Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyponatraemia has been described in association with a number of acute infectious diseases, mainly bacterial and tuberculous meningitis and pneumonia, and has been attributed to inappropriate secretion of arginine vasopressin (AVP). The mechanism of inappropriate AVP production is uncertain, but there is experimental evidence to suggest that fever may stimulate secretion of AVP into plasma and cerebrospinal fluid. In this study, AVP concentrations in plasma and cerebrospinal fluid from 37 febrile children with infections have been compared with those from 27 afebrile control subjects. Ten of the febrile children had meningitis (eight bacterial, two viral) and the remainder a variety of other infectious diseases. Seventy four per cent of febrile infected children were hyponatraemic (serum sodium less than 135 mmol/l) compared with only 8% of the afebrile controls. Plasma AVP concentrations were significantly higher in the febrile patients (median 2.92 pmol/l, range 1.0-23.25, n = 28) than in controls (median 1.67 pmol/l, range 0.57-6.0, n = 14) but there was no significant difference in cerebrospinal fluid AVP concentrations. There was no difference in plasma AVP concentrations between patients with meningitis and those with infections not involving the central nervous system. Careful attention should be paid to fluid and electrolyte balance in all children with acute infections.
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PMID:Plasma and cerebrospinal fluid arginine vasopressin in patients with and without fever. 152 19

The mechanism of hyponatremia associated with pneumonia has not been definitely established. Moreover, renal water excretion was never systematically investigated in cases of pneumonia without hyponatremia. We therefore studied nine consecutive patients breathing spontaneously (nasal oxygen in five), with acute infectious pneumonia and normal plasma sodium concentration. All the patients were previously healthy. Water loads were administered during illness and after recovery. Extracellular fluid volume, arterial blood pressure, PaO2, and PaCO2 were identical during and after pneumonia. By contrast, renal water excretion was markedly impaired during pneumonia and returned to normal values after recovery. This was attested to by a significant decrease in minimum urine osmolality together with significant increases in the percentage of the excreted water load and the maximum free water clearance, after resolution of the pneumonia. Plasma arginine vasopressin values were significantly higher during pneumonia than after recovery despite similar plasma sodium concentrations, both before and after water load. A positive correlation between plasma arginine vasopressin and minimum urine osmolality was found during pneumonia. Thus, impairment in renal water excretion appeared to be due to resetting of the vasopressin osmostat and could not be attributed to any recognized nonosmotic stimulus for vasopressin secretion. On the other hand, these defects varied in severity depending on the extent of the pneumonia and persisted until clearing of alveolar opacities, accounting for their protracted course in some patients. We conclude that water excretion is impaired in most if not in all patients with acute infectious pneumonia (especially if extended), and that the administration of hypotonic solutions should be avoided in these patients.
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PMID:Acute infectious pneumonia is accompanied by a latent vasopressin-dependent impairment of renal water excretion. 305 74

We report a 42-year-old woman with severe motor and intellectual disabilities (SMID) who showed partial central diabetes insipidus during severe pneumonia. Serum sodium levels were previously within the upper normal range from 140 to 147 mEq/L. During pneumonia, however, serum sodium rose rapidly to reach 185 mEq/L. The daily urinary volume exceeded the daily intake of water. Nasal administration of 1-desamino-8-D-arginine vasopressin (DDAVP) reduced the daily urinary volume and the serum sodium level to normal ranges. Consequently, we diagnosed her as having central diabetes insipidus (DI). She required a smaller dose of DDAVP (2.5 microg/day) than usual DI (5-15 microg/day) to maintain normal urinary volume and the serum sodium level for seven months. After the nasal administration of DDAVP was discontinued, the serum sodium levels again returned to within the upper normal range. A water deprivation study demonstrated poor elevation of both plasma antidiuretic hormone (ADH) level (range, 0.5-2.0 pg/ml) and urine osmolarity (peak level, 552 mOsm/kgH2O) despite the elevation of plasma osomolarity, suggesting latent partial central DI. Water balance and serum electrolyte levels should be closely monitored in cases of SMID.
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PMID:[Case of severe motor and intellectual disabilities presenting with partial central diabetes insipidus triggered by infection]. 1546 Oct 31

Neurohormones (NHs) in the cascade of the arginine vasopressin (AVP) system have drawn particular attention in the recent years. Copeptin, the C-terminal portion of provasopressin, is a novel NH of the AVP system, and is known to be co-released with AVP from hypothalamus (neurohypophysis). As a surrogate marker of the AVP system, copeptin has gradually replaced AVP in several clinical studies largely due to its structural and methodological advantages. Copeptin has been regarded as a marker of non-specific stress response, and has also been suggested to have clinical implications in a variety of non-cardiovascular (pneumonia, sepsis, etc.) and cardiovascular conditions (heart failure and acute coronary syndromes (ACSs, etc.)). However, current data on relation of copeptin with other cardiovascular conditions ( arrhythmias, etc.) are still insufficient. The present review primarily focuses on general features of copeptin, its general clinical implications, and specifically aims to cover its potential clinical value in a variety of cardiovascular conditions.
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PMID:Copeptin and cardiovascular disease: a review of a novel neurohormone. 2329 58