SIADH and Hyponatremia with Theophylline

2002 ◽  
Vol 36 (7-8) ◽  
pp. 1180-1182 ◽  
Author(s):  
Evagelos N Liberopoulos ◽  
George H Alexandridis ◽  
Dimitris S Christidis ◽  
Moses S Elisaf
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Underlying Mechanism ◽  
Urinary Sodium ◽  
Case Summary ◽  
Possible Cause ◽  
Stimulation Of

OBJECTIVE: To report a case of possible theophylline-induced hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). CASE SUMMARY: An 88-year-old man developed severe symptomatic hyponatremia (serum sodium 112 mEq/L) associated with inappropriate natriuresis (urinary sodium 58 mEq/L) temporally related to the initiation of theophylline. The patient fulfilled the criteria for the diagnosis of SIADH after all other causes of hyponatremia were excluded. Furthermore, no other drugs or conditions that could have evoked SIADH were found. DISCUSSION: Theophylline has rarely been associated with hyponatremia. A thiazide-like action of the drug on the stimulation of SIADH could be the underlying mechanism for SIADH. CONCLUSIONS: Theophylline should be considered as a possible cause of hyponatremia.

Combined Treatment of Severe Hyponatremia Due to Inappropriate Antidiuretic Hormone Secretion

PEDIATRICS ◽  
1982 ◽  
Vol 69 (5) ◽  
pp. 610-612
Author(s):  
Zvi Weizman ◽  
Kalman Goitein ◽  
Yair Amit ◽  
Uri Wald ◽  
Heddy Landau
Keyword(s):  
Antidiuretic Hormone ◽  
Hypertonic Saline ◽  
Serum Sodium ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Urinary Sodium ◽  
Surgical Removal ◽  
Hypertonic Saline Solution ◽  
Deoxycorticosterone Acetate ◽  
Low Serum

A 6-year-old girl developed generalized seizures followed by coma, five days after surgical removal of a craniopharyngioma. Low serum sodium levels and low serum osmolality with inappropriately high urinary sodium output confirmed the diagnosis of inappropriate antidiuretic hormone (ADH) secretion. Treatment with 3% hypertonic saline solution and repeated doses of furosemide (1 mg/kg) improved her clinical condition; serum sodium levels, however, rose slowly and urinary excretion remained high. Deoxycorticosterone acetate (DOCA), 4 mg/sq m/day, was added to the above regimen. A striking clinical improvement was noted. Serum sodium levels returned to normal with a concomitant sharp decline in urinary sodium output. The clinical course of this patient demonstrates the efficacy of the addition of deoxycorticosterone acetate to hypertonic saline and furosemide in the treatment of severe, lifethreatening hyponatremia due to the syndrome of inappropriate antidiuretic hormone seretion.

Delayed Recurrent SIADH Associated with SSRIs

2002 ◽  
Vol 36 (7-8) ◽  
pp. 1175-1177 ◽  
Author(s):  
Zeev H Arinzon ◽  
Yehoshua A Lehman ◽  
Zeev G Fidelman ◽  
Irina I Krasnyansky
Keyword(s):  
Elderly Patients ◽  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Probability Scale ◽  
Depressed Woman ◽  
Case Summary

BACKGROUND: Depression is a common problem in elderly patients and is frequently treated with selective serotonin-reuptake inhibitors (SSRIs). OBJECTIVE: To report a case of delayed recurrent hyponatremia after switching from one SSRI to another. CASE SUMMARY: An 87-year-old depressed woman began treatment with fluvoxamine. One week later, she was diagnosed with hyponatremia, most likely syndrome of inadequate antidiuretic hormone. Following discontinuation of fluvoxamine, the serum sodium concentration normalized. Later, she began treatment with paroxetine. Sixteen months after initiating paroxetine, she developed symptomatic recurrent hyponatremia. After paroxetine was discontinued, the sodium concentration normalized. DISCUSSION: In this case, unlike those previously reported, hyponatremia recurred 16 months after a different SSRI was initiated. The Naranjo probability scale indicates a probable relationship between recurrent hyponatremia and paroxetine. The mechanism of SSRI-induced hyponatremia is multifactorial. CONCLUSIONS: This case illustrates that replacement of one SSRI with another can cause delayed, recurrent hyponatremia in elderly patients. Plasma sodium concentrations must be monitored, not only in the first weeks of treatment, but throughout the full course.

