SIADH secundario a adenocarcinoma seroso de ovario tratado con tolvaptán / SIADH secondary to serous ovarian adenocarcinoma treated with tolvaptan

La hiponatremia es la alteración electrolítica más frecuente en el medio hospitalario, y en un 30% de los casos se debe a un síndrome de secreción inapropiada de vasopresina (SIADH). El SIADH está descrito como cuadro paraneoplásico endocrinológico en múltiples tumores, entre los que excepcionalmente se encuentra el de ovario y las neoplasias ginecológicas en general. Presentamos un caso de SIADH paraneoplásico por un citoadenocarcinoma seroso de ovario de alto grado, estadio IV. Se trata del primer caso de SIADH crónico por cáncer de ovario tratado con Tolvaptán. En el presente caso el objetivo de eunatremia se alcanzó con una dosis baja de acuarético, lo que apoya la elevada sensibilidad, ya previamente documentada, de los SIADH tumorales al tratamiento con Tolvaptán.

Hyponatremia is the most common electrolyte disturbance in hospitals, and 30% of cases are due to syndrome of inappropriate secretion of antidiuretic hormone (SIADH). SIADH is described as an endocrine paraneoplastic syndrome in multiple tumors including, ovary and gynecological malignancies in general, although these are exceptional. We report a case of paraneoplastic SIADH for high-grade serous ovarian cystoadenocarcinoma stage IV. This is the first case of chronic SIADH for ovarian cancer treated with Tolvaptan. In this case the target of eunatremia was reached with a low dose of aquaretic, which supports the high sensitivity, as previously documented, of paraneoplasic SIADH to Tolvaptan.

Comparison of the frequency and complications of inappropriate antidiuretic hormone secretion in patients with septic and aseptic meningitis

Due to the high prevalence of syndrome of Inappropriate Antidiuretic Hormone Secretion [SIADH]. This study was carried out to evaluate the prevalence and relevant parameters of SIADH in children with septic and aseptic meningitis hospitalized at Kashan Shahid Beheshti Hospital between 1996 and 2006. This descriptive study was conducted on 230 patients with meningitis hospitalized in the pediatric wards of Kashan Shahid Beheshti Hospital between 1996 and 2006. Relevant information [age, gender, type of meningitis, serum sodium and potassium, urine specific gravity [USG], blood sugar, blood urea nitrogen, serum creatinin, hydration condition] was collected from patients' records. Data was analyzed using Mann-Whitney and Kappa [2] tests. Out of 230 patients with meningitis, 33 had incomplete records and only 197 patients were recruited for this study. Sixty eight cases [34.5%] suffered from SIADH. It was more frequent among 1-2 year old children. According to this research, SIADH was diagnosed in 57% of the 121 patients with hyponatremia, 58.7% of the 167 patients with USG> 1.004, 74% of the 93 patients with serum osmolity <280 mOs/l and 100% of the patients with BUN <10 mg%. Due to the high prevalence of SIADH in septic and aseptic meningitis and its complication, it is recommended to restrict fluid therapy and monitor serum sodium, urine specific gravity and other diagnostic tests for SIADH

Hyponatremia and brain injury: absence of alterations of serum brain natriuretic peptide and vasopressin / Hiponatremia e traumatismo cranioencefálico: ausência de alteração sanguínea do peptídeo natriurético cerebral e hormônio antidiurético

OBJECTIVE: To study any possible relation between hyponatremia following brain injury and the presence of cerebral salt-wasting syndrome (CSWS) or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and if vasopressin, brain natriuretic peptide (BNP) and aldosterone have a role in its mechanism. METHOD: Patients with brain injury admitted to the intensive care unit were included and had their BNP, aldosterone and vasopressin levels dosed on day 7. RESULTS: Twenty six adult patients were included in the study. Nine (34.6 percent) had hyponatremia and presented with a negative water balance and higher values of urinary sodium, serum potassium and diuresis than patients with normonatremia. The serum levels of BNP, aldosterone, and vasopressin were normal and no relation was observed between plasma sodium and BNP, aldosterone or vasopressin. CONCLUSION: The most likely cause of hyponatremia was CSWS and there was no correlation between BNP, aldosterone and vasopressin with serum sodium level.

OBJETIVO: Estudar a possível relação entre a hiponatremia seguindo traumatismo cranioencefálico e a presença da síndrome cerebral perdedora de sal (SCPS) ou a síndrome da secreção inapropriada do hormônio antidiurético (SSIHAD), e se a vasopressina, peptídeo natriurético cerebral (BNP) e aldosterona têm um papel nesse mecanismo. MÉTODO: Foram incluídos pacientes com traumatismo cranioencefálico admitidos na unidade de terapia intensiva e foram dosados no sétimo dia seguindo o trauma, BNP, aldosterona e vasopressina. RESULTADOS: Vinte e seis pacientes foram incluídos no estudo. Nove (34,6 por cento) tiveram hiponatremia e apresentaram um balanço hídrico mais negativo e altos valores de sódio urinário, potássio sérico e diurese quando comparados com o grupo que apresentou normonatremia. Os níveis séricos de BNP, aldosterona e vasopressina foram normais e não foi observada relação entre o sódio sérico e BNP, aldosterona e vasopressina. CONCLUSÃO: A causa mais provável da hiponatremia foi a SCPS e não houve correlação entre BNP, aldosterona e vasopressina com o nível sérico de sódio.

