Syndrome of inappropriate secretion of antidiuretic hormone in nasopharynx carcinoma

The syndrome of inappropriate secretion of antidiuretic hormone (ADH) or SIADH has been reported in various disorders. We report a pediatric patient with nasopharynx carcinoma who may have developed a clinical SIADH with severe hyponatremia and generalized seizure during the administration of intravenous hydration. We propose that the inappropriately high plasma level of ADH led to the inability to excrete sufficient amounts of free water during a hyperhydration protocol with a relatively hypotonic fluid, which resulted in acute hyponatremia and central nervous system involvement. To avoid this complication, intravenous hydration before chemotherapy in children with nasopharynx carcinoma should be performed at a slower infusion rate and with a sodium chloride concentration of more than half isotonic.     

Hepatic steatosis during treatment with zidovudine and lamivudine in an HIV-positive patient

BACKGROUND: Polydipsia-hyponatremia is a poorly understood disorder that causes considerable mortality and morbidity. Hyponatremia in polydipsia-hyponatremia has been attributed to disturbances in antidiuretic hormone (ADH) function. Improvements in polydipsia-hyponatremia during clozapine treatment offered the chance to see if levels of ADH and other hormones associated with osmoregulation changed with improvement in biochemical and clinical measures of polydipsia-hyponatremia. METHOD: In this preliminary, longitudinal study, we studied 2 male schizophrenic patients (DSM-III-R) who had polydipsia-hyponatremia. Measures were (1) biochemical and clinical: serum sodium and osmolality, urine osmolality and specific gravity, normalized diurnal weight gain, and estimated urine volume and (2) endocrine: ADH, angiotensin II, atrial natriuretic peptide, and prolactin. Measures were collected during 2 months of baseline (typical neuroleptic) and 6 months of clozapine treatment. RESULTS: Single-case statistical procedures showed significant changes in sodium levels (a.m. and p.m.), estimated urine volume, and a.m. urine specific gravity in both patients and significantly decreased diurnal weight gain in 1 patient. Both serum and urine osmolality showed improvement, but values did not reach statistical significance. Low baseline ADH levels persisted through 6 months of clozapine treatment and showed no changes in the context of improvements in serum sodium and osmolality. No significant changes were seen in levels of angiotensin II and atrial natriuretic peptide. CONCLUSION: Given the limitations of this study, there is some evidence to suggest that the improvements in serum sodium and osmolality during clozapine treatment of polydipsia-hyponatremia may not be related to serum levels of ADH, although altered ADH receptor function cannot be ruled out. These data need to be extended in larger samples.     

Chlorpropamide-induced hyponatremia

A 29-year-old woman with severe idiopathic diabetes insipidus, while being treated by a combination of chlorpropamide and chlorothiazide, developed the syndrome of inappropriate secretion of ADH (SIADH) following an overdose of chlorpropamide. The syndrome resolved as the serum chlorpropamide level fell. This report demonstrates that a chlorpropamide-induced SIADH can occur in a patient with idiopathic diabetes insipidus, and it appears that the antidiuretic effect of the drug is dose-related.     

Hypouricemia in patients with meningitis

Serum urate and sodium concentrations were measured in 23 patients with acute viral and bacterial meningitis. Serum urate level was 3.0 +/- 0.2 mg/dl (mean +/- S.D.) (3.6 +/- 1.2 mg/dl in male and 2.5 +/- 0.9 mg /dl in female) on admission, but gradually elevated with improvements of meningitis. It turned to 4.8 +/- 0.2 mg/dl after recovery, and the value on admission was significantly lower than that after recovery (p < 0.0001). Serum sodium level was 137.6 +/- 2.9 mEq/l on admission and 139.7 +/- 2.7 mEq/l after recovery; also lower in the former (p < 0.01). These results show that patients develop transient hypouricemia, which may be explained by SIADH (syndrome of inappropriate secretion of ADH), although SIADH is subclinical in most cases of meningitis.     

Recurrent hypernatremia; a proposed mechanism in a patient with absence of thirst and abnormal excretion of water

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.     

Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm

BACKGROUND: Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states. METHODS: To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH. RESULTS: Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume. CONCLUSION: Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.     

