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Results for “Atrophy”

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PubMed1999

MIB-1 expression is useful in distinguishing dysplasia from atrophy in elderly women.

Both atrophic and dysplastic cervical squamous epithelia show lack of maturation, nuclear crowding, and increased nuclear/cytoplasmic ratio. Because of these similarities, distinguishing dysplasia from atrophy in cervical biopsies from elderly patients is often problematic. Because dysplasia shows increased proliferation and atrophy has decreased proliferation, the possible utility of MIB-1 in distinguishing dysplasia from atrophy was evaluated. One or more of the following criteria were present in all nine cases with dysplasia and in none of the 17 cases with atrophy: MIB-1 expression in > 20% of cells in the basal one-third of the epithelium, > 5% of cells in the middle one-third of the epithelium, and > 1% of cells in the upper one-third of the epithelium. MIB-1 immunostaining is useful in distinguishing dysplasia from atrophy.

Aged↗

PubMed1996

Quantitative assessment of cerebral atrophy during and after treatment in children with acute lymphoblastic leukemia.

RATIONALE AND OBJECTIVES: The authors evaluate quantitatively brain atrophy induced by central nervous system prophylaxis in children treated for acute lymphoblastic leukemia during and after therapy completion. METHODS: Measurements of the width of the subarachnoid compartments were performed in 243 brain computed tomography (CT) examinations of 196 children examined during (125) and/or after (71) treatment for acute lymphoblastic leukemia without central nervous system involvement. Data were compared with normative data. RESULTS. Diffuse brain atrophy was observed in 74% and 65% of the CT examinations performed during and after cessation of treatment, respectively. The highest incidence of brain atrophy (78%) occurred during the administration of intrathecal chemotherapy. All children younger than 2 years of age exhibited brain atrophy. CONCLUSIONS: Brain atrophy is the principal CT finding in the majority of children treated for acute lymphoblastic leukemia and it can be attributed mainly to intrathecal chemotherapy. This finding can be observed long after therapy completion.

Adolescent↗

PubMed1998

Extreme right lobar atrophy of the liver: a rare complication of autoimmune hepatitis.

Lobar atrophy is a rare morphologic change of the liver. We describe a 73-year-old woman with mild liver dysfunction and history of Sjögren's syndrome who had right hepatic lobar atrophy. Serum biochemistry levels were as follows: albumin, 4.5 g/dl; total bilirubin, 1.0 mg/dl; alanine aminotransferase, 25 international units/l; aspartate aminotransferase, 27 international units/l; alkaline phosphatase, 333 international units/l; and gamma-glutamyl transpeptidase, 332 international units/l. Serological data were as follows: rheumatoid factor, 27.9; anti-nuclear antibody, 1:640; and antismooth muscle antibody, 1:80. Viral markers for hepatitis B were all negative. Anti-hepatitis C virus (anti-c-100) was negative. Portal hypertension developed thereafter, and the patient died of hepatic failure at age 76. Postmortem examination revealed autoimmune hepatitis with moderate fibrosis, portal vein thrombus, and complete obstruction of the right hepatic duct due to hepatolithiasis. Terminal hepatic failure resulted from combination of decreased hepatic volume due to the right lobar atrophy, exacerbation of autoimmune hepatitis in the remnant left hepatic lobe, decreased portal venous blood flow due to thrombosis, portal hypertension, and cholangitis with hepatolithiasis. This is the first reported case of hepatic lobar atrophy due to autoimmune hepatitis. From a clinical standpoint, patients with hepatic lobar atrophy, even if asymptomatic, should be followed up with careful attention to progression of liver diseases, portal hypertension, and biliary complications.

Aged↗

PubMed1997

No evidence for axonal atrophy in human diabetic polyneuropathy.

