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Arq. neuropsiquiatr ; 72(5): 378-382, 05/2014. tab
Article in English | LILACS | ID: lil-709367


To describe a series of 129 consecutive patients submitted to the resection of pituitary tumors using the endoscopic transsphenoidal approach in a public medical center. Method: Retrospective analysis based on the records of patients submitted to the resection of a pituitary tumor through the endoscopic transsphenoidal approach between 2004 and 2009. Results: One hundred and twenty-nine records were analyzed. The tumor was non-secreting in 96 (74.42%) and secreting in 33 patients (22.58%). Out of the secretory tumors, the most prevalent was the growth hormone producer (7.65%), followed by the prolactinoma, (6.98%). Eleven patients developed cerebral spinal fluid (CSF) fistulas, and four of them developed meningitis. One patient died due to intracerebral hemorrhage in the postoperative period. Conclusion: The endoscopic transsphenoidal approach to sellar tumors proved to be safe when the majority of the tumors were non-secreting. The most frequent complication was CSF. This technique can be done even in a public hospital with financial limits, since the health professionals are integrated. .

Descrever uma série de 129 pacientes submetidos à ressecção de tumor de hipófise com acesso endoscópico transesfenoidal em um serviço de público referência em Belo Horizonte. Método: Análise retrospectiva realizada por análise dos prontuários de pacientes submetidos à ressecção de tumor de hipófise com acesso endoscópico transesfenoidal entre os anos 2004 e 2009. Resultados: Foram avaliados 129 prontuários. O tumor era não secretante em 96 (74,42%) e secretante em 33 pacientes (22,58%). Dos tumores secretores, o de maior prevalência foi o produtor de hormônio do crescimento: 15 pacientes (7,65%). Onze pacientes desenvolveram fístula liquórica. Um paciente faleceu devido hemorragia intracerebral no pós-operatório. Conclusão: O acesso endoscópico transfenoidal aos tumores selares mostrou-se seguro numa população em que a maioria dos tumores era não secretante. A principal complicação encontrada foi fístula liquórica. Esta técnica é passível de utilização em hospital público mesmo com limites financeiros desde que haja integração multiprofissional. .

Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Adenoma/surgery , Natural Orifice Endoscopic Surgery/methods , Pituitary Neoplasms/surgery , Adenoma , Adrenocorticotropic Hormone/metabolism , Growth Hormone/metabolism , Pituitary Neoplasms , Reproducibility of Results , Retrospective Studies , Sphenoid Sinus/surgery , Treatment Outcome , Thyrotropin/metabolism
Medicina (B.Aires) ; 73(6): 579-84, Dec. 2013.
Article in Spanish | LILACS, BINACIS | ID: biblio-1165169


Serum cortisol measurement is a very useful tool in the biochemical evaluation of adrenocortical function. Since this hormone circulates in blood mainly linked to binding globulins but is also partially free, it can be measured not only in the blood but also in urine, saliva and other biological fluids and tissues. Basal determinations as well as dynamic testing may be performed to evaluate the circadian variations, to estimate the diurnal cortisol secretion and to analyze its relations with other components of the hypothalamic-pituitary-adrenal axis. Measurements of cortisol in blood, saliva and urine may reflect the cortisol secretion at the time of sample collection or during a 24 h span. Recently, it has been proposed the determination of cortisol in tissues such as hair and nails like a means of evaluating the hormonal status during prolonged periods. The aim of this paper is to update the methodology for measuring cortisol and its usefulness for the clinical diagnosis of troubles of the hypothalamic-pituitary-adrenal axis.

Hydrocortisone/analysis , Saliva/chemistry , Hypothalamo-Hypophyseal System/metabolism , Pituitary-Adrenal System/metabolism , Enzyme-Linked Immunosorbent Assay , Hydrocortisone/blood , Hydrocortisone/urine , Adrenocorticotropic Hormone/metabolism , Humans , Circadian Rhythm/physiology , Transcortin/physiology , Ultrafiltration
Article in English | WPRIM | ID: wpr-148462


Congenital adrenal insufficiency is caused by specific genetic mutations. Early suspicion and definite diagnosis are crucial because the disease can precipitate a life-threatening hypovolemic shock without prompt treatment. This study was designed to understand the clinical manifestations including growth patterns and to find the usefulness of ACTH stimulation test. Sixteen patients with confirmed genotyping were subdivided into three groups according to the genetic study results: congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH, n=11), congenital lipoid adrenal hyperplasia (n=3) and X-linked adrenal hypoplasia congenita (n=2). Bone age advancement was prominent in patients with CAH especially after 60 months of chronologic age (n=6, 67%). They were diagnosed in older ages in group with bone age advancement (P<0.05). Comorbid conditions such as obesity, mental retardation, and central precocious puberty were also prominent in this group. In conclusion, this study showed the importance of understanding the clinical symptoms as well as genetic analysis for early diagnosis and management of congenital adrenal insufficiency. ACTH stimulation test played an important role to support the diagnosis and serum 17-hydroxyprogesterone levels were significantly elevated in all of the CAH patients. The test will be important for monitoring growth and puberty during follow up of patients with congenital adrenal insufficiency.