The mechanism and effect of chronic electrical stimulation of the globus pallidus for treatment of Parkinson disease

2004 ◽  
Vol 100 (6) ◽  
pp. 997-1001 ◽  
Author(s):  
Mitsuhiro Ogura ◽  
Naoyuki Nakao ◽  
Ekini Nakai ◽  
Yuji Uematsu ◽  
Toru Itakura
Keyword(s):  
Electrical Stimulation ◽  
Parkinson Disease ◽  
Globus Pallidus ◽  
Rating Scale ◽  
Underlying Mechanism ◽  
Clinical Effects ◽  
Content Type ◽  
Chronic Electrical Stimulation ◽  
Fine Print ◽  
Stimulation Of

Object. Although chronic electrical stimulation of the globus pallidus (GP) has been shown to ameliorate motor disabilities in Parkinson disease (PD), the underlying mechanism remains to be clarified. In this study the authors explored the mechanism for the effects of deep brain stimulation of the GP by investigating the changes in neurotransmitter levels in the cerebrospinal fluid (CSF) during the stimulation. Methods. Thirty patients received chronic electrical stimulation of the GP internus (GPi). Clinical effects were assessed using the Unified PD Rating Scale (UPDRS) and the Hoehn and Yahr Staging Scale at 1 week before surgery and at 6 and 12 months after surgery. One day after surgery, CSF samples were collected through a ventricular tube before and 1 hour after GPi stimulation. The concentration of neurotransmitters such as γ-aminobutyric acid (GABA), noradrenaline, dopamine, and homovanillic acid (HVA) in the CSF was measured using high-performance liquid chromatography. The treatment was effective for tremors, rigidity, and drug-induced dyskinesia. The concentration of GABA in the CSF increased significantly during stimulation, although there were no significant changes in the level of noradrenaline, dopamine, and HVA. A comparison between an increased rate of GABA concentration and a lower UPDRS score 6 months postimplantation revealed that the increase in the GABA level correlated with the stimulation-induced clinical effects. Conclusions. Stimulation of the GPi substantially benefits patients with PD. The underlying mechanism of the treatment may involve activation of GABAergic afferents in the GP.

scholarly journals AMP-activated protein kinase can induce apoptosis of insulin-producing MIN6 cells through stimulation of c-Jun-N-terminal kinase

2003 ◽  
Vol 30 (2) ◽  
pp. 151-161 ◽  
Author(s):  
BA Kefas ◽  
Y Cai ◽  
Z Ling ◽  
H Heimberg ◽  
L Hue ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Beta Cells ◽  
Caspase 3 ◽  
Underlying Mechanism ◽  
Beta Cell Line ◽  
Sequential Activation ◽  
Low Glucose ◽  
Jnk Activation ◽  
Amp Activated Protein Kinase ◽  
Stimulation Of

