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PubMed2001

Verbal retention lateralizes patients with unilateral temporal lobe epilepsy and bilateral hippocampal atrophy.

PURPOSE: To examine the lateralization utility of preoperative verbal retention in patients with and without bilateral hippocampal atrophy. METHODS: The sample consisted of 74 patients with EEG-defined unilateral temporal lobe epilepsy (TLE) who had also undergone volumetric magnetic resonance imaging (MRI). Verbal retention was operationalized by the Logical Memory percentage retention subtest (LM%) of the Wechsler Memory Scale. Patients were divided into groups with (a) bilaterally normal hippocampal volumes, (b) unilateral atrophy, or (c) bilateral atrophy. Two different thresholds (empirically derived vs. normative) were used to lateralize on the basis of LM%. LM% lateralization was then examined by group using chi2, sensitivity, positive predictive values, and odds ratios. Analyses were also conducted separately in the subset of patients who were seizure free after surgery. RESULTS: Mean LM% performance was significantly lower in patients with left versus right TLE in the subset with bilateral hippocampal atrophy (p = 0.018), but not in patients with a normal MRI (p = 0.918) or unilateral atrophy (p = 0.087). The odds of a correct lateralization by LM% increased from 1.67 in patients with normal MRI to 36.11 in patients with bilateral hippocampal atrophy. The power of a right and left lateralization prediction by LM% was 100% and 75%, respectively, in patients with bilateral hippocampal atrophy. Similar results were obtained when analysis was restricted to patients who were seizure free after surgery. CONCLUSIONS: Preoperative verbal retention as measured by LM% may provide meaningful lateralization information in patients who are difficult to lateralize via MRI.

Adolescent↗

PubMed1998

Nutritional status of newly diagnosed celiac disease patients before and after the institution of a celiac disease diet--association with the grade of mucosal villous atrophy.

No systematic studies have been carried out on the association of nutritional status with the severity of mucosal villous atrophy in newly diagnosed celiac disease patients. We examined the nutritional status of 40 adult patients with newly diagnosed celiac disease classified according to the grade of villous atrophy: partial, subtotal, and total. Nutritional status was determined by food records as well as by anthropometric and biochemical measurements. Anthropometric results did not differ among the three atrophy groups, but serum ferritin and erythrocyte folate were lower in patients with total villous atrophy than in the other groups. Most of the abnormal biochemical values were normalized during 1 y of a gluten-free diet; villous atrophy healed concomitantly. To conclude, patients with total mucosal villous atrophy at diagnosis had low erythrocyte folate and serum ferritin values, but no other major differences were found in nutritional status among celiac disease patients with different grades of villous atrophy.

Adolescent↗

PubMed2003

Homocysteine and brain atrophy on MRI of non-demented elderly.

Patients with Alzheimer's disease have higher plasma homocysteine levels than controls, but it is uncertain whether higher plasma homocysteine levels are involved in the early pathogenesis of the disease. Hippocampal, amygdalar and global brain atrophy on brain MRI have been proposed as early markers of Alzheimer's disease. In the Rotterdam Scan Study, a population-based study of age-related brain changes in 1077 non-demented people aged 60-90 years, we investigated the association between plasma homocysteine levels and severity of hippocampal, amygdalar and global brain atrophy on MRI. We used axial T(1)-weighted MRIs to visualize global cortical brain atrophy (measured semi-quantitatively; range 0-15) and a 3D HASTE (half-Fourier acquisition single-shot turbo spin echo) sequence in 511 participants to measure hippocampal and amygdalar volumes. We had non-fasting plasma homocysteine levels in 1031 of the participants and in 505 of the participants with hippocampal and amygdalar volumes. Individuals with higher plasma homocysteine levels had, on average, more cortical atrophy [0.23 units (95% CI 0.07-0.38 units) per standard deviation increase in plasma homocysteine levels] and more hippocampal atrophy [difference in left hippocampal volume -0.05 ml (95% CI -0.09 to -0.01) and in right hippocampal volume -0.03 ml (95% CI -0.07 to 0.01) per standard deviation increase in plasma homocysteine levels]. No association was observed between plasma homocysteine levels and amygdalar atrophy. These results support the hypothesis that higher plasma homocysteine levels are associated with more atrophy of the hippocampus and cortical regions in elderly at risk of Alzheimer's disease.