In rats with streptozin-induced diabetes mellitus, the caliber of distal myelinated fiber (MF) axons in relation to the number of myelin lamellae is smaller than in controls. This finding usually has been attributed to axonal atrophy, but shrinkage or maldevelopment has also been considered. For human diabetic polyneuropathy (DP), axonal atrophy has been assumed by some investigators, but convincing evidence has not been demonstrated. We morphometrically evaluated transverse sections of 33 sural nerves from carefully evaluated diabetic patients > or = 30 years old without (8 patients) or with (25 patients) DP and compared them with 24 nerves from healthy subjects > or = 30 years old. Nerves from diabetic patients and controls were obtained under identical conditions and processed and evaluated in the same way, using an observer blind to the disease condition. Using computer digitization of electron micrographs, we evaluated the axonal area, perimeter, index of circularity, number of myelin lamellae, and frequency of adaxonal sequestration of 50.4 (mean) +/- 5.8 (SD) MF per sural nerve for healthy subjects and diabetic patients > or = 30 years old. The regression lines of the natural log (In) of axonal area on number of myelin lamellae of diabetic patients (with or without DP) were not significantly different from the regression lines of nerves of healthy subjects for large MFs-the most reliable group in which to recognize atrophy. Likewise, the regression lines of index of circularity (IC) (an index that is decreased with atrophy or shrinkage) on number of myelin lamellae for large fibers was not significantly different between the disease and control groups. The rate of adaxonal sequestration was not significantly higher in DP than in healthy subjects. These results do not support the hypothesis that axonal atrophy occurs in human DP. For small MF, or all MF, some significant differences in regression lines of In axonal area or IC on number of lamellae were found, but these changes are probably explained by events of remyelination and axonal regeneration, which can affect these relationships and are known to occur in DP.

Adult↗

PubMed2006

Autosomal dominant pericentral retinochoroidal atrophy.

PURPOSE: To describe a family pedigree with a newly described hereditary retinal disease. METHODS: Five family members were examined, and a fifth deceased family member was identified through review of old medical records. RESULTS: Five individuals had annular or arcuate pericentral areas of retinal (younger members) or choroidal (older members) atrophy and spared maculae with good visual acuity and normal retinal periphery. Two of the four examined affected family members were symptomatic only for field loss; the other two were asymptomatic. No nyctalopia was reported by any affected individual. Fluorescein angiography revealed hyperfluorescence in the affected areas in the family members with retinal atrophy and hypofluorescence in affected areas in family members with choroidal atrophy. Visual field scotomas were dense and corresponded to the areas of retinal and/or choroidal atrophy. Full-field electroretinograms were normal for two family members and were reduced for one family member with the most advanced retinal and choroidal changes. The scotopic response was only mildly reduced in the fourth examined family member. CONCLUSIONS: We believe that we have identified a pedigree with a previously undescribed autosomal dominant hereditary retinal disease characterized by arcuate retinal and retinochoroidal atrophy and normal visual acuity.

Adult↗

PubMed1992

Experimental study of denervated muscle atrophy following severance of posterior rami of the lumbar spinal nerves.

The morphologic changes in denervation atrophy of paravertebral muscles after severance of the posterior rami in cats were investigated, using histochemical methods and electromyography. Using a paraspinal approach, three branches of the posterior rami on the left side were cut under microscopy at one, two, or three levels (L2 approximately L4). Muscle atrophy was evaluated, using the percent wet weight and the percent diameter of muscle fibers as parameters. Myosine ATPase stain was used to observe reinnervation. Four weeks after surgery, the range and severity of muscle atrophy increased proportionally to the number of posterior rami severed. Muscle atrophy was revealed at one or two levels caudal to the injured nerve level. At 12 and 24 weeks, muscle atrophy recovered gradually. In more than two-level injury groups, however, recovery of percent wet weight reached up to 80% even after 24 weeks, despite the fact of reinnervation demonstrated in some parts of the denervated muscles.

Animals↗

PubMedDate not supplied

Glucocorticoid-induced muscle atrophy. The role of exercise in treatment and prevention.

Glucocorticoids have catabolic effects on skeletal muscle. These effects demonstrate fiber type specificity: Type IIB fibers are most susceptible and type I fibers least susceptible to the atrophy effects of glucocorticoids. Exercise training has been used frequently to counteract glucocorticoid-induced muscle atrophy. Studies have demonstrated that both resistance exercise and endurance exercise are effective in attenuating this atrophy. The cellular mechanisms mediating the attenuating effect of exercise on glucocorticoid-induced atrophy are not completely understood. More research is needed to further elucidate the details of these mechanisms and to determine the most efficacious exercise protocols for deterring glucocorticoid-induced muscle atrophy. Exercise evaluation of patients with glucocorticoid-induced myopathy and subsequent exercise prescription must be individualized and based on the patient's initial muscle function and medical status.

