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PubMed2006

Different types of atrophy in the prostate with and without adenocarcinoma.

OBJECTIVES: The purpose of this study was to evaluate, according to a classification proposed by a working group, the extent and type of atrophy lesions in radical prostatectomy specimens obtained from patients with prostatic carcinoma and benign prostatic hyperplasia (BPH), and to compare the prevalence and types of atrophy between two investigated groups. METHODS: Histologic analysis of 1096 slides from 50 patients with carcinoma and 277 slides from 31 patients with BPH was performed to evaluate, according to the new prostatic atrophy classification, the number of foci and type of atrophic lesions. RESULTS: Age, Gleason grade, and TNM showed no significant correlation with the number of proliferative atrophy (PA) and proliferative inflammatory atrophy (PIA) foci (p>0.05). PIA was significantly more frequent in prostates with carcinoma (1.63 vs 1.27 atrophic lesions per slide) (p<0.001), whereas PA displayed an increased frequency in BPH (2.28 vs 0.76 atrophic lesions per slide) (p<0.001). CONCLUSIONS: We confirmed that PA and PIA are common findings in prostates with and without carcinoma, but the question of whether inflammation produces tissue damage and PA or whether some other insult induces the tissue damage and atrophy directly, with inflammation occurring secondarily, is still unresolved.

Adenocarcinoma↗

PubMed2005

SOGC clinical practice guidelines. The detection and management of vaginal atrophy. Number 145, May 2004.

OBJECTIVE: To support the practitioner in the diagnosis of vaginal atrophy and in the management of the related symptoms. OPTIONS: The modalities of evaluation range from basic pelvic examination, examination of the vulva, and laboratory tests. OUTCOMES: A comprehensive approach to the detection of vaginal atrophy and a discussion of available therapeutic and nontherapeutic options. EVIDENCE: Published opinions of experts, supplemented by evidence from clinical trials, where appropriate. VALUES: The quality of the Force on the Periodic Health Examination. BENEFITS, HARMS AND COSTS: Diagnosis of vaginal atrophy is often a challenge because women are unwilling to report symptoms, which have the potential to significantly decrease their quality of life. Increased clinical suspicion is the first step in the diagnosis of vaginal atrophy, which will prompt the initiation of safe therapies with proven efficacy. RECOMMENDATIONS: (1) Health-care providers should routinely assess postmenopausal women for the symptoms and signs of vaginal atrophy, a common condition that exerts significant negative effects on quality of life. (III-C) (2) Regular sexual activity should be encouraged to maintain vaginal health. (II-2B) (3) Women experiencing recurrent urinary tract infections should be instructed that consumption of pure cranberry-lingonberry juice, rather than cranberry drink, will decrease their risk of urinary infections. (I-A) (4) Vaginal moisturizers applied on a regular basis have an efficacy equivalent to local hormone replacement for the treatment of local urogenital symptoms such as vaginal itching, irritation, and dyspareunia, and should be offered to women wishing to avoid the use of hormone replacement therapy. (I-A) (5) Women experiencing vaginal atrophy can be offered any of the following effective vaginal estrogen replacement therapies: conjugated equine estrogen (CEE) cream (I-A), a sustained-release intravaginal estradiol ring (I-A), or a low-dose estradiol tablet. (I-A) (6) Although systematic absorption of estrogen can occur with local preparations, there is insufficient data to recommend annual endometrial surveillance in asymptomatic women using local estrogens. (III-C) (7) For menopausal women experiencing recurrent urinary tract infections and who have no contraindication to local hormone replacement, vaginal estrogen therapy should be offered. (I-A) VALIDATION: These guidelines have been reviewed by the joint committee of Clinical Practice Gynaecology and Urogynaecology and approved by the Execute and Council of the Society of Obstetricians and Gynaecologists of Canada. SPONSOR: The Society of Obstetricians and Gynaecologists of Canada.

Aging↗

PubMed2003

Whole-brain atrophy in multiple sclerosis measured by two segmentation processes from various MRI sequences.