Aged↗

PubMed2005

Interleukin 1B proinflammatory genotypes protect against gastro-oesophageal reflux disease through induction of corpus atrophy.

BACKGROUND AND AIMS: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease (GORD) is controversial but it is accepted that GORD is associated with increased exposure to gastric acidity. The proinflammatory interleukin (IL)-1B polymorphisms increase the risk of hypochlorhydria and gastric atrophy. We examined the association between proinflammatory cytokine gene polymorphisms, presence of gastric atrophy, and risk of GORD in H pylori positive and negative subjects in Japan. METHODS: We studied 320 consecutive dyspeptic patients without peptic ulcers or cancers. GORD symptoms were scored using the Carlsson-Dent questionnaire and erosive oesophagitis was assessed endoscopically. H pylori infection was diagnosed by urea breath test, histological examination, and serology. Gastric atrophy was assessed histologically, and polymorphisms in the IL-1B, IL-10, and tumour necrosis factor alpha (TNF-A) genes were genotyped. RESULTS: Two hundred and eight patients were H pylori positive and 112 were negative. One hundred and eight (34%) were found to have erosive oesophagitis by endoscopic criteria (grade A: 78; grade B: 23; grade C: 6; grade D: 1). Erosive oesophagitis and GORD symptoms were significantly more common in H pylori negative compared with H pylori positive subjects (p<0.05). H pylori positive subjects were more likely to have corpus gastric atrophy than H pylori negative subjects (p<0.001). Among H pylori positive patients, those without erosive oesophagitis or GORD symptoms were significantly more likely to have corpus atrophy than subjects with erosive oesophagitis or GORD symptoms (p<0.05). Among H pylori positive patients, subjects homozygous for the proinflammatory allele IL-1B-511T had a significantly lower risk of erosive oesophagitis (odds ratio (OR) 0.06 (95% confidence interval (CI) 0.006-0.51); p=0.01) and GORD symptoms (OR 0.10 (95% CI 0.01-0.85); p=0.04) compared with those homozygous for the -511C allele, while none of the two other proinflammatory cytokine gene polymorphisms had significant correlations with erosive oesophagitis or GORD symptoms. CONCLUSIONS: A proinflammatory IL-1B genotype is associated with increased risk of atrophy and decreased risk of GORD in H pylori infected subjects in Japan. These data indicate that in some genetically predisposed subjects, H pylori infection may protect against GORD through induction of gastric atrophy.

Adult↗

PubMedDate not supplied

Plasma ghrelin concentration correlates with the levels of serum pepsinogen I and pepsinogen I/II ratio--a possible novel and non-invasive marker for gastric atrophy.

BACKGROUND/AIMS: Ghrelin, a novel growth-hormone-releasing peptide, has been reported to be localized mainly in the A-like cells in the gastric fundic mucosa. With the extension of gastric inflammation caused by H. pylori infection, gastric mucosal atrophy extends from the antrum to the corpus, which is the predominant site of localization of the ghrelin-producing A-like cells. The present study was designed to investigate the correlation between the plasma ghrelin levels and the extent of gastric mucosal atrophy in patients with chronic gastritis caused by H. pylori infection. METHODOLOGY: Sixty-nine patients with dyspeptic symptoms were enrolled for the study. Of these, 41 patients were confirmed to become negative for H. pylori after therapy to eradicate the infection. The other 28 patients were diagnosed as positive for H. pylori infection. Blood samples were collected from all the patients after 12 hours of fasting, before upper gastrointestinal endoscopy was performed. The plasma levels of total and active ghrelin, as well as the serum levels of pepsinogen I (PGI) and pepsinogen II (PGII) were measured by radioimmunoassay. Based on endoscopic assessment, the atrophic changes in the gastric mucosa were classified as open-type atrophy or closed-type atrophy. RESULTS: There were no significant differences in the plasma total and active ghrelin levels between H. pylori-positive and H. pylori-eradicated (negative) patients. The serum levels of PGI correlated well with the plasma levels of total ghrelin (p<0.01, r=0.38) and active ghrelin (p<0.05, r=0.29). The ratio of serum PGI to PGII level (PG I/II ratio) also correlated well with the plasma level of total ghrelin (p<0.05. r=0.31) and active ghrelin (p<0.05, r=0.27). The plasma levels of total as well as active ghrelin were significantly decreased in patients with low PG levels as compared with those in patients with high PG levels (PGI > 70 ng/mL or PGI/II >3.0). The plasma levels of total as well as active ghrelin were also significantly decreased in patients with endoscopically diagnosed open-type atrophy as compared with those in patients with endoscopically diagnosed closed-type atrophy (p < 0.01), especially in the H. pylori-eradicated cohorts. CONCLUSIONS: The plasma levels of ghrelin, which correlated well with the serum levels of PGI as well as the PGI/II ratio, decreased with increasing extent of gastric mucosal atrophy, suggesting that it could be a potentially useful non-invasive marker for chronic atrophic gastritis.