Hyponatremia and hypernatremia: disorders of water balance.

Total body water and tonicity is tightly regulated by renal action of antidiuretic hormone (ADH), reninangiotensin-aldosterone system, norepinephrine and by the thirst mechanism. Abnormalities in water balance are manifested as sodium disturbances--hyponatremia and hypernatremia. Hyponatremia ([Na+ < 136 meq/ l]) is a common abnormality in hospitalized patients and is associated with increased morbidity and mortality. A common cause of hyponatremia is impaired renal water excretion either due to low extracellular fluid volume or inappropriate secretion of ADH. Clinical assessment of total body water and urine studies help in determining cause and guiding treatment of hyponatremia. Acute and severe hyponatremia cause neurological symptoms necessitating rapid correction with hypertonic saline. Careful administration and monitoring of serum [Na+] is required to avoid overcorrection and complication of osmotic demyelination. Vasopressin receptor antagonists are being evaluated in management of euvolemic and hypervolemic hyponatremia. Hypematremia ([Na+] > 145 meq/l) is caused by primary water deficit (with or without Na+ loss) and commonly occurs from inadequate access to water or impaired thirst mechanism. Assessment of the clinical circumstances and urine studies help determine the etiology, while management of hypernatremia involves fluid resuscitation and avoiding neurological complications from hypernatremia or its correction. Frequent monitoring of [Na+] is of paramount importance in the treatment of sodium disorders that overcomes the limitations of prediction equations.

Pontine and extrapontine osmotic myelinolysis after the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with fluoxetine: case report

Osmotic demyelination syndrome (ODS) may be precipitated by aggressive correction of a hypo or hyper-osmolar states. We describe the case of a 53-year-old woman that was started on fluoxetine 20 mg/day for depression and nine days later was found to have fluoxetine-induced syndrome of inappropriate secretion of antidiuretic hormone. After hyponatremia correction the mental status of the patient gradually improved, but subsequently she had intermittent difficulty in speaking, naming objects, memory deficits and psychomotor slowness. Magnetic resonance revealed bilateral symmetric hyperintense lesions in the basal ganglia, temporal lobe and hippocampal formation compatible with ODS. These symptoms gradually resolved and she was discharged home without any deficits. Two months later, a new image showed lesion in pons and the other lesions had disappeared. Fluoxetine therapy had never been related with a complication like that.

A síndrome de desmielinização osmótica (SDO) pode ser precipitada pela correção agressiva de um estado hiper ou hipoosmolar. Nós descrevemos o caso de mulher de 53 anos que havia iniciado o uso de fluoxetina 20 mg/dia para depressão e que nove dias depois foi diagnosticada como tendo síndrome da secreção inapropriada de hormônio antidiurético induzida por fluoxetina. Depois da correção da hiponatremia o estado mental da paciente gradualmente melhorou, mas subsequentemente ela apresentou dificuldade intermitente para fala e para nomear objetos, déficits de memória recente e lentidão psicomotora. Ressonância magnética revelou lesões hiperintensas bilaterais e simétricas na região dos gânglios da base, lobo temporal e hipocampo compatíveis com SDO. Estes sintomas gradualmente se resolveram e a paciente foi de alta sem qualquer déficit. Dois meses mais tarde uma nova imagem cerebral mostrou lesão na ponte e ausência das lesões antigas. Até onde sabemos a terapia com fluoxetina nunca foi relacionada a uma complicação tardia como esta.

Severe hyponatraemia: current concepts on pathogenesis and treatment.

Severe hyponatraemia (serum sodium <120 mEq/L) is a serious electrolyte disorder associated with life-threatening neurological complications. It develops most often when the ability of the kidney to excrete free water is impaired. The initial adaptation of the brain to hyponatraemia includes loss of water, sodium, potassium and chloride into the cerebrospinal fluid and the late adaptation consists of the loss of organic osmolytes. Adaptation of the brain to hyponatraemia causes potential problems during therapy, as re-adaptation requires a considerably longer time. Rapid correction of hyponatraemia may lead to the development of the osmotic demyelination syndrome. Though the ideal treatment for severe hyponatraemia remains controversial, a consensus regarding therapeutic guidelines has emerged. The rate of correction and the type of infusate depend on the duration and cause of the hyponatraemia, clinical presentation, volume status, renal function and the serum potassium level. The prognosis of the osmotic demyelination syndrome is rather dismal although several therapeutic modalities have been tried.