We have recently shown that conditions known to activate AMP-activated protein kinase (AMPK) in primary beta-cells can trigger their apoptosis. The present study demonstrates that this is also the case in the MIN6 beta-cell line, which was used to investigate the underlying mechanism. Sustained activation of AMPK was induced by culture with the adenosine analogue AICA-riboside or at low glucose concentrations. Both conditions induced a sequential activation of AMPK, c-Jun-N-terminal kinase (JNK) and caspase-3. The effects of AMPK on JNK activation and apoptosis were demonstrated by adenoviral expression of constitutively active AMPK, a condition which reproduced the earlier-described AMPK-dependent effects on pyruvate kinase and acetyl-coA-carboxylase. The effects of JNK activation on apoptosis were demonstrated by the observations that (i). its inhibition by dicumarol prevented caspase-3 activation and apoptosis, (ii). adenoviral expression of the JNK-interacting scaffold protein JIP-1/IB-1 increased AICA-riboside-induced JNK activation and apoptosis. In primary beta-cells, AMPK activation was also found to activate JNK, involving primarily the JNK 2 (p54) isoform. It is concluded that prolonged stimulation of AMPK can induce apoptosis of insulin-producing cells through an activation pathway that involves JNK, and subsequently, caspase-3.

Collecting Duct Na+/K+-ATPase Activity Is Correlated with Urinary Sodium Excretion in Rat Nephrotic Syndromes

2000 ◽  
Vol 11 (4) ◽  
pp. 604-615 ◽  
Author(s):  
GEORGES DESCHÊNES ◽  
ALAIN DOUCET
Keyword(s):  
Nephrotic Syndrome ◽  
Atpase Activity ◽  
Sodium Excretion ◽  
Collecting Duct ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Brattleboro Rats ◽  
Sodium Retention ◽  
Puromycin Aminonucleoside ◽  
Stimulation Of

Abstract. In puromycin aminonucleoside (PAN)-treated nephrotic rats, sodium retention is associated with increased Na+/K+-ATPase activity in the cortical collecting ducts (CCD). This study was undertaken to determine whether stimulation of Na+/K+-ATPase in the CCD is a feature of other experimental nephrotic syndromes, whether it might be responsible for renal sodium retention, and whether it is mediated by increased plasma vasopressin levels or activation of calcineurin. For this purpose, the time courses of urinary excretion of sodium and protein, sodium balance, ascites, and Na+/K+-ATPase activities in microdissected CCD were studied in rats with PAN or adriamycin nephrosis or HgCl2nephropathy. The role of vasopressin and calcineurin in PAN nephrosis were evaluated by measuring these parameters in Brattleboro rats and in rats treated with cyclosporin or tacrolimus. Despite different patterns of changes in urinary sodium and protein excretion in the three nephrotic syndrome models, there was a linear relationship between CCD Na+/K+-ATPase activities and sodium excretion in all three cases. The results also indicated that there was no correlation between proteinuria and sodium retention, but ascites was present only when proteinuria was associated with marked reduction of sodium excretion. Finally, the lack of vasopressin in Brattleboro rats or the inhibition of calcineurin by administration of either cyclosporin or tacrolimus did not prevent development of the nephrotic syndrome in PAN-treated rats or stimulation of CCD Na+/K+-ATPase. It is concluded that stimulation of Na+/K+-ATPase in the CCD of nephrotic rats might be responsible for sodium retention and that this phenomenon is independent of proteinuria and vasopressin and calcineurin activities.

Possible Cefotaxime-Induced Stevens–Johnson Syndrome

2003 ◽  
Vol 37 (6) ◽  
pp. 812-814 ◽  
Author(s):  
Evagelos N Liberopoulos ◽  
George L Liamis ◽  
Moses S Elisaf
Keyword(s):  
Case Control Study ◽  
Causality Assessment ◽  
Clinical Manifestations ◽  
Underlying Mechanism ◽  
Upper Urinary Tract ◽  
Stevens Johnson Syndrome ◽  
Case Summary ◽  
Johnson Syndrome ◽  
Increased Risk ◽  
Control Study