Exercise Therapy↗

PubMed1999

Spinal muscular atrophy: molecular pathophysiology.

Spinal muscular atrophy is an autosomal recessive disease characterized by motor neurone loss, muscle atrophy and weakness. Deletion or mutation of the SMN1 gene reduces intracellular survival motor neurone protein levels causes spinal muscular atrophy, most likely by interfering with spliceosome assembly. A range of clinical severity and corresponding survival motor neurone levels is seen because of the presence of copies of the transcriptionally inefficient SMN2 gene and possibly other modifying genes. The delineation of SMN1 as the gene that causes spinal muscular atrophy and the identification of genes that modify spinal muscular atrophy raise the prospect of gene therapy or in-vivo gene activation treatment for this frequently fatal disorder.

Autoantigens↗

PubMed2002

Secondary axon atrophy and neurological dysfunction in demyelinating neuropathies.

PURPOSE OF THE REVIEW: Secondary axonal atrophy is common in most if not all demyelinating neuropathies and is likely responsible for the majority of clinical symptoms. We review clinical, electrophysiological and morphological evidence for secondary axonal atrophy in demyelinating neuropathies and summarize recent hypotheses on possible pathomechanisms. RECENT FINDINGS: Elucidation of genetic defects responsible for hereditary demyelinating neuropathies and insights into axon-Schwann cell interactions have allowed longitudinal studies of genetically defined demyelinating neuropathies and research into the pathomechanism of secondary axonal atrophy. SUMMARY: There is ample clinical electrophysiological and electropathological evidence that secondary axonal atrophy is found in hereditary and demyelinating neuropathies. Recognizing secondary axonal atrophy as a main cause for clinical disability in demyelinating neuropathies is important for the clinician and may reveal a therapeutic target common to all different forms of demyelinating neuropathies.

Atrophy↗

PubMed2005

Differentiating high-grade cervical intraepithelial lesion from atrophy in postmenopausal women using Ki-67, cyclin E, and p16 immunohistochemical analysis.

OBJECTIVE: In postmenopausal women, differentiating high-grade cervical intraepithelial neoplasia (CIN 2,3) from atrophic uterine cervical squamous epithelium histologically may pose a diagnostic challenge. Recent studies have indicated the value of using a combination of Ki-67, cyclin E, and p16 immunohistochemical analysis in recognizing CIN 2,3. In this study, we compared the staining features of Ki-67, cyclin E, and p16 in cervix specimens from postmenopausal women to distinguish CIN 2,3 from atrophy. METHODS: Twenty-six formalin-fixed paraffin-embedded archival cervical specimens (4 biopsy, 8 laser cone, and 14 total hysterectomy samples) were selected from 25 women 50 to 80 years of age (mean = 64 years). Cases included CIN 2,3 (n = 10), atrophy (n = 9), and coexistent CIN 2,3 and atrophy (n = 6). Slides were stained with monoclonal antibodies to Ki-67, cyclin E, and p16 using the avidin-biotin-peroxidase method. Strength of staining was graded as 1+ to 3+. Pattern of staining was described as diffuse, patchy, or scattered. Ki-67 staining restricted to the basal/parabasal zone was scored as negative. RESULTS: All CIN 2,3 cases demonstrated variable positivity for Ki-67, cyclin E, and p16. Most CIN 2,3 cases showed strong p16 (81.3%) and Ki-67 (75.0%) reactivity, while only 31.3% of them showed strong cyclin E activity. Some CIN 2,3 cases demonstrated strong p16 but weak Ki-61 and cyclin E reactivity. All atrophic epithelia were negative for p16, cyclin E, and Ki-67. In coexistent CIN 2,3 and atrophy cases, the three-antibody panel clearly demarcated the transition from benign to neoplastic epithelia. CONCLUSION: P16 is the most valuable marker followed by Ki-67 for differentiating CIN 2,3. While cyclin E appears to add limited value on these two markers. Therefore, although the three-antibody immunohistochemical panel (p16, Ki-67, and cyclin E) can be a valuable adjunct to routine hematoxylin-eosin staining, it is also possible to use the two-antibody panel (p16 and Ki-67) to effectively distinguish CIN 2,3 from atrophy in postmenopausal women.