Recent MRI and pathologic studies have drawn attention to the destructive nature of the multiple sclerosis (MS) disease process, including the early occurrence of axonal and neuronal loss, leading to macroscopic brain and spinal cord atrophy. Measurement of brain atrophy from MRI has emerged as a potential outcome measure and marker of disease severity in MS and neurodegenerative diseases such as Alzheimer's. However, the optimal method for quantifying atrophy has not been established, including the choice of pulse sequence and segmentation algorithm employed. Using two different MRI scanners to ensure generalizability of results, we compared the reproducibility of four pulse sequences and two analysis methods (fully automated [FA] and semi-automated [SA]) when obtaining brain parenchymal fraction (BPF), a normalized measure of whole-brain atrophy, in patients with MS (n=13) and normal controls (n=2). In order to ensure the validity of our fully automated analysis technique, we also used it to evaluate the atrophy rate over nine months in 57 MS patients from the placebo arm of a clinical trial. All pulse sequences were capable of yielding reproducibility of around 1% coefficient of variation (CoV) or better. The best reproducibility was obtained using 2D multi-slice sequences (conventional spin echo [SE] and fluid-attenuated inversion recovery [FLAIR]), with fully automated analysis. Fully automated analysis of the longitudinal data (conventional spin echo) showed an atrophy rate of -0.5% change in BPF per year, in line with previous findings from a similar cohort of patients. In conclusion, BPF measurement is affected by both pulse sequence and segmentation method. Automated measurement has high reproducibility especially when 2D sequences are used. Semi-automated measurement may have increased accuracy, but with a decreased efficiency and reliability.

Adult↗

PubMed2004

Association of fatigue and brain atrophy in multiple sclerosis.

Functional imaging studies have demonstrated a relationship between fatigue and altered cerebral activation patterns in multiple sclerosis patients, but no relationship between fatigue and brain atrophy has been demonstrated. We hypothesized that the subjective complaint of fatigue would predict the severity of destructive brain pathology. We assessed the relationship between fatigue and brain atrophy longitudinally in a cohort of 134 patients previously enrolled in a 2-year clinical trial of interferon beta-1a and re-evaluated 8 years after randomization into the trial. Brain atrophy was measured using the brain parenchymal fraction (BPF), and disability was measured using the Multiple Sclerosis Functional Composite at baseline, year 2 and year 8. Fatigue was measured using the Sickness Impact Profile's Sleep and Rest Scale (SIPSR) at baseline, year 2 and year 8. Linear regression analyses were used to assess the relationship between changes in fatigue and atrophy progression. Worsening fatigue on the SIPSR during the initial 2 years was significantly associated with progressive brain atrophy over the subsequent 6 years. The relationships between fatigue and brain atrophy were independent of changes in disability, mood, or other MRI characteristics. This suggests that the subjective complaint of fatigue is linked to destructive pathologic processes in RRMS patients.

Atrophy↗

PubMed2006

Differential changes in respiratory capacity and ischemia tolerance of isolated mitochondria from atrophied and hypertrophied hearts.

