Carcinoma de próstata y síndrome de secreción inadecuada de hormona antidiurética / Prostate carcinoma and syndrome of inappropriate antidiuretic hormone secretio

El cáncer de próstata es una causa extremadamente rara de síndrome de secreción inadecuada de hormona antidiurética (SIADH). Se trata de tumores agresivos asociados a un síndrome que puede aparejar consecuencias graves. Un paciente de 64 años fue diagnosticado de adenocarcinoma de próstata Gleason 4+3: 7 en 2014 y recibió terapia de bloqueo hormonal. En 2015 debió ser ingresado por hiponatremia sintomática y se le diagnosticó un SIADH, sin otra causa probable más que el cáncer de próstata. Sufrió rápida progresión de su enfermedad oncológica, llamativamente cuando su PSA se encontraba en valores normales, y falleció al corto plazo. Existe gran variabilidad clínica e histopatológica de los casos informados en la literatura de asociación de carcinoma de próstata y SIADH, sin embargo, todos coinciden en la agresividad de estos tumores. Estas características se presentan en tumores con diferenciación neuroendocrina, frecuentemente resistentes al tratamiento hormonal y que pueden presentar síndromes paraneoplásicos como el SIADH. El perfil de sus alteraciones moleculares se encuentra en estudio para el desarrollo de terapias target. La asociación de adenocarcinoma de próstata y SIADH es muy infrecuente y podría implicar diferenciación neuroendocrina. Por tal motivo es esencial una nueva biopsia del tumor o de sus metástasis a la progresión de la enfermedad para poder conducir un tratamiento adecuado de acuerdo a sus características morfológicas, inmunohistoquímicas y, en un futuro, moleculares.

Prostate cancer is an extremely rare cause of syndrome of inappropriate antidiuretic hormone (SIADH) secretion. These tend to be aggressive tumors and SIADH can carry serious clinical consequences. A 64 years old patient was diagnosed with Gleason 4+3: 7 prostate adenocarcinoma in December 2014 and received hormonal blockade therapy. By March 2015 he was admitted for symptomatic hyponatremia and SIADH secretion was diagnosed, with no other probable cause than prostate cancer. He suffered a rapid progression of his oncologic disease, surprisingly with PSA in normal range, and died in the short term. There is great clinical and histopathological variability in the cases reported in the literature of association of prostate carcinoma and SIADH. However, they all agree on the aggressiveness of these tumors. This characteristic is present in tumors that have neuroendocrine features. They are frequently resistant to hormonal treatment and may present with paraneoplastic syndromes such as SIADH. The profile of its molecular alterations is under study for the development of target therapies. The association of prostate adenocarcinoma and SIADH is very uncommon and could involve neuroendocrine differentiation. For this reason, it is essential to perform a new biopsy of the tumor or its metastases at the progressive disease in order to conduct an appropriate treatment according to its morphological, immunohistochemical and, in the future, molecular characteristics.

Encefalopatía perdedora de sal en romboencefalitis por listeria / Cerebral salt wasting syndrome associated with Listeria monocytogenes encephalitis. Report of one case

Hyponatremia is common in patients with severe neurological diseases and is often secondary to a syndrome of inappropriate antidiuretic hormone secretion (SIADH). However, in some patients, hyponatremia is due to cerebral salt wasting syndrome (CSWS). SIADH and CSWS treatments are opposite and misdiagnosis can lead to increased morbidity and mortality. We report a 52 years old female with a rhom-boencephalitis caused by Listeria Monocytogenes (LM), ventriculitis and abscesses in cerebellum and brainstem. It was associated with hyponatremia, hypotension, increased natriuresis, hypouricemia, and low creatinine and blood urea nitrogen levels. Large amounts ofsodium were needed and the condition persisted after hospital discharge. Hyponatremia is common in central nervous system involvement by LM, however we are not aware of CSWS reports of this condition.

