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Hyperuricemia

MedGen UID:
149260
Concept ID:
C0740394
Disease or Syndrome
Synonyms: High blood uric acid level; Hyperuricaemia
SNOMED CT: Hyperuricemia (35885006); Uricacidemia (35885006)
 
HPO: HP:0002149

Definition

An abnormally high level of uric acid in the blood. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVHyperuricemia

Conditions with this feature

Hereditary fructosuria
MedGen UID:
42105
Concept ID:
C0016751
Disease or Syndrome
Following dietary exposure to fructose, sucrose, or sorbitol, untreated hereditary fructose intolerance (HFI) is characterized by metabolic disturbances (hypoglycemia, lactic acidemia, hypophosphatemia, hyperuricemia, hypermagnesemia, hyperalaninemia) and clinical findings (nausea, vomiting, and abdominal distress; chronic growth restriction / failure to thrive). While untreated HFI typically first manifested when fructose- and sucrose-containing foods were introduced in the course of weaning young infants from breast milk, it is now presenting earlier, due to the addition of fructose-containing nutrients in infant formulas. If the infant ingests large quantities of fructose, the infant may acutely develop lethargy, seizures, and/or progressive coma. Untreated HFI may result in renal and hepatic failure. If identified and treated before permanent organ injury occurs, individuals with HFI can experience a normal quality of life and life expectancy.
Glycogen storage disease, type VII
MedGen UID:
5342
Concept ID:
C0017926
Disease or Syndrome
Glycogen storage disease VII is an autosomal recessive metabolic disorder characterized clinically by exercise intolerance, muscle cramping, exertional myopathy, and compensated hemolysis. Myoglobinuria may also occur. The deficiency of the muscle isoform of PFK results in a total and partial loss of muscle and red cell PFK activity, respectively. Raben and Sherman (1995) noted that not all patients with GSD VII seek medical care because in some cases it is a relatively mild disorder.
Lesch-Nyhan syndrome
MedGen UID:
9721
Concept ID:
C0023374
Disease or Syndrome
HPRT1 disorders, caused by deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGprt), are typically associated with clinical evidence for overproduction of uric acid (hyperuricemia, nephrolithiasis, and/or gouty arthritis) and varying degrees of neurologic and/or behavioral problems. Historically, three phenotypes were identified in the spectrum of HPRT1 disorders: Lesch-Nyhan disease (LND) at the most severe end with motor dysfunction resembling severe cerebral palsy, intellectual disability, and self-injurious behavior; HPRT1-related neurologic dysfunction (HND) in the intermediate range with similar but fewer severe neurologic findings than LND and no self-injurious behavior; and HPRT1-related hyperuricemia (HRH) at the mild end without overt neurologic deficits. It is now recognized that these neurobehavioral phenotypes cluster along a continuum from severe to mild.
Partial hypoxanthine-guanine phosphoribosyltransferase deficiency
MedGen UID:
82770
Concept ID:
C0268117
Disease or Syndrome
HPRT1 disorders, caused by deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGprt), are typically associated with clinical evidence for overproduction of uric acid (hyperuricemia, nephrolithiasis, and/or gouty arthritis) and varying degrees of neurologic and/or behavioral problems. Historically, three phenotypes were identified in the spectrum of HPRT1 disorders: Lesch-Nyhan disease (LND) at the most severe end with motor dysfunction resembling severe cerebral palsy, intellectual disability, and self-injurious behavior; HPRT1-related neurologic dysfunction (HND) in the intermediate range with similar but fewer severe neurologic findings than LND and no self-injurious behavior; and HPRT1-related hyperuricemia (HRH) at the mild end without overt neurologic deficits. It is now recognized that these neurobehavioral phenotypes cluster along a continuum from severe to mild.
Glucose-6-phosphate transport defect
MedGen UID:
78644
Concept ID:
C0268146
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys, resulting in hepatomegaly and renomegaly. The two subtypes (GSDIa and GSDIb) are clinically indistinguishable. Some untreated neonates present with severe hypoglycemia; more commonly, however, untreated infants present at age three to four months with hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia, hypertriglyceridemia, and/or hypoglycemic seizures. Affected children typically have doll-like faces with fat cheeks, relatively thin extremities, short stature, and protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function can lead to a bleeding tendency with frequent epistaxis. Untreated GSDIb is associated with impaired neutrophil and monocyte function as well as chronic neutropenia after the first few years of life, all of which result in recurrent bacterial infections and oral and intestinal mucosal ulcers. Long-term complications of untreated GSDI include growth retardation resulting in short stature, osteoporosis, delayed puberty, gout, renal disease, pulmonary hypertension, hepatic adenomas with potential for malignant transformation, polycystic ovaries, pancreatitis, and changes in brain function. Normal growth and puberty is expected in treated children. Most affected individuals live into adulthood.
