atrophy with a combination of ipsilateral Fuchs' heterochromic cyclitis and retinal vascular abnormalities. Recently, evidence was found for a neurovascular defect in hemifacial atrophy. Our case not only supports the (clinical) association between Fuchs' heterochromic cyclitis and hemifacial atrophy, but the retinal vascular abnormalities found in this patient add further support to the existence of a neurovascular defect. These findings and our short review of the literature point to the hypothesis of a common sympathetic defect, implicated in the aetiology of both Fuchs' heterochromic cyclitis and progressive hemifacial atrophy. It has to be borne in mind, however, that Fuchs' heterochromic cyclitis has been reported in association with other diseases. It seems likely that although Fuchs' heterochromic cyclitis is a single clinical entity, it may have more than one cause.

Adult↗

PubMed2002

Impact of Helicobacter pylori on the development of vitamin B12 deficiency in the absence of gastric atrophy.

BACKGROUND: Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. MATERIALS AND METHODS: Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori-infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. RESULTS: There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p <.01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p <.001). CONCLUSION: The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Adolescent↗

PubMed2001

Atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach: a reality or merely an hypothesis?

The results of recent investigations have suggested that the old hypothesis of an atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach needs to be qualified. The most common cause of intestinal metaplasia is Helicobacter pylori gastritis. The consequence of this intestinal metaplasia is focal atrophy. Helicobacter pylori infection may also trigger an autoimmune gastritis of the corpus mucosa, with atrophy and intestinal metaplasia. Most intestinal metaplasias are only 'paracancerous' but not 'precancerous' lesions. Diffuse gastric carcinomas, such as the signet ring cell carcinoma, arise independently of intestinal metaplasia. Histogenetically, numerous carcinomas of the stomach are primarily of the gastric type, and may secondarily change into the intestinal type.High-grade intra-epithelial neoplasias (dysplasias) detected during the biopsy-based diagnostic work-up appear to be a marker for carcinoma and must, therefore, be removed endoscopically. The detection of intestinal metaplasia in routinely obtained biopsy material is subject to sampling error and is, therefore, not a suitable marker for an increased risk of a gastric carcinoma developing. As an alternative, the concept of gastritis of the carcinoma phenotype, which is more frequently found in early gastric carcinomas and in the relatives of gastric carcinoma patients, has been developed. In this concept, the diffuse parameters of grade and activity of the gastritis in the antrum and corpus, which are independent of sampling error, are subjected to a comparative analysis. A risk gastritis of the carcinoma phenotype is diagnosed when the grade and activity of the gastritis in the corpus are at least equally as pronounced as in the antrum. Currently, this concept is being tested in a prospective ongoing study. Future studies must show whether, and if so which, immunohistochemical or molecular-genetically detectable changes can be applied as risk markers in the diagnostic work-up. Helicobacter pylori eradication probably does not lead to complete regression of the intestinal metaplasia and ensuing focal atrophy. However, eradication of H. pylori does lead to the normalization of changes that can lead to mutations of the stem cells of the gastric mucosa (free radicals, nitric oxide, cell proliferation and vitamin C secretion).

Gastric Mucosa↗

PubMed2005

Microsurgical dermal-fat retransfer for progressive hemifacial atrophy.

Although the etiology of progressive hemifacial atrophy, Romberg's disease, is still unknown, it typically manifests during emotionally salient times, such as the period before the age of 20 years. It involves not only the subcutaneous tissue and skin but also the muscles and osteocartilaginous framework later. Treatment for the atrophy is, in general, recommended after progression of the disease ceases; otherwise, many augmentations will be required after re-atrophy. However, it has recently been reported that well-vascularized tissue might maintain its volume even in the progressive stage, and that progression might be interrupted by vascularized tissue transplantation. The authors report a case reconstructed with free vascularized dermal-fat re-transfer 13 years after a first reconstruction with free-flap transfer, because the primarily over-corrected region had gradually atrophied and the patient desired further treatment. Even though disease progression could not be completely controlled in this case, free vascularized tissue transfer should be considered for mentally fragile young patients, because the free flap is the best among the procedures for Romberg's disease for maintaining volume.

Adipose Tissue↗

PubMed2005

Long-term follow-up in atrophic body gastritis patients: atrophy and intestinal metaplasia are persistent lesions irrespective of Helicobacter pylori infection.

BACKGROUND: Long-term outcome of atrophic body gastritis has not yet been defined. AIM: To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. METHODS: Overall 106 atrophic body gastritis patients with > or = 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology according to the Sydney System. RESULTS: At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P < 0.0001, RR = 26.7). CONCLUSIONS: Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.

Adult↗

PubMed1994

Progressive hemifacial atrophy with agenesis of the head of the caudate nucleus.

We describe a woman with right hemifacial atrophy, a high palate, partial left motor seizures, and mild atrophy of the left arm. CT scan showed asymmetrical lateral ventricles and MRI (magnetic resonance imaging) showed atrophy of the right cerebral hemisphere and agenesis of the head of the right caudate nucleus. To our knowledge, this is the first report of Parry-Romberg syndrome associated with structural abnormalities of the basal nuclei documented by MRI. We suggest that a neurovascular aetiology can explain the spectrum of segmental defects associated with hemifacial atrophy.

