Dissertations / Theses on the topic 'Cushing's syndrome'
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Ritchie, Catherine Marian. "Aspects of hypertension in endocrine disease." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357488.
Full textGroenewald, Liechka. "The prevalence of sleep apnea in patients with Cushing's syndrome." Diss., University of Pretoria, 2020. http://hdl.handle.net/2263/77081.
Full textDissertation (MSc)--University of Pretoria, 2020.
Physiology
MSc
Restricted
Luzi, Nicole. "An Enzymology and Inhibition Study of a cAMP-Dependent Protein Kinase Linked to ACTH-Independent Cushing's Syndrome." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6058.
Full textCrespo, Martín Iris. "Neuropsychological evaluation of patients with acromegaly and Cushing’s syndrome: Long-term effects." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/392681.
Full textThe studies described in this thesis focus on the neuropsychological consequences in patients who have suffered Cushing’s syndrome (CS, due to glucocorticoid excess) and acromegaly (due to excess of growth hormone -GH-). It is known that prolonged exposure to glucocorticoids may have long-lasting adverse effects in CS patients who do not completely return to premorbid level of functioning and quality of life despite long-term cure. On the other hand, in acromegalic patients, potential long-lasting effects of GH on the brain affecting personality, cognition and behaviour have not been considered until recently. Making a choice is a common behavior in daily life and requires selecting one option among several alternative possibilities. The Iowa Gambling Task (IGT) is a measurement of decision making that mimics real-life risk taking situations since it involves uncertainty, reward and punishment. Frontal cortex has a key role in the IGT because it has the ability to coordinate processing among its millions of neurons in order to direct them towards future goals and advantageous decisions. The aims of these studies were to evaluate memory and decision making in patients with CS and acromegaly, and explore their relationship with frontal cortex and affective disorders. Thirty-five CS patients and thirty-five matched controls were evaluated using the IGT and 3Tesla magnetic resonance imaging (MRI) to assess frontal cortical thickness. Thirty-one patients with acromegaly and thirty-one healthy controls were evaluated using the IGT, Rey Auditory Verbal Learning Test (RAVLT), State-Trait Anxiety Inventory (STAI) and Beck Depression Inventory-II (BDI-II). In the first study, CS patients presented an altered decision-making strategy compared to controls, choosing a lower number of the safer cards and higher number of riskier cards. They showed more difficulties than controls to learn the correct profiles of wins and losses for each card group. In whole brain analysis, CS patients showed decreased cortical thickness in the left superior frontal cortex, left precentral cortex, left insular cortex, left and right rostral anterior cingulate cortex, and right caudal middle frontal cortex compared to controls. In the second study, acromegalic patients showed impairments in delayed verbal memory and more anxiety and depressive symptoms than controls. Regarding the IGT, acromegalic patients presented an altered decision-making strategy compared to controls, choosing a lower number of the safer cards and higher number of the riskier cards. Multiple correlations between anxiety and depressive symptoms and performance in memory and decision making were found. These studies show impaired decision making in both CS and acromegalic patients. They selected more disadvantageous choices than advantageous choices. Whereas healthy controls gradually learned to favor the advantageous decks, patients with acromegaly and CS continued to experience large punishment throughout training. We have not found a direct relationship between poor decision making and frontal cortical thinning in CS patients, opposite to previous studies on other clinical conditions. Decision deficits on the IGT were correlated with memory deficits in CS and acromegalic patients. Moreover, acromegalic patients show affective alterations (anxiety and depressive symptoms) that influenced delayed memory and decision making.
Pires, Encuentra Patricia. "Anomalías de la sustancia blanca cerebral en el síndrome de cushing en relación a sintomatología psiquiátrica y rendimiento cognitivo." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457523.
Full textCushing’s syndrome (CS) is an endocrine disorder due to prolonged exposure to cortisol. This endogenous hypercortisolism determines endocrine, cognitive and psychiatric symptoms. A few imaging studies have investigated brain structures in patients with CS and have observed brain damage. The aims of the studies described in this thesis were to explore the microstructure of cerebral white matter (WM), a topic hardly investigated up to now in CS, and to evaluate neuropsychiatric symptoms (depression and anxiety) and cognitive impairment (information processing speed) and their relationship with the WM. Diffusion Tensor Imaging (DTI) is a Magnetic Resonance (MR) imaging technique that allows noninvasive, in vivo study of the brain by assessing the motion of water molecules along and across neural axons. Different DTI maps show WM architecture and can depict microstructural WM abnormalities. Fractional anisotropy (FA) reflects WM integrity, while increases in mean diffusivity (MD) may be caused by demyelination or edema. Decreases in axial diffusivity (AD) indicate axonal loss, while increased radial diffusivity (RD) is related to demyelination. Thirty-five patients with CS and 35 healthy control volunteers were included in these studies. In the first study, a DTI analysis was performed comparing patients with CS with healthy controls, followed by a second analysis in which patients were separated into active CS, remitted CS, and cured CS. Results revealed widespread reductions in whole brain FA, increases in MD and RD and partially also of AD in patients with CS compared to healthy controls. The subgroup analysis demonstrated this same pattern of WM damage in patients with active, remitted and cured CS, suggesting an early onset and persistent damage of brain WM microstructure. DTI alterations seemed to be independent of concomitant hypercortisolism and the presence or absence of other cardiovascular risk factors included into the analysis like hypertension, dyslipidemia, and obesity. Our aim in the second study was to investigate mood disturbances and cognitive impairment in CS patients, and their relationship to WM alterations on DTI. We hypothesized that mood disturbances, evaluated using the Beck Depression Inventory II (BDI-II) and State-Trait Anxiety Inventory (STAI), would be greater in CS patients than in controls, and related to widespread WM alterations on DTI. We additionally hypothesized that CS patients would show abnormalities in information processing speed, evaluated using the Symbol Digit Modalities Test (SDMT), possibly related to WM alterations, since WM state has been related to connectivity function. Results showed greater mood disturbances (depression and anxiety symptoms), but no differences in information processing speed scores, in CS patients compared to healthy controls. In the case-control DTI study, depressive symptoms correlated negatively with FA and positively with RD, a pattern which is linked to loss of myelin and axonal integrity. FA and AD correlated positively with information processing speed. These results indicate that WM integrity are associated with better information processing in CS patients and controls.