17-alpha-Hydroxyprogesterone/blood , Disorder of Sex Development, 46,XY/drug therapy , Adolescent , Adrenal Hyperplasia, Congenital/drug therapy , Adrenal Insufficiency/congenital , Adrenocorticotropic Hormone/metabolism , Bone Development/genetics , Child , Child, Preschool , DAX-1 Orphan Nuclear Receptor/genetics , Female , Genetic Diseases, X-Linked/drug therapy , Genotype , Glucocorticoids/therapeutic use , Humans , Intellectual Disability/complications , Male , Mineralocorticoids/therapeutic use , Obesity/complications , Phosphoproteins/genetics , Puberty, Precocious/complications , Retrospective Studies , Steroid 21-Hydroxylase/genetics
Rev. chil. endocrinol. diabetes ; 5(1): 6-12, ene. 2012. graf, ilus
Article in Spanish | LILACS | ID: lil-640646


Background: Circadian cortisol production results from the interaction of the circadian production of ACTH, the autonomic nervous system and intrinsic factors within the gland. An additional regulator is the neuro-hormone melatonin. In human adrenal gland cultures, melatonin inhibited ACTH stimulated cortisol production and Per1 mRNA expression. ACTH actions on the adrenal involve early and late responses. Aim: To investigate the effects of melatonin on the time course of ACTH stimulated cortisol production and of Per1 expression in the lamb adrenal gland. Material and Methods: Adrenal glands and plasma of five newborn lambs were obtained. Adrenal glands were cut in 15 mg explants. Three of these explants were stored for RNA extraction. The rest of explants were using in different culture protocols with ACTH and melatonin. Results: Lambs had an in vivo a circadian variation in plasma cortisol and in adrenal Per1 expression. In vitro, ACTH stimulated an early and late increase in cortisol production and an early increase in Per1 expression reaching a maximum at 3 hours of treatment. Melatonin inhibited the early Per1 response to ACTH without affecting the early ACTH stimulated cortisol production. However, melatonin inhibited the late response of cortisol production to ACTH. Conclusions: The inhibitory actions of melatonin on Per1 response to ACTH may contribute to the inhibitory effects of melatonin on adrenal steroidogenic response to ACTH.

Animals , Adrenal Glands/metabolism , Hydrocortisone/metabolism , Adrenocorticotropic Hormone/metabolism , Melatonin/metabolism , Period Circadian Proteins , RNA, Messenger/metabolism , Circadian Rhythm , Culture Techniques , Sheep , Time Factors
Arq. bras. endocrinol. metab ; 55(5): 295-302, June 2011. ilus, graf
Article in English | LILACS | ID: lil-604158


In the last two decades there was important evolution on the knowledge of the function of the hypothalamic-pituitary-adrenal axis. In the last decade, the expression "relative adrenal insufficiency" (RAI) was created, and more recently "critical illness-related corticosteroid insufficiency" (CIRCI) was used to designate those patients in which cortisol production was not sufficiently increased in stress situations. Patients with CIRCI have elevated hospital morbidity and mortality. Currently, there is a wide discussion about diagnostic criteria for this dysfunction. Besides basal cortisol, some publications now study the role of other tests, such as cortrosyn test - either in low (1 μg) or high doses (250 μg); free cortisol, salivary cortisol, metyrapone test and others. With this review, we aimed at summarizing the results of the most influent papers that intended to define diagnostic criteria for CIRCI. We also suggest an approach for CIRCI diagnosis and make it clear that the decision about steroid therapy in septic shock patients is matter apart from RAI.

