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Increased serum pyruvate

MedGen UID:
376596
Concept ID:
C1849488
Finding
Synonym: Increased serum pyruvic acid
 
HPO: HP:0003542

Definition

An increased concentration of pyruvate in the blood. [from HPO]

Conditions with this feature

Pyruvate carboxylase deficiency
MedGen UID:
18801
Concept ID:
C0034341
Disease or Syndrome
Pyruvate carboxylase (PC) deficiency is characterized in most affected individuals by failure to thrive, developmental delay, recurrent seizures, and metabolic acidosis. Three clinical types are recognized: Type A (infantile form), in which most affected children die in infancy or early childhood. Type B (severe neonatal form), in which affected infants have hepatomegaly, pyramidal tract signs, and abnormal movement and die within the first three months of life. Type C (intermittent/benign form), in which affected individuals have normal or mildly delayed neurologic development and episodic metabolic acidosis.
MERRF syndrome
MedGen UID:
56486
Concept ID:
C0162672
Disease or Syndrome
MERRF (myoclonic epilepsy with ragged red fibers) is a multisystem disorder characterized by myoclonus (often the first symptom) followed by generalized epilepsy, ataxia, weakness, exercise intolerance, and dementia. Onset can occur from childhood to adulthood, occurring after normal early development. Common findings are ptosis, hearing loss, short stature, optic atrophy, cardiomyopathy, cardiac dysrhythmias such as Wolff-Parkinson-White syndrome, and peripheral neuropathy. Pigmentary retinopathy, optic neuropathy, diabetes mellitus, and lipomatosis have been observed.
Acetyl-CoA acetyltransferase-2 deficiency
MedGen UID:
90995
Concept ID:
C0342735
Disease or Syndrome
Pyruvate dehydrogenase E1-alpha deficiency
MedGen UID:
326486
Concept ID:
C1839413
Disease or Syndrome
Genetic defects in the pyruvate dehydrogenase complex are one of the most common causes of primary lactic acidosis in children. Most cases are caused by mutation in the E1-alpha subunit gene on the X chromosome. X-linked PDH deficiency is one of the few X-linked diseases in which a high proportion of heterozygous females manifest severe symptoms. The clinical spectrum of PDH deficiency is broad, ranging from fatal lactic acidosis in the newborn to chronic neurologic dysfunction with structural abnormalities in the central nervous system without systemic acidosis (Robinson et al., 1987; Brown et al., 1994). Genetic Heterogeneity of Pyruvate Dehydrogenase Complex Deficiency PDH deficiency can also be caused by mutation in other subunits of the PDH complex, including a form (PDHXD; 245349) caused by mutation in the component X gene (PDHX; 608769) on chromosome 11p13; a form (PDHBD; 614111) caused by mutation in the PDHB gene (179060) on chromosome 3p14; a form (PDHDD; 245348) caused by mutation in the DLAT gene (608770) on chromosome 11q23; a form (PDHPD; 608782) caused by mutation in the PDP1 gene (605993) on chromosome 8q22; and a form (PDHLD; 614462) caused by mutation in the LIAS gene (607031) on chromosome 4p14.
Mitochondrial myopathy-lactic acidosis-deafness syndrome
MedGen UID:
343245
Concept ID:
C1855033
Disease or Syndrome
A rare metabolic myopathy presenting during childhood, and characterized clinically by growth failure, severe muscle weakness, and moderate sensorineural deafness and biochemically by metabolic acidosis, elevated serum pyruvate concentration, hyperalaninemia and hyperalaninuria. There have been no further descriptions in the literature since 1973.
Pyruvate dehydrogenase E3-binding protein deficiency
MedGen UID:
343383
Concept ID:
C1855553
Disease or Syndrome