Nakken, Gary N. "The Effects of Excess Corticosterone on LKB1 and AMPK Signaling in Skeletal Muscle of Rats." BYU ScholarsArchive, 2008. https://scholarsarchive.byu.edu/etd/1963.
Full textGonzález, Ramírez Mar 1991. "Bioinformatic analysis of epigenetic regulatory mechanisms in development and disease." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/671370.
Full textUna regulació apropiada de l’expressió gènica és necessària per a un correcte desenvolupament i homeòstasi dels organismes. Els mecanismes epigenètics representen una informació addicional, a més de la seqüència genètica, crucial per al correcte funcionament de cada cèl·lula. Les modificacions d’histones, que modulen i s’associen a activació o repressió transcripcionals, són una característica epigenètica important. Gràcies al modelatge predictiu, hem estudiat quines modificacions d’histones es relacionen millor amb la funció dels enhancers o promotors en cèl·lules mare embrionàries de ratolí, durant la diferenciació i en el desenvolupament animal. Hem trobat que modificacions d’histones diferents es relacionen millor amb enhancers o promotors, respectivament. Hem estudiat el rol dels poised enhancers durant la diferenciació i el desenvolupament. Hem vist que l’activació dels poised enhancers no és exclusiva del llinatge neural, sinó un mecanisme implicat en la diferenciació de tot tipus cel·lular. Hem caracteritzat el paisatge epigenètic de la síndrome de Cushing. Hem trobat alteracions epigenètiques i transcripcionals després d’una remissió de la malaltia a llarg termini, relacionades amb una profunda alteració del ritme circadiari. Aquestes troballes prometen ser rellevants per a futurs avenços terapèutics.
Bathon, Kerstin [Verfasser], Davide [Gutachter] Calebiro, Martin [Gutachter] Fassnacht, and Caroline [Gutachter] Kisker. "Mutations in protein kinase A catalytic subunit as a cause of adrenal Cushing's syndrome: mechanisms and functional consequences / Kerstin Bathon ; Gutachter: Davide Calebiro, Martin Fassnacht, Caroline Kisker." Würzburg : Universität Würzburg, 2019. http://d-nb.info/1196532966/34.
Full textAlencar, Guilherme Asmar. "Aspectos clínicos e moleculares da hiperplasia adrenal macronodular independente de ACTH em sua forma familial." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-03122013-091817/.
Full textINTRODUCTION: ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a rare disease characterized by functioning adrenal macronodules and increased, autonomous and sustained cortisol production. This condition is an uncommon cause of Cushing\'s syndrome (CS). While the sporadic form of the disease appears to be the most frequent, the true prevalence of its familial form is unknown. Despite being a known clinical entity for almost 50 years, the pathophysiological process that leads to AIMAH, the predisposing genetic alterations and important clinical, laboratory and radiological aspects of the disease have not been fully clarified. The recent identification of a large group of relatives with familial AIMAH allowed the accomplishment of the present study. OBJECTIVES: The following were the aims of this study: 1) characterize the development of familial AIMAH through correlations between clinical manifestations, laboratory data and radiological findings; 2) investigate the possible association between AIMAH and the occurrence of intracranial meningioma; 3) characterize the metabolic activity of the adrenal glands in this disease; 4) define the inheritance pattern of the disease in the family studied; and 5) map chromosomal regions and loci potentially related to the genetic etiology of familial AIMAH. METHODS: 96 members of the family studied were initially subjected to a detailed clinical and laboratory evaluation. Computed tomography (CT) scans were performed for the radiological characterization of the adrenal glands. Magnetic resonance imaging scans and 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) scans were performed on patients with both forms of the disease (familial and sporadic) to investigate the presence of intracranial meningioma and characterize the metabolic activity of the adrenal glands, respectively. In vivo studies for aberrant hormone receptors were also conducted on those patients with familial AIMAH. In another phase of the study, different molecular biology techniques were employed to investigate the genetic etiology of familial AIMAH. For such, sequencing of the ACTH receptor gene (MC2R), a linkage study using specific microsatellite markers, a single nucleotide polymorphism (SNP)-based genome-wide linkage study and the sequencing of suspect genes were performed. RESULTS: The evaluation of the family revealed the diagnosis of 15 cases of the disease (7 women and 8 men) in three consecutive generations. AIMAH was transmitted to subsequent generations by both genders and half of the siblings were affected in some segments of the family. Mean age at diagnosis was 52.8 +-11.3 years (range: 32 to 74 years) and about 86% (12/14) of the patients exhibited subclinical CS. Both midnight salivary cortisol and 24-hour urinary cortisol demonstrated low sensitivity (21% and 14%, respectively) for the diagnosis of familial AIMAH. Plasma ACTH levels were low ( < 10 pg/ml) in 46% (5/11) of patients with the disease. In about 62% (8/13) of cases, serum dehydroepiandrosterone sulphate (DHEAS) levels were below the normal range. Simple logistic regression models revealed that the probability (odds ratio) of an individual having the disease in the family was greater in the presence of plethora, progressive weight gain or after the diagnosis of diabetes or prediabetes. Adrenal thickening associated with the presence of bilateral nodules was the most common radiological finding in familial AIMAH. However, radiological abnormalities were found in only one of the adrenal glands in one third of the patients (5/15). Throughout the in vivo studies for aberrant hormone receptors, distinct responses were frequently observed among the individuals with familial AIMAH. One third (5/15) of the patients who underwent magnetic resonance imaging scans had typical images of intracranial meningiomas. The 18F-FDG-PET/CT scan revealed increased metabolic activity of the hyperplastic adrenals in patients with both overt and subclinical CS. The molecular studies delimited genomic regions on chromosomes 16 and 11 potentially related to the genetic cause of familial AIMAH. Some suspected genes (GPR56, GPR97 and GPR114), located in these genomic regions, were sequenced, but no mutations were found. CONCLUSIONS: In the extended family studied, AIMAH followed an autosomal dominant pattern of inheritance and subclinical CS was the most common presentation of the disease. The 1 mg overnight dexamethasone suppression test proved to be the screening test of choice for the initial evaluation of patients suspected to have familial AIMAH, due mainly to the low sensitivity of midnight salivary cortisol and 24-hour urinary cortisol as screening tests. A normal level of plasma ACTH was a common laboratory finding in familial AIMAH. Low serum levels of DHEAS proved to be a relatively early finding associated with the subclinical CS determined by the disease. Adrenal CT scans revealed different radiological patterns among patients with familial AIMAH, with a fairly frequent rate of asymmetry between glands. The distinct responses observed throughout the in vivo studies for aberrant hormone receptors, among family members, favor the hypothesis that these receptors may be an epiphenomenon resulting from cell proliferation and dedifferentiation. An increased prevalence of intracranial meningioma was demonstrated in both the familial and sporadic forms of AIMAH. For the first time, it was shown that AIMAH may exhibit increased 18FFDG uptake on the PET/CT scan, similarly to adrenal carcinoma and metastasis. The main genomic regions potentially associated with familial AIMAH were delimited on chromosome 16 (16p12.1, 16p11.2, 16q12.1, 16q13 and 16q21) and chromosome 11 (11q23.1) (reference genome: NCBI36/hg18)
Aulinas, Masó Anna. "Investigation of the telomere maintenance system in Cushing’s syndrome: A contribution to the phenomena of early ageing and specific morbidity." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/298320.
