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Hypotension

MedGen UID:
5715
Concept ID:
C0020649
Finding
Synonym: Hypotensive disorder
SNOMED CT: Low blood pressure (45007003); Hypotension (45007003); Hypopiesis (45007003); Arterial hypotension (45007003)
 
HPO: HP:0002615
Monarch Initiative: MONDO:0005468

Definition

Low Blood Pressure, vascular hypotension. [from HPO]

Conditions with this feature

Corticosterone 18-monooxygenase deficiency
MedGen UID:
82784
Concept ID:
C0268293
Disease or Syndrome
CMO type I deficiency is an autosomal recessive disorder caused by a defect in the penultimate biochemical step of aldosterone biosynthesis, the 18-hydroxylation of corticosterone (B) to 18-hydroxycorticosterone (18-OHB). This enzymatic defect results in decreased aldosterone and salt-wasting. In CMO I deficiency, aldosterone is undetectable, whereas its immediate precursor, 18-OHB, is low or normal. These patients have an increased ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998). The CYP11B2 gene product also catalyzes the final step in aldosterone biosynthesis: the 18-oxidation of 18-OHB to aldosterone. A defect in that enzymatic step results in CMO type II deficiency (610600), an allelic disorder with an overlapping phenotype but distinct biochemical features. 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).
Familial hypokalemia-hypomagnesemia
MedGen UID:
75681
Concept ID:
C0268450
Disease or Syndrome
Gitelman syndrome (GTLMNS) is an autosomal recessive renal tubular salt-wasting disorder characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. It is the most common renal tubular disorder among Caucasians (prevalence of 1 in 40,000). Most patients have onset of symptoms as adults, but some present in childhood. Clinical features include transient periods of muscle weakness and tetany, abdominal pains, and chondrocalcinosis (summary by Glaudemans et al., 2012). Gitelman syndrome is sometimes referred to as a mild variant of classic Bartter syndrome (607364). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.
Carnitine acylcarnitine translocase deficiency
MedGen UID:
91000
Concept ID:
C0342791
Disease or Syndrome
Carnitine-acylcarnitine translocase (CACT) is a critical component of the carnitine shuttle, which facilitates the transfer of long-chain fatty acylcarnitines across the inner mitochondrial membrane. CACT deficiency causes a defect in mitochondrial long-chain fatty acid ß-oxidation, with variable clinical severity. Severe neonatal-onset disease is most common, with symptoms evident within two days after birth; attenuated cases may present in the first months of life. Hyperammonemia and cardiac arrhythmia are prominent in early-onset disease, with high rates of cardiac arrest. Other clinical features are typical for disorders of long-chain fatty acid oxidation: poor feeding, lethargy, hypoketotic hypoglycemia, hypotonia, transaminitis, liver dysfunction with hepatomegaly, and rhabdomyolysis. Univentricular or biventricular hypertrophic cardiomyopathy, ranging from mild to severe, may respond to appropriate dietary and medical therapies. Hyperammonemia is difficult to treat and is an important determinant of long-term neurocognitive outcome. Affected individuals with early-onset disease typically experience brain injury at presentation, and have recurrent hyperammonemia leading to developmental delay / intellectual disability. Affected individuals with later-onset disease have milder symptoms and are less likely to experience recurrent hyperammonemia, allowing a better developmental outcome. Prompt treatment of the presenting episode to prevent hypoglycemic, hypoxic, or hyperammonemic brain injury may allow normal growth and development.
Analbuminemia
MedGen UID:
164210
Concept ID:
C0878666
Finding