Concentrations of antidiuretic hormone in plasma during human sodium restriction

Negative sodium balance was produced in 10 human volunteers. Body weight, plasma sodium, osmolality, hematocrit, renin activity (PRA), and antidiuretic hormone (ADH) concentrations were determined before, during, and after sodium restriction. Body weight declined and PRA rose during the period of low sodium intake. Plasma sodium concentration and osmolality did not change. A statistically significant change in ADH was not observed. It is suggested that a decrease in ADH was prevented by a rising titer of renin and contraction of the extracellular space.     

Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.     

A case of prostatic ductal adenocarcinoma with endometrioid features, associated with rectal invasion and multiple liver metastases

A 66-year-old man was admitted with destructive arthropathy, and calcium pyrophosphate dihydrate was demonstrated in the synovial fluid specimen. He was found to have a hyponatremia. The serum sodium concentration was 121 mmol/l, plasma arginine vasopressin (AVP) 6.6 pmol/l, and serum interleukin (IL)-6 96 pg/l. The clinical findings suggest the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). However, destructive arthropathy with increased values of C-reactive protein and IL-6 is the only background of SIADH in this patient. We suggest the possibility that IL-6 produced at inflammatory lesions may have stimulated an excessive release of AVP resulting in the hyponatremia and hypochloremia of SIADH.     

Serum CA125 measurement is useful in 3 cases with pericardial effusion

Previously we reported that serum CA125 level is elevated in cases of pericardial effusion. We report three cases in which serum CA125 measurement is useful for assessing clinical status. In case 1, a 19-year-old came to our hospital for cardiac tamponade. Moderate degree of pericardial effusion and high CA125 level were observed. After the pericardectomy the serum CA125 level was normalized and pericardial effusion disappeared. Case 2, a 50-year-old man with mesothelioma and in whom serum CA125 level was elevated with pericardial effusion. After cardiac drainage his condition improved, with decreased CA125 level. However, later the CA125 level rose and recurrent localized pericardial effusion with worsening condition was observed. In case 3, in a 78-year-old woman with pericardial effusion no recurrence was observed after pericardial drainage. Her CA125 value was normal. These results indicated that measurement of CA125 value is a useful marker for assessing the clinical course of this disease.     

Differences between supine and sitting Frank-lead electrocardiograms

In babies ranging in age from 1 to 25 weeks and in children between 1 and 14 years, plasma renin activity and urinary aldosterone activity were determined in relation to urinary sodium excretion. A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. A second stimulus was observed in the influence of the hypothalamo-neurohypophyseal system, when the plasma renin activity was suppressed by administration of antidiuretic hormone and sodium excretion increased due to a decreased aldosterone activity. Our study suggests that there exists a feedback between the renin-angiotensin-aldosterone system and ADH release and that this feedback plays an important role in the regulation of water and electrolyte balance in the young infant.     

Effects of diuretic therapy on electrolyte and acid-base homeostasis

The use of diuretics leads to a negative sodium and fluid balance without primary effects on serum sodium concentration. This parameter is regulated by the activity of the antidiuretic hormone (ADH) system. Secondary changes in other electrolyte systems and in acid base homeostasis also are induced by diuretic therapy. Especially diuretic induced hypokalemia is important as it is responsible for the excess mortality observed in patients with diuretic treated essential hypertension and cardiac abnormalities. All adverse metabolic effects of diuretic therapy are, in contrast to the antihypertensive action, dose dependent. Changes in fluid and electrolyte metabolism induced by diuretics occur within the first 2 or 3 weeks after initiation of medication. Counterregulatory mechanisms are activated and a new steady state is established. Serial laboratory determinations after this period are not necessary as long as this steady state is not affected by additional events (like a change in therapy or diet as well as the occurrence of vomiting or diarrhea).     

