Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 65-year-old lady who presented with acute confusion and profound hyponatraemia (plasma sodium of 97 mmol/L). Five years earlier she had developed sepsis and was found to have hyponatraemia, thought to be due to syndrome of inappropriate antidiuretic hormone secretion. The patient was lost to follow-up. The patient was covered with steroids and investigations confirmed primary adrenal failure with flat response of cortisol to adrenocorticotropic hormone (ACTH) stimulation and very high level of ACTH. Adrenal auto-antibodies were negative and a computed tomography of the adrenals showed bilateral adrenal calcifications, suggestive of previous haemorrhage or infarction. Bilateral adrenal calcification due to haemorrhage/infarction usually does not present with severe hyponatraemia; however, adrenal insufficiency should be excluded in all cases of severe hyponatraemia. In suspected cases, patients should be treated with steroids, even when symptoms or signs are absent, while results of investigations are awaited.
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PMID:An unusual case of profound hyponatraemia and bilateral adrenal calcifications. 1979 4

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) remains a challenging disorder to diagnose and treat. Three cases are presented to illustrate these challenges. The first two cases had drug-induced SIADH secondary to a selective serotonin reuptake inhibitor (for depression) or carbamazepine (for trigeminal neuralgia). The third case had SIADH possibly secondary to bronchiectasis. The lowest serum sodium concentrations ranged between 118 and 124 mmol/L in the three cases. Hyponatraemia was not acute and severe symptoms were absent. However, several mild neurological symptoms were present. In the first case, hyponatraemia likely contributed to a fall, which resulted in a fracture of the odontoid process of the axis. The other two cases also had gait disturbances, in addition to nausea, headache, impaired memory, difficulty concentrating and confusion. In at least two of the cases, the underlying cause of SIADH was impossible to reverse. Traditional treatment for SIADH with fluid restriction and demeclocycline failed, caused side effects or increased duration of hospital stay. These examples suggest a need for better treatment options. The introduction of the vasopressin-receptor antagonists for SIADH may be a welcome new therapy to overcome some of these challenges.
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PMID:The clinical challenge of SIADH-three cases. 1988 33

The occurrence of a syndrome of inappropriate antidiuretic hormone secretion (SIADH) with sodium valproate has been rarely described in the literature. We present a 46-year-old patient, admitted to the Emergency Room for confusion and acute agitation. The exploration showed a severe hyponatraemia induced by sodium valproate, prescribed for a type I bipolar disorder. This article addresses both somatic and psychiatric issues in the differential diagnosis of confusion and agitation.
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PMID:[Inappropriate antidiuretic hormone secretion induced by sodium valproate]. 2022 1

Vasopressin promotes renal water reabsorption decreasing excretion of free water to dilute plasma and lower serum osmolality. We have good understanding of the causes, mechanisms and consequences of this vasopressin-dependent renal water movement. In comparison, vasopressin actions on renal electrolytes including sodium excretion and its consequences have been less well understood. This is so for investigation and discussions of the renal actions of vasopressin are framed primarily around water metabolism rather than any direct effect on salt handling. The fact that water moves in biological systems, to include the mammalian kidney, only by osmosis passively down its concentration gradient is implicit in such discussion but often not overtly addressed. This can cause confusion. Moreover, although vasopressin action on renal sodium excretion via the V2 receptor is critical to water transport, it is masked easily being situational--for instance, dependent on hydration state. It is now clear that an increase in sodium reabsorption along the distal nephron (CNT + CD) mediated by activation of the epithelial Na(+) channel (ENaC) by vasopressin makes an important contribution to maintenance of the axial corticomedullary osmotic gradient necessary for maximal water reabsorption. Thus, we need to modify slightly our understanding of vasopressin and its renal actions to include the idea that while vasopressin decreases free water excretion to dilute plasma, it does this, in part, by promoting sodium reabsorption and consequently decreasing sodium excretion via ENaC activated along the distal nephron.
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PMID:Vasopressin regulation of renal sodium excretion. 2073 86

Sodium, the most important extracellular fluid electrolyte, is the focus of several homeostatic mechanisms that regulate fluid and electrolyte balance. Hyponatremia is a common electrolyte abnormality caused by an actual sodium deficiency or extracellular compartment fluid excess. Clinical symptoms are related with acuity and speed with which this abnormality is established. The symptoms are mainly neurological and neuromuscular disorders (headache, confusion, stupor, seizures, coma) due to brain cells edema. Hyponatremia due to sodium deficiency is caused by sodium loss from kidney (nephritis, diuretics, mineralocorticoid deficiency) and / or extrarenal (vomiting, diarrhea, burns). Hyponatremia due to water excess seems to be the most common and it is attributable to cirrhosis, nephrotic syndrome, heart failure, infusion 5% glucose solutions and drugs that stimulate ADH secretion. It was recently highlighted the role of inflammation and IL-6 in the non-osmotic ADH release. Hyponatremia is considered also marker of phlogosis. Acute (<48 h) and severe (<125 mEq/ L) hyponatremia is a medical emergency that requires prompt correction. Patients with chronic hyponatremia have a high risk of osmotic demyelination syndrome if rapid correction of the plasmatic sodium occurs. In combination with conventional therapy, a new class of drugs, vasopressin receptors antagonists (AVP-R antagonists) would be able to increase the excretion of electrolyte-free water and the serum sodium concentration.
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PMID:[Hyponatremic syndrome]. 2236 42