Analbuminemia (ANALBA) is a rare autosomal recessive disorder manifested by the presence of a very low amount of circulating serum albumin. Affected individuals have few clinical symptoms other than mild edema, hypotension, fatigue, and occasionally a peculiar lower body lipodystrophy (mainly in adult females). The most common biochemical finding is a gross hyperlipidemia, with a significant increase in the total and LDL cholesterol concentrations, but normal concentrations of HDL cholesterol and triglycerides. Analbuminemia often leads to fetal or neonatal death in sibs in families of analbuminemic individuals, which may explain the rarity of the trait (summary by Caridi et al., 2014).
Deficiency of aromatic-L-amino-acid decarboxylase
MedGen UID:
220945
Concept ID:
C1291564
Disease or Syndrome
Aromatic L-amino acid decarboxylase deficiency (AADCD) is an autosomal recessive inborn error in neurotransmitter metabolism that leads to combined serotonin and catecholamine deficiency (Abeling et al., 2000). The disorder is clinically characterized by vegetative symptoms, oculogyric crises, dystonia, and severe neurologic dysfunction, usually beginning in infancy or childhood (summary by Brun et al., 2010).
Autosomal dominant pseudohypoaldosteronism type 1
MedGen UID:
260623
Concept ID:
C1449842
Disease or Syndrome
Autosomal dominant pseudohypoaldosteronism type I (PHA1A) 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 pseudohypoaldosteronism type I (see PHA1B1, 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.
Chuvash polycythemia
MedGen UID:
332974
Concept ID:
C1837915
Disease or Syndrome
Familial erythrocytosis-2 (ECYT2) is an autosomal recessive disorder characterized by increased red blood cell mass, increased serum levels of erythropoietin (EPO; 133170), and normal oxygen affinity. Patients with ECYT2 carry a high risk for peripheral thrombosis and cerebrovascular events (Cario, 2005). Familial erythrocytosis-2 has features of both primary and secondary erythrocytosis. In addition to increased circulating levels of EPO, consistent with a secondary, extrinsic process, erythroid progenitors may be hypersensitive to EPO, consistent with a primary, intrinsic process (Prchal, 2005). For a general phenotypic description and a discussion of genetic heterogeneity of familial erythrocytosis, see ECYT1 (133100).
Bartter disease type 3
MedGen UID:
335399
Concept ID:
C1846343
Disease or Syndrome
Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal (or neonatal) forms of Bartter syndrome (e.g., BARTS1, 601678) typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). Genetic Heterogeneity of Bartter Syndrome Antenatal Bartter syndrome type 1 (601678) is caused by loss-of-function mutations in the butmetanide-sensitive Na-K-2Cl cotransporter NKCC2 (SLC12A1; 600839). Antenatal Bartter syndrome type 2 (241200) is caused by loss-of-function mutations in the ATP-sensitive potassium channel ROMK (KCNJ1; 600359). One form of neonatal Bartter syndrome with sensorineural deafness, Bartter syndrome type 4A (602522), is caused by mutation in the BSND gene (606412). Another form of neonatal Bartter syndrome with sensorineural deafness, Bartter syndrome type 4B (613090), is caused by simultaneous mutation in both the CLCNKA (602024) and CLCNKB (602023) genes. Also see autosomal dominant hypocalcemia-1 with Bartter syndrome (601198), which is sometimes referred to as Bartter syndrome type 5 (Fremont and Chan, 2012), caused by mutation in the CASR gene (601199). See Gitelman syndrome (GTLMN; 263800), which is often referred to as a mild variant of Bartter syndrome, caused by mutation in the thiazide-sensitive sodium-chloride cotransporter SLC12A3 (600968).
Cobalamin C disease
MedGen UID:
341256
Concept ID:
C1848561
Disease or Syndrome
Disorders of intracellular cobalamin metabolism have a variable phenotype and age of onset that are influenced by the severity and location within the pathway of the defect. The prototype and best understood phenotype is cblC; it is also the most common of these disorders. The age of initial presentation of cblC spans a wide range: In utero with fetal presentation of nonimmune hydrops, cardiomyopathy, and intrauterine growth restriction. Newborns, who can have microcephaly, poor feeding, and encephalopathy. Infants, who can have poor feeding and slow growth, neurologic abnormality, and, rarely, hemolytic uremic syndrome (HUS). Toddlers, who can have poor growth, progressive microcephaly, cytopenias (including megaloblastic anemia), global developmental delay, encephalopathy, and neurologic signs such as hypotonia and seizures. Adolescents and adults, who can have neuropsychiatric symptoms, progressive cognitive decline, thromboembolic complications, and/or subacute combined degeneration of the spinal cord.
