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Pathological Study (pathological + study)
Selected AbstractsPathological study of idiopathic portal hypertension with an emphasis on cause of death based on records of Annuals of Pathological Autopsy Cases in JapanJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2007Seiko Sawada Abstract Background and Aim:, Idiopathic portal hypertension (IPH) is thought to be benign if bleeding gastroesophageal varices can be controlled or prevented. A recent autopsy of a woman with IPH who died of hemorrhagic intestinal infarction related to mesenteric thrombosis prompted the authors to examine the terminal antemortem features and causes of death of IPH. Methods:, Autopsy cases registered as IPH from 1986 to 1997 were surveyed in the records of the Annuals of Pathological Autopsy Cases in Japan, with permission from the Japanese Society of Pathology. The records of 65 of these cases were collected and examined pathologically. Results:, It was found that the most frequent cause of death in these cases was (i) bacterial infection (20 cases). The next three causes of death were directly or indirectly related to hepatic disease or its altered portal hemodynamics as follows: (ii) progressive hepatic failure (16 cases); (iii) massive hemorrhage from ruptured gastroesophageal varices (11 cases); and (iv) hemorrhagic intestinal infarction due to mesenteric venous thrombosis (5 cases). Although portal venous thrombosis was closely associated with (iv), (ii) and (iii) seemed not to be associated with portal venous thrombosis. In addition, intracranial hemorrhage and other heterogeneous factors were identified as the cause of death in five cases and eight cases, respectively. Conclusion:, These results suggest that progressive hepatic failure and intestinal hemorrhagic infarction should be considered in addition to rupture of gastroesophageal varices when monitoring patients with IPH. Clinicians should be also aware of severe bacterial infection and intracranial hemorrhage as a fatal complication of IPH. [source] Parasellar Solitary Fibrous Tumor of Meninges: Magnetic Resonance Imaging Features With Pathologic CorrelationJOURNAL OF NEUROIMAGING, Issue 3 2004Chung-Ping Lo MD ABSTRACT Solitary fibrous tumor (SFT) is a benign mensenchymal neoplasm of spindle-cell origin. The authors report the case of a 50-year-old man with SFT arising from the meninges of the left parasellar region with cavernous sinus involvement. The tumor was demonstrated isointense on T1-weighted and heterogeneously hypointense on T2-weighted magnetic resonance imaging (MRI) with strong contrast enhancement. The preoperative MRI diagnosis was meningioma or hemangiopericytoma. Pathological study revealed an SFT that stained positive immuno-histochemically for CD34 and vimentin. [source] Clinical,Pathological study of levodopa complicationsMOVEMENT DISORDERS, Issue 2 2002Azi H. Rajput FRCPC Abstract We sought to determine the continued benefit and the pattern of motor complications of long-term levodopa treatment in Parkinson's disease. Patients were evaluated between 1968 and 1996. Only those who had an adequate levodopa trial and in whom autopsy revealed Lewy body Parkinson's disease were included. Total levodopa and mean daily dose were calculated in each case. Dyskinesia, wearing-off and on-off were collectively classified as motor adverse effects and reported as cumulative incidence. Forty-two patients (male, 30; female, 12) with mean 15.9 years of illness and 9.1 years follow-up received on average 500-mg levodopa daily over 9.8 years. Seventeen of 21 patients assessed during the last 18 months of life reported some motor benefit. Adverse effects were seen in 71.4% of patients. The most common was dyskinesia, in 61.9%; wearing-off in 35.7%; and on-off in 16.7% of patients. The earliest adverse effect was dyskinesia and the last to emerge was on-off. Isolated dyskinesia was seen in 35.7% and wearing-off in 7.1% of patients; 15.5% of patients developed dyskinesia after 2.6 years and 31% after 6.4 years on levodopa. We concluded that levodopa benefit declined and adverse effects increased with time. Dyskinesia was the earliest and the most common isolated adverse effect. © 2002 Movement Disorder Society. [source] Prenatal Marfan syndrome: report of one case and review of the literaturePRENATAL DIAGNOSIS, Issue 8 2006K. R. M. Lopes Abstract Objectives Our objective was to