Biomarkers↗

PubMed1990

[Atrophy of the mandible and maxilla as complication of treatment and healing of jaw fractures].

The authors discuss in the light of literature data the causes of bone atrophy and report two own cases of extensive atrophy of the mandible and atrophy of the maxilla developed during treatment of their fractures. Parallel mandibular atrophy in a patient aged 67 years was observed 3 years after surgical union of fractured fragments of the edentulous mandible with metal plates. The cause of atrophy is related by the authors to prolonged malnutrition of the patient who had partial gaestrectomy 24 years earlier, and his failure to observe the suggested mandible immobilization during the required length of time. Considerable degree of maxilla atrophy in a 34-year-old man developed during treatment of a Le Fort III maxilla fracture. The atrophy affected mainly the apical base of the alveolar process, and it was observed 4 months after fracture. The cause was not systematic, prolonged without informing the stomatologist, and excessive traction was exerted by the rubber band in the chin-sling used for the treatment of the fracture. The treatment used in this case permitted to restore in the maxilla the proportions of bone structures approaching the normal ones.

Adult↗

PubMed1994

[A case of progressive hemifacial atrophy associated with immunological abnormalities].

We reported a case of progressive hemifacial atrophy associated with immunological abnormalities. This patient, a 35-year-old woman, had a history of high fever of unknown etiology associated with anemia and leukocytopenia at the age of 19. Eight months later, right hemifacial atrophy, alopecia and partial lipodystrophy of the right upper arm were developed. And the progression had stopped in the latter twenties. At the age of 35, she visited our hospital because of the hemifacial atrophy. Physical examination revealed right hemifacial atrophy, large alopecia at parietal and right temporal region, and partial lipodystrophy of the right upper arm. CT, MRI and ultrasound tomography of the head and the arm showed skin and scalp atrophy, temporal muscle atrophy and decrease of subcutaneous soft tissues. There was no autonomic dysfunction. Serum IgG was increased, and RA factor, anti-nuclear antibody, anti-DNA antibody and LE cell were positive. In this case, immunological abnormalities were considered to be related to the pathogenesis of hemifacial atrophy.

Adult↗

PubMed1994

Is cranial computerized tomography useful in the diagnosis of multiple system atrophy?

Cranial computer tomographic (CT) images of 33 patients with multiple system atrophy (MSA) and of 40 age-matched controls were blindly analyzed by two neuroradiologists. All patients had autonomic dysfunction, all but one had parkinsonism, and 13 had cerebellar signs. The scans were judged entirely normal in 21%. Moderate or severe infratentorial atrophy was found in 42%. Cerebellar atrophy was present in 39%, and pontine atrophy was present in 18%. Of the 13 patients with cerebellar signs, only eight had cerebellar atrophy. Of the 20 patients without cerebellar signs, five had cerebellar atrophy. Supratentorial involvement was much less common and less severe. Thus, CT demonstrated system involvement that was not evident clinically in five of 33 cases (15%). However, in all five the clinical diagnosis was already evident from the presence of both autonomic and pyramidal signs in addition to parkinsonism. We conclude that CT imaging is of limited diagnostic use in individual patients with MSA.

