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Hyponatremia

MedGen UID:
6984
Concept ID:
C0020625
Finding; Pathologic Function
Synonyms: Hyponatremias
SNOMED CT: Hyponatremia (89627008)
 
OMIM®: 613508
HPO: HP:0002902

Definition

A disorder characterized by laboratory test results that indicate a low concentration of sodium in the blood. [from NCI]

Conditions with this feature

Cystinosis
MedGen UID:
1207
Concept ID:
C0010690
Disease or Syndrome
Nephropathic cystinosis in untreated children is characterized by renal tubular Fanconi syndrome, poor growth, hypophosphatemic rickets, impaired glomerular function resulting in complete glomerular failure, and accumulation of cystine crystals in almost all cells, leading to cellular destruction and tissue dysfunction. The typical untreated child has short stature, light complexion, rickets, and photophobia. Failure to thrive is generally noticed after approximately age six months; signs of renal tubular Fanconi syndrome (polyuria, polydipsia, dehydration, and acidosis) appear as early as age six months; corneal crystals can be present before age one year and are always present after age 16 months. Prior to the use of renal transplantation and cystine-depleting therapy, the life span in nephropathic cystinosis was no longer than ten years. With these therapies, affected individuals can survive at least into the mid-forties or fifties with satisfactory quality of life. Intermediate cystinosis is characterized by all the typical manifestations of nephropathic cystinosis, but onset is at a later age. Renal glomerular failure occurs in all untreated affected individuals, usually between ages 15 and 25 years. The non-nephropathic (ocular) form of cystinosis is characterized only by photophobia resulting from corneal cystine crystal accumulation.
Familial dysautonomia
MedGen UID:
41678
Concept ID:
C0013364
Congenital Abnormality
Familial dysautonomia (FD) affects the development and survival of sensory, sympathetic, and parasympathetic neurons. It is a debilitating disease present from birth. Neuronal degeneration progresses throughout life. Affected individuals have gastrointestinal dysfunction, vomiting crises, recurrent pneumonia, altered sensitivity to pain and temperature perception, and cardiovascular instability. About 40% of individuals have autonomic crises. Hypotonia contributes to delay in acquisition of motor milestones. Older individuals often have a broad-based and ataxic gait that deteriorates over time. Life expectancy is decreased.
Lowe syndrome
MedGen UID:
18145
Concept ID:
C0028860
Disease or Syndrome
Lowe syndrome (oculocerebrorenal syndrome) is characterized by involvement of the eyes, central nervous system, and kidneys. Dense congenital cataracts are found in all affected boys and infantile glaucoma in approximately 50%. All boys have impaired vision; corrected acuity is rarely better than 20/100. Generalized hypotonia is noted at birth and is of central (brain) origin. Deep tendon reflexes are usually absent. Hypotonia may slowly improve with age, but normal motor tone and strength are never achieved. Motor milestones are delayed. Almost all affected males have some degree of intellectual disability; 10%-25% function in the low-normal or borderline range, approximately 25% in the mild-to-moderate range, and 50%-65% in the severe-to-profound range of intellectual disability. Affected males have varying degrees of proximal renal tubular dysfunction of the Fanconi type, including bicarbonate wasting and renal tubular acidosis, phosphaturia with hypophosphatemia and renal rickets, aminoaciduria, low molecular-weight (LMW) proteinuria, sodium and potassium wasting, and polyuria. Fanconi syndrome is usually not clinically apparent in the first few months of life, but symptoms may appear by age six to 12 months. Glomerulosclerosis associated with chronic tubular injury usually results in slowly progressive chronic renal failure and end-stage renal disease after age ten to 20 years.
Hereditary coproporphyria
MedGen UID:
57931
Concept ID:
C0162531
Disease or Syndrome
Hereditary coproporphyria (HCP) is an acute (hepatic) porphyria in which the acute symptoms are neurovisceral and occur in discrete episodes. Attacks typically start in the abdomen with low-grade pain that slowly increases over a period of days (not hours) with nausea progressing to vomiting. In some individuals, the pain is predominantly in the back or extremities. When an acute attack is untreated, a motor neuropathy may develop over a period of days or a few weeks. The neuropathy first appears as weakness proximally in the arms and legs, then progresses distally to involve the hands and feet. Some individuals experience respiratory insufficiency due to loss of innervation of the diaphragm and muscles of respiration. Acute attacks are associated commonly with use of certain medications, caloric deprivation, and changes in female reproductive hormones. About 20% of those with an acute attack also experience photosensitivity associated with bullae and skin fragility.
