A 61-year-old woman presented with a right mandibular tumor and was diagnosed with DLBCL clinical stage IIIA from the biopsy results of the tumor and CT examination. An initial rituximab was administrated a week after the first CHOP treatment. During the infusion of rituximab, she exhibited disorientation, seizure, and consciousness disturbance. Hyponatremia due to SIADH and hypertension were coincidentally observed. MRI revealed T2 and FLAIR hyperintense signals involving the bilateral occipital, parietal, frontal lobes and the cerebellum that were consistent with reversible posterior leukoencephalopathy syndrome (RPLS). Her consciousness level recovered in parallel with corrections in serum sodium levels and blood pressure. Although she presented with transient cortical blindness, all neurological abnormalities disappeared 40 hours after the occurrence of seizure. She received a further 7 cycles of CHOP followed by 7 cycles of rituximab treatment with no relapse of RPLS. After irradiation for a residual abdominal tumor, she has maintained complete remission for 2 years. Although RPLS is a rare complication of rituximab-CHOP chemotherapy, it should be considered in patients with DLBCL who present with acute neurological deterioration.

Direct measurement of arginine-vasopressin/antidiuretic hormone (AVP/ADH) concentrations is not included in the standard diagnostic procedures for paraneoplastic syndrome of inappropriate ADH secretion (SIADH). Here, we evaluate the potential of copeptin measurement as a surrogate marker of AVP/ADH secretion for the direct diagnosis of suspected SIADH in cancer patients. Forty-six unselected cancer patients with serum sodium concentrations permanently below 135 mmol/L were included in this study. We compared standard diagnostic criteria for SIADH to the measurement of plasma copeptin in relation to osmolality. Normative data for comparison were constructed from 24 healthy controls studied under basal conditions, experimental dehydration, and hypotonic hypervolemia as well as from 222 hospital patients with no suspicion of an altered ADH regulation. Log transformation of copeptin revealed a linear relationship to plasma osmolality in the controls (R = 0.495, p < 0.001). Compared to these normative data, copeptin levels in most cancer patients were inappropriately high for plasma osmolality and were not significantly correlated. These results, suggestive for paraneoplastic SIADH, could be confirmed by conventional diagnostic procedures for SIADH. Current strategies to diagnose SIADH are difficult to perform under outpatients conditions. Our approach allows screening from a single plasma sample for true paraneoplastic ADH oversecretion and thus rapid selection for a specific therapy with an AVP receptor antagonist.

Several cases of syndrome of inappropriate antidiuresis induced by anti-Parkinson agents have been reported. Our previous study demonstrated that pergolide and pramipexole stimulated elevation of plasma arginine vasopressin (AVP) levels in some patients with Parkinson's disease (PD), but that levodopa/carbidopa (300/30 mg/day) did not affect plasma AVP levels in treatment-naïve PD patients. On the basis of the binding profile of ropinirole to monoamine receptors, we hypothesized that ropinirole does not stimulate AVP secretion. The aim of this study was to test this hypothesis.Inclusion criteria were patients with probable PD suffering from a wearing-off phenomenon and who had been treated using levodopa/carbidopa with or without entacapone, but not with other classes of anti-Parkinson agents. Patients were excluded if they had at least one condition that could be associated with high AVP levels. Ropinirole was initiated at 0.5 mg 3 times daily, and daily dosages were increased by 1.5 mg/day on a biweekly basis up to 6 mg/day. Plasma AVP levels were determined every two weeks. Effects of escalating ropinirole dosage on plasma AVP levels were evaluated using a one-way analysis of variance for repeated measures, an a priori Dunnett multiple comparison test, and a regression analysis.Of 16 patients enrolled, 11 patients (four males and seven females) completed the study. There was no statistically significant dose-response relationship between the ropinirole dosage and plasma AVP levels.A minimal therapeutic dosage of ropinirole did not affect plasma AVP levels in patients with PD taking levodopa.

We report the case of a 54-year old man with slowly progressive symmetrical weakness of the proximal legs and atactic gait. The diagnostic work-up is reviewed. It revealed the diagnosis of a Lambert-Eaton myasthenic syndrome(LEMS) and SIADH caused by a small cell lung cancer (SCLC).