Lethal congenital glycogen storage disease of heart
MedGen UID:
337919
Concept ID:
C1849813
Disease or Syndrome
A rare glycogen storage disease with fetal or neonatal onset of severe cardiomyopathy with non-lysosomal glycogen accumulation and fatal outcome in infancy. Patients present with massive cardiomegaly, severe cardiac and respiratory complications and failure to thrive. Non-specific facial dysmorphism, bilateral cataracts, macroglossia, hydrocephalus, enlarged kidneys and skeletal muscle involvement have been reported in some cases.
Corticosteroid-binding globulin deficiency
MedGen UID:
343831
Concept ID:
C1852529
Disease or Syndrome
Corticosteroid-binding globulin deficiency is a condition with subtle signs and symptoms, the most frequent being extreme tiredness (fatigue), especially after physical exertion. Many people with this condition have unusually low blood pressure (hypotension). Some affected individuals have a fatty liver or experience chronic pain, particularly in their muscles. These features vary among affected individuals, even those within the same family.\n\nMany people with corticosteroid-binding globulin deficiency have only one or two of these features; others have no signs and symptoms of the disorder and are only diagnosed after a relative is found to be affected.\n\nSome people with corticosteroid-binding globulin deficiency also have a condition called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The features of ME/CFS are prolonged fatigue that interferes with daily activities, as well as general symptoms, such as sore throat or headaches.
Tubulointerstitial kidney disease, autosomal dominant, 2
MedGen UID:
358137
Concept ID:
C1868139
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease – MUC1 (ADTKD-MUC1) is characterized by slowly progressive tubulointerstitial disease that leads to end-stage renal disease (ESRD) and the need for dialysis or kidney transplantation. The rate of loss of kidney function for individuals is variable within and between families, with a median age of onset of end-stage renal disease (ESRD) of 46 years (range: ages 20-70 years). There are no other systemic manifestations.
Cardiomyopathy, familial restrictive, 3
MedGen UID:
382807
Concept ID:
C2676271
Disease or Syndrome
Familial restrictive cardiomyopathy is a genetic form of heart disease. For the heart to beat normally, the heart (cardiac) muscle must contract and relax in a coordinated way. Oxygen-rich blood from the lungs travels first through the upper chambers of the heart (the atria), and then to the lower chambers of the heart (the ventricles).\n\nAdults with familial restrictive cardiomyopathy typically first develop shortness of breath, fatigue, and a reduced ability to exercise. Some individuals have an irregular heart beat (arrhythmia) and may also experience a sensation of fluttering or pounding in the chest (palpitations) and dizziness. Abnormal blood clots are commonly seen in adults with this condition. Without treatment, approximately one-third of adults with familial restrictive cardiomyopathy do not survive more than five years after diagnosis.\n\nIn people with familial restrictive cardiomyopathy, the heart muscle is stiff and cannot fully relax after each contraction. Impaired muscle relaxation causes blood to back up in the atria and lungs, which reduces the amount of blood in the ventricles.\n\nFamilial restrictive cardiomyopathy can appear anytime from childhood to adulthood. The first signs and symptoms of this condition in children are failure to gain weight and grow at the expected rate (failure to thrive), extreme tiredness (fatigue), and fainting. Children who are severely affected may also have abnormal swelling or puffiness (edema), increased blood pressure, an enlarged liver, an abnormal buildup of fluid in the abdominal cavity (ascites), and lung congestion. Some children with familial restrictive cardiomyopathy do not have any obvious signs or symptoms, but they may die suddenly due to heart failure. Without treatment, the majority of affected children survive only a few years after they are diagnosed.
