FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2474508749> ?p ?o ?g. }

• W2474508749 endingPage "A19" @default.
• W2474508749 startingPage "A17" @default.
• W2474508749 abstract "A 45-year-old woman presented with impaired cognition. Her medical history included diffuse large B-cell non-Hodgkin lymphoma (Ann Arbor stage IV) involving the thyroid and mesentery, which was diagnosed in spring 2014 and treated with 3 cycles of R-CHOP (rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisolone) chemotherapy. Two months later, a positron emission tomography scan revealed a partial response to the chemotherapy. One month after the scan, the patient experienced partial loss of consciousness. She was intubated and transferred to the intensive care unit. Magnetic resonance imaging of the brain revealed a large number of hyperintense areas, mainly affecting the white matter of the frontal lobes, basal ganglia, and brainstem (Fig 1). Lumbar punctures did not provide evidence of infectious meningitis. A cytometric analysis of cerebrospinal fluid revealed 8 cells/μL, but no lymphomatous involvement. In the cerebrospinal fluid, interleukin 6 (IL-6) and IL-10 levels were moderately elevated, as one would expect in meningeal lymphoma. On day 5 of hospitalization, despite hydration with normal saline solution, the patient developed hypo-osmolar (240 mOsm/kg) hyponatremia (sodium, 117 mmol/L). Serum uric acid levels were low (1.14 mg/dL). There was no evidence of kidney, thyroid, or adrenal deficiency. Urine output was between 4 and 5 L/24 h, with high urine sodium levels (197 mmol/L) and high urine osmolality (549 mOsm/kg). The patient had low blood pressure, tachycardia, and a low central venous pressure of 7 cmH2O.■What are the causes of hyponatremia in non-Hodgkin lymphoma?■What is the diagnosis in this patient?■What is the pathophysiology of the disease?■How should the patient be treated? Although rare, hyponatremia has nevertheless been reported during the course of non-Hodgkin lymphoma. Most cases of hyponatremia in patients with lymphoma are due to the induction or exacerbation of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) by chemotherapy (eg, the cyclophosphamide and vincristine used in CHOP protocols). The presence of lymphomatous brain lesions may also cause SIADH.1Cabanillas F. Metabolic abnormalities in lymphoma.Clin Lymphoma. 2002; 3: S32-S36Abstract Full Text PDF PubMed Google Scholar Last, a case of adrenocorticotropic insufficiency and hyponatremia caused by lymphomatous infiltration of the pituitary gland has been reported. In this case, the diagnosis of SIADH appears unlikely given the clinical findings of volume depletion and the brisk urine output. Hyponatremia in these circumstances can be explained by a cerebral salt-wasting syndrome. Cerebral salt-wasting syndrome has many causes: primary or secondary brain tumors, ischemic or hemorrhagic stroke, brain trauma, infectious meningitis, encephalitis, and subarachnoid hemorrhage. To distinguish between SIADH and cerebral salt-wasting syndrome, the physician should first evaluate the effective blood volume (Table 1). The radioisotope dilution method is the gold standard but remains difficult to implement in routine clinical practice. In patients with low plasma volume evidenced by signs of volume depletion, negative water and sodium balances, elevated hematocrit, and low central venous pressure, cerebral salt-wasting syndrome can be suspected.2Leonard J. Garrett R.E. Salottolo K. et al.Cerebral salt wasting after traumatic brain injury: a review of the literature.Scand J Trauma Resusc Emerg Med. 2015; 23: 98Crossref PubMed Scopus (38) Google ScholarTable 1A Comparison of CSWS and SIADHCSWSSIADHClinical parameters Plasma volume↓Unchanged/↑ Weight↓↑ Heart rate↑Unchanged Signs of dehydrationPresentAbsent Central venous pressure↓Unchanged/↑ DiuresisUnchanged/↑Unchanged/↓ Water balanceNeutral/negativeNeutral/positiveBiochemical parameters Plasma sodium↓↓ Plasma osmolarity↓↓ Urine sodium↑↑ Urinary osmolarity↑↑ Sodium balanceNegativeVariable Fractional excretion of phosphorus↑Unchanged/↑ ReninUnchanged/↓Unchanged/↓ Aldosterone↓Unchanged/↓ Plasma uric acid↓↓ Fractional excretion of uric acidUnchanged/↓Unchanged/↓ Natriuretic peptidesUnchanged/↑UnchangedDiagnostic tests Isotonic saline solutionAmeliorates hyponatremiaExacerbates hyponatremia Loop diureticsExacerbates hyponatremiaAmeliorates hyponatremiaAbbreviations: CSWS, cerebral salt-wasting syndrome; SIADH, syndrome of inappropriate secretion of antidiuretic hormone. Open table in a new tab Abbreviations: CSWS, cerebral salt-wasting syndrome; SIADH, syndrome of inappropriate secretion of antidiuretic hormone. The pathophysiology of cerebral salt-wasting syndrome is still not well understood, but features the increased secretion of natriuretic factors such as atrial natriuretic peptide and brain natriuretic peptide.2Leonard J. Garrett R.E. Salottolo K. et al.Cerebral salt wasting after traumatic brain injury: a review of the literature.Scand J Trauma Resusc Emerg Med. 2015; 23: 98Crossref PubMed Scopus (38) Google Scholar However, an increase in fractional