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A survey of factors affecting the recruitment and retention of Medical Laboratory Scientific Officers in Pathology.

OBJECTIVE: To survey the perceptions and attitudes of Medical Laboratory Scientific Officer (MLSO) staff in Pathology to explain difficulties in recruitment and retention and inform attempts to solve the difficulties. DESIGN: Questionnaire to a defined group of MLSOs. SETTING: The Laboratory Medicine Directorate, Aberdeen Royal Infirmary. SUBJECTS: MLSO1 and MLSO2 staff currently or recently working in Pathology (histopathology) in Aberdeen. RESULTS: The survey return rate was 100%. Opportunities for career development in Pathology are poor, this being the worst feature of working in Pathology. Remuneration is poor and is a disincentive to remaining in the speciality. MLSOs feel undervalued in relation to other health care workers. Many have concerns about laboratory organisation, but find a sociable and supportive environment that provides job satisfaction. Staff seek work in other laboratories because of opportunities for promotion, learning new skills and increased pay, although pay in specialities other that Pathology is greater only because of shift working in these disciplines. There is a need to increase public awareness of MLSOs' central role in providing and maintaining excellence in Pathology services. CONCLUSION: MLSO staff have concerns about their career structure and salary scales. The responsibility of MSLOs in Pathology for quality assurance and managing MLAs is not recognised. These factors form a disincentive to working in Pathology laboratories and threaten our ability to staff the service and to maintain the turnover and quality of Pathology services. These issues require to be addressed nationally and rapidly to prevent the continuing decline in MLSO numbers. Matters of local organisation might be addressed by trusts and departments, but recognition of the need to resource changes would require reflection in budgets.

Career Mobility↗

[A life dedicated to pathology: Hamdi Suad Aknar].

Hamdi Suad Aknar [1873-1936] was one of the pioneers of pathological anatomy and cancer researches in Türkiye. He completed his education in the military medical school in 1899. Then he started to work at Gülhane, which was a school for training military physicians as interns and residents. He was sent to Germany by Robert Rieder, head of Gülhane, for further education. He got his specialization certificate at the University of Leipzig. When he returned to Gülhane he was appointed as an instructor and started courses of pathological anatomy. He taught pathology at the Mekteb-i Tibbiye-i Mülkiye and the Darulfünun Medical School, too. In 1933, as a result of the university reform, he was dismissed. When he died, he was the head of the pathological anatomy laboratory of the Gureba Hospital in Istanbul. When he returned from Germany, Aknar modernized the laboratory of the pathological anatomy department of Gülhane, which was the first in its field in Türkiye. He founded a pathology museum, which consisted of 1800 macroscopic pieces, in the medical school and prepared a collection of microscopic pieces, as well. He concentrated on cancer research and studied in the field of cell and tissue pathology. He founded a cancer research department in his laboratory in the university. The Society for Research and Strugle Against Cancer (Kanser Mücadele ve Taharri Cemiyeti) was established in 1932, on Hamdi Suad's proposal. He wrote two textbooks for students: General Pathological Anatomy (Teşrih-i Marazi-i Umumi) and Autopsy and Pathological Anatomy Diagnosis and Its Importance in Forensic Medicine (Feth-i Meyyit ve Teşrih-i Marazi Teşhisi ve Tibb-i Adlide Ehemmiyeti.) He was granted a prize of service by the Turkish Scientific and Technical Research Foundation (Türkiye Bilimsel ve Teknik Araştirma Kurumu) in 1974, 38 years after his death.

History, 19th Century↗

[Between science and moral injury--dead human bodies' treatment in anatomy and pathology during early modern times].

