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Human papillomavirus (HPV) in the postmenopausal age group is complex. Not only is there a more serious risk of disease progression because of decreased clearance of virus (1) and more [...], Context.--Human papillomavirus (HPV) in the postmenopausal age group is complex, with infected patients in this age group at increased risk of progressing to invasive disease and showing decreased clearance of the virus. Additionally, atrophic changes of the cervix can make histologic distinction of high-grade squamous intraepithelial lesions (HSILs) difficult. Objective.--To determine morphologic and ancillary testing characteristics of atrophy and HSIL in postmenopausal patients. Design.--Files of patients at least 65 years of age were examined, with 81 patients (109 cases [53 benign, 56 HSIL]) included in the study. Results of morphology, immunostaining (p16 and Ki-67), and HPV RNA in situ hybridization (ISH) were noted on all cases with available material. Results.--Atrophy was present in 96 of 109 cases (88%) overall. Coarse nuclear chromatin was noted in none of the benign cases, in 19 of 30 HSIL biopsies (63%), and in 24 of 26 HSIL excisions (92%). All benign cases were negative for p16 and ISH. In the HSIL cases, 45 of 53 (89%) were positive for p16, and of cases with sufficient tissue for ISH, 44 of 45 (98%) were positive. Of the ISH/p16 discordant cases (n = 7), most were p16 negative/ISH positive (6 of 7; 86%), whereas 1 of 7 (14%) was p16 positive and ISH negative. A majority of HSIL cases showed near-fullthickness elevation of Ki-67 (45 of 54; 83%), whereas mitotic figures were less elevated. Conclusions.--In postmenopausal patients with HSIL, mitotic activity is not reliably elevated, but Ki-67 is consistently high. ISH is a more direct method of HPV detection and should be considered in cases where morphology and immunolabeling show discordance. doi: 10.5858/arpa.2021-0426-OA

Vulvovaginal atrophy (WA) is a common and underreported condition associated with decreased estrogenization of the vaginal tissue. Symptoms include dryness, irritation, soreness, and dyspareunia with urinary frequency, urgency, and urge [...]

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1177/1051228405279988 Byline: Kazuo Abe (1), Tachio Hikita (1), Masaru Yokoe (1), Masahito Mihara (1), Saburo Sakoda (1) Keywords: Multiple system atrophy (MSA); MRI Abstract: ABSTRACT Patients with multiple system atrophy (MSA) may show the 'cross' sign in the pontine base that has been considered as an expression of the degeneration of pontine neurons and transverse pontocerebellar fibers. However, correlations between pontine base atrophy and existence of 'cross' sign have not been fully investigated. The authors studied 68 patients with MSA (47 MSA-C [predominantly cerebellar ataxia], 21 MSA-P [predominantly parkinsonism], mean [[+ or -]SD ] 58.7 [+ or -] 10.9 years). T1-weighted (T1W) sagittal and axial images and T2-weighted (T2W) axial images were obtained for all patients and controls. To measure the areas of pontine basis and cerebellar vermis, the authors used midsagittal T1W images and analyzed a bit map transformed on a computer. They classified atrophy in the pontine base into 3 grades. There is significant correlation between atrophies of pontine base and existence of the cross sign. All patients with a smaller area of pontine base 2 standard deviations below those of normal controls had the cross sign. This supports that existence of the cross sign depends only on the extent of pontine base atrophies. Author Affiliation: (1)From the Department of Neurology, Graduate School of Medicine, Osaka University. Article History: Received October 8, 2004, and in revised form April 4, 2005. Accepted for publication April 8, 2005. Article note: Address correspondence to Dr Kazuo Abe, D-4, Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail: abe@neurol.med.osaka-u.ac.jp.

Multiple system atrophy (MSA) is a fatal neuro-degenerative disorder presenting with autonomic failure-and motor impairment, primarily comprising L-dopa-resistant parkinsonism but occasionally involving cerebellar ataxia. These features result from progressive multisystem neuronal loss that is associated with oligodendroglial [alpha]-synuclein inclusions. The growing number of animal models for MSA reflects the search for a preclinical test-bed for elucidating MSA pathogenesis and for developing novel therapeutic interventions. Here, the currently available MSA animal models will be reviewed and leads for future research will be identified.

The case of a 79-year-old woman is evaluated in a neurology clinic because of difficulty walking and cognitive change. The diagnosis and treatment of the disease is presented. The issue of advance directives with regard to life-sustaining treatment with the patient after the diagnosis of multiple-system atrophy is discussed.

Background: Formal laboratory testing of autonomic function is reported to distinguish between patients with Parkinson's disease and those with multiple system atrophy (MSA), but such studies segregate patients according to [...]

The 3 most common pathologic diagnoses in neurodegenerative disorders are Alzheimer disease (AD), dementia with Lewy bodies (DLB or LBD), and frontotemporal lobar degeneration (FTLD). Almost 20 years ago, Mirra [...], Context.--Autopsy evaluation of the brain of a patient with frontotemporal dementia (FTD) can be daunting to the general pathologist. At some point in their training, most pathologists learn about Pick disease, and can recognize Pick bodies, the morphologic hallmark of Pick disease. Pick disease is a type of frontotemporal lobar degeneration (FTLD), the general category of pathologic process underlying most cases of FTD. The 2 major categories of pathologic FTLD are tauopathies (FTLD-tau) and ubiquitinopathies (FTLD-U). Pick disease is one of the FTLD-tau subtypes and is termed FTLD-tau (PiD). Objective.--To 'demystify' FTLDs, and to demonstrate that subtypes of FTLD-tau and FTLD-U can be easily determined by following a logical, stepwise, histochemical, and immunohistochemical investigation of the FTD autopsy brain. Data Sources.--Previously published peer-reviewed articles. Conclusions.--The hope is that this article will be a useful reference for the general pathologist faced with performing a brain autopsy on a decedent with frontotemporal dementia. (Arch Pathol Lab Med. 2013;137:314-325; doi: 10.5858/arpa.2012-0075-RA)

Atrophic gastritis is seen as the result of long standing Helicobacter pylon infection and recent studies have shown that circulating IgG antibodies to CagA are associated with this condition. Gastric [...]

A 21-year-old man with a history of hemochromatosis and chronic heart failure presented with a 6-month history of weight loss (13.5 kg), fatigue, and generalized weakness. On physical examination, he [...]