Meningoencefalitis tuberculosa en niños: Diez años de experiencia en el Hospital Nacional Cayetano Heredia / Tuberculosis meningoencephalitis in children: Ten years experience at Hospital Nacional Cayetano Heredia

Se presenta 70 niños diagnosticados de MEC TBC entre enero de 1982 y diciembre de 1991. El analisis demostro una ocurrencia de 9.4 casos por año, Siendo los escolares el grupo etareo mas afectado, asi como el contacto tuberculoso, el hacinamiento y la desnutrición los antecedentes mas importantes. El tiampo con compromiso de conciencia transcurrido previo a la hospitalización fue el factor que determino el estadio clínico de ingreso y la condición de alta. La letalidad encontrada fue de 14.3 por ciento

Secreçäo inapropriada de hormônio antidiurético e tuberculose pulmonar ativa / Secretion of inappropriate antidiuretic hormone and active pulmonary tuberculosis

Relata-se o caso de um paciente com 48 anos de idade, com tuberculose pulmonar ativa e síndrome de secreçäo inapropriada de hormônio antidiurético (SIHAD). O presente caso preenche os requisitos necessários para o diagnóstico de SIHAD: hipoosmolalidade plasmática (Posm com variaçäo de 230 a 259 mOsm/kgH2O), hiperosmolalidade urinária (Uosm com variaçäo de 680 a 750 mOsm/kgH2O), perda urinária de sódio (UNa, variaçäo de 188 a 178 mEq/1), com hiponatremia (PNa variando entre 113 a 132 mEq/l), funçöes renal e adrenal normais, ausência de insuficiência cardíaca e hepática e, por último, a dosagem do hormônio antidiurético (HAD = 6 pg/ml - RIE) inapropriadamente aumentada para os baixos níveis da osmolalidade plasmática. O paciente evoluiu bem tanto com o tratamento instituído para a tuberculose pulmonar com o esquema tríplice, como com aquele voltado para a SIHAD com restriçäo hídrica, administraçäo de infusäo de cloreto de sódio e diurético

Hiperplasia gigante de ganglios linfáticos (enfermedad de Castleman) con neuropatía periférica y síndrome de secreción inadecuada de hormona antidiurética / Giant lymph node hyperplasia (Castleman's disease) with peripheral nerve diseases and syndrome of inappropriate secretion of antidiuretic hormone

Se presenta un caso clínico de enfermedad de Castleman localizada en el mediastino simulando um timoma. Castleman describió por primera vez la hiperplasia gigante de ganglios linfáticos. Esta entidad presenta dos tipos histopatológicos con formas de transición entre ambos. Son destacables los síntomas y signos de neuropatía periférica. Como hecho original encontramos asociado un síndrome de secreción inadecuada de hormona antidiurética que cede totalmente con la extirpación del tumor. La histología demostró una hiperplasia gigante de ganglios linfáticos tipo II (hialino-vascular) con formación de seudo-corpúsculos de Hassall

Síndrome de secreción inapropiada de hormona antidiurética en niños con meningitis purulenta / Syndrome of inappropiate secrecion of antidiuretic hormone in children with bacterial meningitis

Se estudiaron 20 niños con edades entre uno y 20 meses, con diagnóstico de meningoencefalitis purulenta. Tres pacientes presentaron hiponatremina y otras alteraciones séricas y urinarias características del síndrome de secreción inapropiada de hormona antidiurética (SSHAD). Estos pacientes tuvieron mayor frecuencia de crisis convulsivas y de puntaje menor de 7 en el índice de Glasgow. Con excepción de los valores de sodio sérico, no se observaron diferencias estadíticamente significativas entre los niños con y sin SSIHAD, en los valores promedio de los siguientes parámetros: potasio, urea, creatinina y osmolalidad séricos, sódio, potasio, urea, creatinina y osmolalidad urinarias, depuración osmolar, fracción excretad del sodio filtrado (FENa), relación U/P de osmolalidad y relación potasio/sodio urinarios. Sin embargo, uno de los niños con SSIHAD mostró valores muy elevados de la FENa y en todos los casos los valores de este índice fue mayor de 1. Por consiguiente, la FENa, puede convertirse en un dato más de sospecha del SSIHAD si se encuentra por encima de la unidad.

Síndrome de secrección inapropiada de hormona antidiurética en niños con meningitis purulenta / Syndrome of inappropriate antidiuretic hormone secretion in children with purulent meningitis

Se estudian 60 niños con meningitis purulenta con el objetivo de evaluar la incidência de Síndrome de Secreción Inapropiada de Hormona Antideurética (SSIHAD). El diagnóstico de esta complicación se apoyó en el hallazgo de hiponatremia, hipoosmolaridad sérica y aumento de la densidad urinaria en ausencia de deshidratación o enfermedad suprarrenal. 17 niños llevaron los criterios diagnósticos del síndrome, 28%. Se analizam los mecanismos fisiopatológicos envueltos en la génesis del SSIHAD