Pyruvate dehydrogenase deficiency is characterized by the buildup of a chemical called lactic acid in the body and a variety of neurological problems. Signs and symptoms of this condition usually first appear shortly after birth, and they can vary widely among affected individuals. The most common feature is a potentially life-threatening buildup of lactic acid (lactic acidosis), which can cause nausea, vomiting, severe breathing problems, and an abnormal heartbeat. People with pyruvate dehydrogenase deficiency usually have neurological problems as well. Most have delayed development of mental abilities and motor skills such as sitting and walking. Other neurological problems can include intellectual disability, seizures, weak muscle tone (hypotonia), poor coordination, and difficulty walking. Some affected individuals have abnormal brain structures, such as underdevelopment of the tissue connecting the left and right halves of the brain (corpus callosum), wasting away (atrophy) of the exterior part of the brain known as the cerebral cortex, or patches of damaged tissue (lesions) on some parts of the brain. Because of the severe health effects, many individuals with pyruvate dehydrogenase deficiency do not survive past childhood, although some may live into adolescence or adulthood.
GRACILE syndrome
MedGen UID:
400428
Concept ID:
C1864002
Disease or Syndrome
GRACILE syndrome is an autosomal recessive lethal disorder characterized by fetal growth retardation, lactic acidosis, aminoaciduria, cholestasis, and abnormalities in iron metabolism. Patients develop fulminant lactic acidosis during the first day of life. Despite intensive care, about half of affected infants die during the first days of life, and the remainder within 4 months of life. Finnish and British patients have been reported, with slightly different phenotypes; the British patients have additional features of complex III deficiency and neurologic symptoms (Visapaa et al., 2002).
Glycogen storage disease due to lactate dehydrogenase M-subunit deficiency
MedGen UID:
419152
Concept ID:
C2931743
Disease or Syndrome
Lactate dehydrogenase deficiency is a condition that affects how the body breaks down sugar to use as energy in cells, primarily muscle cells.\n\nThere are two types of this condition: lactate dehydrogenase-A deficiency (sometimes called glycogen storage disease XI) and lactate dehydrogenase-B deficiency.\n\nPeople with lactate dehydrogenase-A deficiency experience fatigue, muscle pain, and cramps during exercise (exercise intolerance). In some people with lactate dehydrogenase-A deficiency, high-intensity exercise or other strenuous activity leads to the breakdown of muscle tissue (rhabdomyolysis). The destruction of muscle tissue releases a protein called myoglobin, which is processed by the kidneys and released in the urine (myoglobinuria). Myoglobin causes the urine to be red or brown. This protein can also damage the kidneys, in some cases leading to life-threatening kidney failure. Some people with lactate dehydrogenase-A deficiency develop skin rashes. The severity of the signs and symptoms among individuals with lactate dehydrogenase-A deficiency varies greatly.\n\nPeople with lactate dehydrogenase-B deficiency typically do not have any signs or symptoms of the condition. They do not have difficulty with physical activity or any specific physical features related to the condition. Affected individuals are usually discovered only when routine blood tests reveal reduced lactate dehydrogenase activity.
Severe X-linked mitochondrial encephalomyopathy
MedGen UID:
463103
Concept ID:
C3151753
Disease or Syndrome
Combined oxidative phosphorylation deficiency-6 (COXPD6) is an X-linked recessive severe encephalomyopathic disorder with onset in utero or in infancy. Affected patients have hypotonia and severely impaired psychomotor development associated with variably decreased enzymatic activity of mitochondrial respiratory complexes in skeletal muscle or fibroblasts. More variable features may include sensorimotor neuropathy, seizures, severe muscle weakness, abnormal signals in the basal ganglia, hypertrophic cardiomyopathy, deafness, swallowing difficulties, and respiratory insufficiency. Death in childhood may occur (summary by Berger et al., 2011). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).
Mitochondrial myopathy with reversible cytochrome C oxidase deficiency
MedGen UID:
463248
Concept ID:
C3151898
Disease or Syndrome