Aged↗

PubMed2004

Basal forebrain atrophy is a distinctive pattern in dementia with Lewy bodies.

We determined brain atrophy patterns in dementia with Lewy bodies and Alzheimer's disease using voxel-based morphometry, an indirect volumetry. Ten patients with dementia with Lewy bodies, 10 patients with Alzheimer's disease and 10 controls were included. All groups were matched for age; sex and global differences in voxel intensities were included as confounding covariates. We observed basal forebrain atrophy discriminating dementia with Lewy bodies from Alzheimer's disease. Compared to controls, atrophy of lateral prefrontal cortex and left premotor cortex was seen in dementia with Lewy bodies whereas atrophy of the medial temporal cortex, posterior parietal cortex, thalamus and temporo-occipital areas was observed in Alzheimer's disease. Atrophy of insular cortex was found in both patient groups.

Aged↗

PubMed2006

Simulation of tissue atrophy using a topology preserving transformation model.

We propose a method to simulate atrophy and other similar volumetric change effects on medical images. Given a desired level of atrophy, we find a dense warping deformation that produces the corresponding levels of volumetric loss on the labeled tissue using an energy minimization strategy. Simulated results on a real brain image indicate that the method generates realistic images of tissue loss. The method does not make assumptions regarding the mechanics of tissue deformation, and provides a framework where a pre-specified pattern of atrophy can readily be simulated. Furthermore, it provides exact correspondences between images prior and posterior to the atrophy that can be used to evaluate provisional image registration and atrophy quantification algorithms.

Algorithms↗

PubMed1977

Corticosteroid-induced dermal atrophy in the rat.

Corticosteroid-induced dermal atrophy has been studied in the rat using daily application of ethanolic solutions to small areas of flank skin. After 12 days of treatment, the degree of atrophy was determined by comparing the weights of skin plugs (16 mm diameter) taken from the treated areas with contralaterally paired control areas. Doses can be adjusted so that systemic effects are minimized and only local effects are observed. Hydrocortisone, hydrocortisone butyrate, dexamethasone, betamethasone, desonide and triamcinolone acetonide all produce atrophy in the rat, and the degree of thinning is dose dependent. Potencies in the dermal atrophy assay compare directly with topical anti-inflammatory potencies in the rat, and the presence of fluorine in the steroid molecule is not a determining factor in the production of atrophy.

Administration, Topical↗

PubMed1991

New aspects of the mechanism of corticosteroid-induced dermal atrophy.

Glucocorticoids are effective for the treatment of various inflammatory skin diseases, but their long-term use may lead to serious side-effects such as osteoporosis and skin atrophy. The incidence of skin atrophy following application of potent corticosteroids is especially high among children and the elderly. During recent years the effects of glucocorticoids on connective tissue have been elucidated, and it is evident that skin atrophy is mostly due to a decrease in collagen synthesis. Since collagen is the most abundant protein in the skin, the inhibition of its synthesis leads to atrophy. This review discusses the molecular mechanisms of glucocorticosteroid-induced skin atrophy and therapeutic possibilities.

Aged↗

PubMed1996

The effect of minimum luminal nutrition on bacterial translocation and atrophy of the jejunum during parenteral nutrition.