Malignant hyperthermia, susceptibility to, 1
MedGen UID:
443948
Concept ID:
C2930980
Finding
Malignant hyperthermia susceptibility (MHS) is a pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism. Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics (i.e., halothane, isoflurane, sevoflurane, desflurane, enflurane), either alone or in conjunction with a depolarizing muscle relaxant (specifically, succinylcholine). The triggering substances cause uncontrolled release of calcium from the sarcoplasmic reticulum and may promote entry of extracellular calcium into the myoplasm, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate. Affected individuals experience acidosis, hypercapnia, tachycardia, hyperthermia, muscle rigidity, compartment syndrome, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk for cardiac arrhythmia or even cardiac arrest, and myoglobinuria with a risk for renal failure. In nearly all cases, the first manifestations of MH (tachycardia and tachypnea) occur in the operating room; however, MH may also occur in the early postoperative period. There is mounting evidence that some individuals with MHS will also develop MH with exercise and/or on exposure to hot environments. Without proper and prompt treatment with dantrolene sodium, mortality is extremely high.
Chromosome 5q12 deletion syndrome
MedGen UID:
816612
Concept ID:
C3810282
Disease or Syndrome
PDE4D haploinsufficiency syndrome is a rare syndromic intellectual disability characterized by developmental delay, intellectual disability, low body mass index, long arms, fingers and toes, prominent nose and small chin.
Renal tubular dysgenesis of genetic origin
MedGen UID:
1826125
Concept ID:
C5681536
Disease or Syndrome
An instance of renal tubular dysgenesis that is caused by a modification of the individual's genome.
Autosomal recessive pseudohypoaldosteronism type 1
MedGen UID:
1823950
Concept ID:
C5774176
Disease or Syndrome
Autosomal recessive pseudohypoaldosteronism type I, including PHA1B1, 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). Hanukoglu and Hanukoglu (2016) provided a detailed review of the ENaC gene family, including structure, function, tissue distribution, and associated inherited diseases.
Pseudohypoaldosteronism, type IB2, autosomal recessive
MedGen UID:
1824028
Concept ID:
C5774255
Disease or Syndrome
Autosomal recessive pseudohypoaldosteronism type IB2 (PHA1B2) 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).
Mitochondrial trifunctional protein deficiency 2
MedGen UID:
1841010
Concept ID:
C5830374
Disease or Syndrome
The mitochondrial trifunctional protein, composed of 4 alpha and 4 beta subunits, catalyzes 3 steps in mitochondrial beta-oxidation of fatty acids: long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), long-chain enoyl-CoA hydratase, and long-chain thiolase activities. Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. Clinically, classic trifunctional protein deficiency can be classified into 3 main clinical phenotypes: neonatal onset of a severe, lethal condition resulting in sudden unexplained infant death (SIDS; 272120), infantile onset of a hepatic Reye-like syndrome, and late-adolescent onset of primarily a skeletal myopathy (summary by Spiekerkoetter et al., 2003). Some patients with MTP deficiency show a protracted progressive course associated with myopathy, recurrent rhabdomyolysis, and sensorimotor axonal neuropathy. These patients tend to survive into adolescence and adulthood (den Boer et al., 2003). See mitochondrial trifunctional protein deficiency-1 (609015), caused by mutation in the HADHA gene (600890), the alpha subunit of mitochondrial trifunctional protein.