The syndrome of inappropriate secretion of vasopressin (SIADH) (author's transl)

The syndrome of inappropriate ADH secretion ("SIADH") was first recognized 1935 by Roth et al. and described in detail 1957 by Schwartz et al. The clinical symptoms (hyponatremia, hypertonicity of urine and inability to excrete a water load) are caused by inadequately elevated ADH secretion under a variety of situations and diseases. Some recent work was focused on the pathogenesis of this syndrome and new clinical findings (low plasma levels of uric acid and potassium) as well as special forms ("SIADH" without elevated vasopressin levels in plasma) are thought to be of relevance. New therapeutical recommendations will be discussed.     

Effects of various ambient temperatures and of heating and cooling the hypothalamus and cervical spinal cord on antidiuretic hormone secretion and urinary osmolality in pigs

1. Plasma ADH concentration, urinary and plasma osmolality and haematocrit were measured in young pigs placed in cold, thermoneutral, warm and hot ambient temperatures. In some experiments a thermode placed in the hypothalamus or over the cervical spinal cord was heated or cooled at various ambient temperatures. 2. Plasma ADH concentration remained at a low level (0-5--5 muu. ml.-1) over 2 hr or 3 hr periods when the pigs were in cold, thermoneutral or warm ambient temperatures. A hot environment, which caused a marked rise in the pigs' rectal temperature, was associated with a large rise in plasma ADH level. 3. The rise in plasma ADH level which occurred during an increase in body temperature was consistently and completely suppressed by simultaneous cooling of the thermode in the pre-optic region to 5 to 10 degrees C. When the thermode was in the region of the supraoptic nucleus the rise in ADH was only partly suppressed, and when it was over the cervical cord it was only sometimes suppressed. 4. Cooling the thermodes in any position at a cold or thermoneutral ambient temperature, or heating them at a thermoneutral or warm ambient temperature, caused no consistent change in ADH. 5. A diuresis, with a urinary flow-rate of at most 1 ml. min-1 and minimal urinary osmolality of 53 m-osmole kg-1, was observed on only three occasions, twice during cooling of a thermode in the hypothalamus and once after the end of a period when the thermode was heated. In each case, the plasma ADH was less than 2 muu. ml.-1. 6. A slight rise of haematocrit in cold ambient conditions and a slight fall in the warm were observed. Otherwise changes in haematocrit were trivial, and a shift of water between vascular system and interstitium could not be invoked to account for changes in ADH levels. Observed variation of plasma osmolality was also slight.     

Electroencephalographic findings in epilepsy in Asir region of southern Saudi Arabia

People recovering from pneumonia are often weak for no apparent reason. Clinical features such as postural hypotension, arrhythmia and syndrome of inappropriate ADH have, in other circumstances, been attributed to impaired autonomic function. The aim of this study was to see whether elderly patients with pneumonia had impaired autonomic cardiovascular reflexes and, if so, how long this persisted. We compared healthy elderly controls, elderly controls with trauma (fractured femoral neck) and elderly patients with pneumonia. Thirty-eight subjects were studied in a series of cardiovascular autonomic function tests. Results suggest that elderly people have a high prevalence of impaired cardiovascular autonomic reflexes in the immediate post-pneumonic phase, and that this improves significantly after six weeks, with a further improvement by six months. Elderly patients recovering from pneumonia are predisposed to the adverse effects of drugs and other factors which can further impair autonomic cardiovascular reflexes.     

Finding a balance point: a process central to understanding family caregiving in Taiwanese families