In this essay the history of anatomy and pathology between the 16th and the 19th century is focused under the two aspects of scientific development and of moral injury. In anatomy, which came along as a special field of theoretical medicine in 16th century, the human corpse was used as a suitable and to an increasing degree legitimate model of the healthy living body. About two hundred years later, even pathology started to be transformed into pathological anatomy. While anatomists were dealing with the structure of the healthy body pathological anatomists were interested in the morbid changes of the human corpse; the pathologist perceived the dead body as a static model of the dynamic pathological process in the living patient. Anatomy came along in the era of Renaissance and Humanism not least because of a close connection between science and the fine arts, whereas its practical relevance during the 16th and the 17th century resulted from a preparatory function for army surgery. The corpses of executed criminals, infanticides, and of unmarried mothers who had died from natural causes were often used for anatomical purposes including public autopsy. Pathological anatomy, however, unfolded its power not until the end of the 18th and the beginning of the 19th century when a new medical institution had been established: the clinic. The physical methods of examination such as percussion and auscultation of the patient's body could now be reviewed by the results of a post-mortem autopsy. The growing influence of pathological anatomy during 19th century medicine was reflected by a modified perception and evaluation of disease: The spatial dimensions of the visible findings received priority to the chronological development of the process of disease with the consequence of a heightened risk of separating the pathological structures from the suffering patient's biographical context. For the gain to scientism pathological anatomy had to tolerate a loss of reality, replacing the complexity of "heart and soul" by a reductionist model of the dead body.

Anatomy↗

[Advances in molecular oncologic pathology].

Molecular oncologic pathology is a relatively new discipline. It integrates molecular biology with oncologic pathology. Different from the morphology-based traditional diagnostic pathology, molecular oncologic pathology relies on molecular evidences. Complementary to and based on traditional diagnostic pathology, molecular oncologic pathology further predicts the biological behavior of a given tumor and also guides the therapy. This review elaborated the basic concepts and theories of molecular oncologic pathology. It listed several cases to illustrate the clinical applications of molecular oncologic pathology, and to explain how molecular oncologic pathology assists clinicians in cancer diagnosis, treatment, prognostication, and most importantly, cancer prevention.

Humans↗

Informatics as a separate section within a department of pathology.

Departments of pathology should be reorganized to include a separate section of pathology informatics (PI) in addition to the traditional sections of clinical pathology and anatomic pathology. PI is the discipline of medical informatics as practiced within pathology and encompasses a rich mix of activities. The primary role of specialists working in clinical pathology and anatomic pathology would be to create information, whereas that of informaticians in a section of PI would be to add value to the created information by processing it and communicating it to users. The four major benefits associated with a PI section would be as follows: (1) enhanced productivity and efficiency in the development of alignment and impact applications; (2) better management of the information product of pathology and the informaticians themselves; (3) increased political power and influence for pathology; and (4) increased awareness and sophistication on the part of departmental leaders about information processing. Departmental benefits from the proposed organizational change would thus be calibrated in terms of the ability of the revamped department to harness and exploit new information technology.

Clinical Laboratory Information Systems↗

The effect of interinstitution anatomic pathology consultation on patient care.

OBJECTIVE: To determine the effect of routine interinstitution anatomic pathology consultation on patient evaluation and treatment. DESIGN: All interinstitution anatomic pathology consultation diagnoses made during a 1-year period were compared with the original pathologic diagnoses. Patients with discrepant diagnoses were evaluated after an interval of 1 year to determine the correct clinical diagnosis. The relevance of the pathologic consultation to furthering medical evaluation and treatment was determined from a review of the medical record and when necessary from consultation with the patient's physician. SETTING: Patients referred to a university hospital. MAIN OUTCOME MEASURES: We determined the number of patients with discrepant pathologic diagnoses and whether these diagnoses changed the planned surgical procedure, chemotherapy, radiation therapy, or medical evaluation. RESULTS: Seventy-one (9.1%) discrepant diagnoses were identified among the 777 patients. Of these 71 patients, 45 (63%) demonstrated a change in therapy or clinical evaluation as a result of the interinstitution anatomic pathology consultation. In five of these patients the consultation diagnosis was in error. There was a significantly greater percentage of discordant diagnoses among the cytology and fine-needle aspiration biopsies (21%) as compared with the surgical pathology specimens (7.8%; P < .001). CONCLUSIONS: Routine interinstitution anatomic pathology consultation resulted in a change in patient evaluation or treatment in 45 (5.8%) of the 777 cases reviewed. Our interinstitution anatomic pathology consultation policy appears to provide useful diagnostic information, which should contribute to improved patient care. However, when a discrepancy is identified, additional consultation or evaluation should be considered.