Infantile mitochondrial myopathy due to reversible COX deficiency is a rare mitochondrial disorder characterized by onset in infancy of severe hypotonia and generalized muscle weakness associated with lactic acidosis, but is distinguished from other mitochondrial disorders in that affected individuals recover spontaneously after 1 year of age (summary by Mimaki et al., 2010). See also transient infantile liver failure (LFIT; 613070), which is a similar disorder.
Mitochondrial pyruvate carrier deficiency
MedGen UID:
766521
Concept ID:
C3553607
Disease or Syndrome
Mitochondrial pyruvate carrier deficiency is an autosomal recessive metabolic disorder characterized by delayed psychomotor development and lactic acidosis with a normal lactate/pyruvate ratio resulting from impaired mitochondrial pyruvate oxidation (summary by Bricker et al., 2012).
Mitochondrial complex III deficiency nuclear type 5
MedGen UID:
767522
Concept ID:
C3554608
Disease or Syndrome
Mitochondrial complex III deficiency is a genetic condition that can affect several parts of the body, including the brain, kidneys, liver, heart, and the muscles used for movement (skeletal muscles). Signs and symptoms of mitochondrial complex III deficiency usually begin in infancy but can appear later.\n\nMost people with mitochondrial complex III deficiency have a buildup of a chemical called lactic acid in the body (lactic acidosis). Some affected individuals also have buildup of molecules called ketones (ketoacidosis) or high blood glucose levels (hyperglycemia). Abnormally high levels of these chemicals in the body can be life-threatening.\n\nThe severity of mitochondrial complex III deficiency varies widely among affected individuals. People who are mildly affected tend to have muscle weakness (myopathy) and extreme tiredness (fatigue), particularly during exercise (exercise intolerance). More severely affected individuals have problems with multiple body systems, such as liver disease that can lead to liver failure, kidney abnormalities (tubulopathy), and brain dysfunction (encephalopathy). Encephalopathy can cause delayed development of mental and motor skills (psychomotor delay), movement problems, weak muscle tone (hypotonia), and difficulty with communication. Some affected individuals have a form of heart disease called cardiomyopathy, which can lead to heart failure. \n\nMitochondrial complex III deficiency can be fatal in childhood, although individuals with mild signs and symptoms can survive into adolescence or adulthood.
Perrault syndrome 5
MedGen UID:
863744
Concept ID:
C4015307
Disease or Syndrome
Perrault syndrome is characterized by sensorineural hearing loss (SNHL) in males and females and ovarian dysfunction in females. SNHL is bilateral and ranges from profound with prelingual (congenital) onset to moderate with early-childhood onset. When onset is in early childhood, hearing loss can be progressive. Ovarian dysfunction ranges from gonadal dysgenesis (absent or streak gonads) manifesting as primary amenorrhea to primary ovarian insufficiency (POI) defined as cessation of menses before age 40 years. Fertility in affected males is reported as normal (although the number of reported males is limited). Neurologic features described in some individuals with Perrault syndrome include learning difficulties and developmental delay, cerebellar ataxia, and motor and sensory peripheral neuropathy.
Encephalopathy, neonatal severe, with lactic acidosis and brain abnormalities
MedGen UID:
1624694
Concept ID:
C4540052
Disease or Syndrome
NELABA is a severe autosomal recessive metabolic disorder characterized by onset at birth of progressive encephalopathy associated with increased serum lactate. Affected individuals have little or no psychomotor development and show brain abnormalities, including cerebral atrophy, cysts, and white matter abnormalities. Some patients die in infancy (summary by Habarou et al., 2017).
Mitochondrial complex 1 deficiency, nuclear type 2
MedGen UID:
1648466
Concept ID:
C4748737
Disease or Syndrome
Mitochondrial complex 1 deficiency, nuclear type 4
MedGen UID:
1648324
Concept ID:
C4748753
Disease or Syndrome