Nas últimas décadas, houve uma importante evolução no conhecimento sobre a função do eixo hipotálamo-pituitária-adrenal. Na última década, foi cunhada a expressão "insuficiência adrenal relativa" (IAR) e, mais recentemente, a expressão "insuficiência adrenal relacionada à doença grave" (CIRCI) foi utilizada para designar aqueles pacientes nos quais a produção de cortisol não era suficientemente elevada em situações de estresse. Pacientes com CIRCI apresentam elevada morbidade e mortalidade em hospitais. Atualmente, há uma ampla discussão sobre os critérios de diagnóstico para essa desordem. Além do cortisol basal, algumas publicações analisaram o papel de outros testes, tais como o teste de estímulo com ACTH (cortrosina), com doses baixas (1 mg) ou altas (250 mg), cortisol livre, cortisol salivar, teste da metirapona e outros. O objetivo desta revisão foi resumir os resultados dos artigos mais importantes que buscaram definir os critérios de diagnóstico para a CIRCI. Também sugerimos uma abordagem para o diagnóstico da CIRCI e deixamos claro que a decisão sobre a terapia com esteroides em pacientes em choque séptico é uma questão separada da IAR.

Humans , Adrenal Insufficiency/diagnosis , Critical Care , Adrenal Insufficiency/drug therapy , Adrenocorticotropic Hormone/metabolism , Arginine Vasopressin/metabolism , Critical Illness , Corticotropin-Releasing Hormone/metabolism , Cosyntropin , Hydrocortisone/analysis , Hydrocortisone/deficiency , Metyrapone , Pituitary Gland/physiopathology , Steroids/administration & dosage , Steroids/physiology
Rev. bras. psiquiatr ; 29(supl.1): s3-s6, maio 2007.
Article in Portuguese | LILACS | ID: lil-452225


OBJETIVO: Este artigo discute a ativação diferencial do eixo hipotálamo-pituitária-adrenal no transtorno de ansiedade generalizada e no transtorno de pânico. MÉTODO: Resultados de recentes revisões da literatura são resumidos e discutidos. RESULTADOS: Os resultados de estudos experimentais que dosaram o hormônio adrenocorticotrópico, o cortisol e a prolactina mostram que ataques de pânico naturais, bem como os provocados por agentes panicogênicos seletivos - como lactato de sódio e dióxido de carbono -, não ativam o eixo hipotálamo-pituitária-adrenal. Agonistas do receptor de colecistocinina do tipo B, como o peptídeo colecistocinina-4 e a pentagastrina, elevam os hormônios de estresse, independentemente da ocorrência de um ataque de pânico, parecendo ativar diretamente o eixo hipotálamo-pituitária-adrenal. O antagonista benzodiazepínico flumazenil não eleva o nível dos hormônios de estresse; porém, este agente farmacológico não induz ataques de pânico de modo consistente. Agentes farmacológicos que aumentam a ansiedade em pacientes de pânico (cafeína, ioimbina, agonistas serotonérgicos), assim como em pessoas saudáveis, elevam o nível dos hormônios de estresse. CONCLUSÕES: Além das diferenças na sintomatologia e na resposta farmacológica, o transtorno de ansiedade generalizada e o transtorno de pânico afetam os hormônios de estresse de modo distinto. Enquanto a ansiedade antecipatória e o transtorno de ansiedade generalizada ativam tanto o eixo hipotálamo-pituitária-adrenal como o simpático-adrenal, o ataque de pânico causa acentuada ativação simpática; porém, afeta pouco o eixo hipotálamo-pituitária-adrenal.

OBJECTIVE: This article focuses on the differential activation of the hypothalamic-pituitary-adrenal axis in generalized anxiety disorder and panic disorder. METHOD: The results of recently reported reviews of the literature are summarized and discussed. RESULTS: The results of experimental studies that assayed adrenocorticotropic hormone, cortisol and prolactin show that real-life panic attacks, as well as those induced by selective panicogenic agents such as lactate and carbon dioxide, do not activate the hypothalamic-pituitary-adrenal axis. Agonists of the cholecystokinin receptor B such as the cholecystokinin-4 peptide and pentagastrin increase stress hormones regardless of the occurrence of a panic attack and, thus, seem to activate the hypothalamic-pituitary-adrenal axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increase anxiety in both normal people and panic patients (caffeine, yohimbine, serotonergic agonists) raise stress hormone levels. CONCLUSIONS: In addition to the differences in symptomatology and pharmacological response, generalized anxiety disorder and panic disorder affect stress hormones in distinct ways. While anticipatory anxiety and generalized anxiety disorder activate both the hypothalamic-pituitary-adrenal and the sympathoadrenal axes, panic attack causes major sympathetic activation, but has little effect on the hypothalamic-pituitary-adrenal axis.