In spite of opposing changes in rates of adenosine triphosphate turnover, hypertrophy and atrophy of the heart are accompanied by the same changes in gene expression, resembling a fetal genotype. Fetal hearts are characterized by increased ischemia tolerance. We assessed respiratory capacity of mitochondrial subpopulations from unloaded and pressure-overloaded hearts before and after 15 minutes of normothermic ischemia. Unloading was achieved by heterotopic rat heart transplantation and overloading by aortic banding. Respiratory chain gene expression (NADH dehydrogenase, cytochrome c oxidase [COX]) were analyzed by reverse transcriptase-polymerase chain reaction. Subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM) were isolated by differential centrifugation. Citrate synthase was used as mitochondrial marker enzyme. Adenosine diphosphate-stimulated oxygen consumption (state 3) was measured with a Clark-type electrode. Unloading resulted in atrophy, overloading in hypertrophy. State 3 was reduced in atrophied hearts both in SSM and IFM (SSM: 204 +/- 79 vs 804 +/- 147 natoms oxygen min(-1) mL(-1), P < .001; IFM: 468 +/- 158 vs 1141 +/- 296 natoms oxygen min(-1) mL(-1), P < .05), but was unchanged in hypertrophied hearts. NADH dehydrogenase and COX expression was also decreased with atrophy and was unchanged with hypertrophy. Ischemia caused decreased recovery of citrate synthase in isolates of SSM (P < .05) but not of IFM. State 3 in control hearts was reduced in IFM (-41%, P < .01) and SSM (-19%, not significant). This ischemia-induced decrease was less pronounced in SSM (-2%) and IFM (-22%) of atrophied and IFM (-23%) of hypertrophied hearts. Subsarcolemmal mitochondria of hypertrophied hearts displayed the greatest ischemia-induced decrease of state 3 (-32%, P < .05). In conclusion, (1) long-term changes in workload differentially affect maximal respiratory capacity and ischemia tolerance of isolated mitochondria. The changes are not parallel to the changes in energy requirements. (2) Mitochondria of atrophied hearts appear to be more resistant against ischemia than controls.

Adenosine Diphosphate↗

PubMed2006

The effect of glutamine on prevention of glucocorticoid-induced skeletal muscle atrophy is associated with myostatin suppression.

Excess glucocorticoids (GCs) cause muscle atrophy. Glucocorticoid-induced muscle atrophy is associated with increased intramuscular myostatin expression. Myostatin is a negative regulator of skeletal muscle mass. Glutamine prevents GC-induced muscle atrophy. We hypothesized that glutamine effect on reversal of GC-induced muscle atrophy is mediated in part by suppression of myostatin. We administered daily to male Sprague-Dawley rats dexamethasone, dexamethasone plus glutamine, saline or saline plus glutamine, all pair-fed. Animals were killed on day 5. Body weight and weights of gastrocnemius muscles were measured. Myostatin expression was measured by Northern and Western blots, and was compared with glyceraldehyde-3-phosphate dehydrogenase. Myoblast C2C12 cells were exposed to dexamethasone, or dexamethasone and glutamine, and their myostatin messenger RNA and protein expression compared with glyceraldehyde-3-phosphate dehydrogenase. Myostatin promoter activity was measured by luciferase activity of transfected C2C12 cells, grown in medium including dexamethasone, or dexamethasone plus glutamine. Rats that received dexamethasone showed significant body and muscle weight loss accompanied by an increase in intramuscular myostatin expression, compared with their saline-treated controls. Pair-fed rats given dexamethasone plus glutamine had significantly less reduction in body and muscle weights and lower myostatin expression when compared with those treated with dexamethasone alone. In C2C12 myoblast cells, addition of glutamine to dexamethasone prevented the hyperexpression of myostatin induced by dexamethasone. Myostatin promoter activity increased in cells exposed to dexamethasone, but this increase was partially blocked by addition of the glutamine. Administration of glutamine partially prevents GC-induced myostatin expression and muscle atrophy, providing a potential mechanism for the prevention of muscle atrophy induced by glucocorticoids.

Animals↗

PubMed2006

Cerebellar cortical atrophy in experimental autoimmune encephalomyelitis.

Brain atrophy measured by MRI is an important correlate with clinical disability and disease duration in multiple sclerosis (MS). Unfortunately, neuropathologic mechanisms which lead to this grey matter atrophy remain unknown. The objective of this study was to determine whether brain atrophy occurs in the mouse model, experimental autoimmune encephalomyelitis (EAE). Postmortem high-resolution T2-weighted magnetic resonance microscopy (MRM) images from 32 mouse brains (21 EAE and 11 control) were collected. A minimum deformation atlas was constructed and a deformable atlas approach was used to quantify volumetric changes in neuroanatomical structures. A significant decrease in the mean cerebellar cortex volume in mice with late EAE (48-56 days after disease induction) as compared to normal strain, gender, and age-matched controls was observed. There was a direct correlation between cerebellar cortical atrophy and disease duration. At an early time point in disease, 15 days after disease induction, cerebellar white matter lesions were detected by both histology and MRM. These data demonstrate that myelin-specific autoimmune responses can lead to grey matter atrophy in an otherwise normal CNS. The model described herein can now be used to investigate neuropathologic mechanisms that lead to the development of gray matter atrophy in this setting.