Adult↗

PubMed2004

Pathological substrate for regional distribution of increased atrophy rates in progressive supranuclear palsy.

BACKGROUND: Most magnetic resonance imaging (MRI) studies of progressive supranuclear palsy (PSP) are cross-sectional and lack post mortem confirmation of the diagnosis. MRI features described previously in PSP correspond to regions of pathological involvement demonstrated in separate studies, but serial MRI with pathological follow up has not been undertaken. OBJECTIVE: To investigate whether regions of increased atrophy rates demonstrated in PSP during life using fluid registered serial MRI correspond with pathological findings in confirmed PSP. METHODS: A 59 year old male presented with a six month history of balance problems and dysarthria. He had a symmetrical, levodopa unresponsive akinetic-rigid syndrome with a vertical supranuclear gaze palsy. A clinical diagnosis of probable PSP was made. His disease progressed relentlessly and he died five years after onset. Two serial MRI scans undertaken during life were reviewed and fluid (non-linear) registration of the images carried out. Post mortem histopathological analysis of the brain was undertaken to definitively confirm the diagnosis and compare regional pathology with the serial imaging. RESULTS: Fluid registration demonstrated greatest rates of atrophy in the brainstem and frontal cortex, in keeping with the distribution of pathology seen at autopsy. CONCLUSION: Fluid registration of serial MRI allows the topography and rates of regional atrophy in PSP to be delineated in life. Atrophy patterns correlated well with regional pathological load. These observations suggest that serial MRI with registration may help differentiate PSP from clinically similar conditions and supports its use as a surrogate marker of disease progression.

Brain↗

PubMed2002

Clinical and genetic heterogeneity in peroneal muscular atrophy associated with vocal cord weakness.

BACKGROUND: The peroneal muscular atrophy syndrome is the most common inherited disorder of the peripheral nervous system and has extensive clinical and genetic heterogeneity. Cranial nerve involvement is rare, though there are distinct peroneal muscular atrophy syndromes in which vocal cord paralysis is a characteristic feature. Among these dHMN-VII and HMSN-IIC are clinically similar but are differentiated by sensory involvement in HMSN-IIC. The gene for dHMN-VII, designated DHMNVP, has been localised to chromosome 2q14, but the location of the gene for HMSN-IIC is currently unknown. It has been suggested that dHMN-VII and HMSN II-C are allelic disorders. OBJECTIVE: To assess the contribution of the dHMN-VII predisposition gene to peroneal muscular atrophy syndromes associated with vocal cord weakness. METHODS: Linkage analysis of microsatellite markers at chromosome 2q14 was undertaken on two families, one affected by HMSN-IIC and a second manifesting vocal cord paralysis and sensorineural deafness in addition to distal muscular atrophy. RESULTS: Two-point LOD scores at chromosome 2q14 markers encompassing the DHMNVP gene were negative in both families. CONCLUSIONS: These results suggest that at least one further gene predisposing to distal muscular weakness in association with vocal cord paralysis is likely to exist, and that dHMN-VII and HMSN-IIC are unlikely to be allelic disorders. Analyses of further HMSN-IIC families are required to confirm this.

Charcot-Marie-Tooth Disease↗

PubMed2006

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei.

Skeletal muscle atrophy is associated with an increase in apoptosis, and we showed previously that endonuclease G (EndoG) is localized to nuclei following unloading. The goal of this study was to determine whether the onset of apoptosis in response to disuse was consistent with the hypothesis that EndoG is involved in myofiber nuclear loss. Atrophy was induced by hindlimb suspension for 12 h or 1, 2, 4 and 7 days in 6-mo-old rats. Soleus myofiber cross-sectional area decreased significantly by 2 days, whereas muscle mass and muscle-to-body mass ratio decreased by 4 and 7 days, respectively. By contrast, a significant increase in apoptosis, evidenced by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive nuclei, occurred as early as 12 h after suspension, preceding the elevation in muscle atrophy F-box gene expression. The early increase in apoptosis appeared to be specific to myofiber nuclei, whereas TUNEL-positive interstitial cells did not become significantly elevated until 2 days after suspension. Furthermore, TUNEL-positive myofiber nuclei colocalized with EndoG as early as 12 h after suspension, and no such localization was observed in interstitial cells. Although no significant change in total activated caspase-3, -7, or -12 protein abundance was apparent, activated caspase-3 was expressed in interstitial cells undergoing apoptosis, some of which were endothelial cells. These data indicate that apoptosis is an early, and therefore possibly causative, event in the process of muscle atrophy, and that EndoG nuclear translocation is specific for myofiber nuclear apoptosis, whereas interstitial cells may undergo apoptosis via a more classical, caspase-dependent pathway.

Active Transport, Cell Nucleus↗

PubMedDate not supplied

Usefulness of simple measures of temporal lobe atrophy in probable Alzheimer's disease.