Animals , Humans , Hypothalamo-Hypophyseal System/physiopathology , Panic Disorder/physiopathology , Pituitary-Adrenal System/physiopathology , Stress, Psychological/physiopathology , Adrenocorticotropic Hormone/metabolism , Carbon Dioxide/metabolism , Disease Models, Animal , Hypothalamo-Hypophyseal System/metabolism , Lactic Acid/metabolism , Panic Disorder/metabolism , Panic Disorder/psychology , Pituitary-Adrenal System/metabolism , Prolactin/metabolism , Stress, Psychological/metabolism
Rev. bras. psiquiatr ; 29(supl.1): s7-s12, maio 2007.
Article in Portuguese | LILACS | ID: lil-452226


OBJETIVO: Os autores realizaram uma revisão tradicional da literatura sobre os achados neurobiológicos das disfunções do eixo hipotálamo-pituitária-adrenal associados ao transtorno de estresse pós-traumático. MÉTODO: Os achados científicos relevantes foram descritos de acordo com a ordem cronológica de publicação e as características dos estudos, se eram pré-clínicos, relacio-nados à violência precoce como fator de risco e, finalmente, achados clínicos em pacientes portadores de transtorno de estresse pós-traumático. RESULTADOS: Foi encontrada uma literatura rica de achados a respeito de disfunções do eixo hipotálamo-pituitária-adrenal e transtorno de estresse pós-traumático. Os achados mostraram que o transtorno de estresse pós-traumático está associado a disfunções deste eixo e de estruturas cerebrais como o córtex pré-frontal, hipocampo e amídala. Os pacientes com transtorno de estresse pós-traumático apresentam um aumento da responsividade dos receptores de glicocorticóides, sugerindo que a inibição do feedback negativo tem um papel importante na fisiopatologia do quadro. Estudos pré-clínicos com modelos animais de deprivação maternal evidenciaram que, dependendo de quando o trauma ocorre, a disfunção do eixo será diferente. Os estudos clínicos mostram que o estresse precoce está relacionado ao desenvolvimento de psicopatologia durante a vida adulta. CONCLUSÕES: As disfunções do eixo hipotálamo-pituitária-adrenal relacionadas ao transtorno de estresse pós-traumático são evidências robustas e os mecanismos subjacentes a ele são cada vez mais compreendidos.

OBJECTIVE: To review the literature on neurobiological findings related to hypothalamic-pituitary-adrenal axis dysfunctions associated with posttraumatic stress disorder. METHOD: The relevant scientific findings were described according to the date of publication and the characteristics of the studies: preclinical studies, studies on early life violence as a risk factor, and clinical findings related to patients diagnosed with posttraumatic stress disorder. RESULTS: A rich literature on hypothalamic-pituitary-adrenal axis dysfunctions and posttraumatic stress disorder was found. Neurobiological findings showed that posttraumatic stress disorder is associated with hypothalamic-pituitary-adrenal axis dysfunctions and other brain-related structures: prefrontal cortex, hippocampus, and amygdala. Posttraumatic stress disorder patients have low plasma levels of cortisol and present increased responsivity of glucocorticoid receptors, suggesting that the inhibition of negative feedback plays a significant role in the disorder pathology. Preclinical studies using animal models of maternal deprivation showed that depending on the moment the trauma occurred during the development, different hypothalamic-pituitary-adrenal axis dysfunctions were produced. Clinical studies showed that early life stress is related to the development of psychopathologies during adulthood. CONCLUSIONS: There is robust evidence of hypothalamic-pituitary-adrenal axis dysfunctions related to posttraumatic stress disorder, and the mechanisms underlying this association are being better understood.

Animals , Humans , Crime Victims/psychology , Hypothalamo-Hypophyseal System/physiopathology , Pituitary-Adrenal System/physiopathology , Stress Disorders, Post-Traumatic/physiopathology , Violence/psychology , Adrenocorticotropic Hormone/metabolism , Amygdala/pathology , Amygdala/physiopathology , Corticotropin-Releasing Hormone/metabolism , Evidence-Based Medicine , Hippocampus/pathology , Hippocampus/physiopathology , Risk Factors , Survivors , Stress Disorders, Post-Traumatic/psychology
Rev. bras. psiquiatr ; 29(supl.1): s13-s18, maio 2007. ilus
Article in Portuguese | LILACS | ID: lil-452227