Biopsy↗

Clinically undetected motor neuron disease in pathologically proven frontotemporal lobar degeneration with motor neuron disease.

BACKGROUND: Frontotemporal lobar degeneration with motor neuron disease (FTLD-MND) is a pathological entity characterized by motor neuron degeneration and frontotemporal lobar degeneration. The ability to detect the clinical signs of dementia and motor neuron disease in pathologically confirmed FTLD-MND has not been assessed. OBJECTIVES: To determine if all cases of pathologically confirmed FTLD-MND have clinical evidence of frontotemporal dementia and motor neuron disease, and to determine the possible reasons for misdiagnosis. METHOD: Review of historical records and semiquantitative analysis of the motor and extramotor pathological findings of all cases of pathologically confirmed FTLD-MND. RESULTS: From a total of 17 cases of pathologically confirmed FTLD-MND, all had clinical evidence of frontotemporal dementia, while only 10 (59%) had clinical evidence of motor neuron disease. Semiquantitative analysis of motor and extramotor pathological findings revealed a spectrum of pathological changes underlying FTLD-MND. Hippocampal sclerosis, predominantly of the subiculum, was a significantly more frequent occurrence in the cases without clinical evidence of motor neuron disease (P<.01). In addition, neuronal loss, gliosis, and corticospinal tract degeneration were less severe in the other 3 cases without clinical evidence of motor neuron disease. CONCLUSIONS: Clinical diagnostic sensitivity for the elements of FTLD-MND is modest and may be affected by the fact that FTLD-MND represents a spectrum of pathological findings, rather than a single homogeneous entity. Detection of signs of clinical motor neuron disease is also difficult when motor neuron degeneration is mild and in patients with hippocampal sclerosis.

Adult↗

Pathology associated with sporadic Parkinson's disease--where does it end?

Parkinson's disease (PD) is a multisystem disorder in which predisposed neuronal types in specific regions of the human peripheral, enteric, and central nervous systems become progressively involved. A staging procedure for the PD-related inclusion body pathology (i.e., Lewy neurites and Lewy bodies) in the brain proposes that the pathological process begins at two sites and progresses in a topographically predictable sequence in 6 stages. During stages 1-2, the inclusion body pathology remains confined to the medulla oblongata, pontine tegmentum, and anterior olfactory structures. In stages 3-4, the basal mid- and forebrain become the focus of the pathology and the illness reaches its symptomatic phase. In the final stages 5-6, the pathological process is seen in the association areas and primary fields of the neocortex. To date, we have staged a total of 301 autopsy cases, including 106 cases with incidental pathology and 176 clinically diagnosed PD cases. In addition, 163 age-matched controls were examined. 19 of the 301 cases with PD-related pathology displayed a pathological distribution pattern of Lewy neurites and Lewy bodies that diverged from the staging scheme described above. In these cases, olfactory structures and the amygdala were predominantly involved in the virtual absence of brain stem pathology. Most of the divergent cases (17/19) had advanced concomitant Alzheimer's disease-related neurofibrillary changes (stages IV-VI).

Animals↗

Alpha-synuclein pathology in Parkinson's and Alzheimer's disease brain: incidence and topographic distribution--a pilot study.

