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.     

Hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

The syndrome of inappropriate ADH secretion (SIADH), also recently referred to as the "syndrome of inappropriate antidiuresis", is an often underdiagnosed cause of hypotonic hyponatremia, resulting for instance from ectopic release of ADH in lung cancer or as a side-effect of various drugs. In SIADH, hyponatremia results from a pure disorder of water handling by the kidney, whereas external Na+ balance is usually well regulated. Despite increased total body water, only minor changes of urine output and modest edema are usually seen. Renal function and acid-base balance are often preserved, while neurological impairment may range from subclinical to life-threatening. Hypouricemia is a distinguishing feature. The major causes and clinical variants of SIADH are reviewed, with particular emphasis on iatrogenic complications and hospital-acquired hyponatremia. Effective treatment of SIADH with water restriction, aquaretics, or hypertonic saline + loop diuretics, as opposed to worsening of hyponatremia during parenteral isotonic fluid administration, underscores the importance of an early accurate diagnosis and careful follow-up of these patients.     

Herpes zoster ophthalmicus and syndrome of inappropriate antidiuretic hormone secretion

Presented here is a case of syndrome of inappropriate antidiuretic hormone secretion (SIADH) that developed in an elderly woman with single dermatomal herpes varicella zoster ophthalmicus without evidence of varicella-zoster encephalitis or dissemination. This is only the third such case reported in the English language literature to date, and it affirms that SIADH can develop in patients with herpetic involvement of just a single dermatome and corrects with resolution of the herpetic lesions.     

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.     

Mesothelioma associated with the syndrome of inappropriate secretion of antidiuretic hormone

A patient with a malignant mesothelioma developed the syndrome of inappropriate secretion of antidiuretic hormone. The electrolyte abnormalities were corrected by treatment with demethylchlortetracycline. Arginine vasopressin concentrations were increased in serum and urine. It is suggested that the syndrome might have been mediated by secretion of antidiuretic hormone from the posterior pituitary, because arginine vasopressin was not detected in the patient's tumor using a sensitive radioimmunoassay.     

Esophageal small-cell carcinoma with syndrome of inappropriate secretion of antidiuretic hormone

Small-cell carcinoma (SCC) of the esophagus is rare, and its clinical characteristics remain poorly understood. A 54-year-old man was given a diagnosis of esophageal SCC and underwent esophagectomy. Four months after surgery, he was admitted to our hospital because of rapidly developing hyponatremia. Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) due to extensive recurrence of SCC was diagnosed. Combined chemotherapy with irinotecan and cisplatin has dramatically reduced metastatic tumors, and it was concomitantly effective for SIADH. This case demonstrates that esophageal SCC could induce SIADH as a paraneoplastic syndrome and that the above combined chemotherapy was feasible and effective.     

抗利尿激素分泌不适当综合征的诊断和治疗

抗利尿激素分泌不适当综合征(syndrome of inappropriate antidiuretic hormone secretion,简称SIADH)是指体内细胞外液的渗透压已降低,但仍有抗利尿激素(ADH)分泌,而使体内水分潴留,表现为稀释性低血钠,而尿钠和尿渗透压升高的临床综合征.     

Demeclocycline treatment in the syndrome of inappropriate antidiuretic hormone secretion.

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.     

Porphyria and inappropriate antidiuretic hormone syndrome

We report the case of a 37-years-old woman with inappropriate antidiuretic hormone syndrome due to an attack of acute porphyria. The patient was admitted to our hospital for abdominal pain, sleepiness and pink urine. Family and personal history were normal. Seven days before the admission the patient had a laparoscopy operation for endometriosis in her left ovary. The patient had had two normal pregnancies. The physical examination was normal, the skin turgor was good and no edema was present, the blood pressure was 140/90 mmHg. Her serum sodium was 114 mEq/L, serum osmolality 243 mOsm/kg, urine sodium 146 mEq/L and urine osmolality 457 mOsm/kg. Values from laboratory examination revealed a normal peripheral haematogram, a normal kidney function, normal liver, adrenal and thyroid function. The urine tested for amino-levulinic acid, coproporphyrin and uroporphyrin was strongly positive. These findings are compatible with Porphyria Variegata or Coproporphyria Hereditary. A diagnosis of Porphyria acute with SIADH was made, and water fluid restriction, i.v. hypertonic saline infusion and furosemide to correct the hyponatremia was begun. In 1966, lesions of the median eminence of the hypothalamus and both hypothalamic -hypophyseal tracts were described in a patient with Porphyria acute intermittent and SIADH. It was suggested that SIADH occurred because of damage to these areas of the brain from excessive exposure to porphyrins.     

Plasma atrial natriuretic hormone levels in patients with the syndrome of inappropriate antidiuretic hormone secretion

This study explored whether atrial natriuretic hormone (ANH) might be involved in the escape from salt and water retention that occurs in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Sixteen patients with low serum Na+ concentrations [123 +/- 1 (+/- SE) mmol/L] were studied. Each patient excreted urine that was hyperosmolar (mean, 391 +/- 4 mosmol/kg) in relation to serum osmolality (mean, 258 +/- 4 mosmol/kg). Sodium excretion (81 +/- 20 mmol/L) also was inappropriate to the low serum Na+ level. The probable causes of SIADH were head trauma (4), pneumonia (5), lung cancer (3), and chlorpropamide therapy (4). In the nontumor patients, plasma and/or urinary vasopressin (AVP) concentrations were in the normal range, but inappropriate for serum osmolality. Urinary AVP values of 50 pg/mL or more (greater than 46 pmol/L) were found in the three tumor patients. The mean plasma ANH concentration was 6-fold higher than that in normal subjects [296 +/- 51 vs. 51 +/- 13 pg/mL (100 +/- 20 vs. 17 +/- 4 pmol/L); P less than 0.01]. Six SIADH patients were studied again after brief (1-3 days) water restriction. Although serum osmolality increased in each, their plasma AVP concentrations decreased very little, and urinary AVP excretion and plasma ANH did not change. These results indicate that plasma ANH levels are markedly increased in patients with SIADH. Their increased ANH secretion may antagonize water retention resulting from the inappropriate AVP secretion.     

Angiotropic B-cell lymphoma with hemophagocytic syndrome associated with syndrome of inappropriate secretion of antidiuretic hormone

 A case of angiotropic B-cell lymphoma associated with hemophagocytic syndrome (HPS) has been reported. In addition to fever, pancytopenia, hepatosplenomegaly, and lack of lymphadenopathy, unique clinical features, such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and pulmonary infarction, were manifested. Both soluble interleukin-2 receptor (sIL-2R) and IL-6 were elevated in the patient's sera in addition to an increase of serum lactate dehydrogenase and ferritin. In contrast, tumor necrosis factor-α and interferon-γ were within normal ranges. Serum antibodies against Epstein-Barr virus and cytomegalovirus showed a past infection pattern. An autopsy examination revealed systemic intravascular proliferation of lymphoma cells with a B-cell phenotype, confirming the diagnosis of angiotropic B-cell lymphoma. Moreover, SIADH was suggested to result from the infiltration of tumor cells into the pituitary gland. Triple association of angiotropic B-cell lymphoma, HPS and SIADH is quite rare. Therefore, the present case seems to be helpful for clarifying the mechanism for HPS of non-Hodgkin's lymphoma with B-cell origin. Received: 22 June 1999 / Accepted: 25 February 2000