Bilateral massive adrenal hemorrhage

Rao, R. Govinda

doi:10.1016/s0025-7125(16)30087-6

Cited by 104 publications

(93 citation statements)

References 133 publications

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“…Other researchers, however, used doses up to 300 mg/kg trilostane/d in rats and reported a dose-dependent increase in adrenal weight, but no adrenal necrosis [1,28,29]. Notably, our study is the first study to report long-term therapy with trilostane (4 months), as in all other studies trilostane was administered for only [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] days.…”

Section: Methodsmentioning

confidence: 76%

“…Stress-mediated increased ACTH-secretion is presumed to be one factor leading to adrenal hemorrhage and necrosis in individuals with severe infections, septicemia or other illnesses such as burns [14].…”

Section: Methodsmentioning

confidence: 99%

“…Although ACTH is an important physiologic hormone, the suspicion exists that it can have deleterious effects if present in excessive amounts in animals and humans. First, in human medicine, both, stress-mediated increases in ACTH during severe infections and septicemia and the therapeutic administration of huge doses (> 1 mg/d) of exogenous ACTH seemed associated with the risk of adrenal hemorrhage and necrosis [12][13][14]. Second, rats treated intermittently with high doses of a purified bovine ACTH preparation, showed degeneration, focal necrosis and hemorrhage in the adrenal glands [15].…”

Section: Introductionmentioning

confidence: 99%

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Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Burkhardt

Guscetti

Boretti

et al. 2011

Domestic Animal Endocrinology

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-Ruckstuhl, N S (2011). Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats. Domestic Animal Endocrinology, 40(3):155-164. Postprint available at: http://www.zora.uzh.ch Posted at the Zurich Open Repository and Archive, University of Zurich. http://www.zora.uzh.ch Originally published at: Burkhardt, W A; Guscetti, F; Boretti, F S; Todesco, A I; Aldajarov, N; Lutz, T A; Reusch, C E; Sieber-Ruckstuhl, N S (2011). Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats. Domestic Animal Endocrinology, 40(3):155-164.Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats AbstractAdrenal necrosis has been reported as a complication of trilostane application in dogs with hyperadrenocorticism. One suspicion was that necrosis results from the increase of adrenocorticotropic hormone (ACTH) during trilostane therapy. The aim of the current study was to assess the effects of ACTH and trilostane on adrenal glands of rats. For experiment 1, 36 rats were divided into 6 groups. Groups 1.1 to 1.4 received ACTH in different doses (60, 40,20, and 10 μg/d) infused subcutaneously with osmotic minipumps for 16 wk. Group 1.5 received saline, and group 1.6 received no therapy. For experiment 2, 24 rats were divided into 3 groups. Group 2.1 and 2.2 received 5 and 50 mg/kg trilostane/d orally mixed into chocolate pudding for 16 wk. Eight control rats received pudding alone. At the end of the experiments, adrenal glands were assessed for necrosis by histology and immunohistochemistry; levels of endogenous ACTH and nucleosomes were assessed in the blood. Rats treated with 60 μg ACTH/d showed more hemorrhage and vacuolization and increased numbers of apoptotic cells in the adrenal glands than rats treated with 20 or 10 μg ACTH/d, trilostane, or control rats. Rats treated with 60 μg ACTH/d had a higher amount of nucleosomes in the blood compared with rats treated with 10 μg ACTH/d, trilostane, or saline. We conclude that in healthy rats ACTH, but not trilostane, causes adrenal degeneration in a dose-dependent manner. Results of this study support the hypothesis that adrenal gland lesions seen in trilostane-treated dogs are caused by ACTH and not by trilostane. Results of this study support the hypothesis that adrenal gland lesions seen in trilostanetreated dogs are caused by ACTH and not trilostane.

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Section: Methodsmentioning

confidence: 76%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Burkhardt

Guscetti

Boretti

et al. 2011

Domestic Animal Endocrinology

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“…En la serie publicada por Rao la HS sucede después de cirugía, quemaduras o trauma en 112 casos. La cirugía más relacionada con HS es la cardiaca a "corazón abierto" y la cirugía traumatológica, sobre todo la colocación de prótesis o reconstrucción, como en nuestro caso (6,7).…”

Section: Discussionunclassified

“…Del global de 431 pacientes de la serie de Rao fallece el 80%. Pero si diferenciamos los casos anteriores al año 1980, de 343 pacientes descritos antes sólo sobreviven 9, mientras que de los 88 pacientes posteriores a 1980 sobreviven el 75% (6). Se ha descrito recuperación de la función endocrina en la HS traumática (33), y en un único caso ocasionado por un anticoagulante lúpico (34).…”

Section: Fig 1 Tac Que Muestra Suprarrenales Agradadas De Forma Bilunclassified

Insuficiencia suprarrenal aguda por hemorragia suprarrenal bilateral como primera manifestación de un síndrome antifosfolípido: A propósito de un caso y revisión

García

Arberas

Blanco

et al. 2002

An. Med. Interna (Madrid)