Hyponatremia is a clinically relevant disorder. Ten to twenty per cent of patients in hospitals are affected by it. Hyponatremia is found to occur in almost every clinical department. Recently, vasopressin antagonists have been licensed to treat hyponatremia of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). They provide physicians with the first specific and effective therapy of this hyponatremia. This opens up new avenues for clinical research into the symptoms, findings and consequences of hyponatremia.

Hyponatremia is one of the most common electrolyte disturbances in cancer patients. Patients with extremely severe symptomatic hyponatremia need treatment with the administration of hypertonic saline. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a significant cause of cancer-related hyponatremia. A prospective study at a dedicated cancer hospital in Belgium demonstrated that SIADH was the most common cause of hyponatremia (30.4%). Ectopic ADH production by malignant cells (especially in small-cell lung cancer), several anticancer drugs (cyclophosphamide, ifosfamide, vincristine, cisplatin, et al.), stress from surgery, pain, and nausea, may cause SIADH in cancer patients. The second most common cause of hyponatremia in the Belgian investigation was sodium depletion (28.7%). In addition to gastrointestinal losses of sodium (vomiting, diarrhea), salt wasting syndrome (SWS) must be considerd as a cause of sodium depletion. Cerebral salt wasting syndrome (CSWS) with severe central nervous system diseases and renal salt wasting syndrome (RSWS) with cisplatin administration are especially important. Although identifying SWS or SIADH as the cause of hyponatremia is difficult, the treatment strategy for SWS is basically different from that for SIADH. Fluid restriction is generally prescribed for the hyponatremia associated with SIADH, and fluid replacement is indicated for the volume depletion associated with SWS. Furthermore, central nervous system disease and cisplatin administration, may cause both SWS and SIADH. This fact complicates the differential diagnosis, and careful management is necessary.

The syndrome of inappropriate ADH secretion (SIADH), also termed ''syndrome of inappropriate antidiuresis (SIAD)'', is an often unrecognized cause of hypotonic hyponatremia, arising from ectopic release of ADH in lung cancer or as a side effect of various drugs. In SIADH, hyponatremia results from selectively impaired water excretion by the kidney, whereas the external Na+ balance is normally regulated. Despite the increase in total body water, only a slight reduction of urine output and modest edema are usually seen. Renal function and acid-base balance are generally preserved, while subclinical neurological impairment may occasionally become life-threatening, when hyponatremia has an abrupt onset. The major clinical variants of SIADH are reviewed here, with particular emphasis on causes, iatrogenic complications and hospital-acquired hyponatremia. Effective treatment of SIADH is based on water restriction, hypertonic saline plus loop diuretics, or aquaretics. Worsening of hyponatremia may result from parenteral isotonic fluid administration, emphasizing the importance of an early diagnosis and careful follow-up of these patients.

Severe hyponatremia is a critical electrolyte abnormality in allogeneic stem cell transplantation (allo-SCT) recipients and >50% of cases of severe hyponatremia are caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Here, we present a patient with rapidly progressive severe hyponatremia as an initial sign and symptom of human herpesvirus-6-associated post-transplantation acute limbic encephalitis (HHV-6 PALE) after allo-SCT. A 45-year-old woman with acute lymphoblastic leukemia received unrelated bone marrow transplantation from a one locus-mismatched donor at the DR locus. On day 21, she developed a generalized seizure and loss of consciousness with severe hyponatremia, elevated serum antidiuretic hormone (ADH), and decreased serum osmolality. A high titer of HHV-6 DNA was detected in cerebrospinal fluid. Treatment with foscarnet sodium and hypertonic saline was started with improvement of neurological condition within several days. Although an elevated serum ADH, low serum osmolality, and high urinary osmolality persisted for 2 months, she had no other recurrent symptoms of encephalitis. Our experience suggests that hyponatremia accompanied by SIADH should be recognized as a prodromal or concomitant manifestation of HHV-6 PALE, and close monitoring of serum sodium levels in high-risk patients for HHV-6 PALE is necessary for immediate diagnosis and treatment initiation.