Professional guidelines

PubMed

Schlapbach LJ, Watson RS, Sorce LR, Argent AC, Menon K, Hall MW, Akech S, Albers DJ, Alpern ER, Balamuth F, Bembea M, Biban P, Carrol ED, Chiotos K, Chisti MJ, DeWitt PE, Evans I, Flauzino de Oliveira C, Horvat CM, Inwald D, Ishimine P, Jaramillo-Bustamante JC, Levin M, Lodha R, Martin B, Nadel S, Nakagawa S, Peters MJ, Randolph AG, Ranjit S, Rebull MN, Russell S, Scott HF, de Souza DC, Tissieres P, Weiss SL, Wiens MO, Wynn JL, Kissoon N, Zimmerman JJ, Sanchez-Pinto LN, Bennett TD; Society of Critical Care Medicine Pediatric Sepsis Definition Task Force
JAMA 2024 Feb 27;331(8):665-674. doi: 10.1001/jama.2024.0179. PMID: 38245889Free PMC Article
Wieling W, Kaufmann H, Claydon VE, van Wijnen VK, Harms MPM, Juraschek SP, Thijs RD
Lancet Neurol 2022 Aug;21(8):735-746. doi: 10.1016/S1474-4422(22)00169-7. PMID: 35841911Free PMC Article
Bornstein SR, Allolio B, Arlt W, Barthel A, Don-Wauchope A, Hammer GD, Husebye ES, Merke DP, Murad MH, Stratakis CA, Torpy DJ
J Clin Endocrinol Metab 2016 Feb;101(2):364-89. Epub 2016 Jan 13 doi: 10.1210/jc.2015-1710. PMID: 26760044Free PMC Article

Recent clinical studies

Etiology

Wieling W, Kaufmann H, Claydon VE, van Wijnen VK, Harms MPM, Juraschek SP, Thijs RD
Lancet Neurol 2022 Aug;21(8):735-746. doi: 10.1016/S1474-4422(22)00169-7. PMID: 35841911Free PMC Article
Dani M, Dirksen A, Taraborrelli P, Panagopolous D, Torocastro M, Sutton R, Lim PB
Clin Med (Lond) 2021 May;21(3):e275-e282. doi: 10.7861/clinmed.2020-1044. PMID: 34001585Free PMC Article
Palma JA, Kaufmann H
Continuum (Minneap Minn) 2020 Feb;26(1):154-177. doi: 10.1212/CON.0000000000000816. PMID: 31996627Free PMC Article
Mol A, Bui Hoang PTS, Sharmin S, Reijnierse EM, van Wezel RJA, Meskers CGM, Maier AB
J Am Med Dir Assoc 2019 May;20(5):589-597.e5. Epub 2018 Dec 21 doi: 10.1016/j.jamda.2018.11.003. PMID: 30583909
Luciano GL, Brennan MJ, Rothberg MB
Am J Med 2010 Mar;123(3):281.e1-6. doi: 10.1016/j.amjmed.2009.06.026. PMID: 20193838

Diagnosis

Wieling W, Kaufmann H, Claydon VE, van Wijnen VK, Harms MPM, Juraschek SP, Thijs RD
Lancet Neurol 2022 Aug;21(8):735-746. doi: 10.1016/S1474-4422(22)00169-7. PMID: 35841911Free PMC Article
Dani M, Dirksen A, Taraborrelli P, Panagopolous D, Torocastro M, Sutton R, Lim PB
Clin Med (Lond) 2021 May;21(3):e275-e282. doi: 10.7861/clinmed.2020-1044. PMID: 34001585Free PMC Article
Palma JA, Kaufmann H
Continuum (Minneap Minn) 2020 Feb;26(1):154-177. doi: 10.1212/CON.0000000000000816. PMID: 31996627Free PMC Article
Ricci F, De Caterina R, Fedorowski A
J Am Coll Cardiol 2015 Aug 18;66(7):848-860. doi: 10.1016/j.jacc.2015.06.1084. PMID: 26271068
Luciano GL, Brennan MJ, Rothberg MB
Am J Med 2010 Mar;123(3):281.e1-6. doi: 10.1016/j.amjmed.2009.06.026. PMID: 20193838