Adult↗

PubMedDate not supplied

Electro-oculogram in multiple system and late onset cerebellar atrophies.

The present investigation uses electrooculogram to evaluate multiple system atrophy (MSA) and late onset cerebellar atrophies (LOCAs), both idiopathic (ILOCA) and late onset autosomal dominant cerebellar ataxia (ADCA). Forty cases were clinically examined using scales for cerebellar, pyramidal, parkinsonian, mental status and neuroimaging quantitative evaluations. The patients were classified into three groups: olivopontocerebellar atrophy (OPCA), striatonigral degeneration (SND), Shy-Drager syndrome (SDS), and LOCA. We have used direct current electro-oculography in order to establish their validity in making the diagnosis. Cerebellar signs were significantly correlated with impaired VOR-fix gain and OKN, abnormalities of saccades, and reduced smooth pursuit gain (p < 0.05). Pons atrophy was significantly correlated with impaired VOR-fix gain (p < 0.01), abnormalities of saccades (p < 0.01), and reduced smooth pursuit gain (p < 0.05). Cerebellar hemisphere atrophy was significantly correlated only with impaired VOR-fix gain (p < 0.05), and medulla oblongata atrophy only with abnormalities of saccades (p < 0.05). Gaze-evoked nystagmus was found in 42.8% of patients with OPCA, and only in 14.2% with SND, but was not found in LOCA patients (t test, p < 0.05). In patients with OPCA, the combination of gaze-evoked nystagmus, abnormalities of sinusoidal VOR and reduced OKN gain measurements was very frequent, while infrequent in both LOCA (Fisher's exact test, p < 0.05) and SND subjects (p < 0.01). SDS also showed abnormalities of the oculomotor system.

Adult↗

PubMed1998

Essential iris atrophy, pigment dispersion, and glaucoma in DBA/2J mice.

PURPOSE: To characterize ocular abnormalities associated with iris atrophy in DBA/2J mice and to determine whether mice of this strain develop elevated intraocular pressure (IOP) and glaucoma. METHODS: Different approaches, including slit-lamp biomicroscopy, ophthalmoscopic examination, ultrasound backscatter microscopy, and histology were used to examine the eyes of DBA/2J mice ranging from 2 to 30 months old. IOP was measured in DBA/2J mice of different ages. RESULTS: DBA/2J mice were found to develop pigment dispersion, iris transillumination, iris atrophy, anterior synechias, and elevated IOP. IOP was elevated in most mice by the age of 9 months. These changes were followed by the death of retinal ganglion cells, optic nerve atrophy, and optic nerve cupping. The prevalence and severity of these lesions increased with age. Optic nerve atrophy and optic nerve cupping was present in the majority of mice by the age of 22 months. CONCLUSIONS: DBA/2J mice develop a progressive form of secondary angle-closure glaucoma that appears to be initiated by iris atrophy and the associated formation of synechias. This mouse strain represents a useful model to evaluate mechanisms of pressure-related ganglion cell death and optic nerve atrophy, and to evaluate strategies for neuroprotection.

Aging↗

PubMed1999

Multiple system atrophy: the putative causative role of environmental toxins.

BACKGROUND: Whereas a number of studies have investigated the putative role of environmental toxins in the pathogenesis of idiopathic Parkinson disease, the possibility of such a role in multiple system atrophy has received little attention. DESIGN AND SETTING: Review of records of patients examined in the Parkinson's Disease Center and Movement Disorder Clinic, Baylor College of Medicine, Houston, Tex, from July 1, 1977, to February 4, 1998. PATIENTS: We reviewed 100 consecutive medical records of patients who satisfied the diagnostic criteria for multiple system atrophy formulated by the Consensus Committee of the American Autonomic Society and the American Academy of Neurology. INTERVENTION: The type and amount of toxin exposure were verified by history and examination of records whenever possible. Severity of parkinsonism was assessed by clinical rating scales. MAIN OUTCOME MEASURE: Development of multiple system atrophy after environmental toxin exposure. RESULTS: Eleven patients had a notable history of heavy exposure to environmental toxins. One patient with multiple system atrophy confirmed by postmortem evaluation was exposed to high concentrations of malathion, diazinon, and formaldehyde, while the other patients with multiple system atrophy had well-documented high exposures to agents including n-hexane, benzene, methyl isobutyl ketone, and pesticides. The case studied pathologically demonstrated extensive advanced glial changes, including glial cytoplasmic inclusions in deep cerebellar white matter, brainstem, cortex (superior frontal, insula) and putamen, with notable cell loss and depigmentation of the substantia nigra and locus ceruleus. CONCLUSION: While many studies report a possible role of environmental toxins in Parkinson disease, such a role is even more likely in multiple system atrophy, as this is a sporadic disease.