To study the incidence and topographic distribution of alpha-synuclein-positive inclusions in Parkinson's disease (PD), dementia with LB (DLB), and Alzheimer's disease (AD), 206 brains of elderly patients, including 53 patients with clinical PD, 110 autopsy-proven AD cases, 22 with dementia with LB (DLB), 1 case with essential tremor, and 20 age-matched controls were investigated using alpha-synuclein immunohistochemistry. For technical reasons, the olfactory system was not studied. In all PD brains, alpha-synuclein-positive inclusions and neuronal losses were present in medullary and pontine nuclei, locus coeruleus, and substantia nigra, with additional lesions in amygdala (24%), allocortex (58%), cingulate area (34%), and isocortex (26.5%). All PD cases corresponded to pathology stage 4-6 suggested by Braak et al. (2003, Neurobiol Aging 24:197). In most cases of DLB, the distribution of alpha-synuclein pathology and neurodegeneration corresponded to stages 5 and 6 of PD pathology. The case with essential tremor and 48.2% of the AD cases showed no LB pathology; in the other AD brains alpha-synuclein-positive inclusions were seen in various brain areas. None of the controls showed LB pathology. Among 12 cases of incidental Lewy body disease (without clinical parkinsonian signs), 7 corresponded morphologically to PD stage 3 or 4. In further 6 AD cases, 2 with parkinsonian symptoms, considerable damage to locus coeruleus, substantia nigra, nucleus basalis and allocortex with preservation of the medullary nuclei was seen. The preliminary data largely confirm the Braak staging of brain pathology, although some of the clinical PD cases corresponded to stage 3 often considered as "preclinical". In addition, some cases without demonstrable involvement of medullary nuclei showed extensive PD-like pathology in other brain areas, suggesting deviation from the proposed stereotypic expansion pattern and that incidental LB pathology may affect solely the locus coeruleus and substantia nigra. Striking similarity of LB pathology between DLB and PD suggests close morphological relationship between both disorders. Widespread LB lesions occurred in many sporadic AD cases without parkinsonian symptoms, the pathogenesis and clinical impact of which are unclear. The relationship between AD and PD with particular reference to alpha-synuclein-positive lesions needs further elucidation [corrected].

Aged↗

The ubiquitin-binding protein p62 identifies argyrophilic grain pathology with greater sensitivity than conventional silver stains.

The routine diagnosis of argyrophilic grain disease is fraught by the lack of availability of an easily applied reproducible stain that can highlight the grain pathology with sensitivity and with minimal background. The Gallyas silver iodide technique is not widely used and, even in experienced hands, is difficult to perform due to inconsistencies inherent in silver-based techniques on thin sections. Grain pathology can be detected using immunohistochemistry for phosphorylated tau protein, but the grain pathology is most often masked by background tau-positive material; leading to problems with interpretation, especially for practitioners seeing small numbers of cases. There is a need for a reliable immunohistochemical stain that can detect grain pathology and provide a clear contrast between grains and other tau-positive neurodegenerative pathologies. We have investigated the novel ubiquitin-binding protein p62 as a potential biomarker for grain pathology in argyrophilic grain disease. Four cases of argyrophilic grain disease, in which the pathology was determined using the Gallyas silver iodide technique, were re-assessed using paraffin-embedded sections immunostained with antibodies specific for p62. We found that the detection of grain pathology was more sensitive than with silver-based techniques and that the resolution of the pathology was significantly improved. We suggest that p62 could be used to replace the Gallyas technique in the routine diagnosis of argyrophilic grain disease.

Adaptor Proteins, Signal Transducing↗

Anorectal pathology in HIV/AIDS-infected patients has not been impacted by highly active antiretroviral therapy.

PURPOSE: The aim of this study was to determine if the prevalence and distribution of anorectal pathology in HIV-infected patients treated by colorectal surgeons have changed after the introduction of highly active antiretroviral therapy. METHODS: The Los Angeles County-University of Southern California HIV Clinic is solely dedicated to the care of HIV patients. A colorectal clinic was established within this environment in 1991 and has served as the exclusive provider for the care of anorectal pathology in these patients. A prospective database of patients treated at this clinic was reviewed for two 18-month periods. The first group (early period) was composed of patients treated between January 1994 through June 1995, before the institution of more effective antiretroviral therapy. The second group (later period) consisted of patients treated between January 2001 through June 2002, after the introduction of highly active antiretroviral therapy. Data were tabulated for HIV-related anorectal pathologies, such as anal ulcer and anogenital condyloma, and non-HIV-related pathologies, including fissure, fistula in ano, hemorrhoids, perianal abscess, and other pathologies, for each of the two time periods. RESULTS: A total of 117 individual patients with anorectal pathology were treated in the early period and 109 received care in the later period, of which 107 were able to be evaluated. The pathology was distributed as follows for the early vs. late periods: 33 vs. 33 percent for ulcer, 30 vs. 34 percent for condyloma, 9 vs. 4 percent for fissure, 6 vs. 6 percent for fistula, 4 vs. 5 percent for hemorrhoids, 3 vs. 3 percent for abscess, and 15 vs. 16 percent for all other anorectal pathology. There was no statistically significant difference in any of these groups. CONCLUSION: The prevalence and distribution of both HIV-related and non-HIV-related anorectal pathology seen in our HIV patients have not been altered by the introduction of highly active antiretroviral therapy.

Acquired Immunodeficiency Syndrome↗

Vascular pathologies and cognition in a population-based cohort of elderly people.

The MRC Cognitive Function and Ageing Study (CFAS) is a prospective longitudinal study of a population-based cohort of elderly people in six UK sites, evaluated using psychometric instruments and questionnaires to elucidate physical and mental health. Data from the core study includes prevalence and incidence rates for dementia and longitudinal measures of cognitive decline together with data on genetic risk factors for dementia. A neuropathology study runs in collaboration with the core study based on premortem counselling of individual respondents or carers. Analysis of pathological data from the first 209 accumulated brain donations showed that both Alzheimer-type pathologies (ATP) and vascular pathologies (including congophilic amyloid angiopathy (CAA)) were common in both demented and non-demented respondents. Although many cases fulfil conventional diagnostic criteria for the pathological diagnosis of Alzheimer disease, the data differ from those published from conventional studies of hospital or memory clinic cohorts. In particular, there are individuals whose total burden of pathology is inappropriately high or low compared with their clinical dementia status, even when all pathologies are considered in a multivariable model of dementia risk factors (25% of respondents misdiagnosed from pathology findings). Vascular pathology is so common that few dementia cases lack a mixed component of both ATP and vascular lesions (pure AD cases, 21%). More recently, the study has examined white matter pathology in this cohort as a potential manifestation of small-vessel disease (SVD) in the ageing brain. Using an MRI strategy to image formalin-fixed brain slices, the study shows that white matter lesions (WMLs) are common (94% overall frequency) and are an independent risk factor for dementia using multivariable analysis.

Aged↗

The relation between pathological worrying and fatigue in a working population.

OBJECTIVE: This study aimed to explore cross-sectional and longitudinal associations between pathological worry and fatigue in a working population. METHODS: In employees with very low or very high fatigue levels, psychometrics of the Penn State Worry Questionnaire (PSWQ; measuring pathological worry) and the Checklist Individual Strength (CIS; measuring fatigue) were examined and their cross-sectional and longitudinal associations were explored. RESULTS: Pathological worry and fatigue can be measured as different constructs. However, pathological worry and fatigue were also associated on a cross-sectional level. Pathological worry predicted fatigue level 10 months later, but this association disappeared after adjustment for the cross-sectional association between pathological worry and fatigue. CONCLUSION: Although they can be measured as different constructs, pathological worry and fatigue seem to be associated. When studying longitudinal relations between pathological worry and fatigue, their cross-sectional association should be taken into account. Pathological worry might not be a risk factor for fatigue per se, but might act more like a mediating factor.

Adult↗

Are dopaminergic genes involved in a predisposition to pathological aggression? Hypothesizing the importance of "super normal controls" in psychiatricgenetic research of complex behavioral disorders.