Cardioencephalomyopathy, fatal infantile, due to cytochrome c oxidase deficiency 1
MedGen UID:
1748867
Concept ID:
C5399977
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 2 (MC4DN2) is an autosomal recessive multisystem metabolic disorder characterized by the onset of symptoms at birth or in the first weeks or months of life. Affected individuals have severe hypotonia, often associated with feeding difficulties and respiratory insufficiency necessitating tube feeding and mechanical ventilation. The vast majority of patients develop hypertrophic cardiomyopathy in the first days or weeks of life, which usually leads to death in infancy or early childhood. Patients also show neurologic abnormalities, including developmental delay, nystagmus, fasciculations, dystonia, EEG changes, and brain imaging abnormalities compatible with a diagnosis of Leigh syndrome (see 256000). There may also be evidence of systemic involvement with hepatomegaly and myopathy, although neurogenic muscle atrophy is more common and may resemble spinal muscular atrophy type I (SMA1; 253300). Serum lactate is increased, and laboratory studies show decreased mitochondrial complex IV protein and activity levels in various tissues, including heart and skeletal muscle. Most patients die in infancy of cardiorespiratory failure (summary by Papadopoulou et al., 1999). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Mitochondrial complex 4 deficiency, nuclear type 3
MedGen UID:
1764816
Concept ID:
C5436682
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 3 (MC4DN3) is an autosomal recessive multisystem metabolic disorder with a highly variable phenotype. Some patients present with encephalomyopathic features in early infancy, whereas others may present later in infancy or the first years of life after normal early development. Affected individuals show hypotonia, failure to thrive, and developmental delay or regression with poor eye contact and loss of motor skills with ataxia. Additional features observed in some patients include proximal renal tubulopathy, macrocytic anemia, sensorineural hearing loss, nystagmus, and hypertrophic cardiomyopathy, consistent with systemic involvement. Brain imaging in most patients shows lesions consistent with Leigh syndrome (see 256000). Laboratory studies show increased serum lactate and decreased levels and activity of mitochondrial respiratory complex IV. Most patients die in infancy (summary by Valnot et al., 2000 and Antonicka et al., 2003). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Mitochondrial complex 4 deficiency, nuclear type 18
MedGen UID:
1752734
Concept ID:
C5436720
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 18 (MC4DN18) is an autosomal recessive metabolic disorder that primarily affects skeletal muscle tissue. Affected individuals present in infancy with hypotonia, limb muscle weakness, and high-arched palate. The severity of the disorder is variable: some patients may only have gait difficulties, whereas others may also have significant respiratory insufficiency and cardiomyopathy. Death in infancy has been reported. Patient skeletal muscle shows decreased levels and activity of mitochondrial respiratory complex IV (Inoue et al., 2019). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Leukoencephalopathy, progressive, infantile-onset, with or without deafness
MedGen UID:
1779519
Concept ID:
C5542996
Disease or Syndrome
Infantile-onset progressive leukoencephalopathy with or without deafness (LEPID) is an autosomal recessive complex neurodegenerative disorder with onset of symptoms in infancy or early childhood. Most patients present with sensorineural deafness or hypoacousia and global developmental delay. Affected individuals show episodic regression with progressive motor deterioration resulting in spastic tetraplegia and loss of ambulation, as well as impaired intellectual development with poor or absent speech. Additional more variable features may include poor overall growth with microcephaly, seizures, visual loss, microcytic anemia, and hepatic enlargement or abnormal liver enzymes. Brain imaging shows deep white matter abnormalities consistent with a progressive leukoencephalopathy. The brain and spinal cord are usually both involved; calcifications of these regions are often observed. Laboratory studies show increased serum lactate and deficiencies of mitochondrial respiratory chain complexes, consistent with global mitochondrial dysfunction. Early death often occurs (summary by Itoh et al., 2019).