Acute intermittent porphyria
MedGen UID:
56452
Concept ID:
C0162565
Disease or Syndrome
Acute intermittent porphyria (referred to as AIP in this GeneReview) results from half-normal activity of the enzyme hydroxymethylbilane synthase (HMBS). It is characterized clinically by life-threatening acute neurovisceral attacks of severe abdominal pain without peritoneal signs, often accompanied by nausea, vomiting, tachycardia, and hypertension. Attacks may be complicated by neurologic findings (mental changes, convulsions, and peripheral neuropathy that may progress to respiratory paralysis), and hyponatremia. Acute attacks, which may be provoked by certain drugs, alcoholic beverages, endocrine factors, calorie restriction, stress, and infections, usually resolve within two weeks. Most individuals with AIP have one or a few attacks; about 5% (mainly women) have recurrent attacks (defined as >4 attacks/year) that may persist for years. Other long-term complications are chronic renal failure, hepatocellular carcinoma (HCC), and hypertension. Attacks, which are very rare before puberty, are more common in women than men. All individuals with a genetic change in the gene HMBS that predisposes to AIP are at risk of developing acute attacks; however, most never have symptoms and are said to have latent (or presymptomatic) AIP.
Familial hyperkalemic periodic paralysis
MedGen UID:
68665
Concept ID:
C0238357
Disease or Syndrome
Hyperkalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness or paralysis, usually beginning in infancy or early childhood. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Episodes tend to increase in frequency until mid-adulthood, after which they occur less frequently. Factors that can trigger attacks include rest after exercise, potassium-rich foods such as bananas and potatoes, stress, fatigue, alcohol, pregnancy, exposure to cold temperatures, certain medications, and periods without food (fasting). Muscle strength usually returns to normal between attacks, although many affected people continue to experience mild stiffness (myotonia), particularly in muscles of the face and hands. Most people with hyperkalemic periodic paralysis have increased levels of potassium in their blood (hyperkalemia) during attacks. Hyperkalemia results when the weak or paralyzed muscles release potassium ions into the bloodstream. In other cases, attacks are associated with normal blood potassium levels (normokalemia). Ingesting potassium can trigger attacks in affected individuals, even if blood potassium levels do not go up.
Congenital secretory diarrhea, chloride type
MedGen UID:
78631
Concept ID:
C0267662
Disease or Syndrome
Congenital secretory chloride diarrhea is an autosomal recessive form of severe chronic diarrhea characterized by excretion of large amounts of watery stool containing high levels of chloride, resulting in dehydration, hypokalemia, and metabolic alkalosis. The electrolyte disorder resembles the renal disorder Bartter syndrome (see 607364), except that chloride diarrhea is not associated with calcium level abnormalities (summary by Choi et al., 2009). Genetic Heterogeneity of Congenital Diarrhea Other forms of congenital diarrhea include microvillus inclusion disease (DIAR2; 251850), caused by mutation in the MYO5B gene (606540) on chromosome 18q21; a syndromic form of congenital secretory sodium diarrhea (see DIAR3, 270420), caused by mutation in the SPINT2 gene (605124) on chromosome 19q13.1; malabsorptive congenital diarrhea (DIAR4; 610370), caused by mutation in the NEUROG3 gene (604882) on chromosome 10q21.3; congenital tufting enteropathy (DIAR5; 613217), caused by mutation in the EPCAM gene (185535) on chromosome 2p21; early-onset chronic diarrhea (DIAR6; 614616), caused by mutation in the GUCY2C gene (601330) on chromosome 12p13.1-p12.3; and neonatal-onset chronic diarrhea (DIAR7; 615863) caused by mutation in the DGAT1 gene (604900) on chromosome 8q24.
Corticosterone 18-monooxygenase deficiency
MedGen UID:
82784
Concept ID:
C0268293
Disease or Syndrome
Familial hemophagocytic lymphohistiocytosis
MedGen UID:
78797
Concept ID:
C0272199
Pathologic Function