Full textCushing's syndrome (CS), a rare disease due to excessive cortisol secretion, is associated with increased morbidity and mortality, even after therapy compared to background population and is associated with premature aging processes. On the other hand, telomeres are repetitive DNA sequences, essential to maintain genomic stability. Without telomeres, genetic material could be lost after every cell division; thus, when telomeres are critically short, cell division stops and senescence and apoptosis are induced. To avoid telomere length (TL) attrition an enzymatic complex called telomerase is produced. Telomerase can be regulated by genetic, epigenetic and hormonal factors such as cortisol. Hypercortisolism also occurs in chronic depressive disorders and psychosocial stress, where TL is shorter than in controls. Moreover, TL shortening has also been associated with cardiovascular disease, cardiovascular risk factors (CVRF) and chronic inflammation processes. TL shortening is considered a novel cardiovascular risk marker, and is associated with inflammation biomarkers. Based on these previous evidences, we hypothesized that hypercortisolemia could contribute to premature ageing by inducing accelerated telomere shortening, which in turn could be implied in the persistent morbidity and clinical consequences associated with CS, even years after biochemical remission. Additionally, TL shortening, might be involved in the “low grade” inflammatory state and higher prevalence of CVRF observed in CS. Therefore, this research was designed to answer our hypothesis, being the main aims of this project to investigate TL in CS patients compared to controls, and to evaluate relationships between TL, CVRF and inflammation markers in CS. This is the first research to evaluate TL in this rare disease with a relatively large series of CS patients, which could provide a unique opportunity to examine the effects of hypercortisolism on telomere maintenance. Seventy-seven CS patients were compared with 77 gender-, age-, and smoking-matched controls. Fifteen CS were also evaluated longitudinally, during active disease and after remission of hypercortisolism. Clinical data and blood samples were collected (lipids, adrenal function...). Adiponectin, interleukin-6 (IL6) and C-reactive protein (CRP) were available in a subgroup of patients (n=32). Leukocyte TL was measured by telomere restriction fragment-Southern technique. Mean TL in CS and controls was similar, however in the longitudinal evaluation after adjustment for age, TL was shorter in active disease than after remission. No correlation was found between other circulating cortisol parameters, duration of exposure to hypercortisolism or biochemical cure and TL. We observed that dyslipidemic CS had shorter TL than non-dyslipidemic subjects. After adjustment for age and body mass index, cured and active CS dyslipidemic patients had shorter TL than non-dyslipidemic subjects. Additionally, higher TL shortening was observed in dyslipidemic obese patients who were also hypertensive, compared to those with two or less CVRF. Total-cholesterol and triglycerides negatively correlated with TL, as well as CRP and IL6. No differences in TL according the presence of other CVRF were observed in CS or the control group. The main conclusions are that individual CS patients in whom hypercortisolism is controlled after successful treatment, TL increases despite being on average 3 years older. It would appear therefore that telomerase activity would be induced once hypercortisolism disappears, and this could be one of the mechanisms by which increased morbidity, mortality and biological aging improve when disease is controlled. These preliminary results suggest that hypercortisolism might negatively impact telomere maintenance. Moreover, TL is shortened in dyslipidemic CS patients, further worsened if hypertension and/or obesity coexist and is negatively correlated with increased inflammation markers. Therefore, increased lipids and a “low-grade” inflammation may contribute to TL shortening and consequently to premature ageing and increased morbidity in CS.
Martínez, Momblán Mª Antonia. "Impacto de un programa educativo para el paciente con síndrome de Cushing: Estudio Multicéntrico." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/112025.
Full textINTRODUCTION: Cushing's syndrome (CS) is one of those rare endocrine diseases, is characterized by hypersecretion of cortisol, is caused by a pituitary tumor (Cushing's disease), or more rarely by an adrenal tumor or ectopic. The main cause of morbidity and mortality in the SC is cardiovascular disease, even if patients have been treated effectively (ie, has controlled the hypercortisolism). Despite the many complications that patients may suffer SC and the presence of several cardiovascular risk factors (central obesity, diabetes, ischemic heart disease, hypertension, dyslipidemia, etc.). Potentially dangerous, there are currently no educational programs respond to this educational deficit. For the patient with SC so far no comprehensive care that will address the complexity of this disease and achieve an improved quality of life, decreased morbidity and mortality, increased comfort, convenience and independence in self-care Said aspect allows nursing site frontline action against education in this group of patients, through the development and promotion of specific educational tools that improve the quality of life of these patients. OBJECTIVES: To assess the effectiveness of the educational sessions for patients with Cushing's syndrome and operated outpatient follow the HSCSP and Hospital Clinic of Barcelona, in terms of quality of life, clinical evaluation indicators, level of pain and physical activity, patterns of rest and use of health resources (monitoring conducted between 2010 and 2011). DESIGN, STUDY SCOPE AND SUBJECTS: We performed a multicenter, prospective, randomized, stratified by center. The field study was conducted in two reference centers in Catalonia where care for patients suffering from Cushing's syndrome (CS), one is the Hospital de la Santa Creu i Sant Pau (HSCSP) and the Hospital Clinic of Barcelona. The final sample of 61 patients DATA COLLECTION AND ANALYSIS: Data collection was performed through the patient's history and analyze sociodemographic, anthropometric, laboratory, and clinical and related SC over all educational sessions. So pass same questionnaires at the beginning and end of the educational sessions and were CushingQoL Quality, Questionnaire International Physical Activity Questionnaire (IPAQ), Oviedo Sleep Questionnaire (COS), Fagerström Test for Nicotine Dependence (FTND), Spanish Pain Questionnaire (CDE) Diagnostic Test for Erectile Dysfunction (IIEF 5), Questionnaire on female sexual function (Spanish version of FSFI) Questionnaire brief profile of female sexual function (B-PFSF) and lifestyle questionnaire related overweight and obesity. RESULTS: We present significant improvements in the intervention group compared to control group: pain level (p = 0.0525), improvement in physical activity (p = 0.0072) and lifestyle (p<0.0001). Also confirmed CushingQoL associations with: CushingQoL basal-end (p = 0.0085), improvement in pain (p = 0.053), physical activity (p = 0.0068) and level of rest or sleep (p = 0, 0098). CONCLUSIONS: The educational sessions disrupt the deteriorating quality of life, increasing moderate and vigorous physical activity, promotes adherence analgesic causing a decrease in pain, improved rest patterns and a decrease in the resources consumed in the intervention group.