describe the features of prenatal Marfan syndrome. Methods Doppler fetal echocardiograms were performed. The morphology and rhythm of the fetal heart were examined sequentially. Results The case was referred because of cardiomegaly and dilated great vessels. Sequential Doppler echocardiographic evaluation led to the diagnosis of prenatal Marfan syndrome. The main features are cardiomegaly, dysplastic atrioventricular valves with tricuspid regurgitation and dilated great vessels, which can be aneurysmal at their origin. The fetus died in utero at 39 weeks of gestation because of cardiac failure. Pathological study confirmed the Marfan habitus and complications. Molecular genetic study showed a de novo point mutation in exon 26 of the FBN1 gene. Conclusion We report a case of prenatal Marfan syndrome diagnosed by sequential evaluation of the cardiac signs, which are essential for prenatal diagnosis. The prognosis seems as poor as the neonatal one. The prenatal diagnosis is essential for adequate counselling. Copyright © 2006 John Wiley & Sons, Ltd. [source] Gnathodiaphyseal Dysplasia: A Syndrome of Fibro-Osseous Lesions of Jawbones, Bone Fragility, and Long Bone BowingJOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2001Mara Riminucci Abstract We report an unusual generalized skeletal syndrome characterized by fibro-osseous lesions of the jawbones with a prominent psammomatoid body component, bone fragility, and bowing/sclerosis of tubular bones. The case fits with the emerging profile of a distinct syndrome with similarities to previously reported cases, some with an autosomal dominant inheritance and others sporadic. We suggest that the syndrome be named gnathodiaphyseal dysplasia. The patient had been diagnosed previously with polyostotic fibrous dysplasia (PFD) elsewhere, but further clinical evaluation, histopathological study, and mutation analysis excluded this diagnosis. In addition to providing a novel observation of an as yet poorly characterized syndrome, the case illustrates the need for stringent diagnostic criteria for FD. The jaw lesions showed fibro-osseous features with the histopathological characteristics of cemento-ossifying fibroma, psammomatoid variant. This case emphasizes that the boundaries between genuine GNAS1 mutation-positive FD and other fibro-osseous lesions occurring in the jawbones should be kept sharply defined, contrary to a prevailing tendency in the literature. A detailed pathological study revealed previously unreported features of cemento-ossifying fibroma, including the participation of myofibroblasts and the occurrence of psammomatoid bodies and aberrant mineralization, within the walls of blood vessels. Transplantation of stromal cells grown from the lesion into immunocompromised mice resulted in a close mimicry of the native lesion, including the sporadic formation of psammomatoid bodies, suggesting an intrinsic abnormality of bone-forming cells. [source] The spectrum of cutaneous lesions in rheumatoid arthritis: a clinical and pathological study of 43 patientsJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2003C. M. Magro Introduction:, Rheumatoid arthritis (RA) is an idiopathic arthropathy syndrome that has a propensity to affect the small joints of the hands and feet with extra-articular manifestations comprising skin lesions, neuropathy, pericarditis, pleuritis, interstitial pulmonary fibrosis and a systemic polyarteritis nodosa (PAN)-like vasculitic syndrome. The most widely recognized skin lesion is the rheumatoid nodule. Other skin manifestations are poorly defined. Materials and methods:, Using a natural language search of the authors' outpatient dermatopathology databases, skin biopsies from 43 patients with RA were selected for retrospective analysis in an attempt to define the dermatopathological spectrum of RA and its clinical correlates. Results:, The biopsies were categorized by the dominant histologic pattern, recognizing that in most cases there were additional minor reaction patterns. Palisading and/or diffuse interstitial granulomatous inflammation was the dominant pattern seen in 21 patients; the lesions included nodules, plaques and papules with a predilection to involve skin over joints. Besides interstitial histiocytic infiltrates and variable collagen necrobiosis, these cases also showed interstitial neutrophilia, vasculitis and pauci-inflammatory vascular thrombosis. The dominant morphology in 11 other