Familial hemophagocytic lymphohistiocytosis (FHL) is characterized by proliferation and infiltration of hyperactivated macrophages and T-lymphocytes manifesting as acute illness with prolonged fever, cytopenias, and hepatosplenomegaly. Onset is typically within the first months or years of life and, on occasion, in utero, although later childhood or adult onset is more common than previously suspected. Neurologic abnormalities may be present initially or may develop later; they may include increased intracranial pressure, irritability, neck stiffness, hypotonia, hypertonia, convulsions, cranial nerve palsies, ataxia, hemiplegia, quadriplegia, blindness, and coma. Rash and lymphadenopathy are less common. Other findings include liver dysfunction and bone marrow hemophagocytosis. The median survival of children with typical FHL, without treatment, is less than two months; progression of hemophagocytic lymphohistiocytosis and infection account for the majority of deaths in untreated individuals.
Congenital adrenal hypoplasia, X-linked
MedGen UID:
87442
Concept ID:
C0342482
Congenital Abnormality
X-linked adrenal hypoplasia congenita (X-linked AHC) is characterized by infantile-onset acute primary adrenal insufficiency at an average age of three weeks in approximately 60% of affected individuals. Onset in approximately 40% is in childhood. A few individuals present in adulthood with delayed-onset adrenal failure or partial hypogonadism due to partial forms of X-linked AHC. Adrenal insufficiency typically presents acutely in male infants with vomiting, feeding difficulty, dehydration, and shock caused by a salt-wasting episode. Hypoglycemia (sometimes presenting with seizures) or isolated salt loss may be the first symptom of X-linked AHC. Cortisol may be low or within the normal range, which is inappropriately low for a sick child. In older children, adrenal failure may be precipitated by intercurrent illness or stress. If untreated, adrenal insufficiency is rapidly lethal as a result of hyperkalemia, acidosis, hypoglycemia, and shock. Affected males typically have delayed puberty (onset age >14 years) or arrested puberty caused by hypogonadotropic hypogonadism (HH). Early pubertal development with pubertal arrest has been reported in some cases. Males with classic X-linked AHC are infertile despite treatment with exogenous gonadotropin therapy or pulsatile gonadotropin-releasing hormone (GnRH), although testicular sperm extraction-intracytoplasmic sperm injection (TESE-ICSI) has been successful in one case. Carrier females may very occasionally have symptoms of adrenal insufficiency or hypogonadotropic hypogonadism as a result of skewed X-chromosome inactivation.
Pseudohypoaldosteronism type 1 autosomal dominant
MedGen UID:
260623
Concept ID:
C1449842
Disease or Syndrome
Autosomal dominant pseudohypoaldosteronism type I is characterized by salt wasting resulting from renal unresponsiveness to mineralocorticoids. Patients may present with neonatal renal salt wasting with hyperkalaemic acidosis despite high aldosterone levels. These patients improve with age and usually become asymptomatic without treatment. Some adult patients with the disorder may have elevated aldosterone levels, but no history of clinical disease. This observation suggests that only those infants whose salt homeostasis is stressed by intercurrent illness and volume depletion develop clinically recognized PHA I (summary by Geller et al., 1998). Autosomal recessive PHA (PHA1B; 264350), caused by mutation in any one of 3 genes encoding the epithelial sodium channel (ENaC), is a similar but more severe systemic disorder with persistence into adulthood.
Pseudohypoaldosteronism type 1 autosomal recessive
MedGen UID:
258573
Concept ID:
C1449843
Disease or Syndrome
Autosomal recessive pseudohypoaldosteronism type I is characterized by renal salt wasting and high concentrations of sodium in sweat, stool, and saliva. The disorder involves multiple organ systems and is especially threatening in the neonatal period. Laboratory evaluation shows hyponatremia, hyperkalemia, and increased plasma renin activity with high serum aldosterone concentrations. Respiratory tract infections are common in affected children and may be mistaken for cystic fibrosis (CF; 219700). Aggressive salt replacement and control of hyperkalemia results in survival, and the disorder appears to become less severe with age (review by Scheinman et al., 1999). A milder, autosomal dominant form of type I pseudohypoaldosteronism (PHA1A; 177735) is caused by mutations in the mineralocorticoid receptor gene (MCR, NR3C2; 600983). Gitelman syndrome (263800), another example of primary renal tubular salt wasting, is due to mutation in the thiazide-sensitive sodium-chloride cotransporter (SLC12A3; 600968).
Hyperchlorhidrosis, isolated
MedGen UID:
333560
Concept ID:
C1840437
Finding
Isolated hyperchlorhidrosis is an autosomal recessive condition in which excessive salt wasting in sweat can result in severe infantile hyponatremic dehydration and hyperkalemia (summary by Muhammad et al., 2011).
Nephrogenic syndrome of inappropriate antidiuresis
MedGen UID:
336877
Concept ID:
C1845202
Disease or Syndrome