Machado, Marcio Carlos. "Estudo da expressão do receptor da vasopressina (AVPR1B), do receptor do hormônio liberador de corticotrofina (CRHR1) e do receptor dos secretagogos de GH (GHSR-1a) em pacientes portadores de síndrome de Cushing ACTH-dependente: correlação clínico-molecular." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-31102006-131430/.
Full textINTRODUCTION: The differential diagnosis of ACTH-dependent Cushing\'s syndrome (CS) is one of the major challenges in endocrinology, especially in view of the similar clinical and laboratorial behavior between some carcinoid tumors and Cushing\'s disease (CD). Hence, dynamic tests of ACTH and cortisol release have been carried out with the aim to identify predictive and specific responses for this differential diagnosis. The pattern of the responses has been attributed to receptors overexpression, yet few studies have been undertaken to confirm such association. The aim of the present study was to verify whether ACTH and cortisol release in response to human CRH (hCRH), desmopressin, and GH releasing peptide (GHRP-6) depends on the magnitude of expression of their respective receptors (CRHR1, AVPR1B e GHSR-1a) in samples of tumors from patients with ACTH-dependent CS. PATIENTS AND METHODS: Twenty two patients (20 with CD and 2 with Ectopic ACTH Syndrome [EAS], lung and thymus carcinoid tumors) from the Division of Endocrinology and Metabolism of University of Sao Paulo School of Medicine, median age of 32 years (15-54 years), being 18 females and 4 males, were evaluated between 2002 and 2004. The patients were submitted to dynamic tests with hCRH (100 µg), desmopressin (10 µg) and GHRP-6 (1 µg/kg), with measurement of ACTH and cortisol levels, and also of GH in the case of GHRP-6 stimulation. Twenty one age and sex-matched controls were submitted to the GHRP-6 test. During surgery, tumor fragments were collected and subsequently processed for total mRNA extraction. Gene expression of CRHR1, AVPR1B and GHSR-1a relative to GAPDH was quantitated by real-time qPCR. Tissue samples of normal pituitary, lung and thymus from necropsy were used as controls. RESULTS: Greater expression of GHSR-1a was observed in patients responsive to the GHRP-6 test, both in those with CD and in the one with pulmonary carcinoid tumor. No enhanced expression of receptors CRHR1 and AVPR1B was found in CD patients responsive to the respective dynamic tests, yet there was a strong association between the in vivo responses and the expression of those receptors in the two patients with EAS. GHRP-6 -induced ACTH and cortisol release was more marked in patients with CD as compared with control individuals, but there was overlap of the responses. GH stimulation was observed in control individuals and, to a lesser extent, in patients with CD. CONCLUSIONS: There was greater expression of GHSR-1a in patients with ACTH-dependent CS who responded to GHRP-6, establishing a direct association between receptor gene expression and the in vivo response to the secretagogue in both CD patients and those with EAS. An association between expression of CRHR1 and AVPR1B and the in vivo response to the respective secretagogues was found in patients with EAS but not in those with CD. In view of the response to GHRP-6 in a patient with EAS, we considered the use of this peptide in the differential diagnosis of ACTH-dependent CS of limited value.
Viaud, Jean-François. "Le syndrome de Cushing paranéoplasique à propos de 12 cas." Bordeaux 2, 1995. http://www.theses.fr/1995BOR23075.
Full textMartinez, Emmanuel. "Difficultés et pièges de l'exploration des syndromes de Cushing paranéoplasiques : à propos d'un cas non résolu suivi de janvier 1988 à octobre 1999." Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M150.
Full textList, Jörg V., Stephan B. Sobottka, Angela Hübner, Constanze Bonk, Jan Koy, Thomas Pinzer, and Gabriele Schackert. "Cushing’s Disease in a 7-Month-Old Girl due to a Tumor Producing Adrenocorticotropic Hormone and Thyreotropin-Secreting Hormone." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135392.
Full textDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
Santos, Vives Alicia. "Estudio neuropsicológico, neurorradiológico y clínico en el hipercortisolismo endógeno = Neuropsychological, neuroradiological and clinical study in endogenous hypercortisolism." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/384710.