Therapy

Pruna A, Bonaccorso A, Belletti A, Turi S, Di Prima AL, D'amico F, Zangrillo A, Kotani Y, Landoni G
J Cardiothorac Vasc Anesth 2024 Jan;38(1):268-274. Epub 2023 Oct 1 doi: 10.1053/j.jvca.2023.09.037. PMID: 37880041
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Intern Emerg Med 2023 Jan;18(1):23-30. Epub 2022 Sep 18 doi: 10.1007/s11739-022-03102-w. PMID: 36117230
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Anaesthesia 2020 Jan;75(1):109-121. Epub 2019 Sep 18 doi: 10.1111/anae.14841. PMID: 31531852
CONSENSUS Trial Study Group
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Prognosis

Schuurmans J, van Rossem BTB, Rellum SR, Tol JTM, Kurucz VC, van Mourik N, van der Ven WH, Veelo DP, Schenk J, Vlaar APJ
Intensive Care Med 2024 Apr;50(4):516-525. Epub 2024 Jan 22 doi: 10.1007/s00134-023-07304-4. PMID: 38252288Free PMC Article
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Luciano GL, Brennan MJ, Rothberg MB
Am J Med 2010 Mar;123(3):281.e1-6. doi: 10.1016/j.amjmed.2009.06.026. PMID: 20193838
Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, Suppes R, Feinstein D, Zanotti S, Taiberg L, Gurka D, Kumar A, Cheang M
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Clinical prediction guides

Maheshwari K, Shimada T, Yang D, Khanna S, Cywinski JB, Irefin SA, Ayad S, Turan A, Ruetzler K, Qiu Y, Saha P, Mascha EJ, Sessler DI
Anesthesiology 2020 Dec 1;133(6):1214-1222. doi: 10.1097/ALN.0000000000003557. PMID: 32960954
Dobrocky T, Grunder L, Breiding PS, Branca M, Limacher A, Mosimann PJ, Mordasini P, Zibold F, Haeni L, Jesse CM, Fung C, Raabe A, Ulrich CT, Gralla J, Beck J, Piechowiak EI
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Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD, Grubb BP, Hamdan MH, Krahn AD, Link MS, Olshansky B, Raj SR, Sandhu RK, Sorajja D, Sun BC, Yancy CW
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Recent systematic reviews

Araiza-Garaygordobil D, García-Martínez CE, Burgos LM, Saldarriaga C, Liblik K, Mendoza I, Martinez-Selles M, Scatularo CE, Farina JM, Baranchuk A; Neglected Tropical Diseases and other Infectious Diseases affecting the Heart (the NET‐Heart) project
Cardiovasc J Afr 2021 Sep-Oct 23;32(5):276-283. Epub 2021 Jul 20 doi: 10.5830/CVJA-2021-033. PMID: 34292294Free PMC Article
Yu JT, Xu W, Tan CC, Andrieu S, Suckling J, Evangelou E, Pan A, Zhang C, Jia J, Feng L, Kua EH, Wang YJ, Wang HF, Tan MS, Li JQ, Hou XH, Wan Y, Tan L, Mok V, Tan L, Dong Q, Touchon J, Gauthier S, Aisen PS, Vellas B
J Neurol Neurosurg Psychiatry 2020 Nov;91(11):1201-1209. Epub 2020 Jul 20 doi: 10.1136/jnnp-2019-321913. PMID: 32690803Free PMC Article
Mol A, Bui Hoang PTS, Sharmin S, Reijnierse EM, van Wezel RJA, Meskers CGM, Maier AB
J Am Med Dir Assoc 2019 May;20(5):589-597.e5. Epub 2018 Dec 21 doi: 10.1016/j.jamda.2018.11.003. PMID: 30583909
Wesselink EM, Kappen TH, Torn HM, Slooter AJC, van Klei WA
Br J Anaesth 2018 Oct;121(4):706-721. Epub 2018 Jun 20 doi: 10.1016/j.bja.2018.04.036. PMID: 30236233
Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M; Sepsis Definitions Task Force
JAMA 2016 Feb 23;315(8):775-87. doi: 10.1001/jama.2016.0289. PMID: 26903336Free PMC Article

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