Environmental Pollutants↗

PubMed2001

The effect of brain atrophy on cerebral hypometabolism in the visual variant of Alzheimer disease.

BACKGROUND: Brain glucose metabolic rates measured by positron emission tomography can be more affected by partial volume effects in Alzheimer disease (AD) than in healthy aging because of disease-associated brain atrophy. OBJECTIVE: To determine whether the distinct distribution of cerebral metabolic lesions in patients with the visual variant of AD (AD + VS) represents a true index of neuronal/synaptic dysfunction or is the consequence of brain atrophy. SETTING: Government research hospital. DESIGN: Resting cerebral metabolic rate for glucose was measured with positron emission tomography in a cross-sectional study of AD and AD + VS groups and in healthy control subjects. Segmented magnetic resonance images were used to correct for brain atrophy. PATIENTS: Patients with AD + VS had prominent visual and visuospatial symptoms. There were 15 patients with AD, 10 with AD + VS, and 37 age-matched control subjects. MAIN OUTCOME MEASURE: Measurement of the rate of cerebral glucose metabolism. RESULTS: Before atrophy correction, the AD + VS group, compared with the control subjects, showed hypometabolism in primary and extrastriate visual areas and in parietal and superior temporal cortical areas. Compared with the AD group, the AD + VS group showed hypometabolism in visual association areas. After atrophy correction, hypometabolism remained significantly different between patients and controls and between the 2 AD groups. CONCLUSIONS: The reductions in cerebral hypometabolism represent a true loss of functional activity and are not simply an artifact caused by brain atrophy. The different patterns of hypometabolism indicate the differential development of the lesions between the AD and AD + VS groups.

Aged↗

PubMed2006

Conversion of mild cognitive impairment to Alzheimer disease predicted by hippocampal atrophy maps.

BACKGROUND: While most patients with mild cognitive impairment (MCI) transition to Alzheimer disease (AD), others develop non-AD dementia, remain in the MCI state, or improve. OBJECTIVE: To test the following hypotheses: smaller hippocampal volumes predict conversion of MCI to AD, whereas larger hippocampal volumes predict cognitive stability and/or improvement; and patients with MCI who convert to AD have greater atrophy in the CA1 hippocampal subfield and subiculum. DESIGN: Prospective longitudinal cohort study. SETTING: University of California-Los Angeles Alzheimer's Disease Research Center. PATIENTS: We followed up 20 MCI subjects clinically and neuropsychologically for 3 years. MAIN OUTCOME MEASURE: Baseline regional hippocampal atrophy was analyzed with region-of-interest and 3-dimensional hippocampal mapping techniques. RESULTS: During the 3-year study, 6 patients developed AD (MCI-c), 7 remained stable (MCI-nc), and 7 improved (MCI-i). Patients with MCI-c had 9% smaller left and 13% smaller right mean hippocampal volumes compared with MCI-nc patients. Radial atrophy maps showed greater atrophy of the CA1 subregion in MCI-c. Patients with MCI-c had significantly smaller hippocampi than MCI-i patients (left, 24%; right, 27%). Volumetric analyses showed a trend for greater hippocampal atrophy in MCI-nc relative to MCI-i patients (eg, 16% volume loss). After permutation tests corrected for multiple comparison, the atrophy maps showed a significant difference on the right. Subicular differences were seen between MCI-c and MCI-i patients, and MCI-nc and MCI-i patients. Multiple linear regression analysis confirmed the group effect to be highly significant and independent of age, hemisphere, and Mini-Mental State Examination scores at baseline. CONCLUSIONS: Smaller hippocampi and specifically CA1 and subicular involvement are associated with increased risk for conversion from MCI to AD. Patients with MCI-i tend to have larger hippocampal volumes and relative preservation of both the subiculum and CA1.