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of hyponatremia. The syndrome manifests as an inability to excrete a free water load, with inappropriately concentrated urine and resultant hyponatremia, hypoosmolality, and natriuresis. SIADH occurs in a setting of normal blood volume, without evidence of renal disease or deficiency of thyroxine or cortisol. Although usually transient, SIADH may be chronic; it is often associated with drug use or a lesion in the central nervous system or lung. When the cardinal features of SIADH were defined by Bartter and Schwartz (1967), levels of AVP could not be measured. Subsequently, radioimmunoassays revealed that SIADH is usually associated with measurably elevated serum levels of AVP. Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is characterized by a clinical picture similar to SIADH, but is associated with undetectable levels of AVP (Feldman et al., 2005).
Hemophagocytic lymphohistiocytosis, familial, 2
MedGen UID:
400366
Concept ID:
C1863727
Disease or Syndrome
Familial hemophagocytic lymphohistiocytosis (FHL) is characterized by proliferation and infiltration of hyperactivated macrophages and T-lymphocytes manifesting as acute illness with prolonged fever, cytopenias, and hepatosplenomegaly. Onset is typically within the first months or years of life and, on occasion, in utero, although later childhood or adult onset is more common than previously suspected. Neurologic abnormalities may be present initially or may develop later; they may include increased intracranial pressure, irritability, neck stiffness, hypotonia, hypertonia, convulsions, cranial nerve palsies, ataxia, hemiplegia, quadriplegia, blindness, and coma. Rash and lymphadenopathy are less common. Other findings include liver dysfunction and bone marrow hemophagocytosis. The median survival of children with typical FHL, without treatment, is less than two months; progression of hemophagocytic lymphohistiocytosis and infection account for the majority of deaths in untreated individuals.
Bartter syndrome type 4
MedGen UID:
355430
Concept ID:
C1865270
Disease or Syndrome
Bartter syndrome is a group of very similar kidney disorders that cause an imbalance of potassium, sodium, chloride, and related molecules in the body. In some cases, Bartter syndrome becomes apparent before birth. The disorder can cause polyhydramnios, which is an increased volume of fluid surrounding the fetus (amniotic fluid). Polyhydramnios increases the risk of premature birth. Beginning in infancy, affected individuals often fail to grow and gain weight at the expected rate (failure to thrive). They lose excess amounts of salt (sodium chloride) in their urine, which leads to dehydration, constipation, and increased urine production (polyuria). In addition, large amounts of calcium are lost through the urine (hypercalciuria), which can cause weakening of the bones (osteopenia). Some of the calcium is deposited in the kidneys as they are concentrating urine, leading to hardening of the kidney tissue (nephrocalcinosis). Bartter syndrome is also characterized by low levels of potassium in the blood (hypokalemia), which can result in muscle weakness, cramping, and fatigue. Rarely, affected children develop hearing loss caused by abnormalities in the inner ear (sensorineural deafness). Two major forms of Bartter syndrome are distinguished by their age of onset and severity. One form begins before birth (antenatal) and is often life-threatening. The other form, often called the classical form, begins in early childhood and tends to be less severe. Once the genetic causes of Bartter syndrome were identified, researchers also split the disorder into different types based on the genes involved. Types I, II, and IV have the features of antenatal Bartter syndrome. Because type IV is also associated with hearing loss, it is sometimes called antenatal Bartter syndrome with sensorineural deafness. Type III usually has the features of classical Bartter syndrome.
Normokalemic periodic paralysis, potassium-sensitive
MedGen UID:
356973
Concept ID:
C1868433
Disease or Syndrome
Addison disease
MedGen UID:
357032
Concept ID:
C1868690
Disease or Syndrome
Autoimmune Addison disease affects the function of the adrenal glands, which are small hormone-producing glands located on top of each kidney. It is classified as an autoimmune disorder because it results from a malfunctioning immune system that attacks the adrenal glands. As a result, the production of several hormones is disrupted, which affects many body systems. The signs and symptoms of autoimmune Addison disease can begin at any time, although they most commonly begin between ages 30 and 50. Common features of this condition include extreme tiredness (fatigue), nausea, decreased appetite, and weight loss. In addition, many affected individuals have low blood pressure (hypotension), which can lead to dizziness when standing up quickly; muscle cramps; and a craving