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PubMed2003

Selective caudate atrophy in multiple sclerosis: a 3D MRI parcellation study.

Deep gray matter damage may be an important component of the multiple sclerosis (MS) disease process. We tested whether caudate atrophy occurs in MS, and whether it correlates with conventional MRI or clinical markers of disease progression. Caudate nuclei of 24 MS patients and 10 age-matched healthy controls were traced, normalized, reconstructed and visualized from MRI scans. Normalized bicaudate volume was 19% lower in MS controls ( p< 0.001), an effect that persisted after adjusting for whole-brain atrophy ( p< 0.008). Caudate volume did not correlate with disease duration, physical disability score, whole-brain atrophy, or total T2 hyperintense or T1 hypointense lesion load (all p > 0.05). We conclude that selective caudate atrophy is associated with MS and may occur through direct mechanisms.

Adult↗

PubMedDate not supplied

CT in lobar atrophy of the liver caused by alveolar echinococcosis.

We reviewed the CT findings of 13 patients with histologically proved alveolar echinococcosis of the liver. Seven of these patients had hilar involvement, which caused dilatation of intrahepatic bile ducts and invasion of the portal vein or portal branches. In two of these patients we found marked atrophy of the right lobe and in one patient marked atrophy of the left lobe in addition to various CT findings previously reported for alveolar echinococcosis of the liver. The occurrence of lobar atrophy of the liver caused by alveolar echinococcosis has not been previously reported. We concluded that, when a mass lesion with hilar infiltration causing lobar atrophy is found in endemic areas, alveolar echinococcosis should be considered in the differential diagnosis in addition to malignant neoplasms.

Atrophy↗

PubMed2001

Update on the pathologic approach to the diagnosis of gastritis, gastric atrophy, and Helicobacter pylori and its sequelae.

Biopsy sampling of the gastric mucosa at diagnostic endoscopy provides information that cannot be obtained otherwise. The most common indication for gastric biopsy is the need to know whether the patient is infected with Helicobacter pylori or not and whether the stomach is gastritic or not. Microscopic examination of gastric biopsy specimens gives, in addition to H. pylori status, information about the grade, extent, and topography of gastritis- and atrophy-related alterations in the gastric mucosa. This information provides further possibilities for the assessment of risk and likelihood of various gastric disorders. The presence of atrophy (loss of mucosal glands) results in failures in secretory functions of the corresponding mucosa and leads to errors in the homeostasis of normal gastric physiology. The grade of atrophy of the corpus mucosa linearly correlates with peak and maximal output of acid. The presence of advanced (moderate or severe) corpus atrophy indicates an extremely hypochlorhydric or achlorhydric stomach in which, for example, ordinary peptic ulcer is unlikely or impossible in spite of a possible H. pylori infection. Some well characterized and common topographic phenotypes of H. pylori gastritis and atrophic gastritis can be delineated as follows: Predominance or restriction of the H. pylori-related inflammation in antrum, in association with a nonatrophic corpus mucosa--of which phenotype is the most common--and with an increased risk of peptic ulcer disease, duodenal ulcer in particular ("duodenal ulcer phenotype" of gastritis); the presence of atrophic gastritis in corpus of the stomach ("corpus predominant gastritis"), which indicates a low risk of peptic ulcer and a reduction in the capacity of the patient to secrete acid; the occurrence of advanced atrophic gastritis and intestinal metaplasia multifocally in the stomach (advanced "multifocal atrophic gastritis"), which are features of a gastritis type and which also indicate a low acid secretion capacity and an increased risk of gastric neoplasias ("gastric cancer phenotype of gastritis"), suggesting a need for a careful exclusion of concomitant presence of small focal neoplastic or dysplastic lesions; and the presence of normal and healthy gastric mucosa, which indicates an extremely low risk of both peptic ulcer disease or gastric cancer and, therefore, is a finding of high clinical relevance. The presence of duodenal or gastric ulcer in conjunction with normal, healthy gastric mucosa suggests either aspirin or nonsteroidal antiinflammatory drugs to be the most likely cause of the ulcer.