Mitochondrial complex 2 deficiency, nuclear type 4
MedGen UID:
1782861
Concept ID:
C5543176
Disease or Syndrome
Mitochondrial complex II deficiency nuclear type 4 (MC2DN4) is a severe autosomal recessive disorder characterized by early-onset progressive neurodegeneration with leukoencephalopathy. Acute episodes of neurodegeneration are often triggered by catabolic stress such as infection or fasting.
Mitochondrial complex IV deficiency, nuclear type 22
MedGen UID:
1786100
Concept ID:
C5543491
Disease or Syndrome
Mitochondrial complex IV deficiency nuclear type 22 (MC4DN22) is an autosomal recessive metabolic disorder characterized by neonatal hypertrophic cardiomyopathy, encephalopathy, and severe lactic acidosis with fatal outcome (Wintjes et al., 2021). For a discussion of genetic heterogeneity of mitochondrial complex IV (cytochrome c oxidase) deficiency, see 220110.
Spinocerebellar ataxia, autosomal recessive 30
MedGen UID:
1778853
Concept ID:
C5543620
Disease or Syndrome
Autosomal recessive spinocerebellar ataxia-30 (SCAR30) is a progressive neurologic disorder characterized by childhood-onset global developmental delay with variably impaired intellectual development, motor dysfunction, and cerebellar ataxia. Affected individuals may also have psychiatric abnormalities, such as obsessive behavior, psychotic episodes, or hallucinations. Brain imaging usually shows cerebellar atrophy, although this may be an age-dependent feature (summary by Langer et al., 2018).
Combined oxidative phosphorylation deficiency 28
MedGen UID:
1800504
Concept ID:
C5569081
Disease or Syndrome
Combined oxidative phosphorylation deficiency-28 (COXPD28) is a complex autosomal recessive multisystem disorder associated with mitochondrial dysfunction. The phenotype is variable, but includes episodic metabolic decompensation beginning in infancy that can result in mild muscle weakness, cardiorespiratory insufficiency, developmental delay, or even death. Biochemical studies of patient tissues show variable mitochondrial defects, including decreased activities of respiratory chain enzymes (summary by Kishita et al., 2015). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).
Pyruvate dehydrogenase E3 deficiency
MedGen UID:
1805500
Concept ID:
C5574660
Disease or Syndrome
The phenotypes of dihydrolipoamide dehydrogenase (DLD) deficiency are an overlapping continuum that ranges from early-onset neurologic manifestations to adult-onset liver involvement and, rarely, a myopathic presentation. Early-onset DLD deficiency typically manifests in infancy as hypotonia with lactic acidosis. Affected infants frequently do not survive their initial metabolic decompensation, or die within the first few years of life during a recurrent metabolic decompensation. Children who live beyond the first two to three years frequently exhibit growth deficiencies and residual neurologic deficits (intellectual disability, spasticity, ataxia, and seizures). In contrast, isolated liver involvement can present as early as the neonatal period and as late as the third decade. Evidence of liver injury/failure is preceded by nausea and emesis and frequently associated with encephalopathy and/or coagulopathy. Acute metabolic episodes are frequently associated with lactate elevations, hyperammonemia, and hepatomegaly. With resolution of the acute episodes affected individuals frequently return to baseline with no residual neurologic deficit or intellectual disability. Liver failure can result in death, even in those with late-onset disease. Individuals with the myopathic presentation may experience muscle cramps, weakness, and an elevated creatine kinase.