for salty foods. A characteristic feature of autoimmune Addison disease is abnormally dark areas of skin (hyperpigmentation), especially in regions that experience a lot of friction, such as the armpits, elbows, knuckles, and palm creases. The lips and the inside lining of the mouth can also be unusually dark. Because of an imbalance of hormones involved in development of sexual characteristics, women with this condition may lose their underarm and pubic hair. Other signs and symptoms of autoimmune Addison disease include low levels of sugar (hypoglycemia) and sodium (hyponatremia) and high levels of potassium (hyperkalemia) in the blood. Affected individuals may also have a shortage of red blood cells (anemia) and an increase in the number of white blood cells (lymphocytosis), particularly those known as eosinophils (eosinophilia). Autoimmune Addison disease can lead to a life-threatening adrenal crisis, characterized by vomiting, abdominal pain, back or leg cramps, and severe hypotension leading to shock. The adrenal crisis is often triggered by a stressor, such as surgery, trauma, or infection. Individuals with autoimmune Addison disease or their family members often have another autoimmune disorder, most commonly autoimmune thyroid disease or type 1 diabetes.
Bartter syndrome, type 4b
MedGen UID:
416521
Concept ID:
C2751312
Disease or Syndrome
Bartter syndrome is a group of very similar kidney disorders that cause an imbalance of potassium, sodium, chloride, and related molecules in the body. In some cases, Bartter syndrome becomes apparent before birth. The disorder can cause polyhydramnios, which is an increased volume of fluid surrounding the fetus (amniotic fluid). Polyhydramnios increases the risk of premature birth. Beginning in infancy, affected individuals often fail to grow and gain weight at the expected rate (failure to thrive). They lose excess amounts of salt (sodium chloride) in their urine, which leads to dehydration, constipation, and increased urine production (polyuria). In addition, large amounts of calcium are lost through the urine (hypercalciuria), which can cause weakening of the bones (osteopenia). Some of the calcium is deposited in the kidneys as they are concentrating urine, leading to hardening of the kidney tissue (nephrocalcinosis). Bartter syndrome is also characterized by low levels of potassium in the blood (hypokalemia), which can result in muscle weakness, cramping, and fatigue. Rarely, affected children develop hearing loss caused by abnormalities in the inner ear (sensorineural deafness). Two major forms of Bartter syndrome are distinguished by their age of onset and severity. One form begins before birth (antenatal) and is often life-threatening. The other form, often called the classical form, begins in early childhood and tends to be less severe. Once the genetic causes of Bartter syndrome were identified, researchers also split the disorder into different types based on the genes involved. Types I, II, and IV have the features of antenatal Bartter syndrome. Because type IV is also associated with hearing loss, it is sometimes called antenatal Bartter syndrome with sensorineural deafness. Type III usually has the features of classical Bartter syndrome.
Hyperkaliemic periodic paralysis type 2
MedGen UID:
418942
Concept ID:
C2930895
Disease or Syndrome
Hyperuricemia, pulmonary hypertension, renal failure, and alkalosis
MedGen UID:
462559
Concept ID:
C3151209
Disease or Syndrome
HUPRA syndrome is a severe autosomal recessive multisystem disorder characterized by onset in infancy of progressive renal failure leading to electrolyte imbalances, metabolic alkalosis, pulmonary hypertension, hypotonia, and delayed development. Affected individuals are born prematurely (summary by Belostotsky et al., 2011).
Corticosterone methyloxidase type 2 deficiency
MedGen UID:
483046
Concept ID:
C3463917
Disease or Syndrome
CMO type II deficiency is an autosomal recessive disorder caused by a defect in the final biochemical step of aldosterone biosynthesis, the 18-hydroxylation of 18-hydroxycorticosterone (18-OHB) to aldosterone. This enzymatic defect results in decreased aldosterone and salt-wasting associated with an increased serum ratio of 18-OHB to aldosterone. In CMO II deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-OHB. These patients have a low ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998). The CYP11B2 gene product also catalyzes an earlier step in aldosterone biosynthesis: the 18-hydroxylation of corticosterone to 18-OHB. A defect in that enzymatic step results in CMO type I deficiency (204300), an allelic disorder with an overlapping phenotype but distinct biochemical features. In CMO I deficiency, aldosterone is undetectable, whereas its immediate precursor, 18-OHB, is low or normal (Portrat-Doyen et al., 1998).