Diagnosis of Alzheimer's disease is made on clinical grounds, and the availability of a simple and sensitive quantitative index of the disease might aid in the routine diagnosis. The aim of this study was to assess whether linear measures of brain atrophy as detected by magnetic resonance imaging can be helpful in the differentiation of mild to moderate Alzheimer's disease from nondemented elderly. Measures of global (bifrontal index and interuncal distance) and hippocampal (minimum thickness of the medial temporal lobe, hippocampal height, width of the choroid fissure, and width of the temporal horn) atrophy were taken from 26 cases and 21 controls. Measures of hippocampal atrophy were the most sensitive in the differentiation of cases from controls, and among them width of the temporal horn yielded the highest sensitivity, predicting the disease in 73% of cases with 95% specificity. A compound measure comprising width of the temporal horn, width of the choroid fissure, and hippocampal height increased sensitivity to 85%. These results suggest that selected simple indices of hippocampal atrophy might be useful in the diagnosis of Alzheimer's disease.

Aged↗

PubMed1993

Alkaline Phosphatase, Sucrase, and Insulin-like Growth Factor Receptors are Present in Atrophied Small Bowel 14 Years after Jejunoileal Bypass.

The authors obtained atrophied and hypertrophied small intestinal tissue from a patient undergoing jejunolleal (JI) bypass reversal. Tissue from both segments was examined for insulin, insulin-like growth factor-I (IGF-1) and IGF-11 receptors, and alkaline phosphatase and sucrase. We were interested in the potential of the atrophied segment to respond to luminal stimulation once the food train was re-established. Within the atrophic segment, flow cytometric evaluation of the receptors revealed (expressed as percent positive staining cells): insulin, 17.1%; IGF-1, 33.6%; and IGF-11, 60.8%, while the immunoreactive sucrase was 87.7% and alkaline phosphatase was 88.6%. Actual sucrase activity (expressed as glucose generated) in this segment was 17.9 ng/minl,ug protein and alkaline phosphatase was 28.0 U/L/µg protein as assessed by conventional methods. Receptor evaluation in the hypertrophic segment demonstrated 9.7% positive staining cells for insulin, 26.6% for IGF-I and 70.2% for IGF-11. Immunoreactive sucrase was 91.2% and alkaline phosphatase was 91.4%. Enzyme activity for sucrase was 10.4 ng/min/µg protein and for alkaline phosphatase was 59.4 U/L/µg protein. This data suggests that even in atrophied bowel insulin and IGF receptors as well as sucrase and alkaline phosphatase enzymes are present and may assist in the rapid recovery of the atrophied portion following reversal of the JI bypass.

Journal Article↗

PubMed2005

Matrix metalloproteinase imbalance in muscle disuse atrophy.

Muscle atrophy commonly occurs as a consequence of prolonged muscle inactivity, as observed after cast immobilization, bed rest or space flights. The molecular mechanisms responsible for muscle atrophy are still unknown, but a role has been proposed for altered permeability of the sarcolemma and of the surrounding connective tissue. Matrix metallo-proteinases (MMPs) are a family of enzymes with proteolytic activity toward a number of extracellular matrix (ECM) components; they are inhibited by tissue inhibitors of MMPs (TIMPs). In a rat tail-suspension experimental model, we show that after fourteen days of non-weight bearing there is increased expression of MMP-2 in the atrophic soleus and gastrocnemius and decreased expression of TIMP-2. In the same experimental model the expression of Collagen I and Collagen IV, two main ECM components present in the muscles, was reduced and unevenly distributed in unloaded animals. The difference was more evident in the soleus than in the gastrocnemius muscle. This suggests that muscle disuse induces a proteolytic imbalance, which could be responsible for the breakdown of basal lamina structures such as Collagen I and Collagen IV, and that this leads to an altered permeability with consequent atrophy. In conclusion, an MMP-2/TIMP-2 imbalance could have a role in the mechanism underlying muscle disuse atrophy; more studies are needed to expand our molecular knowledge on this issue and to explore the possibility of targeting the proteolytic imbalance with MMP inhibitors.

Animals↗

PubMed1999

[A case of progressive hemifacial atrophy with Pourfour de Petit syndrome which was successfully treated by stellate ganglion block].

We herein report a 31-year-old woman with progressive hemifacial atrophy. The atrophy at her left face began about ten years ago. She had been in a traffic accident one year before the onset of her facial atrophy. Neurological examination revealed anisocoria (right < left) and retraction of the left eyelid, which thus suggested the presence of Pourfour de Petit syndrome. The pupillary reaction to both cocaine and tyramine were reduced bilaterally. Thermography of the face showed slightly lower surface temperature on the left side. A facial thermal sweat test was normal. These findings indicated local hyperactivity of the sympathetic nervous system at the Th 1-Th2 levels on the left side. A left stellate ganglion block effectively induced an accumulation of the subcutaneus tissue of her face on the left side. This is a very rare case in which local sympathetic hyperactivity is present and has caused progressive hemifacial atrophy.

Adult↗