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INTRODUCCIÓNEn estudios efectuados en autopsias la incidencia global de hemorragia suprarrenal (HS) es de 0,14-1,8% (1). En una serie de 7.500 autopsias se presenta HS en 0,33%, pero si se seleccionan los pacientes fallecidos por shock este porcentaje sube al 15,4% (2). Esto lleva a decir al algunos autores que la HS es muy frecuente en pacientes graves, y que algunos de ellos pueden recuperados con un diagnóstico precoz (3). La HS asociada a síndrome antifosfolipídico (SAF), en relación o no a lupus eritematoso sistémico (LES), es una entidad poco frecuente. En raras ocasiones es la primera manifestación de la enfermedad (4). Actualmente es una causa conocida de insuficiencia suprarrenal a considerar en el estudio etiológico de las alteraciones suprarrenales (5). CASO APORTADOMujer de 59 años con historia previa de poliartritis en metacarpofalángicas e interfalángicas proximales de ambas manos hace años, fotosensibilidad y fenómeno de Raynaud bilateral. Ingresa en el servicio de Traumatología por presentar fractura de cadera izquierda subcapital tras caída casual, siendo intervenida 5 días después del ingreso con colocación de prótesis de Z-Muller. Recibe profilaxis con dalteparina sódica 5.000 unidades subcutáneas diarias. Una semana después de la intervención comienza con dolor abdominal, vómitos, diarrea y anemización (disminución de 4 g/dL en la hemoglobina). Efectuada una ecografía abdominal demuestra la presencia de glándulas suprarrenales con aumento de tamaño patológico, no pudiendo diferenciar si se trata de metástasis o hemorragia. Por presentar deterioro progresivo del nivel de conciencia y en coma (Glasgow 4) se traslada a la UCI. En la analítica practicada destacaba natremia de l10 mEq/L y cortisolemia 1 µg/L. Una tomografía axial computerizada (TAC) craneal demostró un infarto lacunar en el asta frontal del ventrículo izquierdo, y en el EEG existían datos de sufrimiento cerebral muy intenso difuso. La TAC abdominal demostró la presencia de masas suprarrenales bilaterales de 6x7 cm en el lado derecho y 7x8 cm en el izquierdo, compatibles con HS, sin poder descartar metástasis (Fig. 1). Con medidas de soporte y tratamiento sustitutivo hormonal, durante su estancia en UCI, se normaliza el nivel de conciencia, siendo trasladada al Servicio de Medicina Interna para completar el estudio. La exploración física no revelaba otros hallazgos de interés. En la analítica presentaba hemoglobina de 12,7 g/dL, 102.000 plaquetas/mm 3 , VSG de 107 mm en la la hora, APTT de 40,4" (control 32,1"), fosfatasa alcalina 392 U/L, GGT 131 U/L, albúmina 2,8 g/dL, serología de VHB, VHC y VIH negativas, LDH 31

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DNA damage and p21WAF1/CIP1/SDI1 in experimental injury of the rat adrenal cortex and trauma-associated damage of the human adrenal cortex

et al. 1999

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In vivo models are needed to study the reactions of tissues to DNA damage, such as the induction of the cyclin‐dependent kinase inhibitor p21, indicating potential repair of the damage, versus apoptosis, indicating the elimination of the damaged cells. Damage to DNA occurs in tissues during shock, sepsis, and other critical medical conditions. Previous studies have found evidence of damage to the cortex of adrenal glands from organ donors who had undergone severe trauma prior to death. The present experiment studied rats under experimental interventions of clinical relevance to patients with conditions that put them at risk for damage to the adrenal glands. These interventions comprised ischaemia and reperfusion injury, sepsis following caecal ligation and puncture, acute pancreatitis, and administration of chemical agents (zymosan and acrylonitrile). All the interventions caused an increase in p21 mRNA as assessed by northern blotting and in situ hybridization. Increased nuclear p21 protein was shown by immunohistochemistry. All the interventions caused damage to DNA, as shown by labelling of available 3′ termini of single‐strand breaks with terminal transferase. The number of cells undergoing apoptosis, visualized by ligation of a hairpin oligonucleotide probe to double‐strand breaks in DNA, was much lower. In rat adrenal glands, apoptotic cells were infrequent under all the conditions studied. They were more abundant in human organ donor adrenal glands that were previously shown to have extensive DNA damage accompanied by induction of p21. The similarity of the effects of a wide variety of surgical interventions and chemical agents suggest a common pathophysiological mechanism which is not specific to the initiating injury. Experimental injury of the rat adrenal cortex provides a model for investigating the role of organ DNA damage and of mediators of the response to DNA damage, such as p21. Copyright © 1999 John Wiley & Sons, Ltd.

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Bilateral massive adrenal hemorrhage

Cited by 104 publications

References 133 publications

Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Insuficiencia suprarrenal aguda por hemorragia suprarrenal bilateral como primera manifestación de un síndrome antifosfolípido: A propósito de un caso y revisión

DNA damage and p21WAF1/CIP1/SDI1 in experimental injury of the rat adrenal cortex and trauma-associated damage of the human adrenal cortex

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