Animals↗

PubMed2006

The gross motor function measure is a valid and sensitive outcome measure for spinal muscular atrophy.

Spinal muscular atrophy is a genetic disease of the anterior horn cell with high morbidity rate in childhood. Certain drugs may be of benefit and are in or under consideration for Phase II trials. Outcome measures that are age appropriate and representative of disease activity remain under study. Several have not yet been validated for spinal muscular atrophy. The Gross Motor Function Measure is a measure of motor function. We showed previously that the Gross Motor Function Measure is a reliable outcome measure to assess motor function in children with spinal muscular atrophy. By collating our data from 40 spinal muscular atrophy patients, ages 5 through 17 years, we now show the validity of the Gross Motor Function Measure when compared to Quantitative Muscle Testing and ambulatory status in children with spinal muscular atrophy. The median for Gross Motor Function Measure total scores for walkers was 237 (range: 197-261) and for non-walkers, 64 (range: 4-177; P<0.0001) with no distributional overlap. We conclude that the Gross Motor Function Measure is valid and sensitive as an outcome measure for clinical trials in pediatric spinal muscular atrophy.

Adolescent↗

PubMed2004

Reduced expression of aquaporin 4 in human muscles with amyotrophic lateral sclerosis and other neurogenic atrophies.

Aquaporin 4 (AQP4) is a water channel protein that is widely distributed in human tissues. However, the precise functional role of AQP4 in skeletal muscle tissue has not yet been determined. Expression of AQP4 was reported to be reduced in muscle tissue from Duchenne muscular dystrophy patients. In the regenerating phase of skeletal muscle, AQP4 expression was reduced when nerve supply was not present. However, in diseased human muscles with neurogenic atrophy including amyotrophic lateral sclerosis, there has been no data on the changes in AQP4 expression. In the present study, we investigated the expression of AQP4 at mRNA and protein levels in human muscles with neurogenic atrophy. The mean level of AQP4 mRNA was significantly lower in muscles with neurogenic atrophy than that in muscles from normal controls. The myofiber surface immunostaining with anti-AQP4 antibody in muscles with neurogenic atrophy was reduced on the surface of scattered myofibers, small angulated myofibers, and myofibers in small- and large-group atrophy despite the presence of dystrophin. Based on the present findings, we conclude that the expression of AQP4 is affected by nerve supply and is down-regulated in human muscles with neurogenic atrophy.

Amyotrophic Lateral Sclerosis↗

PubMed2004

gamma-Diketone neuropathy: axon atrophy and the role of cytoskeletal protein adduction.

Multifocal giant neurofilamentous axonal swellings and secondary distal degeneration have been historically considered the hallmark features of gamma-diketone neuropathy. Accordingly, research conducted over the past 25 years has been directed toward discerning mechanisms of axonal swelling. However, this neuropathological convention has been challenged by recent observations that swollen axons were an exclusive product of long-term 2.5-hexanedione (HD) intoxication at lower daily dose-rates (e.g., 175 mg/kg/day); that is, higher HD dose-rates (e.g., 400 mg/kg/day) produced neurological deficits in the absence of axonal swellings. The observation that neurological toxicity can be expressed without axonal swelling suggests that this lesion is not an important pathophysiological event. Instead, several research groups have now shown that axon atrophy is prevalent in nervous tissues of laboratory animals intoxicated over a wide range of HD dose-rates. The well-documented nerve conduction defects associated with axon atrophy, in conjunction with the temporal correspondence between this lesion and the onset of neurological deficits, strongly suggest that atrophy has pathophysiological significance. In this commentary, we present evidence that supports a pathognomonic role for axon atrophy in gamma-diketone neuropathy and suggests that the functional consequences of this lesion mediate the corresponding neurological toxicity. Previous research has demonstrated that HD interacts with proteins via formation of pyrrole adducts. We therefore discuss the possibility that this chemical process is essential to the mechanism of atrophy. Evidence presented in this review suggests that "distal axonopathy" is an inaccurate classification and future nosological schemes should be based on the apparent primacy of axon atrophy.