We hypothesize that pathological aggression, a complex behavioral disorder, in adolescents may in part involve polymorphisms of the dopaminergic system. While a number of neurotransmitter systems must be involved, due to polygenic inheritance, one major pathway should involve the dopaminergic system. Advances in our knowledge of the neurobiology of aggression and violence have given rise to rational pharmacological treatments for these behaviors. The main biological systems that are known to be involved are certain reward neurotransmitters including: serotonin, opioid peptides, gamma-aminobutyric acid, and the catecholamines (dopamine and norepinephrine). It is our notion that pathological aggressive behavior is in part similar mechanistically to other forms of impulsive behaviors such as pathological gambling. By analogy to drug dependence, it has been speculated that the underlying pathology in pathological gambling is a reduction in the sensitivity of the reward system. While studying pathological gamblers and controls during a guessing game using functional Magnetic Resonance Imaging, Reuter et al. observed a reduction of ventral striatal and ventromedial prefrontal activation in the pathological gamblers that were negatively correlated with gambling severity. Subsequently, linking hypo activation of these areas to disease severity. A positive correlation of both the dopamine D2 receptor gene (DRD2) and the dopamine transporter gene (DAT1) polymorphisms were observed with pathological violence in adolescents in a blinded clinical trial. Thus, this and other cited work preliminary suggest a role for both the DRD2 and DAT genes in pathological aggressive behavior. We further hypothesize that follow-up gene research in this area, albeit premature, resulting in confirmation of positive correlations with dopaminergic polymorphisms, and utilizing highly screened controls (eliminating any addictive, compulsive and impulsive behaviors in both proband and family) may have important ramifications in our young population.

Adolescent↗

Clinical and pathologic tumor size in renal cell carcinoma; difference, correlation, and analysis of the influencing factors.

OBJECTIVES: To investigate the relation between the clinical and pathologic size and to identify the factors that affect this relationship. The clinical size of the tumor is essential for choosing the appropriate treatment in renal cell carcinoma. The pathologic size, on the other hand, is an important prognostic indicator. METHODS: We reviewed the charts of 291 open nephrectomy patients treated for nonmetastatic renal cell carcinoma. Clinical size was defined as the largest diameter on contrast-enhanced computed tomography. Pathologic size was defined as the largest diameter on pathologic examination. The clinical and pathologic sizes were compared, and their correlation was analyzed. The effect of various clinical and pathologic factors on the percentage of the size difference (%Delta(size)) was analyzed. RESULTS: The mean clinical and pathologic size was 5.4 +/- 3.2 and 5.3 +/- 3.3 cm, respectively. The difference was not significant (P = 0.1679). The clinical and pathologic size also correlated highly (r = 0.9540; P <0.0001). The estimated blood loss, local tumor extension, and cell type had significant influence on the %Delta(size) (P = 0.0018, 0.0415, and 0.0079, respectively). Additionally, in approximately one half of the patients with the greatest size difference, features such as cystic masses, hemorrhage, pyelonephritis, localization near or invasion of the collecting system, cysts or dilated calices adjacent to the tumor, and multiple cysts within the kidney were present, which were identified as factors that might have influenced the accuracy of the clinical size. CONCLUSIONS: The overall accuracy of the clinical size and its correlation with the pathologic size was acceptable. However, the presence of the above-mentioned factors should be taken into consideration during the interpretation of clinical tumor size.

Carcinoma, Renal Cell↗

Dendritic spine pathology: cause or consequence of neurological disorders?

Altered dendritic spines are characteristic of traumatized or diseased brain. Two general categories of spine pathology can be distinguished: pathologies of distribution and pathologies of ultrastructure. Pathologies of spine distribution affect many spines along the dendrites of a neuron and include altered spine numbers, distorted spine shapes, and abnormal loci of spine origin on the neuron. Pathologies of spine ultrastructure involve distortion of subcellular organelles within dendritic spines. Spine distributions are altered on mature neurons following traumatic lesions, and in progressive neurodegeneration involving substantial neuronal loss such as in Alzheimer's disease and in Creutzfeldt-Jakob disease. Similarly, spine distributions are altered in the developing brain following malnutrition, alcohol or toxin exposure, infection, and in a large number of genetic disorders that result in mental retardation, such as Down's and fragile-X syndromes. An important question is whether altered dendritic spines are the intrinsic cause of the accompanying neurological disturbances. The data suggest that many categories of spine pathology may result not from intrinsic pathologies of the spiny neurons, but from a compensatory response of these neurons to the loss of excitatory input to dendritic spines. More detailed studies are needed to determine the cause of spine pathology in most disorders and relationship between spine pathology and cognitive deficits.