Hiponatremia: conceitos básicos e abordagem prática / Hyponatremia: basic concepts and practical approach

Hyponatremia is the most common electrolyte imbalance in hospitalized patients. It is associated with several unfavorable endpoints such as: the need for intensive care, longer hospital stay, higher hospitalization costs, discharge to long-term care facilities, and mortality. It is still not clear if there is a direct causal relationship or if hyponatremia is simply a marker of disease severity. Nevertheless, it is quite clear that improper management of a hyponatremic patient may result in severe neurologic damage or death. This paper addresses the basic pathophysiologic concepts about hyponatremia followed by a practical approach to its diagnosis and management.

Hiponatremia é o distúrbio hidroeletrolítico mais comum em pacientes hospitalizados. A presença de hiponatremia está associada a uma série de desfechos desfavoráveis, tais como: necessidade de internamento em unidade de terapia intensiva, hospitalização prolongada e de maior custo, transferência para abrigos e mortalidade. Ainda não está claro se existe relação de causalidade direta ou se a hiponatremia é apenas um marcador de gravidade da doença de base. No entanto, sabe-se que o manejo inadequado de um paciente hiponatrêmico pode causar graves danos neurológicos ou até mesmo a morte. Neste manuscrito, os conceitos básicos sobre a fisiopatologia da hiponatremia serão revisados, seguido de uma abordagem prática sobre sua investigação e tratamento.

Enfrentamiento de la hiponatremia: Más allá de la corrección del sodio. A propósito de un caso clínico / Secondary adrenal insufficiency presenting as hyponatremia: Report of one case

Hyponatremia can be a marker of an underlying disease. We report a 52 years-old male with Diabetes Mellitus who consulted for an episode of nausea and vomiting lasting four days. His baseline serum sodium was 118 mEq/L. He had no neurological deficit. Hyponatremia was initially interpreted in context of gastrointestinal fluid loss but correction with saline solution was poor. His urine sodium was 105 mEq/L and his urine osmolality was 281 mOsm/L, so an Inappropriate Secretion of Antidiuretic Hormone Syndrome was suspected. Later, we found that the patient had a two year history of fatigue, weakness, anorexia, frequent nausea, vomiting and diarrhea, loss of libido and decreased axillary and pubic hair. Thyroid-Stimulating Hormone (TSH) was normal and serum Cortisol < 1 µg/dL. A CT scan showed a sellar mass compatible with a macroadenoma. There was also a moderately high serum prolactin and low testosterone, thyroxin and growth hormone levels. The visual fi eld exami-nation showed right temporal hemianopsia. The patient was treated with steroids with a very good clinical response and serum sodium normalization. Subsequently a transsphenoidal excision of the tumor was performed and replacement of the other hormones was started. Now the patient remains asymptomatic.

Cerebral salt wasting syndrome in tuberculous meningitis

Case of a seventy year old female, who developed cerebral salt wasting syndrome in association with Tuberculous Meningitis is presented

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.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) and neurological crisis due to acute intermittent porphyria, successfully treated with haemodialysis.

We report an eighteen year old female, a case of acute intermittent porphyria with syndrome of inappropriate antidiuretic hormone secretion, as presenting feature for its rarity. The neurological crisis was successfully treated with haemodialysis.

Syndromes related to sodium and arginine vasopressin alterations in post-operative neurosurgery

BACKGROUND: Cerebral salt wasting syndrome (CSWS), syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI) are frequently found in postoperative neurosurgery. PURPOSE: To identify these syndromes following neurosurgery. METHOD: The study included 30 patients who had been submitted to tumor resection and cerebral aneurysm clipping. Sodium levels in serum and urine and urine volume were measured daily up to the 5th day following surgery. Plasma arginine vasopressin (AVP) was measured on the first, third and fifth days post-surgery. RESULTS: CSWS was found in 27/30 patients (90 percent), in 14 (46.7 percent) of whom it was associated with a reduction in the levels of plasma AVP (mix syndrome). SIADH was found in 3/30 patients (10 percent). There was no difference between the two groups of patients. CONCLUSION: CSWS was the most common syndrome found, and in half the cases it was associated with DI. SIADH was the least frequent syndrome found.