Professional guidelines

PubMed

Hussein NA, Ebied SA, Nour HA, Zaki UK, El-Kotishy SM, Salem TM
Eur J Pharmacol 2021 Jan 15;891:173668. Epub 2020 Oct 22 doi: 10.1016/j.ejphar.2020.173668. PMID: 33098833
Du C, Wei H, Zhang M, Hu M, Li Z, Zhang C, Luo X, Liang Y
J Pediatr Endocrinol Metab 2020 Jul 28;33(7):923-930. doi: 10.1515/jpem-2019-0453. PMID: 32623374
Tarnopolsky MA, Raha S
Med Sci Sports Exerc 2005 Dec;37(12):2086-93. doi: 10.1249/01.mss.0000177341.89478.06. PMID: 16331134

Recent clinical studies

Etiology

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Devis-Jauregui L, Eritja N, Davis ML, Matias-Guiu X, Llobet-Navàs D
Autophagy 2021 May;17(5):1077-1095. Epub 2020 May 13 doi: 10.1080/15548627.2020.1752548. PMID: 32401642Free PMC Article
Beynon RA, Richmond RC, Santos Ferreira DL, Ness AR, May M, Smith GD, Vincent EE, Adams C, Ala-Korpela M, Würtz P, Soidinsalo S, Metcalfe C, Donovan JL, Lane AJ, Martin RM; ProtecT Study Group; PRACTICAL consortium
Int J Cancer 2019 Apr 15;144(8):1918-1928. Epub 2018 Dec 7 doi: 10.1002/ijc.31929. PMID: 30325021Free PMC Article
Sookoian S, Pirola CJ
World J Gastroenterol 2015 Jan 21;21(3):711-25. doi: 10.3748/wjg.v21.i3.711. PMID: 25624707Free PMC Article
Wall BT, Stephens FB, Constantin-Teodosiu D, Marimuthu K, Macdonald IA, Greenhaff PL
J Physiol 2011 Feb 15;589(Pt 4):963-73. Epub 2011 Jan 4 doi: 10.1113/jphysiol.2010.201343. PMID: 21224234Free PMC Article

Diagnosis

Caramelo I, Coelho M, Rosado M, Cardoso CMP, Dinis A, Duarte CB, Grãos M, Manadas B
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Front Cell Infect Microbiol 2022;12:999627. Epub 2022 Dec 22 doi: 10.3389/fcimb.2022.999627. PMID: 36619742Free PMC Article
Hsu CC, Senussi NH, Fertrin KY, Kowdley KV
Hepatol Commun 2022 Aug;6(8):1842-1854. Epub 2022 Jun 14 doi: 10.1002/hep4.2012. PMID: 35699322Free PMC Article
Duft RG, Castro A, Bonfante ILP, Lopes WA, da Silva LR, Chacon-Mikahil MPT, Leite N, Cavaglieri CR
Nutr Metab Cardiovasc Dis 2022 Jan;32(1):269-278. Epub 2021 Oct 9 doi: 10.1016/j.numecd.2021.09.024. PMID: 34906412
Sookoian S, Pirola CJ
World J Gastroenterol 2015 Jan 21;21(3):711-25. doi: 10.3748/wjg.v21.i3.711. PMID: 25624707Free PMC Article

Therapy

Xu Y, Shao M, Fang X, Tang W, Zhou C, Hu X, Zhang X, Su KP
Brain Behav Immun 2022 Jan;99:119-129. Epub 2021 Sep 24 doi: 10.1016/j.bbi.2021.09.014. PMID: 34563620
Chang WC, So J, Lamon-Fava S
Sci Rep 2021 Aug 11;11(1):16324. doi: 10.1038/s41598-021-95590-7. PMID: 34381108Free PMC Article
Beynon RA, Richmond RC, Santos Ferreira DL, Ness AR, May M, Smith GD, Vincent EE, Adams C, Ala-Korpela M, Würtz P, Soidinsalo S, Metcalfe C, Donovan JL, Lane AJ, Martin RM; ProtecT Study Group; PRACTICAL consortium
Int J Cancer 2019 Apr 15;144(8):1918-1928. Epub 2018 Dec 7 doi: 10.1002/ijc.31929. PMID: 30325021Free PMC Article
Wall BT, Stephens FB, Constantin-Teodosiu D, Marimuthu K, Macdonald IA, Greenhaff PL
J Physiol 2011 Feb 15;589(Pt 4):963-73. Epub 2011 Jan 4 doi: 10.1113/jphysiol.2010.201343. PMID: 21224234Free PMC Article
Johansson S, Vedin A, Wilhelmsson C
Epidemiol Rev 1983;5:67-95. doi: 10.1093/oxfordjournals.epirev.a036265. PMID: 6357823