Patients with acute hyponatraemia present with neurologic symptoms resulting from cerebral oedema induced by water movement into the brain. The author reports a male patient who presented to our emergency department with headache for 3 days and confusion for a day. The reported patient was on two immunosuppressive drugs, namely prednisone and azathiorprine for his ulcerative colitis. Laboratory data were consistent with syndrome of inappropriate antidiuretic hormone secretion (SIADH) which was appropriately corrected; however his mental status deteriorated. The patient's initial presentation was considered to be secondary to hyponatraemia. There was lapse of 36 h where the hyponatraemia was corrected; however the cause of the SIADH was not investigated. On further investigation of the patient a diagnosis of cryptococcal meningitis was ascertained. This case highlights the importance of considering a central nervous system infection in an immuno-suppressed patients presenting with hyponatraemia secondary to SIADH.
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PMID:Hyponatraemia masking the diagnosis of cryptococcal meningitis. 2266 27

In the central nervous system (CNS) of domestic animals, numerous specialized normal structures, unusual cell types, findings of uncertain or no significance, artifacts, and various postmortem alterations can be observed. They may cause confusion for inexperienced pathologists and those not specialized in neuropathology, leading to misinterpretations and wrong diagnoses. Alternatively, changes may mask underlying neuropathological processes. "Specialized structures" comprising the hippocampus and the circumventricular organs, including the vascular organ of the lamina terminalis, subfornical organ, subcommissural organ, pineal gland, median eminence/neurohypophyseal complex, choroid plexus, and area postrema, are displayed. Unusual cell types, including cerebellar external germinal cells, CNS progenitor cells, and Kolmer cells, are presented. In addition, some newly recognized cell types as of yet incompletely understood significance and functionality, such as synantocytes and aldynoglia, are introduced and described. Unusual reactive astrocytes in cats, central chromatolysis, neuronal vacuolation, spheroids, spongiosis, satellitosis, melanosis, neuromelanin, lipofuscin, polyglucosan bodies, and psammoma bodies may represent incidental findings of uncertain or no significance and should not be confused with significant microscopic changes. Auto- and heterolysis as well as handling and histotechnological processing may cause postmortem morphological changes of the CNS, including vacuolization, cerebellar conglutination, dark neurons, Buscaino bodies, freezing, and shrinkage artifacts, all of which have to be differentiated from genuine lesions. Postmortem invasion of micro-organisms should not be confused with intravital infections. Awareness of these different changes and their recognition are a prerequisite for identifying genuine lesions and may help to formulate a professional morphological and etiological diagnosis.
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PMID:Nonlesions, unusual cell types, and postmortem artifacts in the central nervous system of domestic animals. 2269 22

Community-acquired pneumonia (CAP) is the leading cause of death from infectious diseases worldwide, with an incidence of 0.3 to 0.5% in the adult population. A new diagnostic and prognostic approach relies on evaluation of biomarkers as an expression of the host's inflammatory response against the microorganism. C-reactive protein (CRP), procalcitonin (PCT), and cytokines are the most frequently studied, whereas pro-adrenomedullin (pro-ADM), pro-vasopressin (pro-VNP), and others are currently obtaining promising results. Their usefulness for diagnosis is limited, although PCT has been successfully used to guide prescription of antibiotics in patients with suspected CAP. Nevertheless, the accuracy of PCT in distinguishing between bacterial or viral infection and safely withholding antibiotics in CAP is the subject of debate. Analysis of systemic biomarkers in addition to clinical scores [Pneumonia Severity Index (PSI) or CURB-65 (confusion, urea, respiratory, blood pressure, >65 years)/CRB-65 (confusion, respiratory, blood pressure)] has been shown to improve 30 day mortality prediction and absence of severe complications. Pro-ADM is probably the biomarker that correlates most strongly with mortality prediction. During treatment, ~15% of hospitalized CAP patients develop treatment failure, and almost 6% may manifest rapidly progressive pneumonia. Initially increased and persistent raised levels of biomarkers and cytokines have been shown to identify patients at risk of treatment failure, thereby aiding clinical management. Data from the literature appear to support the use of biomarkers in routine clinical practice to improve the decision making in CAP.
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PMID:Biomarkers and community-acquired pneumonia: tailoring management with biological data. 2271 12

Pregabalin, a molecule with similar structure of GABA neurotransmitter, initially developed as an antiepileptic, is now commonly used in the treatment of painful peripheral neuropathies. We report an 82-year-old man who presented with confusion, urinary incontinence and gait instability. He was receiving pregabalin for a left L5 radicular pain. Laboratory tests at admission revealed a profound hyponatremia (117 mmol/L) that was corrected by fluid restriction and pregabalin withdrawal. According to the patient and laboratory outcome, we established the diagnosis of inappropriate antidiuretic hormone secretion due to pregabalin. The test of Naranjo demonstrated a probable imputability of pregabalin.
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PMID:[Gait instability revealing a syndrome of inappropriate antidiuretic hormone secretion associated to pregabalin]. 2301 93

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a common and multifactorial cause of hyponatremia that is often overlooked. The common pathophysiological mechanism is the increased production and/or action of antidiuretic hormone within the kidney, resulting in hypotonic hyponatremia. Inadequate correction of hyponatremia may have fatal neurological consequences leading to central pontine myelinolysis. We report the case of a patient with a history of recent head trauma, who came to our observation for acute-onset mental confusion secondary to severe hyponatremia due to SIADH of combined etiology.
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PMID:[Severe hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone]. 2354 55


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