Animals↗

PubMed2005

Cerebellar atrophy in temporal lobe epilepsy.

PURPOSE: The goal of this work was to determine the presence and degree of cerebellar atrophy in chronic temporal lobe epilepsy, its clinical seizure correlates, and its association with general cortical atrophy. METHODS: Study participants were 78 persons with temporal lobe epilepsy and 63 age- and gender-matched healthy controls. All subjects underwent high-resolution MRI with manual tracing of the cerebellum. Clinical seizure features and history were obtained by structured interview and review of medical records. RESULTS: The epilepsy group exhibited significant abnormality in cerebellar volume, with mean reductions ranging from 4 to 6.6% depending on adjustments. Significantly more individual subjects with epilepsy exhibited cerebellar atrophy compared with controls across all operational definitions or thresholds of abnormality including z < or = -2.0 (13% TLE, 3.4% controls) and z < or = 1.5 (22% TLE, 3.4% controls). Clinical seizure features reflecting both neurodevelopmental (history of initial precipitating injuries) and severity of course (longer duration, increased number of lifetime generalized tonic-clonic seizures) factors were associated with cerebellar atrophy. Atrophy of the cerebellum could be observed independent of more general (cerebral) atrophic processes. CONCLUSIONS: The presence of cerebellar atrophy is a reflection of the extratemporal abnormalities that can be observed in localization-related temporal lobe epilepsy, which may be due, at least in part, to factors associated with epilepsy chronicity.

Adult↗

PubMed2003

A novel mutation in the OPA1 gene in a Japanese patient with optic atrophy.

PURPOSE: To report a novel mutation of the OPA1 gene in a Japanese patient with optic atrophy and to describe the clinical features of the patient. DESIGN: Observational case report. METHODS: Genomic DNA was extracted from leukocytes of four unrelated Japanese patients with optic atrophy. All the exons and splice sites of the OPA1 gene were amplified by polymerase chain reaction and directly sequenced. RESULTS: One patient with optic atrophy had a heterozygous Arg445His mutation in the OPA1 gene. The Arg445His mutation was detected neither in 110 control subjects nor in the patient's healthy family members. CONCLUSIONS: A novel mutation of the OPA1 gene, similar to those reported in Western countries, was detected in a Japanese patient with optic atrophy. Mutations of the OPA1 gene may contribute to the development of optic nerve atrophy in Japanese cases of optic atrophy.

Adolescent↗

PubMed1998

Usefulness of videoduodenoscopy and vital dye staining as indicators of mucosal atrophy of celiac disease: assessment of interobserver agreement.

BACKGROUND: The present study was designed to determine the diagnostic usefulness of videoduodenoscopic inspection alone and the addition of vital dye staining in the detection of celiac disease. We additionally sought to evaluate interobserver agreement for specific duodenoscopic markers of mucosal atrophy. METHODS: One hundred sixty-seven consecutive subjects who underwent duodenoscopy for intestinal biopsy were included in a prospective controlled study. Endoscopic examination was performed by experienced endoscopists according to a set protocol using methylene blue (1%) dye. All procedures were recorded on videotape, but only 20 (10 with atrophy and 10 normal) were used in a blinded, independent, randomized analysis by five reviewers to evaluate interobserver agreement. Endoscopic signs indicative of mucosal atrophy were as follows: reduction in the number or loss of Kerkring's folds, "scalloped" folds, "mosaic pattern," and visualization of the underlying blood vessels. RESULTS: Eighty-seven patients had celiac disease (57 newly diagnosed, 30 when treated). Seven treated patients had nonatrophic mucosa. In 80 patients the final diagnosis excluded celiac disease. Videoendoscopic inspection alone correctly identified 75 of 80 patients with complete mucosal atrophy and 86 of 87 with normal mucosa. False-negative diagnoses occurred in treated celiac patients with mild atrophy. Mosaic pattern (89%) and scalloped folds (86%) were the most useful endoscopic signs. Vital dye staining, as assessed by experienced endoscopists, provided identical results to those obtained by inspection alone. Sensitivity, specificity, and positive and negative predictive values for the presence of one or more than one feature were 94%, 100%, 100%, and 96%, respectively. The agreement (kappa statistics) among observers was excellent for the mosaic pattern (kappa: 0.76 for both the videoendoscopic inspection alone and dye staining) and the scalloped folds (kappa: 0.83 and 0.76, respectively) and was fair (kappa: 0.41 and 0.59, respectively) for the reduction in the number or loss of duodenal folds. CONCLUSION: This study confirms that videoduodenoscopy is useful in the detection of intestinal atrophy. Dye staining produces a better delineation of scalloped folds and mosaic pattern in the atrophic mucosa, but did not provide additional information to the expert endoscopist. Finally, interobserver agreement was excellent for the most prevalent signs.