Recent clinical studies

Etiology

Geoghegan P, Harrison AM, Thongprayoon C, Kashyap R, Ahmed A, Dong Y, Rabinstein AA, Kashani KB, Gajic O
Mayo Clin Proc 2015 Oct;90(10):1348-55. doi: 10.1016/j.mayocp.2015.07.014. PMID: 26434962
Huang CC, Chung CM, Hung SI, Pan WH, Leu HB, Huang PH, Chiu CC, Lin LY, Lin CC, Yang CY, Li SY, Chen YC, Wu TC, Lin SJ, Chen JW
Medicine (Baltimore) 2015 Aug;94(34):e1422. doi: 10.1097/MD.0000000000001422. PMID: 26313793Free PMC Article
Usala RL, Fernandez SJ, Mete M, Cowen L, Shara NM, Barsony J, Verbalis JG
J Clin Endocrinol Metab 2015 Aug;100(8):3021-31. Epub 2015 Jun 17 doi: 10.1210/jc.2015-1261. [Epub ahead of print] PMID: 26083821Free PMC Article
Williams CN, Riva-Cambrin J, Presson AP, Bratton SL
J Neurosurg Pediatr 2015 May;15(5):480-7. Epub 2015 Feb 27 doi: 10.3171/2014.10.PEDS14368. [Epub ahead of print] PMID: 25723724
Fournier JP, Yin H, Nessim SJ, Montastruc JL, Azoulay L
Am J Med 2015 Apr;128(4):418-25.e5. Epub 2014 Nov 22 doi: 10.1016/j.amjmed.2014.10.046. [Epub ahead of print] PMID: 25460534