Aged↗

PubMed2006

Regional gray matter atrophy in early primary progressive multiple sclerosis: a voxel-based morphometry study.

BACKGROUND: Gray matter (GM) atrophy has been reported in multiple sclerosis (MS). However, little is known about its regional distribution. OBJECTIVE: To investigate the regional distribution of GM atrophy in clinically early primary progressive MS (PPMS). DESIGN AND PATIENTS: Thirty-one patients with PPMS within 5 years of symptom onset (mean age, 43.2 years; median Expanded Disability Status Scale score, 4.5) and 15 healthy control subjects (mean age, 43.7 years) were studied. All subjects underwent a 3-dimensional inversion-recovery fast spoiled gradient-recalled echo sequence that was repeated after 1 year in patients only. Magnetic resonance images underwent an optimized voxel-based morphometric analysis that segments magnetic resonance data volumes in a normalized space and quantifies tissue atrophy on a voxel-by-voxel basis. A lesion mask was created for each patient and used in normalization and segmentation steps to minimize bias from lesions. A multisubject design was used in the cross-sectional study to compare patients with PPMS and controls. A 1-way analysis of variance (within-subjects) design was used in the longitudinal study. RESULTS: At baseline, patients with PPMS displayed bilateral thalamic atrophy compared with controls. In addition, a significant association between lesion load and decreased GM volume was found for the thalami. Loss of GM in the putamen, caudate, thalami, and cortical and infratentorial areas was observed in patients after 1 year of follow-up. CONCLUSIONS: Atrophy is most obvious in deep GM in clinically early PPMS. This may reflect increased sensitivity of these regions to neurodegeneration. Cortical and infratentorial atrophy developed as the disease evolved.

Adult↗

PubMed2005

Recurrence of retinal pigment epithelial changes after macular translocation with 360 degrees peripheral retinectomy for geographic atrophy.

OBJECTIVE: To assess the prevalence of recurrence of macular geographic atrophy (GA) of the retinal pigment epithelium (RPE) after macular translocation with 360 degrees retinectomy (MT360) in one institution. METHODS: A retrospective review of all cases of GA that were treated with MT360 in 1 institution. Demographic and clinical data including the duration of preoperative visual loss, preoperative and postoperative visual acuity, and the prevalence of postoperative foveal RPE atrophy were recorded for these patients, and these data were compared with similar data from patients who underwent MT360 for neovascular age-related macular degeneration (AMD) as part of the prospective Duke Macular Translocation Study, Duke University Eye Center, Durham, NC. RESULTS: Four eyes in 4 patients with GA secondary to AMD underwent MT360 and were compared with 63 eyes in 63 patients who underwent MT360 for neovascular AMD as part of the Duke Macular Translocation Study. The mean duration of preoperative visual loss was higher in the GA group (11.3 months) than in the neovascular AMD group (1.7 months) (P = .08). The prevalence of postoperative foveal RPE atrophy was significantly higher in the GA group (n = 3; 75.0%) than in the neovascular AMD group (n = 5; 8.3%) (P<.01); in the GA group, this corresponded to recurrence of the GA lesions. In contrast, the postoperative RPE atrophy seen in the neovascular AMD group was due to postoperative mechanical forces such as laser therapy or RPE tearing. There was no significant difference in the mean preoperative or postoperative visual acuity in either group. CONCLUSIONS: Subfoveal RPE atrophy can reoccur following MT360 in eyes with nonneovascular AMD and GA; RPE atrophy similar to this has not been found in a large consecutive series of patients with neovascular AMD after MT360. Further research is needed to assess if the potential for visual recovery in eyes with end-stage nonneovascular AMD is outweighed by the possibility of postoperative recurrence of GA.

Aged↗

PubMed2001

Absence of nasal mucosal atrophy with fluticasone aqueous nasal spray.