Mammalian alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases contributing to the synthesis of retinoic acid, the active form of vitamin A involved in growth and development. Xenopus laevis ADH1 and ADH4 genes were isolated using polymerase chain reaction primers corresponding to conserved motifs of vertebrate ADHs. The predicted amino acid sequence of Xenopus ADH1 was clearly found to be an ortholog of ADH1 from the related amphibian Rana perezi. Phylogenetic tree analysis of the Xenopus ADH4 sequence suggested this enzyme is likely to be an ADH4 ortholog, and this classification was more confidently made when based also on the unique expression patterns of Xenopus ADH1 and ADH4 in several retinoid-responsive epithelial tissues. Northern blot analysis of Xenopus adult tissues indicated nonoverlapping patterns of ADH expression, with ADH1 mRNA found in small intestine, large intestine, liver, and mesonephros and ADH4 mRNA found in esophagus, stomach, and skin. These nonoverlapping tissue-specific patterns are identical to those previously observed for mouse ADH1 and ADH4, thus providing further evidence that Xenopus ADH1 and ADH4 are orthologs of mouse ADH1 and ADH4, respectively. During Xenopus embryonic development ADH1 mRNA was first detectable by Northern blot analysis at stage 35, whereas ADH4 mRNA was undetectable through stage 47. Whole-mount in situ hybridization indicated that ADH1 expression was first localized in the pronephros during Xenopus embryogenesis, thus conserved with mouse embryonic ADH1 which is first expressed in the mesonephros. ADH4 expression was not detected in Xenopus embryos by whole-mount in situ hybridization but was localized to the gastric mucosa of the adult stomach, a property shared by mouse ADH4. Conserved expression of ADH1 and ADH4 in retinoid-responsive epithelial tissues of amphibians and mammals argue that these enzymes may perform essential retinoid signaling functions during development of the pronephros, mesonephros, liver, and lower digestive tract in the case of ADH1 and in the skin and upper digestive tract in the case of ADH4.     

Genetic Associations of Alcohol Dehydrogenase With Alcohol Use Disorders and Endophenotypes in White College Students.

Associations of alcohol dehydrogenase (ADH) gene polymorphisms (ADH1B*2 and ADH1C*1) with a lifetime alcohol use disorder (AUD) were examined in White college students. Alcohol-related endophenotypes likely to be influenced by elevations in acetaldehyde were also assessed. Individuals with an ADH1B*2 allele had lower rates of AUDs, consumed a lower maximum number of drinks in a 24-hr period, reported a greater level of response to alcohol, were more likely to have experienced alcohol-induced headaches following 1 or 2 drinks, and reported more severe hangovers than those lacking this allele. These findings are consistent with the hypothesis that enhanced sensitivity to alcohol and lower levels of alcohol use reflect the mechanism by which ADH1B*2 protects against developing an AUD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Miliary tuberculosis presenting with hyponatremia and thrombocytopenia

A 74-year-old woman with miliary tuberculosis had moderately severe hyponatremia due to inappropriate secretion of antidiuretic hormone (SIADH) and very severe thrombocytopenia without other hematologic abnormalities. She was treated with isoniazid, rifampin, ethambutol, prednisone, vincristine and fluid restriction and recovered completely. The SIADH may have been a response by the posterior pituitary to a decrease in intravascular volume resulting from the extensive pulmonary disease or associated hypoxia, or the tuberculous lung may have released ADH or an ADH-like substance. The thrombocytopenia may have resulted from a direct or indirect toxic effect of infection or, less likely, the tuberculosis may have activated latent idiopathic thrombocytopenic purpura.     

Qigong Yangsheng as a complementary therapy in the management of asthma: a single-case appraisal

In Caucasians, a genetic polymorphism is known for some alcohol dehydrogenase (ADH) systems (beta and gamma). Knowledge of population frequencies of the beta and gamma hepatic isozyme variants in France is a prerequisite to understanding any role this genetic variation might play in determining the risk of alcohol-related diseases. For the present study, the ADH phenotypes of 115 French Caucasian control subjects, consisting of 64 men and 51 women, were studied. The beta2 subunit was found to have a very low frequency. The relative frequencies of ADH gamma subunits observed in French Caucasians were found to be in good agreement with those already observed in other Caucasian populations. When gender and age were taken into account, a particular group corresponding to young men (age <50 years) was characterized by a manifest discordance with the comparable female population.     

Roentgen contrast media, source for AOX-contamination of waste water by hospitals]

A 30-year-old HIV-positive man presented with acute hydrocephalus secondary to tuberculous meningitis, for which an external ventricular drain was inserted. He developed marked natriuresis in the postoperative period, which resulted in acute hyponatraemia (131 to 122 mmol/l) and a contraction of his intravascular volume. A diagnosis of cerebral salt wasting syndrome was made, and he responded to sodium and fluid loading. This case highlights the differentiation of cerebral salt wasting syndrome from the more commonly occurring syndrome of inappropriate anti-diuretic hormone secretion as the aetiology of the hyponatraemia.