Adult↗

PubMed2001

Gray matter T2 hypointensity is related to plaques and atrophy in the brains of multiple sclerosis patients.

Cortical and subcortical gray matter hypointensities on T2-weighted MR images (T2WI) occur commonly in MS brains and have been related to disease duration, clinical course, and the level of neurologic disability. These hypointensities have been reported to occur in the thalamus, basal ganglia, and rolandic cortex. We assessed whether T2 hypointensity is associated with the severity of white matter plaques and atrophy of MS brains. In 114 MS patients, hypointensity of the thalamus, putamen, caudate, and sensorimotor cortex was ordinally rated against age- and gender-matched normal controls on 1.5-T MRI fast spin-echo axial T2WI. Regional and global T2 hyperintense and T1 hypointense parenchymal lesion loads were ordinally rated. Enlargement of subarachnoid and ventricular spaces (atrophy) was ordinally rated vs. age- and gender-matched normal controls. T2 hypointensity was highly, positively correlated with many other MRI variables. Regression modeling showed that T2 hypointensity was related to total atrophy, total T2 lesion load, third ventricular enlargement, parietal atrophy, and to a lesser extent, frontal T1 lesions and cerebellar T2 lesions, but not related to gadolinium enhancement. Ordinal ratings of T2 lesions and central atrophy showed high correlations with quantitative computerized assessments. We conclude that gray matter hypointensity on T2WI may reflect pathologic iron deposition and brain degeneration in MS. This T2 hypointensity is associated with brain atrophy and other MR markers of tissue damage. Further study is warranted to determine if T2 hypointensity is predictive of disease course in MS and is a useful surrogate outcome measure in therapeutic trials.

Adolescent↗

PubMed1997

Atrophy of the corpus callosum in chronic alcoholism.

To determine the prevalence of corpus callosum atrophy in chronic alcoholics and its relationship to cognitive function and brain atrophy, a prospective clinicoradiologic study was carried out in 28 right-handed male patients with chronic alcoholism and 14 age- and sex-matched right-handed control subjects. Clinical evaluation, neuropsychological testing and measurement of the midsagittal corpus callosum area and thickness (genu, truncus and splenium), as well as the frontal lobe index and the width of the cortical sulci on T1- and T2-weighted magnetic resonance images were performed. Compared to controls, alcoholics had significantly decreased corpus callosum area and thickness, mainly in the genu. Two-thirds had a corpus callosum area 2 SD below the mean of the control group. The sagittal area of the corpus callosum body correlated negatively with the degree of frontal and cortical atrophies (r = -0.5579 and -0.6853, respectively p < 0.01, both). Alcoholics with corpus callosum atrophy exhibited impairment of visual and logical memories (p < 0.05 both) and those with reduced thickness of the genu showed impairment of frontal lobe tasks (p < 0.05). The reduction of corpus callosum indices (age-corrected) also correlated with the total lifetime dose of ethanol consumed (r = 0.6107, p < 0.001), but was not related to nutritional status or electrolyte imbalance. Atrophy of the corpus callosum is common among alcoholic patients and may reflect the severity and pattern of cortical damage. The degree of this atrophy also correlated with the severity of ethanol intake.