Atrophy↗

PubMed1998

Progressive presumed choriocapillaris atrophy after surgery for age-related macular degeneration.

PURPOSE: The authors sought to evaluate the progression of presumed choriocapillaris atrophy after surgical excision of a subfoveal choroidal neovascular membrane (CNV) in an 80-year-old man with age-related macular degeneration. METHODS: The CNV was excised using a conventional three-port vitrectomy with subretinal dissection. The excised tissue was studied with light and electron microscopy. Preoperative and serial postoperative fluorescein angiograms (FA) and fundus photographs were obtained to study the dissection bed. RESULTS: Seven days after surgery, the FA showed hyperfluorescence in the area previously occupied by the CNV. Six weeks after surgery, this area showed retinal pigment epithelium (RPE) depigmentation, atrophy, or both on clinical examination, and the FA showed presumed choriocapillaris nonperfusion. Seven months after surgery, the area of the RPE depigmentation or atrophy and the corresponding area of presumed choriocapillaris nonperfusion had enlarged. The area of depigmentation or atrophy continued to enlarge for 1 year after surgery. Histologically, the excised CNV specimen disclosed RPE cells but no choriocapillaris. CONCLUSIONS: Presumed choriocapillaris nonperfusion after CNV excision may be due to RPE removal at surgery and may progress postoperatively.

Aged↗

PubMed1993

Oligodendroglial and neuronal inclusions in multiple system atrophy.

Argyrophilic cytoplasmic inclusions of oligodendrocytes have been described in cases of multiple system atrophy (olivopontocerebellar atrophy, striatonigral degeneration, and Shy-Drager syndrome). The oligodendroglial cytoplasmic inclusions are immunolabeled with antiubiquitin antibodies. Ultrastructurally, they appear as granule-associated filaments. They have not been found in other neurological diseases or in normal brains, and are now considered to be early and specific markers of multiple system atrophy. More recently, similar argyrophilic inclusion bodies have been reported in the cytoplasm of neurons and in both oligodendroglial and neuronal nuclei of multiple system atrophy brains. Neuronal and oligodendroglial cytoplasmic inclusions have identical ultrastructural characteristics, but different antigenic properties. The chemical nature of the inclusions is presently unknown and their significance remains controversial: they could be a primary event in the course of the degenerative process or merely an epiphenomenon of some disordered cytoskeletal metabolism.

Corpus Striatum↗

PubMedDate not supplied

Influence of raloxifene on the efficacy of an estradiol-releasing ring for treating vaginal atrophy in postmenopausal women.

OBJECTIVE: To determine the potential interaction of oral raloxifene 60 mg/day on the efficacy of a low-dose, estradiol-releasing vaginal ring used to treat signs and symptoms of vaginal atrophy in postmenopausal women. DESIGN: Randomized, double-blind, placebo-controlled, parallel treatment trial of raloxifene and placebo with open-label 17beta-estradiol ring. At 10 sites in the United States, 91 postmenopausal women with at least two signs of vaginal atrophy were treated with a 17beta-estradiol ring and randomized to receive concomitant raloxifene 60 mg/day or placebo for 6 months. Efficacy of treatments was evaluated by comparing investigator assessments of genitourinary atrophic signs, vaginal maturation value, and participant assessments of vaginal symptoms at 6 months. Other measures included rate and severity of hot flashes and assessment of sexual function. Uterine safety was assessed by endometrial biopsy and transvaginal ultrasound. RESULTS: In women treated with a 17beta-estradiol ring, both the raloxifene and placebo treatment groups showed improvements in signs and symptoms of vaginal atrophy at 6 months, with no significant differences in degree of improvement between groups. There were no signs of endometrial proliferation in either group. CONCLUSIONS: Concomitant administration of raloxifene does not alter the effects of the 17beta-estradiol ring on alleviating signs and symptoms of genitourinary atrophy in postmenopausal women.

Administration, Intravaginal↗

PubMed2003

Urethral atrophy after artificial urinary sphincter placement: is cuff downsizing effective?