OBJETIVO: Revisar os achados recentes sobre a relação entre estresse, eixo hipotálamo-pituitária-adrenal e depressão, na tentativa de explicar um endofenótipo de vulnerabilidade para o desenvolvimento da depressão. MÉTODO: Revisão não sistemática da literatura baseada na hipótese de endofenótipo. RESULTADOS: A depressão está relacionada à hipercortisolemia em muitos pacientes; porém, nem todos os deprimidos apresentam esta alteração na função hipotálamo-pituitária-adrenal. Os primeiros estudos publicados observaram esta hiperativação do eixo hipotálamo-pituitária-adrenal por meio do teste de supressão da dexametasona. Estes resultados não foram largamente replicados em grande parte devido à falta de acurácia desse teste. A hipercortisolemia ocorre freqüentemente em pacientes com depressão grave, do tipo melancólico, psicóticos ou não. Está relacionada a um polimorfismo específico do gene do transportador da serotonina; a história de abuso ou negligência durante a infância ou perda parental precoce; e ao temperamento que resulta em alterações na resposta ao estresse. CONCLUSÕES: As alterações do eixo hipotálamo-pituitária-adrenal dependem de diversos fatores, como gravidade e tipo de depressão, genótipo, história de trauma na infância, temperamento e, provavelmente, resiliência. Todas essas variáveis se relacionam a um endofenótipo vulnerável ao desenvolvimento de depressão.

OBJECTIVE: To review the new findings about stress, hypothalamic-pituitary-adrenal axis and depression trying to explain a possible endophenotype prone to depression. METHOD: Nonsystematic review of the literature based on the endophenotype hypothesis. RESULTS: Depression is linked to hypercortisolemia in many patients, but not all patients present these hypothalamic-pituitary-adrenal axis dysfunction. The dexamethasone suppression test is not the most accurate test to measure the hypothalamic-pituitary-adrenal axis function, and its use in the first studies published probably jeopardized the results. Hypercortisolemia frequently occurs in patients with severe depression, melancholic, either psychotic or nonpsychotic type; it is linked to the presence of a polymorphism in the promoter of the serotonin transporter gene, with a history of childhood abuse or neglect, or other significant stressful experiences like the loss of a parent during childhood and temperament leading to alterations in the response to stress. CONCLUSIONS: The alterations of the hypothalamic-pituitary-adrenal axis depend on many factors like severity and type of depression, genotype, history of exposure to stress, temperament, and probably resilience. All these factors together result in an endophenotype thought to be prone to depression.

Humans , Depressive Disorder, Major/genetics , Glucocorticoids/metabolism , Hypothalamo-Hypophyseal System/physiopathology , Pituitary-Adrenal System/physiopathology , Stress, Psychological/genetics , Adrenocorticotropic Hormone/metabolism , Corticotropin-Releasing Hormone , Depressive Disorder, Major/physiopathology , Dexamethasone , Genetic Predisposition to Disease , Phenotype , Polymorphism, Genetic , Stress, Psychological/physiopathology , Temperament
Rev. bras. psiquiatr ; 29(supl.1): s33-s38, maio 2007. graf, ilus
Article in Portuguese | LILACS | ID: lil-452230


OBJETIVO: Revisar a literatura a respeito da interação entre sono e sistema imunológico. MÉTODO: Busca no Web of Science e no PubMed com os descritores: sono, privação de sono, estresse, eixo hipotálamo-pituitária-adrenal, sistema imunológico e doenças auto-imunes. RESULTADOS: Foram encontrados 588 artigos no Web of Science. As 61 referências mais significativas e mais relacionadas aos objetivos do estudo foram utilizadas. Foram incluídos artigos originais e de revisão. CONCLUSÃO: A privação de sono e o sistema imunológico exercem e sofrem influências mútuas. A privação de sono é considerada um estressor, uma vez que induz a elevação do cortisol em seres humanos - ou da corticosterona em roedores. Os glicocorticóides, por sua vez, exercem um efeito imunossupressor. Por essas razões, foi proposto que o aumento da ativação do eixo hipotálamo-pituitária-adrenal seja um importante mediador das alterações imunológicas observadas em pacientes com insônia ou privados de sono.

OBJECTIVE: To review the literature on the interaction between sleep and the immune system. METHOD: A search on Web of Science and Pubmed database including the keywords sleep, sleep deprivation, stress, hypothalamic-pituitary-adrenal axis, immune system, and autoimmune diseases. RESULTS: On Web of Science, 588 publications were retrieved; 61 references, more significant and closer to our objective, were used, including original articles and review papers. CONCLUSION: Sleep deprivation and immune system exert a bidirectional influence on each other. Since sleep deprivation is considered a stressor, inasmuch as it induces elevation of cortisol or corticosterone levels in humans and rodents, respectively, and given the well-known immunosuppressive effect of glucocorticoids, we propose that increased activation of the hypothalamic-pituitary-adrenal axis is a major mediator of the immune alterations observed in patients with insomnia or in sleep deprived subjects.