OBJECTIVE: To report a case of possible cefotaxime-induced Stevens–Johnson syndrome (SJS). CASE SUMMARY: A 72-year-old woman with an upper urinary tract infection developed erosions and blisters on the skin and the mucous membranes, as well as fever and prostration, soon after the administration of cefotaxime. This presentation is consistent with the features of SJS. Resolution of the clinical manifestations was observed after discontinuation of the drug; all other drugs, infections, or immunologic disorders that could have caused this syndrome were carefully excluded. An objective causality assessment revealed that SJS was possibly associated with the use of cefotaxime. DISCUSSION: Although cephalosporins have been associated with an increased risk for SJS and cefotaxime has been suspected of being associated with SJS in a previous case–control study, this is the first full report for cefotaxime-related SJS in the literature. An immunologically mediated reaction may be the underlying mechanism. CONCLUSIONS: Although cefotaxime administration seems to be the underlying cause of the SJS observed in our patient, establishment of a definite causal relationship requires additional cases and supportive data.

scholarly journals Syndrome of Inappropriate Secretion of Antidiuretic Hormone due to Selective Serotonin Reuptake Inhibitors After Pancreaticoduodenectomy for Carcinoma of the Ampulla of Vater: Case Report

2013 ◽  
Vol 98 (4) ◽  
pp. 289-291
Author(s):  
Ryota Iwase ◽  
Hiroaki Shiba ◽  
Takeshi Gocho ◽  
Yasuro Futagawa ◽  
Shigeki Wakiyama ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Ampulla Of Vater ◽  
Serum Sodium Concentration ◽  
Selective Serotonin ◽  
Inappropriate Secretion

Abstract A 68-year-old man underwent pancreaticoduodenectomy with lymph nodes dissection for carcinoma of the ampulla of Vater. The patient had anxiety neurosis and had been treated with a selective serotonin reuptake inhibitor (SSRI). Postoperatively, SSRI was resumed on postoperative day 2. His serum sodium concentration gradually decreased, and the patient was given a sodium supplement. However, 11 days after the operation, laboratory findings included serum sodium concentration of 117 mEq/L, serum vasopressin of 2.0 pg/mL, plasma osmolality of 238 mOsm/kg, urine osmolality of 645 mOsm/kg, urine sodium concentration of 66 mEq/L, serum creatinine concentration of 0.54 mg/dL, and serum cortisol concentration of 29.1 μg/dL. With a diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the antianxiety neurosis medication was changed from the SSRI to another type of drug. After switching the medication, the patient made a satisfactory recovery with normalization of serum sodium by postoperative day 20.

Hydrogen peroxide stimulates ubiquitin-conjugating activity and expression of genes for specific E2 and E3 proteins in skeletal muscle myotubes

2003 ◽  
Vol 285 (4) ◽  
pp. C806-C812 ◽  
Author(s):  
Yi-Ping Li ◽  
Yuling Chen ◽  
Andrew S. Li ◽  
Michael B. Reid
Keyword(s):  
Skeletal Muscle ◽  
Actinomycin D ◽  
Underlying Mechanism ◽  
Muscle Proteins ◽  
Conjugation System ◽  
Cell Extracts ◽  
Expression Of Genes ◽  
Ubiquitin Conjugation ◽  
Muscle Catabolism ◽  
Stimulation Of

Reactive oxygen species (ROS) are thought to promote muscle atrophy in chronic wasting diseases, but the underlying mechanism has not been determined. Here we show that H2O2 stimulates ubiquitin conjugation to muscle proteins through transcriptional regulation of the enzymes (E2 and E3 proteins) that conjugate ubiquitin to muscle proteins. Incubation of C2C12 myotubes with 100 μM H2O2 increased the rate of 125I-labeled ubiquitin conjugation to muscle proteins in whole cell extracts. This response required at least 4-h exposure to H2O2 and persisted for at least 24 h. Preincubating myotubes with cycloheximide or actinomycin D blocked H2O2 stimulation of ubiquitin-conjugating activity, suggesting that gene transcription is required. Northern blot analyses revealed that H2O2 upregulates expression of specific E3 and E2 proteins that are thought to regulate muscle catabolism, including atrogin1/MAFbx, MuRF1, and E214k. These results suggest that ROS stimulate protein catabolism in skeletal muscle by upregulating the ubiquitin conjugation system.

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