Full textEl síndrome de Cushing endógeno es una enfermedad rara debida a un exceso de cortisol circulante. El exceso crónico de cortisol puede provocar una serie de alteraciones que no en todos los casos revierten tras la curación hormonal, y que incluyen disminución del volumen cerebral, alteraciones neuropsicológicas y del estado de ánimo y riesgo cardiovascular elevado. Esta tesis pretende estudiar algunos de los efectos que provoca el síndrome de Cushing a nivel cerebral, analizando su relación con otros parámetros clínicos. Concretamente, los objetivos de la tesis incluyen por un lado analizar el volumen cerebelar en los pacientes con síndrome de Cushing, así como establecer su relación con el rendimiento neuropsicológico, los niveles de cortisol y otros parámetros clínicos. Por otro lado, se pretende analizar la presencia de lesiones de sustancia blanca cerebral en los pacientes con síndrome de Cushing y la relación entre riesgo cardiovascular, lesiones de sustancia blanca, rendimiento neuropsicológico y volumen cerebral. Se encontraron menores volúmenes del córtex cerebelar bilateral en los pacientes activos, pero no en los pacientes curados, en comparación con los controles. El córtex cerebelar correlacionó positivamente con el rendimiento en memoria visual y la calidad de vida y negativamente con la edad en el momento del diagnóstico y el nivel de triglicéridos circulantes. Los pacientes activos presentaban peor rendimiento a nivel de memoria, y ambos grupos de pacientes presentaban mayores niveles de ansiedad y depresión que los controles sanos. Por otro lado, los pacientes en remisión, pero no los pacientes activos presentaron mayor nivel de lesiones de sustancia blanca cerebral que los controles sanos. Estas lesiones estaban relacionadas con los niveles de tensión diastólica y la duración de la hipertensión. Los pacientes en remisión que tomaban hidrocortisona presentaban mayor nivel de lesiones que los pacientes en remisión que no tomaban el fármaco. Finalmente ambos grupos de pacientes (activos y en remisión) presentaban mayor riesgo cardiovascular que los controles sanos. El riesgo cardiovascular correlacionó negativamente con la función cognitiva y el volumen cerebral en los pacientes en remisión. En conclusión, el síndrome de Cushing determina diferentes comorbilidades en las distintas fases de la enfermedad. Algunas de las alteraciones halladas en los pacientes activos podrían ser al menos parcialmente reversibles, aunque el riesgo cardiovascular asociado a la enfermedad puede llevar a otras comorbilidades en el futuro si no se controla. Estos datos remarcan la importancia de proporcionar un soporte psicológico a los pacientes en caso necesario y de controlar el riesgo vascular para prevenir la posible afectación cerebral futura y reducir el riesgo de complicaciones cardiovasculares.
Caetano, Maria Silvia Santarem [UNIFESP]. "Aumento da probabilidade diagnóstica de Síndrome de Cushing subclínica em amostra de população de pacientes obesos com diabetes mellitus do tipo 2." Universidade Federal de São Paulo (UNIFESP), 2008. http://repositorio.unifesp.br/handle/11600/9000.
Full textA sindrome de Cushing (SC) endogena e rara. Pacientes com SC subclinica (SCS) apresentam hipercortisolismo sem manifestacoes clinicas. SC ocorre em 2-3% de diabeticos mal controlados. Estudamos 103 pacientes adultos obesos ambulatoriais com diabetes mellitus tipo 2 para avaliar alteracoes do cortisol e SCS. Todos coletaram cortisol salivar as 23:00h e cortisol salivar e serico apos teste de supressao com 1mg de dexametasona (DST). Pacientes cujos resultados de qualquer teste estavam no quintil superior (253ng/dL, 47ng/dL e 1,8ƒÊg/dL, respectivamente para cortisol salivar 23:00h e salivar e serico pos-DST) foram reavaliados. Os valores medios desse grupo encontravam-se 2,5 vezes acima dos valores dos demais pacientes. Apos um teste confirmatorio com 2mgx2dias DST a investigacao da SC foi encerrada para 61 pacientes com todos os testes normais e 33 com apenas um teste (falso) positivo. Todos os 8 pacientes com dois testes alterados apresentaram cortisol urinario normal, mas 3 deles mostraram maior probabilidade diagnostica de SCS (hipercortisolismo e alteracoes em exames de imagem). Contudo, o diagnostico final nao pode ser confirmado por cirurgia ou patologia em nenhum deles. Embora nao confirmatorios, os resultados deste estudo sugerem que a prevalencia de SCS seja maior em populacoes de risco do que na populacao geral.
Endogenous Cushing’s syndrome (CS) is unusual. Patients with subclinical CS (SCS) present altered cortisol dynamics without obvious manifestations. CS occurs in 2-3% of obese poorly controlled diabetics. We studied 103 overweight adult outpatients with type 2 diabetes to examine for cortisol abnormalities and SCS. All collected salivary cortisol at 23:00h and salivary and serum cortisol after a 1mg dexamethasone suppression test (DST). Patients whose results were in the upper quintile for each test (253ng/dL, 47ng/dL and 1.8ìg/dL, respectively for the 23:00h and post-DST saliva and serum cortisol) were re-investigated. Average values from the upper quintile group were 2.5- fold higher than in the remaining patients. After a confirmatory 2mgx2day DST the investigation for CS was ended for 61 patients with all normal tests and 33 with only one (false) positive test. All 8 patients who had two abnormal tests had subsequent normal 24h-urinary cortisol, and 3 of them were likely to have SCS (abnormal cortisol tests and positive imaging). However, a final diagnosis could not to be confirmed by surgery or pathology. Although not confirmatory, the results of this study suggest that the prevalence of SCS is considerably higher in populations at risk than in the general population.
TEDE
BV UNIFESP: Teses e dissertações
Leal, Rodolfo Assis Oliveira. "Abordagem ao diagnóstico do hiperadrenocorticismo canino: a importância dos testes funcionais: estudo retrospectivo de 8 casos clínicos." Master's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2008. http://hdl.handle.net/10400.5/943.
Full textA abordagem ao diagnóstico do hiperadrenocorticismo (Síndrome de Cushing) pressupõe a interacção de um conjunto de exames complementares sendo que, os testes funcionais desempenham um papel muito importante a esse nível. Após descrição geral da doença, na presente dissertação, é apresentado um estudo retrospectivo acerca do diagnóstico do hiperadrenocorticismo em 8 canídeos. Conjugando uma boa anamnese, um exame clínico e as alterações, mesmo inespecíficas, dos perfis laboratoriais, a intuição clínica constitui o principal ponto de partida para um bom plano de diagnóstico. A este nível distinguem-se etapas distintas: a confirmação do hiperadrenocorticismo e a pesquisa do seu diagnóstico etiológico. Para confirmação da doença há a destacar três tipos de testes funcionais: o Rácio Cortisol-Creatinina Urinário (RCCU), o Teste de estimulação pela hormona adrenocorticotrófica (ACTH) e o teste de supressão pela dexametasona (em dose baixa). Por seu lado, o diagnóstico etiológico poderá ser efectuado recorrendo ao doseamento de ACTH endógena ou ao teste de supressão pela dexametasona (em dose alta). Ainda que o plano de diagnóstico pressuponha duas etapas, este estudo permitiu concluir que, por vezes, é possível diagnosticar a doença recorrendo apenas a um tipo de teste (como o teste de supressão pela dexametasona em dose baixa) ou por associação de testes numa única abordagem (como a combinação RCCU e o teste de supressão pela dexametasona em dose alta). Tendo em conta a necessidade de exploração do quadro lesional da doença, o recurso subsequente à imagiologia é imperativo, razão pela qual a ultrasonografia constitui uma das principais técnicas de escolha aquando do diagnóstico de hiperadrenocorticismo. Dada a dificuldade em criar linhas gerais fixas para o diagnóstico do hiperadrenocorticismo, a utilização e combinação de testes funcionais deverá ser adequada a cada caso clínico cabendo ao Médico Veterinário a realização de uma correcta aplicação dos mesmos.