Adult↗

PubMed2003

Effect of raloxifene on the response to conjugated estrogen vaginal cream or nonhormonal moisturizers in postmenopausal vaginal atrophy.

OBJECTIVE: To study the effect of raloxifene on the response to conjugated estrogen cream or nonhormonal moisturizer in postmenopausal women with preexisting signs of vaginal atrophy. METHODS: Postmenopausal women with preexisting and untreated vaginal atrophy were enrolled in this parallel, placebo-controlled, randomized study. A total of 187 women were randomized to four treatment groups: daily oral raloxifene (60 mg per day) or a placebo in a double-blind manner plus one application of conjugated estrogen cream (0.5 g) or one applicator full of nonhormonal moisturizer, open label. The conjugated estrogen cream or nonhormonal moisturizer was applied daily for the first 2 weeks, and then twice weekly thereafter for 3 months. Efficacy of treatment regimens on signs and symptoms of vaginal atrophy was evaluated by monitoring objective and subjective parameters. RESULTS: Signs and symptoms of vaginal atrophy improved in all four treatment groups. Raloxifene did not diminish the magnitude of improvement when administered with either vaginal preparation. Conjugated estrogen cream produced a statistically greater improvement in signs (P <.05) but not in individual symptoms or overall satisfaction relative to nonhormonal moisturizer. CONCLUSION: Postmenopausal women with evidence of preexisting vaginal atrophy may use either low-dose conjugated estrogen cream or nonhormonal moisturizer to treat the atrophy concurrently with raloxifene (60 mg per day).

Administration, Intravaginal↗

PubMed1989

Atrophic macular degeneration. Rate of spread of geographic atrophy and visual loss.

The authors studied 50 eyes with atrophic (dry) macular degeneration (geographic atrophy of age-related macular degeneration [GAMD], in 50 consecutive patients for 2 to 6 years (average, 3.4 years). There were 35 women and 15 men ranging in age from 60 to 89 years (average, 73 years). The areas of atrophy tended to follow the disappearance or flattening of soft drusen, pigment epithelial detachment, or reticular mottling of the retinal pigment epithelium. The atrophic areas were multifocal in 20 of the 50 eyes. Atrophy of the retinal pigment epithelium was followed by atrophy of the choriocapillaris. The atrophic areas tended to expand (average rate in one direction, 139 microns per year) and cause gradual loss of central visual acuity. The rate of significant visual loss (from 20/50 or better to 20/100 or worse) was 8% of eyes per year. There was a tendency toward resistance of the spread of atrophy into the fovea. The atrophy tended to expand faster in patients under age 75 and slower in patients aged 75 and over. Subretinal neovascularization developed in ten of the 50 eyes.

Aged↗

PubMedDate not supplied

Association between blood pressure levels over time and brain atrophy in the elderly.

The relation between blood pressure level and degree of global brain atrophy is equivocal. We evaluated past and present blood pressure levels and change in blood pressure over 20 years in relation to the degree of cortical atrophy on magnetic resonance imaging (MRI). In 1995-1996, we measured blood pressure and performed MRI in 1077 nondemented elderly (age 60-90 years). For 513 of these, we had information on a blood pressure level 20 years before. The degree of cortical atrophy was semi-quantitatively scored (range 0-15). In late life, a high (>/=90 mmHg) and low (<65 mmHg) diastolic blood pressure were associated with more cortical atrophy than a diastolic blood pressure level between 65-74 mmHg (adjusted difference 0.60 units (95% confidence interval (CI), 0.18-1.02) and 0.77 units (0.28-1.25), respectively). Persons whose diastolic blood pressure had declined more than 10 mmHg over 20 years had more cortical atrophy than those with stable blood pressure levels (adjusted difference 0.53 units, 0.05-1.02). Both high and declining diastolic blood pressure levels are associated with more global brain atrophy on MRI.

Aged↗