Animals↗

Facilitating survival and recovery by removing autogenic pathology from the clinical picture.

For the most part, the clinical picture is the expression of autogenic pathology and, unless the anatomical insult represents a major structural compromise, it contributes little to the clinical picture. Autogenic pathology created by the processing of peripheral neurological impulses altered by the presence of anatomical insults is created independently of the gravity of the anatomical insults. Even in the presence of a survivable insult, autogenic pathology is often fatal. Each successful resuscitation effort identifies a patient with a survivable insult who almost died before autogenic pathology was removed by cerebral anoxia, and/or electric shock. Similar patients who suffer terminal brain damage cannot be identified. Cardinal receptors furnish the embryo with its first neural contact with its environment. On completion of embryological migration, they occupy a position in the skin overlying the root of their spinal nerve. Cardinal receptors are functionally segmented to the specific distribution of their spinal nerve and use the stable neurological impulses from the skin to furnish the cadence by which peripheral impulses are processed and valued. Selected cardinal receptors may be specifically stimulated by saline infiltration that produces intradermal blebs in the skin overlying their spinal nerve's root. An augmented burst of infiltration pain immediately followed by symptomatic relief identifies monitoring cardinal receptors. The identification of monitoring receptors confirms the presence of pathology found within the specific distribution of their spinal nerve. Peripheral impulses processed within the cadence of highly stimulated cardinal receptors are assigned an insignificant value. Assigning an insignificant value to peripheral impulses altered by the presence of an anatomical insult removes autogenic pathology from the clinical picture. The immediate onset of profound symptomatic relief heralds the removal of autogenic pathology. Visceral pathology is monitored by bilateral pairs of cardinal receptors so it produces discomfort perceived without specific location information. Therefore, the specific visceral distribution has been discounted and is virtually unknown. However, when visceral pathology is correlated with bilateral pairs of monitoring cardinal receptors there are no patient variations.

Aged↗

Preoperative estimation of the pathological breast tumour size by physical examination, mammography and ultrasound: a prospective study on 105 invasive tumours.

OBJECTIVE: The clinical breast tumour size can be assessed preoperatively by physical examination, mammography and ultrasound. At present it is not clear which modality correlates best with the histological invasive breast tumour size. This prospective study aims to determine the most accurate clinical method (physical examination, mammography or ultrasound) to predict the histological invasive tumour size preoperatively. METHODS AND PATIENTS: Between October 1999 and August 2000, 96 women with 105 invasive malignant breast tumours were included in this study. All patients underwent excision and the tumour size was measured on histology. Tumour size was measured by all three modalities in 73 cases. Results were evaluated by calculating correlation coefficients. The examination modalities presenting the best estimation of the pathological tumour size were used in a stepwise linear regression analysis to construct a formula predicting the pathological tumour size from the result of the various diagnostic modalities. RESULTS: The correlation coefficient between ultrasound and pathological size (r=0.68) was significantly better than the correlations between physical examination and pathological size (r=0.42) and mammographic and pathological size (r=0.44). Physical examination overestimates and ultrasound underestimates breast tumour classification. The most accurate prediction formula was: Pathological tumour size (mm) equals sonographic tumour size (mm)+3 mm. CONCLUSION: When comparing physical examination, mammography and ultrasound for the prediction of the pathological size of a malignant breast tumour, ultrasound is the best predictor. The ensuing regression formula determines pathological size as tumour size by ultrasound+3 mm. However, with the wide 95% confidence interval of +/-11 mm, it remains difficult to predict the exact pathological size for an individual invasive breast tumour. A small deviation in millimetres of the tumour size could lead to a change in treatment and to another prognostic estimate.

Adult↗