OBJECTIVE: To evaluate whether 1 year of continuous treatment with intranasal fluticasone propionate would lead to atrophy in the nasal mucosa compared with an active control, oral terfenadine. DESIGN: Prospective, randomized, multicenter, open-label, parallel-group study. SETTING: Two tertiary care academic institutions. PATIENTS: Seventy-five subjects older than 18 years with perennial allergic rhinitis. INTERVENTIONS: Patients received either fluticasone propionate aqueous nasal spray, 200 microg once daily, or terfenadine, 60 mg twice daily, for 1 year. Nasal biopsy specimens were obtained before and after 1 year of treatment and were evaluated for evidence of atrophy. MAIN OUTCOME MEASURES: Epithelial and collagen layer thickness of the nasal mucosa as assessed by light microscopy and the presence and degree of edema, and regularity of collagen fibrils as assessed by electron microscopy. Analyses were performed without knowledge of subject identity or treatment assignment. RESULTS: Neither fluticasone nor terfenadine treatment led to atrophy in the nasal mucosa by clinical or histologic observation. No significant changes from baseline were observed for any assessment of atrophy. In contrast to what would have been expected if atrophy were to occur, mean epithelial layer thickness in the fluticasone group significantly increased compared with terfenadine treatment (P = .03). CONCLUSIONS: Treatment with intranasal fluticasone for 1 year increases the thickness of the nasal epithelium as compared with a year's treatment with terfenadine and does not lead to atrophy in the nasal mucosa. The increased thickness in the fluticasone treatment may represent repair from epithelial damage caused by chronic allergic inflammation.

Administration, Intranasal↗

PubMed2002

Leukemia inhibitory factor is a mediator of Escherichia coli lipopolysaccharide-induced acute thymic atrophy.

Septic shock in animals and humans is associated with thymic atrophy and generalized lymphocyte apoptosis that impairs T cell responses. Injection of animals with E. coli lipopolysaccharide (LPS) mimics bacterial sepsis-induced thymic atrophy. Leukemia inhibitory factor (LIF) induces pituitary ACTH release in vivo, and LIF administration to mice induces acute thymic atrophy. We have investigated the role of LIF in LPS-induced thymic atrophy. LPS significantly elevated serum LIF within 1 h and induced thymic LIF mRNA within 6 h. Moreover, pretreatment of mice with anti-LIF antibody significantly reduced LPS-induced thymic atrophy. Using adrenalectomized mice and 17-day fetal thymic organ cultures treated with the steroidogenic enzyme inhibitor metyrapone, we demonstrated that LIF induced both systemic and intrathymic corticosteroid production. These data demonstrate systemic and intrathymic pathways of E. coli LPS-induced acute thymic atrophy mediated by LIF and corticosteroids.

Adrenal Cortex Hormones↗

PubMed2002

Accelerated hippocampal atrophy in Alzheimer's disease with apolipoprotein E epsilon4 allele.

Although apolipoprotein E epsilon4 is an established risk factor for Alzheimer's disease, its effect on the rate of progression of Alzheimer's disease remains unknown. The purpose of this longitudinal study was to elucidate whether the rate of hippocampal atrophy is a function of the apolipoprotein E genotypes and severity of disease. Fifty-five patients with probable Alzheimer's disease were the subjects. The annual rate of hippocampal atrophy was determined by using magnetic resonance imaging repeated at a 1-year interval. On a two-way analysis of variance, the effect of the apolipoprotein E epsilon4 allele on hippocampal atrophy was significant, but neither the effect of severity nor the interaction term was significant. In further analysis with one-way analysis of variance, the mean annual rate of hippocampal atrophy was significantly different between the groups of patients with (9.76 +/- 4.27%) and without the apolipoprotein E epsilon4 allele (6.99 +/- 4.24%). Apolipoprotein E epsilon4 dose was significantly correlated with the rate of hippocampal atrophy (rs = 0.277, Spearman rank correlation coefficient), suggesting a gene dose effect. The involvement of the apolipoprotein E epsilon4 allele in the progression of hippocampal atrophy has implications for therapeutic approaches in Alzheimer's disease and should be taken into consideration in longitudinal studies including clinical drug trials.

Aged↗