Animals , Humans , Hypothalamo-Hypophyseal System/physiology , Immune System/physiology , Pituitary-Adrenal System/physiology , Stress, Physiological , Sleep Deprivation/physiopathology , Sleep/physiology , Adrenocorticotropic Hormone/metabolism , Circadian Rhythm/physiology , Glucocorticoids/metabolism , Hydrocortisone/metabolism , Sleep, REM , Sleep Deprivation/immunology , Sleep Disorders, Circadian Rhythm/physiopathology , Sleep/immunology
An. acad. bras. ciênc ; 79(1): 87-95, Mar. 2007. ilus
Article in English | LILACS | ID: lil-445588


Rhodnius prolixus Malpighian tubules (MTs) are a good model for fluid and ion secretion studies in view of the dramatic postprandial diuresis, which follows its massive blood meals. Ingestion of a blood meal equals to 10-12 times their initial body mass, leads to rapid activation of high output by excretory system, which eliminates 40-50 percent of the fluid mass. Secretion of ions and water is stimulated 1000-fold by serotonin and diuretic hormone. These hormones cooperate synergistically to activate adenylate cyclase activity from MTs cells, which increase the level of intracellular cAMP. The anti-diuretic hormones have also an important role in the fluid maintenance of Rhodnius prolixus. Several hours after insect feeding occurs a reduction in urine flow, that has been thought to result from a decreased diuretic hormone release or from a novel mechanism of anti-diuresis involving insect cardioacceleratory peptide 2b (CAP2b) and cyclic GMP. In this article it is discussed how the hormone regulation of fluid transport is done in Rhodnius prolixus MTs.

Os túbulos de Malpighi (TMs) de Rhodnius prolixus são reconhecidos por serem excelentes modelos para o estudo da secreção de fluidos e íons devido a grande diurese que ocorre quando esses animais se alimentam de sangue. O inseto, após alimentação, pode aumentar seu peso corporal inicial em até 10-12 vezes, o que leva a rápida ativação do sistema excretor, que elimina 40-50 por cento do fluido corporal. A secreção de íons e água é estimulada 1000 vezes pela serotonina e pelos hormônios diuréticos. Esses hormônios agem sinergicamente ativando a adenil ciclase das células dos TMs, aumentando os níveis intracelulares de AMPc. Os hormônios anti-diuréticos também têm um importante papel na manutenção dos fluídos corporais do Rhodnius prolixus. Várias horas após a alimentação do inseto ocorre uma redução do fluxo urinário, o que foi sugerido ser decorrente da diminuição da liberação dos hormônios diuréticos ou da anti-diurese envolvendo o peptídeo cardioaceleratório 2b (CAP2b) e o GMPc. Neste artigo é discutida a regulação hormonal do transporte de fluido nos MTs de Rhodnius prolixus.

Animals , Diuresis/physiology , Insect Hormones/metabolism , Malpighian Tubules/physiology , Neuropeptides/metabolism , Rhodnius/physiology , Adrenocorticotropic Hormone/metabolism , Cyclic AMP/metabolism , Ion Transport/physiology , Kinins/metabolism , Malpighian Tubules/metabolism , Rhodnius/metabolism , Serotonin/metabolism
Arq. bras. endocrinol. metab ; 51(1): 34-41, fev. 2007. ilus
Article in Portuguese | LILACS | ID: lil-448361


Diversas alterações endócrinas são descritas na obesidade. O eixo corticotrófico encontra-se hiper-responsivo, com maior depuração dos hormônios e nível de cortisol normal. A caracterização do pseudo-Cushing é importante. A leptina parece ser um hormônio permissivo para o desencadeamento da puberdade. Em adultos, as gonadotrofinas são normais, hiperandrogenismo e hiperestrogenismo são encontrados. Nas mulheres, a resistência insulínica é central no desenvolvimento da síndrome dos ovários policísticos (SOP), associada a hiperandrogenemia ovariana. Nos obesos, GH geralmente é baixo e IGF1 normal. A função tireoidiana é habitualmente normal nos obesos.

Several endocrine changes have been described in the obesity state. The corticotropic axis is hyperresponsive and there is enhancement of hormonal clearance, but cortisol levels are within the normal range. It is important to characterize a pseudo-Cushing in obesity. Leptin seems to be a permissive hormone for the beginning of puberty. In adults, gonadotropines are normal, and hyperandrogenism and hyperestrogenism are found. In women, insulin resistance has a central role in polycystic ovarian syndrome (POS), which is associated to ovarian hyperandrogenemia. In obese subjects, growth hormone (GH) is generally low and IGF1 is normal. Thyroid function is commonly normal in obese subjects.