In situations of catabolic stress, the gut becomes atrophic and may have diminished barrier function as evidenced by an increase in bacterial translocation. The aim of this study was to examine the effect of minimum luminal nutrition during parenteral nutrition on the extent of jejunal atrophy and rate of bacterial translocation. Central venous lines were inserted into 30 rats before they underwent randomization to receive nutritional support with: (a) conventional parenteral nutrition; (b) conventional parenteral nutrition with 3 g/day of rat food (i.e., minimum luminal nutrition); or (c) rat food ad libitum. The rats were assessed after 10 days for nutritional status, extent of jejunal atrophy, caecal flora, as well as the extent of bacterial translocation to the mesenteric lymph nodes, liver and spleen. Rats in the rat food ad libitum group lost the smallest amount of weight and had the least amount of jejunal atrophy, yet had a similar rate of bacterial translocation as the parenterally nourished groups. When compared with the conventional parenteral nutrition group, the minimum luminal nutrition group had better preservation of the weight of the small bowel and its isolated mucosa (P < 0.01), but had a similar rate of bacterial translocation. Minimum luminal nutrition reduced the extent of atrophy of the gut but did not affect the incidence of bacterial translocation. It is inferred that there is no direct relationship between the extent of mucosal atrophy and incidence of bacterial translocation.

Animal Feed↗

PubMed2005

Treatment of local, persistent cutaneous atrophy following corticosteroid injection with normal saline infiltration.

BACKGROUND: Injections of corticosteroids are commonly used for a variety a dermatologic conditions but may cause local, persistent cutaneous atrophy, with few therapeutic options. OBJECTIVE: To determine the effectiveness of bacteriostatic normal saline infiltration on the improvement of corticosteroid-induced cutaneous atrophy. MATERIALS AND METHODS: Four patients with corticosteroid-induced atrophy of the skin, two caused by acneiform cysts and one from intramuscular steroid injection, were treated with weekly injections of normal saline directly into the atrophic site. The patients were seen on weekly follow-up visits, and improvement was documented. RESULTS: All four patients demonstrated complete resolution of skin atrophy and restoration of surface contour within 4 to 8 weeks of initial presentation. Injected volumes of normal saline ranged from 5 to 20 cm(3) per treatment session and three to six weekly treatments. The patients were completely satisfied with these results. CONCLUSION: Normal saline infiltration offers a safe, tolerable, relatively rapid, and effective treatment for local, persistent corticosteroid-induced atrophy.

Adrenal Cortex Hormones↗

PubMed1995

Focal intermittent delta activity in patients with mesiotemporal atrophy: a reliable marker of the epileptogenic focus.

We attempted to determine the significance of background abnormalities and their relation with spikes and location of atrophy in 56 patients with temporal lobe epilepsy (TLE) and mesiotemporal atrophy (MTA) assessed by volumetric magnetic resonance imaging (MRI): 35 patients had unilateral (group I) and 21 had bilateral atrophy with lateralized predominance (group II). Trains of delta waves over temporal regions were observed in > or = 90% of patients. They lateralized with accuracy equal to that of the spikes to the site of atrophy (delta 92% or 29 of 32 patients in group I and 63% or 12 of 19 of group II; spikes 85% or 28 of 33 of group I and 65% or 13 of 20 of group II). Delta waves and spikes occurred together in > 85% of cases. With respect to their location, a striking concordance was observed: delta activity almost always occurred ipsilateral with unilateral spiking (90% or 19 of 21 of patients with unilateral and 88% or 7 of 8 of patients with bilateral atrophy) and bilaterally independently with bilateral spiking (67% or 6 of 9 of patients in group I and 100% or 10 of 10 in group II). Furthermore, spiking and delta activity were never in disagreement with respect to lateralization. In TLE related to MTA, delta transients are a reliable indicator of the epileptogenic focus and presumably reflect the epileptogenic process rather than the underlying structural pathology.

Adolescent↗

PubMed1980

Alcoholism and cerebral atrophy: a study of 50 patients with CT scan and psychologic testing.

A study of 50 alcoholic patients was carried out with CT scans of their brains and psychologic testing. These patients were alcohol and drug free, and without neurologic or psychiatric disorders at the time of the examinations. Fifty-eight percent of the patients had cerebral atrophy. There was no correlation between the results of the psychologic testing and cerebral atrophy. The only factor that correlated to a significant degree with cerebral atrophy was the duration of problem drinking. Only the mean duration of problem drinking was statistically significantly longer in the patients with cerebral atrophy compared to those patients with normal CT scans. Implications of this finding of high prevalence of cerebral atrophy in alcoholics is discussed.

Adult↗