ABSTRACT Several functional tests play a major role in the diagnosis of Hyperadrenocorticism. Examining the disease retrospectively as it presented in eight dogs sheds light on the practitioner’s multimodal means of diagnosis, their utility and efficacy. A good history, clinical examination and baseline laboratorial data may lead the practitioner to suspect a case of hyperadrenocorticism. To confirm these suspicions, the following diagnostic tests are available: the Urine Cortisol:Creatinine Ratio (UCCR), the Corticotropin (ACTH) stimulation test and the Low-Dose Dexamethasone Suppression Test. Once hyperadrenocorticism is confirmed, the practitioner must then determine whether the condition is primarily pituitary-dependent, or adrenal-dependent. This etiologic diagnosis can be made using the Plasma Endogenous ACTH Concentration or the High-Dose Dexamethasone Suppression Test. Although both a diagnosis of hyperadrenocorticism should be made as well as a determination of the primary organ responsible for disease, by means of two different testing methods as aforementioned, sometimes, it is possible to diagnose the hyperadrenocorticism with only one functional test (as the low-dose dexametasone suppression test) or with a test’s association (as the combined Urinary Cortisol:Creatinine Ratio and the High-Dose Dexamethasone Suppression Test). Imaging also plays an important role in revealing the pattern of the lesion and characterizing the disease. In fact, ultrasonography represents the most used resource to diagnose the hyperadrenocorticism. Recognising the difficulty to prepare diagnostic guidelines for hyperadrenocorticism, the aforementioned functional tests should be used according with individual clinical cases and the practitioner should recognize the advantages and disadvantages of each one of them.
List, Jörg V., Stephan B. Sobottka, Angela Hübner, Constanze Bonk, Jan Koy, Thomas Pinzer, and Gabriele Schackert. "Cushing’s Disease in a 7-Month-Old Girl due to a Tumor Producing Adrenocorticotropic Hormone and Thyreotropin-Secreting Hormone." Karger, 1999. https://tud.qucosa.de/id/qucosa%3A27645.
Full textDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
Bradarić, Zrinjka [Verfasser]. "Untersuchung zum Equinen Cushing Syndrom und Prüfung der Wirksamkeit von Vitex agnus-castus (Mönchspfeffer) bei der Behandlung des Equinen Cushing Syndroms / Zrinjka Bradarić." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1027815359/34.
Full textCavalcante, Isadora Pontes. "Correlação da expressão de GLUT1, HK1, HK2 e HK3 com alta captação de 18/F-FDG em hiperplasia macronodular adrenal primária." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-12012015-125308/.
Full textIntroduction: Primary macronodular adrenal hyperplasia (PMAH) is a rare cause of Cushing\'s syndrome, characterized by functioning adrenal macronodules and increased cortisol production. Recently, integrated 18F-FDG-PET/CT examination revealed an increased 18F-FDG uptake in patients with PMAH. However, it is still unclear the mechanism by which PMAH would present with a high 18F-FDG uptake in PET/CT. Objectives: The aim of this study was to investigate whether GLUT1, HK1, HK2 and/or HK3 expression would account for the high18F-FDG uptake in PMAH and compare these expressions with ACA and ACC adrenal tisuue. Methods: 12 patients undergoing adrenalectomy for PMAH with previous 18F-FDG-PET/CT. 18F-FDG uptake was quantified as the maximum standardized uptake value (maxSUV). mRNA expression was investigated through quantitative RT-PCR and protein expression was investigated using immunohistochemical studies. PMAH gene and protein expression were compared to 15 patients with ACA and 10 with ACC. Correlations were performed through Pearson\'s correlation coefficient test and comparisons through Kruskal-Wallis test, followed by Dunn adjust. Statistical significance was considered when p < 0.05. Results: All patients with PMAH presented with high 18F-FDG uptake, the range of SUVmax in these patients varied from 3.3 to 8.9 and the nodule sizes varied from 3.5 to 15 cm. There was a strong positive correlation between the nodule size and 18F-FDG uptake. However, no correlation could be established between gene and protein expression of GLUT1, HK1, HK2 and HK3 and 18F-FDG uptake. SLC2A1 and HK2 expression was significantly higher in patients with CCA than in patients with AAC and PMAH. Conclusions: Increased 18F-FDG uptake in PMAH does not arise from the overexpression of GLUT1, HK1, HK2 or HK3. Further investigation is required to elucidate the glycolytic pathway involved in glucose metabolism in PMAH
BOUFFARD, CORINNE. "Reflexions sur l'evolution des conceptions etiopathogeniques et therapeutiques des hypercorticismes surrenaux." Clermont-Ferrand 1, 1988. http://www.theses.fr/1988CLF13026.
Full textKrammer, Clemens [Verfasser], and Martin [Akademischer Betreuer] Reincke. "Kardiovaskuläres Risiko bei Cushing Syndrom und subklinischem Cushing Syndrom : eine klinisch-prospektive Arbeit / Clemens Krammer ; Betreuer: Martin Reincke." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1229835628/34.
Full textLanoux, Patricia. "Syndrome de Cushing et cancer du rein : à propos d'une observation." Reims, 1989. http://www.theses.fr/1989REIMM119.
Full textVergely, Nathalie. "L'ostéocalcine : marqueur périphérique de l'effet osseux du cortisol dans le syndrome de Cushing : à propos de 17 observations." Saint-Etienne, 1992. http://www.theses.fr/1992STET6421.
Full textGonçalves, Francisca Alves Reis Leite. "Estudo preliminar para identificação de potenciais fatores preditores de laminite em cavalos com idade [maior ou igual a] 15 anos, com um fenótipo de disfunção da pars intermedia da pituitária (DPIP)." Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2018. http://hdl.handle.net/10400.5/16058.