Humans , Endocrine Glands/metabolism , Hormones/metabolism , Hypothalamo-Hypophyseal System/metabolism , Obesity/metabolism , Obesity/physiopathology , Adrenocorticotropic Hormone/metabolism , Gonadotropins, Pituitary/metabolism , Growth Hormone/metabolism , Insulin Resistance/physiology , Leptin/metabolism , Thyrotropin/metabolism
Arq. bras. cardiol ; 85(6): 421-424, dez. 2005. ilus
Article in Portuguese | LILACS | ID: lil-419801


Este artigo tem o objetivo de relatar o diagnóstico e a evolução clínica de um paciente de 15 anos portador de uma disfunção congênita da esteroideogênese adrenal, que pode apresentar-se como hipertensão arterial de diagnóstico muitas vezes tardio (adolescência), virilização ou formas perdedoras de sal (nascimento e infância).

Humans , Male , Adolescent , Adrenal Hyperplasia, Congenital , Adrenal Hyperplasia, Congenital , Hypertension/complications , Hypertension/drug therapy , Hypertension/metabolism , Adrenocorticotropic Hormone/metabolism , Puberty, Precocious/enzymology , Puberty, Precocious/pathology
Noise Health ; 2004 Jan-Mar; 6(22): 35-47
Article in English | IMSEAR | ID: sea-122028


Mainly dependent on level and dynamic increase sound produces over-shooting excitations which activate subcortical processing centers (e.g. the amygdala, functioning as fear conditioning center) besides cortical areas (e. g. arousing annoyance, awakenings) as well. In addition there exist very close central nervous connections between subcortical parts of the auditory system (e.g. amygdala) showing typical plasticity effects (sensitization) and the hypothalmic-pituitary-adrenal (HPA)-axis. Using that causal chain noise induce cortisol excretion even below the awakening threshold. Thus repeated noise events (e.g. overflights during night time) may lead to accumulation of the cortisol level in blood. This can happen because its time-constant of exponential decrease is about 50 to 10 times larger than that one for adrenaline and noradrenaline. This fact and the unusual large permeability of cortisol through the cell membranes opens a wide field of connections between stress-dependent cortisol production and the disturbance of a large number of other endocrine processes, especially as a result of long-term stress activation by environmental influences such as environmental noise. Based upon a physiological model calculating the cortisol accumulation starting at a nightly threshold of physiological over-proportional reactions around Lmax = 53 dB(A) the number of tolerable noise events (over-flights in a nightly time range) can be estimated for given indoor peak sound pressure levels, keeping the cortisol increase within the normal range. Examples of results for 8 hours in the night are for instance number and level combinations (NAL-values) of 13 events with 53 dB(A) indoor peak level or 6 events with 70 dB(A) indoor peak level respectively.

Adrenocorticotropic Hormone/metabolism , Aircraft , Amygdala/metabolism , Auditory Perception/physiology , Endocrine System/metabolism , Endorphins/metabolism , Humans , Hydrocortisone/blood , Maximum Allowable Concentration , Noise, Transportation/adverse effects , Occupational Exposure/adverse effects , Pituitary Gland/metabolism , Sleep Wake Disorders/etiology
Arq. bras. endocrinol. metab ; 44(6): 455-70, dez. 2000. ilus, tab
Article in Portuguese | LILACS | ID: lil-277271


Este artigo revisa o potencial papel do tratamento medicamentoso para os adenomas hipofisários secretores de ACTH, TSH e aqueles clinicamente näo-funcionantes (ACNF). Metirapona, mitotano e cetoconazol (preferível por causar menos efeitos colaterais) säo as drogas mais eficazes no controle do hipercortisolismo, mas nenhuma delas supera a eficácia da cirurgia transesfeinodal (TSA). O tratamento medicamentoso da doença de Cushing está, portanto, melhor indicado para pacientes aguardando o efeito pleno da radioterapia ou, como alternativa para esta última, em casos de hipercortisolismo persistente após TSA, e para pacientes com rejeiçäo ou limitaçöes clínicaspara a cirurgia. Outra indicaçäo potencial seria em idosos com microadenomas ou pequenos macroadenomas, ou em casos associados a sela vazia. No que se refere aos adenomas secretores de TSH, os análogos somatostatínicos (SRIFa) proporcionam normalizaçäo dos hormônios tireoidianos em até 95 por cento dos casos. Assim, eles podem se mostrar úteis em casos de insucesso da cirurgia ou como terapia primária de casos selecionados. Ocasonalmente, agonistas dopaminérgicos (DA), sobretudo a cabergolina, também podem ser eficazes. Em contraste, DA e SRIFa raramente induzem uma significante reduçäo das dimensöes dos ACNFs. Por isso, em pacientes com tais tumores, essas drogas devem ser principlamente consideradas diante de contra-indicaçöes ou limitaçöes clínicas para a cirurgia ou quando a cirurgia e a radioterapia tenham sido mal-sucedidas.