INTRODUÇÃO: A síndrome perdedora de sal (SPS), síndrome da secreção inapropriada do hormônio antidiurético (SIADH) e diabetes insipidus (DI) são freqüentemente encontradas no pós-operatório de neurocirurgia. OBJETIVO: Identificar essas síndromes relacionadas à neurocirurgia. MÉTODO: Foram estudados 30 pacientes submetidos à ressecção de tumor (n=19) e clipagem de aneurisma (n=11) cerebral durante os primeiros cinco dias do pós-operatório. Os pacientes foram submetidos a dosagens diárias de sódio sérico e urinário até o 5° dia pós-operatório, com controle de volume urinário neste período e dosagem de arginina-vasopressina (AVP) plasmática no 1°, 3° e 5° dias pós-operatórios. RESULTADOS: A SPS foi encontrada em 27/30 pacientes (90 por cento), em 14/27 (46,7 por cento) associada à diminuição dos níveis de AVP plasmática (síndrome mista). A SIADH foi encontrada em 3/30 pacientes (10 por cento). Não houve diferença entre os dois grupos de pacientes. CONCLUSÃO: A SPS foi a síndrome mais freqüente, em metade de casos associada ao DI. A SIADH foi a menos freqüente.

Revisión a partir de un caso clínico: encefalopatía perdedora de sal secundaria a asfixia por ahorcamiento / Review in relation to a clinical case: cerebral salt wasting secondary to asphyxia by hanging

Siendo la hiponatremia un trastorno frecuente en unidades de tratamiento intensivo en especial neuroquirúrgico, se deben tener en consideración las dos etiologías más frecuentes: SIADH y encepalopatía perdedora de sal. La importancia del diagnóstico diferencial radica en que la forma de aproximación diagnóstica y el tratamiento son diferentes, de tal modo que el manejo inadecuado puede intensificar la hiponatremia poniendo en riesgo vital al paciente. Aún así existen otras causas que pueden aumentar la natriuresis: infusiones prolongadas de soluciones salinas pueden provocar un balance negativo de Na y Cl, por internalización de canales Na/K ATP. Además non todos pacientes con EPS presentan niveles elevados de péptido natriurético cerebral. Por lo que aún está en discusión y no se tiene consenso absoluto respecto de su fisiopatología.

Cerebral Salt Wasting Syndrome After Calvarial Remodeling in Craniosynostosis

Hyponatremia and increased urine output after calvarial remodeling have been noted in pediatric patients with craniosynostosis. If not treated properly, patients develop hypoosmotic conditions that can lead to cerebral edema, increased intracranial pressure, and collapsed circulation. Postoperative hyponatremia after central nervous system surgery is considered as the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Recently, however, cerebral salt wasting syndrome (CSWS) instead of SIADH has been reported frequently. CSWS is associated with a decreased serum sodium level, increased urinary sodium level, increased urine output, decreased ECF volume, increased atrial natriuretic peptide (ANP) level, and increased brain natriuretic peptide (BNP) level. We experienced nine patients with craniosynostosis who underwent calvarial remodeling. By postoperative day 1, the ANP and BNP levels increased by 3-6 folds compared with the preoperative levels. They returned to the normal levels by postoperative day 5. The ADH level was within the normal range even after operation. The urinary sodium level increased in all patients by postoperative day 1 and 3. But the serum sodium level, and serum and urine osmolarity were normal due to appropriate replacement of sodium and fluid. After calvarial remodeling, the potential development of CSWS should be considered and distinguished from SIADH. The patients with CSWS require normal saline resuscitation and should prophylactically receive normal saline.

Cerebral infarction and cerebral salt wasting syndrome in a patient with tuberculous meningoencephalitis.

A 38-year old female with underlying systemic lupus erythematosus was admitted with tuberculous meningoencephalitis. After an initial good response to anti-tuberculous treatment, she developed cerebral infarction and profound hyponatremia. This was due to cerebral salt wasting syndrome, which has only previously been described in 2 cases. The difficulties in diagnosis and management of this case are discussed.

Perdida cerebral de sal: medio siglo de un síndrome no bien definido / Cerebral salt wasting: half a century of a largely undefined syndrome

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls.