A case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) with low plasma concentrations of antidiuretic hormone.

A 66-year-old Japanese man presented with persistent hyponatremia without polydipsia and polyuria. Laboratory examination showed serum sodium of 117 mEq/l, plasma osmolality 239 mosm/kg, urine sodium 108 mEq/l, urine osmolality 577 mosm/kg, and normal levels (less than 2.0 pg/ml) of serum antidiuretic hormone (ADH). ADH release was regulated normally with changes in plasma osmolality. No obvious cause for the syndrome of inappropriate secretion of ADH (SIADH) could be detected. However, 20 months later, the patient had bouts of hematuria and was found to have cancer of the urinary bladder. Increased renal sensitivity to ADH was suspected as the underlying mechanism of SIADH.     

Hyponatremia with increased plasma antidiuretic hormone in a case of hypothyroidism

We report a 70-year-old woman with hypothyroidism and severe hyponatremia. Her plasma antidiuretic hormone (ADH) level was inappropriately high for her low plasma osmolality. Her low serum sodium level was gradually corrected by water restriction and sodium supplementation prior to the initiation of thyroid hormone replacement. After a diagnosis of Hashimoto's thyroiditis had been made, the patient was treated with levothyroxine. Following this treatment, the patient's serum sodium level increased drastically. It is suggested that the elevated plasma ADH level played an important role in the development of hyponatremia in this case.     

Hyponatremia of hypothyroidism. Appropriate suppression of antidiuretic hormone levels.

A hypothyroid, 72-year-old woman with idiopathic hypopituitarism manifested severe hyponatremia, plasma hypoosmolality, and inappropriately elevated urine osmolality suggestive of a syndrome of inappropriate antidiuretic hormone secretions. The hyponatremia did not respond to demeclocycline hydrochloride, and antidiuretic hormone (ADH) levels measured by a specific radioimmunoassay were appropriately suppressed. Subsequent replacement therapy with levothyroxine sodium resulted in correction of the hyponatremia. Thus, both direct assay as well as hormone blockade failed to show an action of ADH in mediating the water retention.     

Safety of pre‐engraftment prophylactic foscarnet administration after allogeneic stem cell transplantation

K. Ishiyama, T. Katagiri, K. Ohata, K. Hosokawa, Y. Kondo, H. Yamazaki, A. Takami, S. Nakao. Safety of pre‐engraftment prophylactic foscarnet administration after allogeneic stem cell transplantation. Transpl Infect Dis 2011. All rights reserved Abstract: Human herpesvirus‐6 (HHV‐6) is a major cause of limbic encephalitis with a dismal prognosis after allogeneic hematopoietic stem cell transplantation (SCT). Because our previous trial of preemptive therapy with foscarnet sodium (phosphonoformic acid; PFA) failed to prevent HHV‐6 encephalitis, we conducted a prospective study to examine the safety of prophylactic PFA administration and elucidate the changes in the plasma HHV‐6 DNA levels in the early post‐SCT period. Plasma HHV‐6 DNA was measured thrice weekly from day 6. PFA, 90 mg/kg/day, was administered from days 7 to 21 after bone marrow or peripheral blood SCT and to day 25 after umbilical cord blood transplantation. Of the 10 patients enrolled, 2 dropped out of the study, 1 because of early death, and 1 with a low glomerular filtration rate. Grade 3 or greater adverse events occurred in 9 of the 10 prophylactic PFA patients and in 7 of the 10 control patients who had clinical backgrounds similar to the study subjects and underwent SCT during the same period. Neurological disorders developed in none of the study subjects but in 4 of the 10 control patients, including 2 with HHV‐6 encephalitis. HHV‐6 reactivation occurred in 3 of the 10 study subjects. The prophylactic PFA regimen was thus safe and it may reduce the risk of limbic encephalitis, but is not considered to be potent enough to prevent HHV‐6 reactivation.     

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by rathke's cleft cyst: a case report

We report a case of a seventy-year-old woman with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by Rathke's cleft cyst. She experienced nausea, vomiting, diarrhea, and headache and disturbance of consciousness induced by hyponatremia at a serum sodium level of 100 mEq/l. In spite of severe hyponatremia, urinary sodium excretion was not suppressed and serum osmolality (270 mOsm/kg) was lower than urine osmolality (304 mOsm/kg), and arginine vasopressin (AVP) remained within normal range. SIADH was diagnosed because she was free from other diseases known to cause hyponatremia such as dehydration, cardiac dysfunction, liver dysfunction, renal dysfunction, hypothyroidism, and adrenal insufficiency. Cranial computed tomographic (CT) scan and cranial magnetic resonance (MR) imaging showed a cystic lesion of approximately 2 cm in diameter in the pituitary gland. These images suggested that the cystic lesion was a Rathke's cleft cyst, which was the cause of SIADH. Water restriction therapy normalized her serum sodium concentration and improved her symptoms. After one year, she suffered from general fatigue, appetite loss, fever, and body weight loss (5 kg/2 months). She had neither hypotension nor hypoglycemia, but her serum sodium level was low and serum cortisol, ACTH, and urine free cortisol were very low. Therefore, secondary adrenal insufficiency was suspected and diagnosed by stimulation tests. After start of hydrocortisone replacement therapy (10 mg/day), her symptoms disappeared. In conclusion, Rathke's cleft cyst should be kept in mind as a potential cause in a patient with SIADH, hypopituitarism, and/or adrenal insufficiency.     

Hyponatremia and syndrome of inappropriate antidiuretic hormone secretion complicating stem cell transplantation

Hyponatremia is a common electrolyte disorder in hospitalized patients. Although there are a few case reports of hyponatremia following stem cell transplantation (SCT), no reports concerning the incidence are currently available. We describe the occurrence of hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following SCT. In a single center analysis of 140 patients, hyponatremia and SIADH were observed in 40 and 11.4% of patients, respectively, following SCT. Risk factors for SIADH included young age, transplantation from an HLA-mismatched or unrelated donor, cord blood transplantation, and graft-versus-host disease prophylaxis with methyl prednisolone. Multivariate analysis revealed that transplantation from an HLA-mismatched donor and performance of SCT in a child below 4 years of age were risk factors for SIADH. For patients who underwent SCT from an HLA-mismatched or unrelated donor, those with SIADH showed a significantly higher overall survival rate (90.9 vs 40.2%) and event-free survival rate (77.8 vs 33.8%) compared to those without SIADH. Overall, our data show that hyponatremia and SIADH are relatively common complications following SCT, especially in children below 4 years of age and after SCT from an HLA-mismatched donor.     

Herpes zoster ophthalmicus and syndrome of inappropriate antidiuretic hormone secretion

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a common consequence of neurologic and pulmonary infections as well as drug intake and many other clinical situations. This report describes SIADH that developed in an elderly woman with single dermatomal herpes varicella zoster ophthalmicus without evidence of varicella zoster encephalitis or dissemination. A 76-year-old woman was admitted to our department for evaluation of left facial pain, confusion and disorientation. Further investigation revealed hyponatremia 112 mEq/L, low serum osmolality, high urine osmolality, normal renal function, normal adrenal and thyroid hormones, and high plasma vasopressin 40 pg/mL. These results indicate that the hyponatremia in this case was due to SIADH and that SIADH was caused by an increased release of vasopressin probably because of the antiviral drug (acyclovir) or infection of varicella zoster virus (VZV) in a single dermatome.     

Inappropriate secretion of antidiuretic hormone:a rare complication after common bile duct exploration

BACKGROUND:The syndrome of inappropriate secretion of antidiuretic hormone(SIADH)as a dilutional hyponatremia is due to a pathological increase of antidiuretic hormone(ADH).It is characterized by hyponatremia and decreased serum osmolarity as well as an increase in urinary osmolarity.The most common etiological factors of this syndrome include diseases or trauma of the central nervous system and malignant tumor or inflammation of the lung.SIADH following abdominal surgery is rare. METHODS:We report the case...     

The pitfall "dehydration" and hyponatremia

Hyponatremia represents a very common disturbance in hospitalized eldery. It correlates with delirium, falls, and intrahospital mortality. Often hyponatremia is ignored or missclassified. The represented algorithm is based on only a few parameters: serum and urine osmolality, and sodium. Treatment of the underlying causes of hyponatremia, e.g., cessation of medications and polypharmacy, is essential. The syndrome of inadequate secretion of antidiuretic hormone (SIADH; hypotonic isovolemic hyponatremia) is also considered.     

Tücke ?Exsikkose“ und Hyponatri?mie

Hyponatremia represents a very common disturbance in hospitalized eldery. It correlates with delirium, falls, and intrahospital mortality. Often hyponatremia is ignored or missclassified. The represented algorithm is based on only a few parameters: serum and urine osmolality, and sodium. Treatment of the underlying causes of hyponatremia, e.g., cessation of medications and polypharmacy, is essential. The syndrome of inadequate secretion of antidiuretic hormone (SIADH; hypotonic isovolemic hyponatremia) is also considered.     

Syndrome of inappropriate secretion of antidiuretic hormone associated with localized herpes zoster ophthalmicus

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with localized herpes zoster is rarely reported and may be under-appreciated. We describe two diabetic men with herpes zoster ophthalmicus (HZO) who developed hyponatremia (114 and 116 mmol/L) during acute illness. Both were euvolemic and had elevated urine osmolality (435 and 368 mmol/kg.H₂O) and sodium (Na⁺) concentration (61 and 63 mmol/L) along with normal cardiac, renal, liver, and endocrine function consistent with the diagnosis of SIADH. Thorough investigation for other causes of SIADH, including detailed physical examination, laboratory studies, and computed tomography of the brain, chest, and abdomen, were negative. Despite antiviral therapy (acyclovir) for herpes zoster, ophthalmoplegia, keratitis, and post-herpetic neuralgia (PHN) developed. Even with fluid restriction and high salt diet, SIADH lasted for 3 to 4 months and resolved concomitantly with resolution of PHN, suggesting an association between SIADH and HZO. These two cases raise the potential for herpes zoster infection, especially HZO, to involve the regulatory pathway of ADH secretion, contributing to SIADH. The presence of PHN, which reflects greater neural damage may, at least in part, explain the prolonged ADH secretion and hyponatremia.     

Inappropriate antidiuretic hormone secretion,abdominal pain and disseminated varicella‐zoster virus infection: an unusual and fatal triad in a patient 13 months post Rituximab and autologous stem cell transplantation

We report a case of varicella‐zoster virus (VZV) infection associated with severe abdominal pain, inappropriate antidiuretic hormone (ADH) secretion (SIADH) and death, 13 months post‐autologous peripheral blood stem cell transplantation (PBSCT). This unusual clinical triad has been reported twice in the setting of allogeneic bone marrow transplantation, however it has not been reported after autologous transplantation and never so long after transplantation. We speculate as to why this occurred, as early recognition might have altered the clinical outcome.     

Paroxetine-induced hyponatremia in an elderly man due to the syndrome of inappropriate secretion of antidiuretic hormone

We report an 82-year old man prescribed paroxetine who had hyponatremia and in whom the syndrome of inappropriate secretion of antidiuretic hormone was diagnosed. He had taken sulpiride for depressed mental status. However, he showed parkinsonism, which was an adverse effect from the treatment of sulpiride. Therefore sulpiride was changed to selective serotonin reuptake inhibitor, paroxetine 10mg daily. His depressed mental status deteriorated after paroxetine treatment started. His depression had not lessened after 12 days, and the dosage was increased to 20mg daily. On the 15th day after starting paroxetine, routine laboratory tests showed that his serum sodium level was 126 mEq/l. We recognized that his confusion and loss of appetite were symptoms of hyponatremia, rather than of worsening depression. Laboratory data revealed hyponatremia, low serum osmolarity (242 mOsm/kg) with a relatively high level of serum antidiuretic hormone, and concentrated urine (439 mOsm/kg). We diagnosed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), associated with paroxetine. The dosage of paroxetine was reduced gradually and the serum sodium level returned to normal on day 2 after medication ceased completely. Paroxetine produces fewer adverse effects than other types of antidepressants. However, its use can be associated with inappropriate secretion of antidiuretic hormone in the body and may lead to SIADH, which is characterized by hyponatremia, a potentially fatal condition that is typically asymptomatic until it becomes severe. SIADH is more likely in some populations, including the elderly. Serum sodium levels should be monitored closely, especially in elderly patients.     

Syndrome of inappropriate antidiuretic hormone secretion associated with acute myeloid leukemia with multilineage dysplasia

A patient having acute myeloid leukemia (AML) with multilineage dysplasia, developed hyponatremia and showed all symptoms of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) through a mechanism similar to tumor lysis. Retrospective immunohistochemical analysis of blast cells was positive for antidiuretic hormone (ADH) protein. According to us, this is the first case report of SIADH in an AML patient with multilineage dysplasia, showing blast cells immunostained for ADH, which clearly demonstrated that the tumor cells produced ADH.     

Encephalitis caused by human herpesvirus‐6B in pancreas‐after‐kidney transplantation

Human herpesvirus‐6 (HHV‐6) is a common pathogen among children, classically presenting with fever and rash that resolves without specific therapy. HHV‐6 can be reactivated in the immunosuppressed patient. After bone marrow and solid organ transplantation, HHV‐6 has been linked to various clinical syndromes, including undifferentiated febrile illness, encephalitis, myelitis, hepatitis, pneumonitis, and bone marrow suppression. However, HHV‐6 encephalitis after pancreatic transplant has rarely been reported. Early diagnosis and treatment of HHV‐6 encephalitis may be important for affected patients. We report the case of a 53‐year‐old pancreas‐after‐kidney transplant recipient who initially presented with high fever and confusion 3 weeks after operation. We managed to save the patient's life and preserve the pancreas graft function. We also review previously reported cases of HHV‐6B encephalitis in solid organ transplant recipients.     

Syndrome of inappropriate secretion of antidiuretic hormone and thrombocytopenia caused by cytomegalovirus infection in a young immunocompetent woman

We report the first case of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with cytomegalovirus (CMV) infection. A 32-year-old woman was admitted to our hospital because of pandysautonomic signs and symptoms. Thrombocytopenia and hyponatremia were present. Serum anti-CMV IgM and IgG antibodies were positive. Despite hyponatremia, urinary osmolality exceeded plasma osmolality and plasma vasopressin levels related to plasma osmolality were high. Restriction of water intake and administration of dimethylchlorotetracycline improved hyponatremia, suggesting this patient had SIADH. In this patient, SIADH may have been caused by acute pandysautonomia that developed following CMV infection.     

Human herpesvirus 6‐related pure red cell aplasia,secondary graft failure,and clinical severe immune suppression after allogeneic hematopoietic cell transplantation successfully treated with foscarnet

E.D. Lagadinou, M. Marangos, M. Liga, G. Panos, E. Tzouvara, E. Dimitroulia, M. Tiniakou, A. Tsakris, N. Zoumbos, A. Spyridonidis. Human herpesvirus 6‐related pure red cell aplasia, secondary graft failure, and clinical severe immune suppression after allogeneic hematopoietic cell transplantation successfully treated with foscarnet.
Transpl Infect Dis 2010: 12: 437–440. All rights reserved. Abstract: Human herpesvirus 6 (HHV‐6) is frequently detected after allogeneic hematopoietic cell transplantation (allo‐HCT); however, the clinical interpretation of HHV‐6 viremia in a transplant patient is challenging as it may signify asymptomatic reactivation, chromosomal integration of the virus genome in the donor or recipient with no clinical significance, or severe HHV‐6 disease. Here we present a case of HHV‐6 disease after allo‐HCT presenting as pure red cell aplasia, secondary graft failure, and severe immunosuppression causing multiple severe bacterial super‐infections. Examination of pre‐transplant patient and donor samples as well as serial determination of HHV‐6 DNA copy numbers after transplantation were necessary to definitively interpret HHV‐6 viremia as active HHV‐6 infection with a causative role in pancytopenia and immune suppression. Foscarnet treatment resulted both in viral load decline and disappearance of HHV‐6‐related bone marrow suppression and predisposition to severe infections. Clinicians should be aware of the wide array of clinical manifestations and the diagnostic pitfalls of post‐transplant HHV‐6 disease. These issues are extremely challenging, as they may result either in dangerous underestimation of HHV‐6 disease or in the institution of unnecessary antiviral therapy. Late bone marrow aplasia and late severe infections after allo‐HCT without other obvious causes may be HHV‐6 related.     

Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.     

Hyponatremia as the Initial Presentation of Cryptococcal Meningitis After Liver Transplantation

Introduction:

Meningoencephalitis is the most common clinical manifestation of cryptococcal infection, as the organism has a propensity to invade the CNS. Patients often present with elevated intracranial pressure, focal motor deficits, altered mentation and internal hydrocephalus. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) has been reported as a notable cause of euvolemic hyponatremia in immunocompromised patients.

Case Presentation:

A 67-year-old male with liver transplantation due to hepatitis C (HCV) related liver cirrhosis developed severe hyponatremia four months after liver transplantation, which was discovered during routine clinic visit. Patient was referred to the emergency department, treated and discharged with normal serum sodium level. Few days later, he presented with dizziness, confusion, ataxia, abnormal muscle movements and leg pain. Laboratory investigations were consistent with SIADH and revealed a sodium level of 115 mmol/L. Brain MRI showed a leptomeningeal enhancement in the superior cerebellar sulci suspicious for infection. Lumbar puncture was performed and consistent with Cryptococcus neoformans infection; therefore, cryptococcal meningitis was diagnosed. Amphotericin B was started for the patient for six weeks followed by fluconazole for one year. His level of consciousness improved significantly, and his serum sodium level slowly returned to its normal baseline over three weeks after starting amphotericin B.

Conclusions:

Symptomatic hyponatremia secondary to SIADH remains a rare complication of cryptococcal meningitis.     

Central Diabetes Insipidus after Syndrome of Inappropriate Antidiuretic Hormone Secretion with Severe Hyponatremia in a Patient with Rathke's Cleft Cyst

A 49-year-old man developed severe hyponatremia associated with transient headache and was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fluid restriction and sodium supplementation corrected the hyponatremia. However, several days later, the patient exhibited hypernatremia with thirst and polyuria. A detailed examination indicated central diabetes insipidus (CDI) with an intrasellar cystic lesion indicative of Rathke''s cleft cyst (RCC). A case of RCC exhibiting headache, hyponatremia, and subsequent hypernatremia has been reported. Our case shows that CDI may appear after SIADH in patients with RCC, especially in those with serum sodium levels that unexpectedly increase rapidly beyond the reference range.