PURPOSE: We reviewed the outcome of cuff downsizing with an artificial urinary sphincter for treating recurrent incontinence due to urethral atrophy. MATERIALS AND METHODS: We analyzed the records of 17 patients in a 7-year period in whom clinical, radiological and urodynamic evidence of urethral atrophy was treated with cuff downsizing. Cuff downsizing was accomplished by removing the existing cuff and replacing it with a 4 cm. cuff within the established false capsule. Incontinence and satisfaction parameters before and after the procedure were assessed by a validated questionnaire. RESULTS: Mean patient age was 70 years (range 62 to 79). Average time to urethral atrophy was 31 months (range 5 to 96) after primary sphincter implantation. Mean followup after downsizing was 22 months (range 1 to 64). Cuff downsizing caused a mean decrease of 3.9 to 0.5 pads daily. The number of severe leakage episodes decreased from a mean of 5.4 to 2.1 The mean SEAPI (stress leakage, emptying, anatomy, protection, inhibition) score decreased from 8.2 to 2.4. Patient satisfaction increased from 15% to 80% after cuff downsizing. In 1 patient an infected cuff required complete removal of the device. CONCLUSIONS: Patient satisfaction and continence parameters improved after cuff downsizing. We believe that this technique is a simple and effective method of restoring continence after urethral atrophy.

Aged↗

PubMed2005

Molecular signaling pathways regulating muscle proteolysis during atrophy.

PURPOSE OF REVIEW: Although a variety of diverse stimuli induce muscle atrophy, there is a surprising number of similarities in the intracellular responses. One prominent response is an increase in muscle proteolysis resulting from stimulation of the ubiquitin-proteasome pathway. Understanding the intracellular signaling pathways that regulate muscle mass should offer insights into the coordination of cellular responses. This review will discuss recent findings on the molecular signaling pathways regulating proteolysis during muscle atrophy. RECENT FINDINGS: The expression of several muscle-specific E3 ubiquitin ligases is consistently increased in conditions causing muscle atrophy. Insulin and insulin-like growth factor-1 act through the phosphoinositide 3-kinase/AKT pathway to suppress the expression of two of these enzymes, MuRF1 and MAFbx/atrogin-1. Efforts to identify targets of the muscle-specific E3 ligases are yielding interesting information. Insulin and insulin-like growth factor-1 also attenuate wasting by inhibiting caspase-3, which cleaves actin to facilitate its destruction by the ubiqutin-proteasome system. Other signaling systems involved in the regulation of muscle mass include the nuclear factor kappa B pathway. SUMMARY: The maintenance of muscle mass requires a delicate balance between catabolic factors and anabolic factors. These signals inversely modulate the activity of several key regulatory pathways including the phosphoinositide-3 kinase/AKT and nuclear factor kappa B systems, which control the transcription of components of the ubiquitin-proteasome proteolytic pathway activity, the activity of caspase-3, and perhaps other proteolytic functions. When levels of insulin or insulin-like growth factor-1 are insufficient or inflammatory cytokine production is increased, muscle atrophy ensues.

Caspase 3↗

PubMed2006

Gene therapy with anabolic growth factors to prevent muscle atrophy.

PURPOSE OF REVIEW: Many situations cause muscle atrophy. When severe, muscle atrophy is associated with an increase in morbidity and mortality. This loss of muscle mass is thought to be due to an imbalance between catabolic and anabolic pathways, resulting in an increase of muscle protein proteolysis and in a decrease in protein synthesis. Changes in muscle levels of muscle growth factors are thought to play a major role in this imbalance. Despite recent better understanding of the metabolic and molecular derangements leading to muscle wasting, therapy of muscle atrophy still has a poor success rate. RECENT FINDINGS: The recent demonstration that changes in local growth factors, such as insulin-like growth factor-I and myostatin, occur during muscle atrophy has stimulated research interest to prevent muscle mass loss by delivering these growth factors or their inhibitors into the muscle. During the last few years, several advances in the field of muscle gene transfer, using electroporation or recombinant adeno-associated viral vectors, have opened novel therapeutic ways to deliver growth factors able to counteract the loss of muscle mass. SUMMARY: Preventing decrease of insulin-like growth factor-I muscle, or inhibiting myostatin action by local genes over-expression, may provide a clinically relevant avenue for the preservation, attenuation or reversal of disease-related muscle loss.

Animals↗

PubMed2006

Subclinical exocrine pancreatic dysfunction resulting from decreased cholecystokinin secretion in the presence of intestinal villous atrophy.

UNLABELLED: The aim of this study was to evaluate the concept that pancreatic dysfunction in patients having gluten sensitivity (celiac disease [CD]) or cow's milk protein enteropathy (CMPE) may result from the lack of pancreatic enzyme stimulation in the absence or decrease of cholecystokinin (CCK) secretion caused by villous atrophy. PATIENTS AND METHODS: The following parameters were measured: plasma CCK in response to a fatty meal and human pancreatic fecal elastase in 24 patients with CD while on gluten-free diet and after gluten provocation and in 12 patients with CMPE at diagnosis and after a 6-month period of cow's milk-free diet. Intestinal mucosa morphology was examined by small bowel biopsy. Sixty-three controls having no organic gastrointestinal problems were investigated once at the time of diagnostic evaluation. RESULTS: Fasting CCK, obtained at a time when patients with CD or CMPE had normal intestinal mucosa, was significantly different from postprandial and comparable to that of the control group. Fasting CCK obtained from patients with villous atrophy was also statistically different, but not significantly, from the postprandial. Fasting and postprandial plasma CCK and fecal pancreatic elastase values from patients having normal intestinal mucosa were significantly higher than those obtained from patients with villous atrophy. Significant correlation of intestinal mucosa morphology and CCK with fecal elastase concentration was documented. CONCLUSION: Exocrine pancreatic dysfunction in individuals having villous atrophy may be the consequence of decreased CCK secretion. Cholecystokinin and pancreatic secretion is restored to normal, with intestinal mucosa regeneration.

Adolescent↗

PubMed2003

Prevention of pectus excavatum for children with spinal muscular atrophy type 1.

To demonstrate the elimination of pectus excavatum and promotion of more normal lung growth and chest wall development by the use of high-span positive inspiratory pressure plus positive end-expiratory pressure (PIP+PEEP), patients with spinal muscular atrophy type 1 with paradoxical breathing were placed on high-span PIP+PEEP when sleeping from the point of diagnosis of spinal muscular atrophy. Although the appearance of pectus excavatum is ubiquitous in untreated infants with spinal muscular atrophy type 1, after institution of high-span PIP+PEEP, pectus resolves and lungs and chest walls grow more normally. High-span PIP+PEEP is indicated for all infants diagnosed with spinal muscular atrophy who demonstrate paradoxical breathing for the purpose of promoting more normal lung and chest development.

Child↗

PubMed2006

Day-of-injury computerized tomography, rehabilitation status, and development of cerebral atrophy in persons with traumatic brain injury.

OBJECTIVE: To compare day-of-injury (DOI) computerized tomography (CT) findings with acute injury severity markers, disability at acute hospital admission and discharge from inpatient rehabilitation, injury severity markers, and degree of postacute cerebral atrophy on magnetic resonance imaging (MRI). DESIGN: Retrospective chart review of 240 consecutive traumatic brain injury (TBI) admissions (mean age 31.7 +/- 15.8 yrs) with moderate-to-severe initial brain injury. All DOI CT abnormalities were qualitatively rated. Disability was assessed using the Disability Rating Scale (DRS) and the FIM measure. In a representative subset, cerebral atrophy was determined by the ventricle-to-brain ratio (VBR) method and quantified from MRI scans 25 or more days postinjury. RESULTS: CT classification resulted in nonsignificant differences in DRS and FIM ratings at the time of discharge from the rehabilitation unit, except in brainstem injury subjects who had significantly higher DRS and lower FIM scores at rehabilitation discharge. At 25 or more days postinjury, presence of any DOI CT abnormality was associated with larger VBR. Increased VBR, as an index of cerebral atrophy, was associated with worse rehabilitation discharge DRS and FIM ratings. CONCLUSIONS: Other than brainstem injury, DOI CT findings relate poorly to rehabilitation outcome. Presence of DOI CT abnormalities were associated with the development of cerebral atrophy, which was associated with poorer rehabilitation discharge DRS and FIM scores.

Activities of Daily Living↗

PubMed2006

The thenar index: an objective assessment and classification of thenar atrophy based on static hand imprints and clinical implications.

BACKGROUND: The aims of this study were to test the effectiveness of the subjective clinical evaluation and to search for any possibility of constituting an objective assessment system for the diagnosis of thenar atrophy based on static hand imprints. METHODS: Static hand imprints were obtained from normal subjects (group A, n = 116) and carpal tunnel syndrome patients with thenar atrophy (group B, n = 26). Thenar index and the bilateral thenar index ratio were defined. Cutoff values were considered by analyses with receiver operating characteristic curves. RESULTS: No statistically significant difference could be demonstrated in thenar index values of dominant and nondominant hands between genders and age groups (p > 0.05). A statistically significant difference was observed between severity groups in group B (p < 0.05). There was a statistically significant difference between thenar index and bilateral thenar index ratio values of groups A and B (p < 0.05). Cutoff values were considered a thenar index of 31 and a bilateral thenar index ratio of 0.8, which revealed acceptable specificity (95.3 percent) and sensitivity (77.4 percent). A new quantitative classification for thenar atrophy severity is proposed. CONCLUSIONS: Understanding the true onset and natural progression of thenar atrophy can only be anticipated with the aid of an objective assessment system. Currently, this method should be regarded as a system for patient records and comparison for presurgical and postsurgical data. The authors believe that the thenar index classification has some merit for future use. It seems that additional objective and scientific evaluation systems and novel approaches are still needed to demystify the true nature of carpal tunnel syndrome.

Adult↗

PubMed2006

Intraoral duct ligation without inclusion of the parasympathetic nerve supply induces rat submandibular gland atrophy.

The atrophic effect of ligating the main duct of the right submandibular gland was examined in rat using a novel intraoral approach that did not include the chorda lingual (CL) nerve. Comparison was made with the effect of duct ligation including the attached CL nerve as carried out in previous studies. In all animals, the contralateral, unligated left submandibular gland was used as a control. At different times (1, 2, 7, 14 and 21 days) after ligation, glands were removed and weighed. Tissue was fixed for morphological analysis and homogenized for biochemical assay of secretory proteins. After 21 days, ligated glands showed a significant decrease in wet weight compared with unligated glands. Weight loss was the greatest (P < 0.05) in glands ligated with the CL nerve included. Light microscopy revealed that following ligation, an initial inflammatory reaction was followed by severe atrophy of acini and granular ducts. The atrophy was less severe when the CL nerve was not ligated. Secretory proteins were decreased from day 1 onwards following duct ligation in both groups. It can be concluded that most of the atrophy induced by duct ligation is independent of damage caused to the parasympathetic nerve supply, although the latter causes a greater atrophy presumably due to denervation.

Animals↗

PubMed2006

Effects of a multilamellar emulsion on glucocorticoid-induced epidermal atrophy and barrier impairment.

Skin atrophy is one of the most frequent side-effects of the topical glucocorticoid. Skin barrier impairment has also been reported as a steroid-induced side effect. Although there have been various studies on preventing or minimizing this atrophogenic effect, little has been reported about preventing barrier impairment. This study was performed to determine the effects of a multilamellar emulsion (MLE) that had a well-ordered lamellar structure on the steroid-induced barrier impairment and epidermal atrophy. To confirm these effects of MLE, 0.05% clobetasol-17-propionate (CP) and 0.05% clobetasol-17-propionate in MLE (MLE/CP) were topically applied to both flanks of hairless mice for 9 days. The topically applied CP induced a significant impairment of the epidermal permeability barrier, and MLE/CP also did not have a preventive effect on this change. However, skinfold thickness studies and histological studies showed that MLE/CP significantly reduced the steroid-induced atrophy. The topical application of MLE/CP was also shown to have a preventive effect on the steroid-induced increase of the stratum corneum (SC) surface pH. In addition, the electron microscopic findings showed relatively well-conserved lamellar bilayers in the skin treated with MLE, as compared to CP only. The results showed that the topical application of MLE immediately after CP treatment prevented the glucocorticoid-induced transepidermal water loss values increase. Light microscopy measurements showed that the skin treated with MLE immediately after CP treatment for 1 week had a slightly lower decline of skin thickness than did the CP-treated skin. These results suggest that MLE should be effective for preventing glucocorticoid-induced epidermal atrophy and for repairing the barrier impairment.

Administration, Topical↗

PubMed1998

Review article: Gastric atrophy and atrophic gastritis--nebulous concepts in search of a definition.

Epidemiological and biological evidence indicates that atrophic gastritis represents an important risk factor for gastric adenocarcinoma of the intestinal type. To estimate an individual subject's risk of gastric cancer, pathologists should be able to diagnose correctly and reliably assess gastric atrophy. However, both anecdotal evidence and recent studies suggest that pathologists have a low level of agreement on gastric atrophy. Moreover, the terms 'gastric atrophy' and 'atrophic gastritis' remain imprecisely defined, further adding confusion to the histopathological imprecision. The use of visual analogue scales proposed in the recently updated Sydney System for the classification and grading of gastritis may eventually help pathologists achieve a greater degree of interobserver agreement on the histopathological features of gastritis. However, this cannot be achieved in the absence of a stringent and widely accepted definition of atrophy. The purpose of this article is to review briefly the possible pathogenetic pathways leading to the development of atrophic changes in the gastric mucosa, explore the issue of its reversibility, and propose a working definition that could contribute to improved diagnostic reproducibility.

Adenocarcinoma↗

PubMed1989

Can villous atrophy be induced by chronic alcohol consumption?

A 43-year-old man presented with loose stools, abdominal pain and a weight loss of 15 kg. Investigations revealed a pancreatic insufficiency and an enteropathy with villous atrophy. Coeliaki was suspected. In spite of treatment with a gluten-free diet in hospital the patient did not improve and the villous atrophy remained unchanged. Other causes than coeliaki to villous atrophy were ruled out. The patient had a heavy consumption of alcohol and after prolonged abstinence the patient gained weight, the pain disappeared and the stools were normalized. The jejunal biopsy was now normal. This case report raises the possibility that enteropathy and villous atrophy may be causally related to alcohol overconsumption.

Adult↗

PubMed1992

Estimation error of Leydig cell numbers in atrophied rat testes due to the assumption of spherical nuclei.

In this study, Leydig cell numbers in control and atrophied testes (induced via subcutaneous implants of testosterone plus 17 beta estradiol for 16 weeks; TE-implanted) of rats, estimated via the fractionator method (independent of any assumptions) were compared to those estimated via the disector (unbiased, but dependent on shrinkage) and Floderus (assumes spherical particles, dependent on shrinkage) methods. Estimates of Leydig cell numbers in control rats produced by all three stereological methods were similar. In rats with atrophied testes, both the fractionator and the disector methods produced significantly lower (P < 0.01; 47% and 41% with fractionator and disector, respectively) Leydig cell number estimates per testis than in the controls. By contrast, the estimates of Leydig cell number in atrophied testes derived via the Floderus equation were not significantly different from those of controls, but larger than those obtained via the fractionator and the disector methods. These results suggested that the assumptions of the Floderus method were violated in the atrophied rat testes. Why was the Floderus method of estimating Leydig cell number applicable to control rats but not to the TE-implanted rats? In an attempt to answer this question the diameter measurement together with its correction factor used in the Floderus equation (i.e. D+t - 2H) was also derived from the data collected for the disector method. The values for D+t - 2H used in the Floderus method and also calculated via the disector method were found to be identical in controls, but for the TE-implanted rats a 32% lower value was obtained with the Floderus equation when compared to the disector. These findings suggested that this estimation error caused an overestimation of Leydig cell numbers in the TE-implanted rat testes.

Animals↗