Prognosis

Salminen A, Määttä AM, Mäntylä P, Leskelä J, Pietiäinen M, Buhlin K, Suominen AL, Paju S, Sattler W, Sinisalo J, Pussinen PJ
J Dent Res 2024 Jan;103(1):13-21. Epub 2023 Nov 15 doi: 10.1177/00220345231203562. PMID: 37968796Free PMC Article
Caramelo I, Coelho M, Rosado M, Cardoso CMP, Dinis A, Duarte CB, Grãos M, Manadas B
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Ceperuelo-Mallafré V, Reverté L, Peraire J, Madeira A, Maymó-Masip E, López-Dupla M, Gutierrez-Valencia A, Ruiz-Mateos E, Buzón MJ, Jorba R, Vendrell J, Auguet T, Olona M, Vidal F, Rull A, Fernández-Veledo S
Front Immunol 2022;13:912579. Epub 2022 Sep 14 doi: 10.3389/fimmu.2022.912579. PMID: 36189213Free PMC Article
Sookoian S, Pirola CJ
World J Gastroenterol 2015 Jan 21;21(3):711-25. doi: 10.3748/wjg.v21.i3.711. PMID: 25624707Free PMC Article
Nakao K, Miyaaki H, Ichikawa T
J Gastroenterol 2014 Apr;49(4):589-93. Epub 2014 Feb 17 doi: 10.1007/s00535-014-0932-4. PMID: 24531873

Clinical prediction guides

Chen L, Wang S, Zhang Y, Li Y, Zhang X, Ma J, Zou X, Yao T, Li S, Chen J, Zhou H, Wu L, Zhou Y, Zhang L
Front Cell Infect Microbiol 2022;12:999627. Epub 2022 Dec 22 doi: 10.3389/fcimb.2022.999627. PMID: 36619742Free PMC Article
Morze J, Wittenbecher C, Schwingshackl L, Danielewicz A, Rynkiewicz A, Hu FB, Guasch-Ferré M
Diabetes Care 2022 Apr 1;45(4):1013-1024. doi: 10.2337/dc21-1705. PMID: 35349649Free PMC Article
Xu Y, Shao M, Fang X, Tang W, Zhou C, Hu X, Zhang X, Su KP
Brain Behav Immun 2022 Jan;99:119-129. Epub 2021 Sep 24 doi: 10.1016/j.bbi.2021.09.014. PMID: 34563620
Beynon RA, Richmond RC, Santos Ferreira DL, Ness AR, May M, Smith GD, Vincent EE, Adams C, Ala-Korpela M, Würtz P, Soidinsalo S, Metcalfe C, Donovan JL, Lane AJ, Martin RM; ProtecT Study Group; PRACTICAL consortium
Int J Cancer 2019 Apr 15;144(8):1918-1928. Epub 2018 Dec 7 doi: 10.1002/ijc.31929. PMID: 30325021Free PMC Article
Sookoian S, Pirola CJ
World J Gastroenterol 2015 Jan 21;21(3):711-25. doi: 10.3748/wjg.v21.i3.711. PMID: 25624707Free PMC Article

Recent systematic reviews

Caramelo I, Coelho M, Rosado M, Cardoso CMP, Dinis A, Duarte CB, Grãos M, Manadas B
World J Pediatr 2023 Jun;19(6):505-548. Epub 2023 Apr 21 doi: 10.1007/s12519-023-00698-7. PMID: 37084165Free PMC Article
Morze J, Wittenbecher C, Schwingshackl L, Danielewicz A, Rynkiewicz A, Hu FB, Guasch-Ferré M
Diabetes Care 2022 Apr 1;45(4):1013-1024. doi: 10.2337/dc21-1705. PMID: 35349649Free PMC Article
Wang Y, Du Z, Chen Y, Liu Y, Yang Z
Medicine (Baltimore) 2021 Feb 26;100(8):e24883. doi: 10.1097/MD.0000000000024883. PMID: 33663117Free PMC Article
Mbuagbaw L, Mursleen S, Irlam JH, Spaulding AB, Rutherford GW, Siegfried N
Cochrane Database Syst Rev 2016 Dec 10;12(12):CD004246. doi: 10.1002/14651858.CD004246.pub4. PMID: 27943261Free PMC Article

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