Adenoma/drug therapy , Adenoma/metabolism , Adrenocorticotropic Hormone/metabolism , Pituitary Neoplasms/drug therapy , Thyrotropin/metabolism , Adenoma/complications , Adenoma/metabolism , Cushing Syndrome/etiology , Somatostatin/analogs & derivatives
Indian J Pediatr ; 2000 Nov; 67(11): 813-8
Article in English | IMSEAR | ID: sea-83560


Steroid 21-hydroxylase deficiency congenital adrenal hyperplasia is the most common cause of genital ambiguity in females at birth. Inhibited formation of cortisol causes increase in the release of ACTH in turn leading to overproduction of adrenal androgens. This predisposes the affected female fetus to prenatal development of genital ambiguity. A large number of patients also have aldosterone insufficiency which manifests after birth in form of inability to conserve sodium and to excrete potassium which can lead to adrenal shock and neonatal death, if left untreated. Prenatal diagnosis is possible using several methods like steroid assay of amniotic fluid and, HLA typing. Recently with advancement more accurate direct molecular genetic techniques have been utilized on chorionic villus samples in first trimester of pregnancy. Prenatal treatment is also possible and pregnancies can be managed by administering dexamethasone to the mother as soon as pregnancy is diagnosed. This suppresses fetal androgen production in genetic females preventing virilization and leading to normal development. Prenatal diagnosis and treatment are highly desirable in families with a positive family history towards birth of a child without features of the disease.

Adrenal Hyperplasia, Congenital/diagnosis , Adrenocorticotropic Hormone/metabolism , Dexamethasone/therapeutic use , Diagnosis, Differential , Female , Humans , Infant, Newborn , Male , Molecular Biology , Pregnancy , Prenatal Diagnosis/methods
Braz. j. med. biol. res ; 33(10): 1121-31, Oct. 2000.
Article in English | LILACS | ID: lil-270215


The release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH.

Humans , Animals , Central Nervous System Infections/metabolism , Hypothalamo-Hypophyseal System/physiology , Pituitary-Adrenal System/physiology , Stress, Physiological/metabolism , Adrenocorticotropic Hormone/metabolism , Atrial Natriuretic Factor/metabolism , Atrial Natriuretic Factor/physiology , Central Nervous System/metabolism , Corticotropin-Releasing Hormone/metabolism , Corticotropin-Releasing Hormone/physiology , Lipopolysaccharides/pharmacology , Nitric Oxide/physiology , Oxytocin/metabolism , Oxytocin/physiology , Vasopressins/metabolism , Vasopressins/physiology
Indian J Exp Biol ; 2000 Jul; 38(7): 663-8
Article in English | IMSEAR | ID: sea-60337


Tissues from 100 cases of breast cancer were analysed immunohistochemically for the presence of adrenocorticotropic hormone (ACTH) or ACTH-like peptides and expression of c-erbB-2 oncoprotein, epidermal growth factor receptor (EGF-R) as well as oestrogen receptor (ER). Immunopositivity for ACTH was found in 15% cases of infiltrating duct carcinoma of the breast, whereas 38% and 36% breast tumours were positive for c-erbB-2 and EGF-R respectively. While 27% cases were positive for ER. The immunoexpressions of all parameters were higher in breast cancer cases with upper age group (45 years or above) than the patients below 45 years of age. A significant correlation was observed between the tumour grade and the expression of c-erbB-2 oncoprotein. Further, a positive association between the immunoexpression of c-erbB-2 and EGF-R was noticed. Interestingly, a statistically significant relationship was found between the immunopositivity of ACTH and ER. The study reflects a probable association of ACTH or ACTH-like peptides in pathological process of breast cancer.

Adrenocorticotropic Hormone/metabolism , Adult , Breast Neoplasms/metabolism , Carcinoma, Ductal, Breast/metabolism , Female , Humans , Immunohistochemistry , Middle Aged , ErbB Receptors/metabolism , Receptor, ErbB-2/metabolism , Receptors, Estrogen/metabolism , Receptors, Growth Factor/metabolism