patients was vasculopathic in nature: pauci-inflammatory vascular thrombosis, glomeruloid neovascularization, a neutrophilic vasculitis of pustular, folliculocentric, leukocytoclastic or benign cutaneous PAN types, granulomatous vasculitis, and lymphocytic vasculitis and finally occlusive intravascular histiocytic foci for which the designation of ,RA-associated intravascular histiocytopathy' is proposed. Rheumatoid factor (RF) positivity and active arthritis were common in this group, with anti-Ro and anticardiolipin antibodies being co-factors contributing to vascular injury in some cases. Immunofluorescent testing in three patients revealed dominant vascular IgA deposition. In nine patients, the main pattern was one of neutrophilic dermal and/or subcuticular infiltrates manifested clinically as urticarial plaques, pyoderma gangrenosum and panniculitis. Conclusions:, The cutaneous manifestations of RA are varied and encompass a number of entities, some of which define the dominant clinical features, such as the rheumatoid papule or subcutaneous cords, while others allude to the histopathology, i.e. rheumatoid neutrophilic dermatosis. We propose a more simplified classification scheme using the adjectival modifiers of ,rheumatoid-associated' and then further categorizing the lesion according to the dominant reaction pattern. Three principal reaction patterns are recognized, namely extravascular palisading granulomatous inflammation, interstitial and/or subcuticular neutrophilia and active vasculopathy encompassing lymphocyte-dominant, neutrophil-rich and granulomatous vasculitis. In most cases, an overlap of the three reaction patterns is seen. Co-factors for the vascular injury that we believe are integral to the skin lesions of RA include RF, anti-endothelial antibodies of IgA class, anti-Ro and anticardiolipin antibodies. [source] Intramyocardial arterial narrowing in dogs with subaortic stenosisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 9 2004T. Falk Earlier studies have described intramyocardial arterial narrowing based on hyperplasia and hypertrophy of the vessel wall in dogs with subaortic stenosis (SAS). In theory, such changes might increase the risk of sudden death, as they seem to do in heart disease in other species. This retrospective pathological study describes and quantifies intramyocardial arterial narrowing in 44 dogs with naturally occurring SAS and in eight control dogs. The majority of the dogs with SAS died suddenly (n=27); nine had died or been euthanased with signs of heart failure and eight were euthanased without clinical signs. Dogs with SAS had significantly narrower intramyocardial arteries (P<0.001) and more myocardial fibrosis (P<0.001) than control dogs. Male dogs and those with more severe hypertrophy had more vessel narrowing (P=0.02 and P=0.02, respectively), whereas dogs with dilated hearts had slightly less pronounced arterial thickening (P=0.01). Arterial narrowing was not related to age, but fibrosis increased with age (P=0.047). Dogs that died suddenly did not have a greater number of arterial changes than other dogs with SAS. This study suggests that most dogs with SAS have intramyocardial arterial narrowing and that the risk of dying suddenly is not significantly related to the overall degree of vessel obliteration. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 43JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003S Amadio Study aim: the Ebf gene family has been implicated in several developmental processes, ranging from B-cell development to neuronal differentiation. As the murine Ebf2 gene is expressed in numerous sites of nervous system, Ebf2-null mice develop hypogonadotropic hypogonadism, due to defective migration of gonadotropin releasing hormone-synthesizing neurons, and a peripheral neuropathy as well. Therefore, we aimed to study whether electrophysiological tests would be able to detect abnormalities of peripheral nerve function. Methods: 2 groups of mice were studied, which consisted of 8 Ebf2-/- mice and 9 age-matched controls. The sciatic nerve was stimulated at the ankle and at the ischiatic notch; the compound motor action potential (cMAP) was recorded from the paw muscles with a pair of needle electrodes to measure the motor conduction velocity (MCV). Results: MCV mean values were lower in Ebf2-/-(21.8 m/sec; SD 2.9) than in controls (35.2 m/sec; SD 2.6) and the difference was significant (p < 