Diagnosis

Usala RL, Fernandez SJ, Mete M, Cowen L, Shara NM, Barsony J, Verbalis JG
J Clin Endocrinol Metab 2015 Aug;100(8):3021-31. Epub 2015 Jun 17 doi: 10.1210/jc.2015-1261. [Epub ahead of print] PMID: 26083821Free PMC Article
Mayer CU, Treff G, Fenske WK, Blouin K, Steinacker JM, Allolio B
Am J Med 2015 Oct;128(10):1144-51. Epub 2015 Apr 23 doi: 10.1016/j.amjmed.2015.04.014. [Epub ahead of print] PMID: 25912199
Pearce EA, Myers TM, Hoffman MD
Wilderness Environ Med 2015 Jun;26(2):189-95. Epub 2015 Feb 23 doi: 10.1016/j.wem.2014.08.007. [Epub ahead of print] PMID: 25736400
Nigro N, Winzeler B, Suter-Widmer I, Schuetz P, Arici B, Bally M, Blum C, Bingisser R, Bock A, Huber A, Müller B, Nickel CH, Christ-Crain M
J Am Geriatr Soc 2015 Mar;63(3):470-5. Epub 2015 Mar 4 doi: 10.1111/jgs.13325. [Epub ahead of print] PMID: 25735607
Pazhayattil GS, Rastegar A, Brewster UC
Am J Kidney Dis 2015 Apr;65(4):623-7. Epub 2014 Dec 24 doi: 10.1053/j.ajkd.2014.09.027. [Epub ahead of print] PMID: 25542410

Therapy

Geoghegan P, Harrison AM, Thongprayoon C, Kashyap R, Ahmed A, Dong Y, Rabinstein AA, Kashani KB, Gajic O
Mayo Clin Proc 2015 Oct;90(10):1348-55. doi: 10.1016/j.mayocp.2015.07.014. PMID: 26434962
Huang CC, Chung CM, Hung SI, Pan WH, Leu HB, Huang PH, Chiu CC, Lin LY, Lin CC, Yang CY, Li SY, Chen YC, Wu TC, Lin SJ, Chen JW
Medicine (Baltimore) 2015 Aug;94(34):e1422. doi: 10.1097/MD.0000000000001422. PMID: 26313793Free PMC Article
Pearce EA, Myers TM, Hoffman MD
Wilderness Environ Med 2015 Jun;26(2):189-95. Epub 2015 Feb 23 doi: 10.1016/j.wem.2014.08.007. [Epub ahead of print] PMID: 25736400
Williams CN, Riva-Cambrin J, Presson AP, Bratton SL
J Neurosurg Pediatr 2015 May;15(5):480-7. Epub 2015 Feb 27 doi: 10.3171/2014.10.PEDS14368. [Epub ahead of print] PMID: 25723724
Fournier JP, Yin H, Nessim SJ, Montastruc JL, Azoulay L
Am J Med 2015 Apr;128(4):418-25.e5. Epub 2014 Nov 22 doi: 10.1016/j.amjmed.2014.10.046. [Epub ahead of print] PMID: 25460534