excretion of phosphate and urea suggests that proximal tubule function is significantly impaired. Natriuretic peptide synthesis takes place in the brain (mainly in the hypothalamus and sympathetic projections) and may therefore be disrupted when these regions are injured. Their effects result in afferent arteriolar dilation and efferent arteriolar constriction, which in turn lead to increased glomerular filtration. They also inhibit sodium reabsorption by the medullary portion of the collecting ducts. Last, the peptides act on the endocrine system, inhibiting the secretion of renin, aldosterone, and eventually antidiuretic hormone.3Cerdà-Esteve M. Cuadrado-Godia E. Chillaron J.J. et al.Cerebral salt wasting syndrome: review.Eur J Intern Med. 2008; 19: 249-254Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar Overall, these effects lead to urinary loss of sodium and water and contraction of extracellular volume. Treatments of cerebral salt-wasting syndrome (volume expansion) and SIADH (fluid restriction) are diametrically opposed. In cerebral salt-wasting syndrome, volume expansion with hypertonic saline solution should target correction of hyponatremia by not more than 8 to 10 mmol/L per day. The rate and volume of infusion within 24 hours are calculated in order to meet these objectives based on the equation shown in Box 1. When serum sodium level has been corrected, even water balance must be maintained with infusion of isotonic saline solution.4Palmer B.F. Hyponatremia in patients with central nervous system disease: SIADH versus CSW.Trends Endocrinol Metab. 2003; 14: 182-187Abstract Full Text Full Text PDF PubMed Scopus (225) Google ScholarBox 1Equation to Estimate the Expected Change in Plasma Sodium After Infusion of Saline SolutionΔNap=(Nai−Nap)/(totalwater+1)WhereΔNap is the desired change in plasma sodium,Nap is the current plasma sodium level,Nai is the sodium concentration in the infusion,and total water is equal to body weight (in kg) × 0.6. ΔNap=(Nai−Nap)/(totalwater+1)WhereΔNap is the desired change in plasma sodium,Nap is the current plasma sodium level,Nai is the sodium concentration in the infusion,and total water is equal to body weight (in kg) × 0.6. In our patient, the persistence of impaired mental status and metabolic disorders despite volume expansion required initiation of high-dose methotrexate (3,000 mg/m2) and corticosteroids, along with continuation of R-CHOP chemotherapy. Shortly afterward, the neurologic disorder resolved and serum sodium and urine parameters normalized. Hypo-osmolar hyponatremia caused by cerebral salt wasting syndrome in the course of a non-Hodgkin lymphoma with brain lesions." @default.
• W2474508749 created "2016-07-22" @default.
• W2474508749 creator A5006320058 @default.
• W2474508749 creator A5023154022 @default.
• W2474508749 creator A5040384789 @default.
• W2474508749 creator A5057090299 @default.
• W2474508749 date "2016-07-01" @default.
• W2474508749 modified "2023-10-10" @default.
• W2474508749 title "Quiz Page July 2016" @default.
• W2474508749 cites W1984348933 @default.
• W2474508749 cites W1998923243 @default.
• W2474508749 cites W2025239380 @default.
• W2474508749 cites W2172937506 @default.
• W2474508749 doi "https://doi.org/10.1053/j.ajkd.2016.03.420" @default.
• W2474508749 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27343809" @default.
• W2474508749 hasPublicationYear "2016" @default.
• W2474508749 type Work @default.
• W2474508749 sameAs 2474508749 @default.
• W2474508749 citedByCount "4" @default.
• W2474508749 countsByYear W24745087492017 @default.
• W2474508749 countsByYear W24745087492020 @default.
• W2474508749 countsByYear W24745087492021 @default.
• W2474508749 crossrefType "journal-article" @default.
• W2474508749 hasAuthorship W2474508749A5006320058 @default.
• W2474508749 hasAuthorship W2474508749A5023154022 @default.
• W2474508749 hasAuthorship W2474508749A5040384789 @default.
• W2474508749 hasAuthorship W2474508749A5057090299 @default.
• W2474508749 hasBestOaLocation W24745087491 @default.
• W2474508749 hasConcept C71924100 @default.
• W2474508749 hasConceptScore W2474508749C71924100 @default.
• W2474508749 hasIssue "1" @default.
• W2474508749 hasLocation W24745087491 @default.
• W2474508749 hasLocation W24745087492 @default.
• W2474508749 hasLocation W24745087493 @default.
• W2474508749 hasOpenAccess W2474508749 @default.
• W2474508749 hasPrimaryLocation W24745087491 @default.
• W2474508749 hasRelatedWork W1506200166 @default.
• W2474508749 hasRelatedWork W1995515455 @default.
• W2474508749 hasRelatedWork W2048182022 @default.
• W2474508749 hasRelatedWork W2080531066 @default.
• W2474508749 hasRelatedWork W2604872355 @default.
• W2474508749 hasRelatedWork W2748952813 @default.
• W2474508749 hasRelatedWork W2899084033 @default.
• W2474508749 hasRelatedWork W3031052312 @default.
• W2474508749 hasRelatedWork W3032375762 @default.
• W2474508749 hasRelatedWork W3108674512 @default.
• W2474508749 hasVolume "68" @default.
• W2474508749 isParatext "false" @default.
• W2474508749 isRetracted "false" @default.
• W2474508749 magId "2474508749" @default.
• W2474508749 workType "article" @default.