Full textCom o aumento da esperança média de vida do cavalo, o aparecimento de doenças como a disfunção da pars intermedia da pituitária (DPIP), também conhecida por síndrome de Cushing, tem-se tornado mais frequente. A laminite é a principal consequência desta doença e manifesta-se sobretudo sob a forma subclínica, com evolução progressiva e carácter crónico. A manifestação clínica de laminite é incapacitante para o cavalo, afetando o seu bem-estar e a sua atividade física. O objetivo deste estudo preliminar foi encontrar fatores que se relacionassem com a rotação da terceira falange (P3) e possibilitassem prever a ocorrência de laminite em cavalos com um fenótipo compatível com DPIP, antecipando a manifestação clínica desta doença e permitindo prevenir as suas consequências. Neste estudo foram incluídos oito cavalos das zonas de Lisboa e Santarém, caracterizados através da realização de um exame clínico geral e específico, um questionário aos proprietários, seguido de recolha de amostras de sangue para hemograma e determinação da concentração plasmática de hormona adrenocorticotrópica (ACTH), bem como para determinação dos níveis séricos de insulina e de glucose plasmática após realização de um teste de glucose oral. Para investigar a existência de laminite foi realizada uma avaliação radiográfica e macroscópica das extremidades distais e a medição da pressão arterial de forma indireta, a partir da artéria coccígea, recorrendo à utilização de um esfigmomanómetro. A partir dos dados obtidos neste estudo foi possível identificar uma correlação positiva, segundo o método de Spearman, entre o aumento da pressão arterial (sistólica e diastólica) e a ocorrência de rotação da terceira falange. Os resultados deste estudo apontam também para a possível existência de um valor de rotação da terceira falange a partir do qual são notáveis alterações macroscópicas da estrutura do casco. Pelo facto de não existirem intervalos de referência para avaliação da concentração basal plasmática da ACTH específicos para a latitude de Portugal, três dos oito equinos obtiveram um resultado duvidoso, reforçando a importância da realização de estudos futuros para obtenção de intervalos adequados.
ABSTRACT - Preliminary study in order to identify potential predictors of laminitis in horses aged ≥ 15 years, with a phenotype for pituitary pars intermedia dysfunction (PPID) - The equine average life expectancy has been increasing and with it the frequency of pathologies like pituitary pars intermedia dysfunction (PPID), also known as equine Cushing’s syndrome. A chronic and progressive appearance of laminitis is the most clinically relevant consequence of this pathology and it drastically affects the horse’s well-being and performance. This preliminary study focused on finding factors related to the rotation of the third phalanx (P3), which could potentially anticipate the occurrence of laminitis in horses with a phenotype for PPID, making it possible to prevent its clinical manifestation and its consequences. This study included eight horses from the districts of Lisbon and Santarém, Portugal. The characterization process of the sample included a general and specific clinical examination, a questionnaire for the owners, followed by blood sample collection for a complete blood count and plasmatic adrenocorticotropic hormone (ACTH) concentration measurement, as well as for measuring the serum insulin and plasma glucose levels after an oral sugar test. To investigate the presence of laminitis we performed a radiological and macroscopic evaluation of the distal extremities and measured the arterial blood pressure in the coccygeal artery (indirect method) with the use of a sphygmomanometer. From the data collected in this study we observed a positive correlation, according to Spearman’s rank correlation coefficient, between the raise in arterial (systolic and diastolic) pressure and the occurrence of rotation of the third phalanx. The results of this study also point to the existence of a possible cut-off value for P3 rotation from which macroscopic deformities of the hoof occur. Because there aren’t specific reference intervals for the evaluation of basal ACTH for Portugal’s latitude, three out of eight horses presented dubious results, reinforcing the importance of future studies to define appropriate reference intervals.
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Leblanc, Martine. "Syndrome de Cushing et apudomatoses : à propos d'une observation." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25273.
Full textDECROUX, BRIGAUD PASCALE. "Efficacite du ketoconazole dans les syndromes de cushing paraneoplasiques : a propos de 2 cas personnels et 10 cas bibliographiques." Lyon 1, 1992. http://www.theses.fr/1992LYO1M071.
Full textNavarranne, Anne. "Syndrome de Cushing par sécrétion ectopique d'ACTH : à propos d'un cas." Bordeaux 2, 1989. http://www.theses.fr/1989BOR23025.
Full textBLANQUET, PATRICIA. "Place du ketoconazole dans le traitement medical du syndrome de cushing." Nice, 1992. http://www.theses.fr/1992NICE6596.
Full textSONGY, LAURENCE. "Le syndrome de cushing : demarche diagnostique a propos de 10 cas." Reims, 1991. http://www.theses.fr/1991REIMM040.
Full textTIERTANT, JEAN. "Syndrome de cushing et grossesse : a propos d'un cas et revue de la litterature." Lille 2, 1994. http://www.theses.fr/1994LIL2M005.
Full textPicon, Aline. "Syndrome de Cushing paranéoplasique et tumeurs neuro-endocrines pulmonaires : pièges et difficultés diagnostiques à propos de trois cas." Montpellier 1, 1996. http://www.theses.fr/1996MON11143.
Full textEspiard, Stéphanie. "Génétique de l'hyperplasie macronodulaire des surrénales : identification et caractérisation du gène ARMC5." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB076/document.