0.001). The mean cMAP amplitude was also decreased in Ebf2-/-(6.2 mV; SD 2.7) as compared to controls (9.3 mV; SD 2.6, p < 0.05). Conclusions: electrophysiological tests demonstrated a sharp decrease of sciatic MCV in Ebf2-/- mouse, as consequence of defective axon sorting, segmental dysmyelination and axonal damage revealed by pathological study. [source] Corticobasal degeneration as cause of progressive non-fluent aphasia: Clinical, radiological and pathological study of an autopsy caseNEUROPATHOLOGY, Issue 6 2006Masaki Takao A Japanese male developed gradual loss of spontaneous speech at age 60. Three years later meaningful speech had deteriorated to the point that it had become restricted to monotonous utterances. Neuropsychological examination at age 62 showed that he had severe non-fluent aphasia. A brain MRI demonstrated mild cortical atrophy with ischemic lesions in the cerebral white matter. He was diagnosed as having primary progressive aphasia. At age 63, he was admitted to the hospital to reevaluate the neurological condition. Neurologic examination showed severe non-fluent aphasia, hyperreflexia, snout and sucking reflexes. No alien hand was observed. He was able to walk, dress, wash himself and use chopsticks as well as name real objects. At age 65, 99mTc-hexamethylpropyleneamine oxime single photon emission computed tomography (HMPAO-SPECT) revealed diffuse cerebral hypoperfusion that was particularly prominent in the left frontal lobe. An MRI showed progressive cortical atrophy with the definite atrophy of the left paracentral gyrus. The hippocampal formation and putamen were also atrophic. He died of pneumonia at age 67. The brain weighed 810 g with atrophy of the frontal lobe, globus pallidus, enlargement of the lateral ventricles and depigmentation of the substantia nigra. Microscopic examination showed severe neuronal loss and gliosis in the cerebral cortex, globus pallidus interna and substantia nigra. Ballooned neurons were observed in the cerebral cortex. Gallyas-Braak method revealed numerous astrocytic plaques and argentophilic threads in the cerebrum. Clinical diagnosis of corticobasal degeneration sometimes is difficult in individuals with atypical clinical presentations. More exact clinical and radiological criteria may warrant a diagnosis of corticobasal degeneration. [source] Pick's disease with Pick bodies combined with progressive supranuclear palsy without tuft-shaped astrocytes: A clinical, neuroradiologic and pathological study of an autopsied caseNEUROPATHOLOGY, Issue 3 2006Lu-Ning Wang We report clinical, neuroradiologic features, and neuropathologic findings of a 76-year-old man with coexistent Pick's disease and progressive supranuclear palsy. The patient presented with loss of recent memory, abnormal behavior and change in personality at the age of 60. The symptoms were progressive. Three years later, repetitive or compulsive behavior became prominent. About 9 years after onset, he had difficulty moving and became bed-ridden because of a fracture of his left leg. His condition gradually deteriorated and he developed mutism and became vegetative. The patient died from pneumonia 16 years after the onset of symptoms. Serial MRI scans showed progressive cortex atrophy, especially in the bilateral frontal and temporal lobes. Macroscopic inspection showed severe atrophy of the whole brain, including cerebrum, brainstem and cerebellum. Microscopic observations showed extensive superficial spongiosis and severe neuronal loss with gliosis in the second and third cortical layers in the frontal, temporal and parietal cortex. There were Pick cells and argyrophilic Pick bodies, which were tau- and ubiquitin-positive in neurons of layers II,III of the above-mentioned cortex. Numerous argyrophilic Pick bodies were observed in the hippocampus, especially in the dentate fascia. In addition, moderate to severe loss of neurons was found with gliosis and a lot of Gallyas/tau-positive globus neurofibrillary tangles in the caudate nucleus, globus pallidus, thalamus, substantia nigra, locus coeruleus and dentate nucleus. Numerous thorned-astrocytes and coiled bodies but no-tuft shaped astrocytes were noted in the basal ganglion, brainstem and cerebellar white matter. In conclusion, these histopathological features were compatible with classical Pick's disease and coexistence with progressive supranuclear palsy without tuft-shaped astrocytes. [source] | ||||||||||