Prognosis

Geoghegan P, Harrison AM, Thongprayoon C, Kashyap R, Ahmed A, Dong Y, Rabinstein AA, Kashani KB, Gajic O
Mayo Clin Proc 2015 Oct;90(10):1348-55. doi: 10.1016/j.mayocp.2015.07.014. PMID: 26434962
Huang CC, Chung CM, Hung SI, Pan WH, Leu HB, Huang PH, Chiu CC, Lin LY, Lin CC, Yang CY, Li SY, Chen YC, Wu TC, Lin SJ, Chen JW
Medicine (Baltimore) 2015 Aug;94(34):e1422. doi: 10.1097/MD.0000000000001422. PMID: 26313793Free PMC Article
Mayer CU, Treff G, Fenske WK, Blouin K, Steinacker JM, Allolio B
Am J Med 2015 Oct;128(10):1144-51. Epub 2015 Apr 23 doi: 10.1016/j.amjmed.2015.04.014. [Epub ahead of print] PMID: 25912199
Fournier JP, Yin H, Nessim SJ, Montastruc JL, Azoulay L
Am J Med 2015 Apr;128(4):418-25.e5. Epub 2014 Nov 22 doi: 10.1016/j.amjmed.2014.10.046. [Epub ahead of print] PMID: 25460534
Yoon J, Ahn SH, Lee YJ, Kim CM
Support Care Cancer 2015 Jun;23(6):1735-40. Epub 2014 Nov 30 doi: 10.1007/s00520-014-2522-7. [Epub ahead of print] PMID: 25433438

Clinical prediction guides

Huang CC, Chung CM, Hung SI, Pan WH, Leu HB, Huang PH, Chiu CC, Lin LY, Lin CC, Yang CY, Li SY, Chen YC, Wu TC, Lin SJ, Chen JW
Medicine (Baltimore) 2015 Aug;94(34):e1422. doi: 10.1097/MD.0000000000001422. PMID: 26313793Free PMC Article
Nigro N, Winzeler B, Suter-Widmer I, Schuetz P, Arici B, Bally M, Blum C, Bingisser R, Bock A, Huber A, Müller B, Nickel CH, Christ-Crain M
J Am Geriatr Soc 2015 Mar;63(3):470-5. Epub 2015 Mar 4 doi: 10.1111/jgs.13325. [Epub ahead of print] PMID: 25735607
Williams CN, Riva-Cambrin J, Presson AP, Bratton SL
J Neurosurg Pediatr 2015 May;15(5):480-7. Epub 2015 Feb 27 doi: 10.3171/2014.10.PEDS14368. [Epub ahead of print] PMID: 25723724
Fournier JP, Yin H, Nessim SJ, Montastruc JL, Azoulay L
Am J Med 2015 Apr;128(4):418-25.e5. Epub 2014 Nov 22 doi: 10.1016/j.amjmed.2014.10.046. [Epub ahead of print] PMID: 25460534
Yoon J, Ahn SH, Lee YJ, Kim CM
Support Care Cancer 2015 Jun;23(6):1735-40. Epub 2014 Nov 30 doi: 10.1007/s00520-014-2522-7. [Epub ahead of print] PMID: 25433438

Recent systematic reviews

Geoghegan P, Harrison AM, Thongprayoon C, Kashyap R, Ahmed A, Dong Y, Rabinstein AA, Kashani KB, Gajic O
Mayo Clin Proc 2015 Oct;90(10):1348-55. doi: 10.1016/j.mayocp.2015.07.014. PMID: 26434962
Corona G, Giuliani C, Verbalis JG, Forti G, Maggi M, Peri A
PLoS One 2015;10(4):e0124105. Epub 2015 Apr 23 doi: 10.1371/journal.pone.0124105. PMID: 25905459Free PMC Article
Nagler EV, Vanmassenhove J, van der Veer SN, Nistor I, Van Biesen W, Webster AC, Vanholder R
BMC Med 2014 Dec 11;12:1. doi: 10.1186/s12916-014-0231-1. [Epub ahead of print] PMID: 25539784Free PMC Article
Verbalis JG, Grossman A, Höybye C, Runkle I
Curr Med Res Opin 2014 Jul;30(7):1201-7. Epub 2014 May 14 doi: 10.1185/03007995.2014.920314. [Epub ahead of print] PMID: 24809970
Atsariyasing W, Goldman MB
Psychiatry Res 2014 Jul 30;217(3):129-33. Epub 2014 Mar 29 doi: 10.1016/j.psychres.2014.03.021. [Epub ahead of print] PMID: 24726819

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