Full textPrimary bilateral macronodular adrenal hyperplasia (PBMAH) is a rare cause of adrenal Cushing’s syndrome and bilateral adrenal tumors. We suspected a genetic origin of the disease on the basis of the report of some familial cases and the involvement of both adrenal glands. The aim of this study was to find a genetic cause of non syndromic PBMAH. To look at chromosomal abnormalities, we use single-nucleotide polymorphism (SNP) arrays and microsatellite markers analysis in a first series of 33 patients all operated for PBMAH. We realize whole genome sequencing of 5 patients (blood and tumor DNAs matched). Then we genotyped by Sanger sequencing the gene Armadillo Repeat Containing 5 (ARMC5) in this first series and 66 additional patients. Clinical data were collected to establish genotype-phenotype correlation. In addition, the cohort of patients of our collaborators at the National Institute Health (Dr. Stratakis, Bethesda, USA) was studied. The effects of ARMC5 inactivation and overexpression and the partners of the protein were sought in cell-culture models. The most frequent somatic alteration was a loss of heterozygosity at 16p observed in tumors of 25% of the patients. The gene ARMC5, located at 16p11.2, was the most frequently mutated by whole genome sequencing: a mutation was found in 4/5 patients. 55% of the patients of the first cohort (33 patients treated by adrenalectomy for PBMAH) had ARMC5 alteration. One patient presented with germline microdeletion of the locus identified by SNP array. Every patient had two events: either a mutation or a deletion at the germline level, either a second mutation or a LOH at the somatic level. We showed that the two events were present on different alleles suggesting that ARMC5 is a tumor suppressor gene. In addition, we showed for several patients that the second hit was different in each adrenal nodules of a same patient. This first cohort included only operated patients with serious forms of the disease. The study of the American cohort and the analysis of the total cohort of our lab including non-operated patients and milder forms showed an alteration of ARMC5 in about 25% of the patients. Genotype-phenotype correlation showed that ARMC5 defects are associated with younger age at the diagnosis, higher hypercortisolism, bigger adrenals and higher number of nodules. In addition, a mutation of ARMC5 was shown in a patient with a PBMAH secreting both aldosterone and cortisol. Analysis of a series of patient affected by primary hyperaldosteronism suggested that ARMC5 may be associated with hypertension especially in African-American subjet. Overexpression of ARMC5 leads in vitro to cell apoptosis. We showed that this apoptosis was reduced when transfecting vector harboring missense mutations or single amino-acid deletion found in our cohort. Invalidation of ARMC5 leads to a decreased steroidogenic enzymes expression, cortisol production and reduced protein kinase A (PKA) activity. We showed that ARMC5 interacts with the calaytic subunit alpha of the PKA dissociated from the cAMP-bound regulatory subunits. More than one quarter of sporadic PBMAH patients present a pathogenic germline ARMC5 defect and these index cases present a more severe disease. Systematic genotyping of ARMC5 may help for early diagnosis of PBMAH, familial counseling, and patients’ management. ARMC5 appears to be a new regulator of PKA and might represent a new target for the development of pharmacological agents controlling PKA function and cortisol production
MAZZA, SYLVIO. "Syndrome de cushing paraneoplasique et tumeur endocrine du pancreas : a propos d'un cas." Reims, 1989. http://www.theses.fr/1989REIMM052.
Full textSandner, Benjamin. "Evaluation des Einflusses anthropometrischer Faktoren und Cytochrom-P450-modulierender Pharmaka auf den Dexamethasonmetabolismus im Rahmen des niedrig dosierten Dexamethason-Suppressionstestes." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-216234.
Full textMODRIC, VINCENT. "Les tassements vertebraux revelateurs d'un syndrome de cushing : a propos de trois observations." Reims, 1989. http://www.theses.fr/1989REIMM055.
Full textMYCINSKI, STANISLAS. "Test au cfr dans les syndromes de cushing : interet diagnostique et pronostique." Lille 2, 1989. http://www.theses.fr/1989LIL2M006.
Full textCaldaguès, Ramos Emmanuelle Baron Remond Sabine. "Discussion étiologique d'un syndrome de Cushing secondaire à une maladie surrénalienne primitive à propos d'un cas /." [S.l.] : [s.n.], 2004. http://theses.univ-nantes.fr/thesemed/SPEcaldagues.pdf.
Full textCaumia-Baillenx, Gyslène. "Association neurofibromatose-tumeur carcinoide-hypergastrinémie : à propos d'un cas clinique." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M070.
Full textDELANDRE, THIERRY. "Syndrome d'hypercorticisme para-neoplasique : a propos d'un cas de carcinome bronchique neuro-endocrine a cellules de type intermediaire." Aix-Marseille 2, 1990. http://www.theses.fr/1990AIX20016.
Full textFernandes, Maria Antónia Fialho. "Clínica de animais de companhia: hiperadrenocorticismo em animais de companhia: desenvolvimento de um caso clínico de síndrome de cushing num felídeo." Master's thesis, Universidade de Évora, 2014. http://hdl.handle.net/10174/13997.
Full textCABALET, DOMINIQUE. "Syndrome de cushing iatrogene chez le nourrisson : a propos de deux observations." Toulouse 3, 1988. http://www.theses.fr/1988TOU31310.
Full textLozès, Marie. "A propos de neuf patients diagnostiqués pour un syndrome de Cushing au centre Hospitalier Universitaire de Pointe-à-Pitre entre 2006 et 2010 : Quel dépistage proposer en médecine générale ?" Antilles-Guyane, 2011. http://www.theses.fr/2011AGUY0406.
Full textCushing syndrome is a rare disease, but its prevalence is underestimated and the diagnosis difficult and often delayed that causes many complications which can be life-threatening. The General Practitionner should be the first to discuss and track it. We studied a series of nine patients diagnosed with Cushing's syndrome at the University Hospital of Pointe-à-Pitre between 2006 and 2010. Of the 9 cases, a single diagnosis of Cushing's syndrome has been referred by general practitioners. The High Authority of Health recommends screening patients with discriminating symptoms such as facio-truncal distribution of fat, signs of hypercatabolism skin, muscle and bone as weIl as children with a slower growth curve, especiaIly if it is associated with paradoxal weight gain. Screening should also detect risk groups such as diabetics impossible to balance, treatment resistant hypertension, osteoporosis without obvious cause, atypical psychiatrie patients and patients with adrenal incidentaloma. First line testing to be conducted are urine free cortisol, 1 mg overnight dexamethaseone suppression test and late-night salivary cortisol. Tests should be repeated for suspeeted cyclic Cushing's syndrome
Leonczuk, Bernadette [Verfasser]. "Langzeitwirkung von Trilostan bei Hunden mit Cushing-Syndrom / Bernadette Leonczuk." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2011. http://d-nb.info/1013353722/34.
Full textRitzel, Katrin [Verfasser]. "Das Cushing Syndrom: Eine Diagnostische und therapeutische Herausforderung / Katrin Ritzel." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1234389177/34.
Full textSolbi, Mohamed. "A propos d'une acromégalie particulière." Montpellier 1, 1994. http://www.theses.fr/1994MON11162.
Full textVARINOT, CORINNE. "Syndrome de cushing de l'enfant et de l'adolescent : a propos de 8 observations." Reims, 1994. http://www.theses.fr/1994REIMM087.
Full textROBIN, PHILIPPE GUY MARCEL. "Les adenomes hypophysaires geants : a propos de deux observations." Clermont-Ferrand 1, 1989. http://www.theses.fr/1989CLF13047.
Full textLehnert, Claudia. "24 hour hormone and serum electrolyte levels of dogs with pituitary-dependent hyperadrenocorticism treated with trilostane." Giessen : VVB Laufersweiler, 2007. http://geb.uni-giessen.de/geb/volltexte/2007/4678/index.html.
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