Hyperphosphatasemia with bone disease
MedGen UID:
75678
Concept ID:
C0268414
Disease or Syndrome
Paget disease of bone-5 is an autosomal recessive, juvenile-onset form of Paget disease, a disorder of the skeleton resulting from abnormal bone resorption and formation. Clinical manifestations include short stature, progressive long bone deformities, fractures, vertebral collapse, skull enlargement, and hyperostosis with progressive deafness. There is phenotypic variability, with some patients presenting in infancy, while others present later in childhood (summary by Naot et al., 2014). For discussion of genetic heterogeneity of Paget disease of bone, see 167250.
Alstrom syndrome
MedGen UID:
78675
Concept ID:
C0268425
Disease or Syndrome
Alström syndrome is characterized by cone-rod dystrophy, obesity, progressive bilateral sensorineural hearing impairment, acute infantile-onset cardiomyopathy and/or adolescent- or adult-onset restrictive cardiomyopathy, insulin resistance / type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and chronic progressive kidney disease. Cone-rod dystrophy presents as progressive visual impairment, photophobia, and nystagmus usually starting between birth and age 15 months. Many individuals lose all perception of light by the end of the second decade, but a minority retain the ability to read large print into the third decade. Children usually have normal birth weight but develop truncal obesity during their first year. Sensorineural hearing loss presents in the first decade in as many as 70% of individuals and may progress to the severe or moderately severe range (40-70 db) by the end of the first to second decade. Insulin resistance is typically accompanied by the skin changes of acanthosis nigricans, and proceeds to T2DM in the majority by the third decade. Nearly all demonstrate hypertriglyceridemia. Other findings can include endocrine abnormalities (hypothyroidism, hypogonadotropic hypogonadism in males, and hyperandrogenism in females), urologic dysfunction / detrusor instability, progressive decrease in renal function, and hepatic disease (ranging from elevated transaminases to steatohepatitis/NAFLD). Approximately 20% of affected individuals have delay in early developmental milestones, most commonly in gross and fine motor skills. About 30% have a learning disability. Cognitive impairment (IQ <70) is very rare. Wide clinical variability is observed among affected individuals, even within the same family.
Primary hypomagnesemia
MedGen UID:
120640
Concept ID:
C0268448
Disease or Syndrome
Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is a progressive renal disorder characterized by excessive urinary Ca(2+) and Mg(2+) excretion. There is progressive loss of kidney function, and in about 50% of cases, the need for renal replacement therapy arises as early as the second decade of life (summary by Muller et al., 2006). Amelogenesis imperfecta may also be present in some patients (Bardet et al., 2016). A similar disorder with renal magnesium wasting, renal failure, and nephrocalcinosis (HOMG5; 248190) is caused by mutations in another tight-junction gene, CLDN19 (610036), and is distinguished by the association of severe ocular involvement. For a discussion of phenotypic and genetic heterogeneity of familial hypomagnesemia, see HOMG1 (602014).
Deficiency of hydroxymethylglutaryl-CoA lyase
MedGen UID:
78692
Concept ID:
C0268601
Disease or Syndrome
3-Hydroxy-3-methylglutaryl-CoA lyase deficiency is a rare autosomal recessive disorder with the cardinal manifestations of metabolic acidosis without ketonuria, hypoglycemia, and a characteristic pattern of elevated urinary organic acid metabolites, including 3-hydroxy-3-methylglutaric, 3-methylglutaric, and 3-hydroxyisovaleric acids. Urinary levels of 3-methylcrotonylglycine may be increased. Dicarboxylic aciduria, hepatomegaly, and hyperammonemia may also be observed. Presenting clinical signs include irritability, lethargy, coma, and vomiting (summary by Gibson et al., 1988).
Phosphate transport defect
MedGen UID:
87455
Concept ID:
C0342749
Disease or Syndrome
Glycogenosis due to glucose-6-phosphatase deficiency (G6P) type b, or glycogen storage disease (GSD) type 1b, is a type of glycogenosis due to G6P deficiency (see this term).
Renal cysts and diabetes syndrome
MedGen UID:
96569
Concept ID:
C0431693
Disease or Syndrome
The 17q12 recurrent deletion syndrome is characterized by variable combinations of the three following findings: structural or functional abnormalities of the kidney and urinary tract, maturity-onset diabetes of the young type 5 (MODY5), and neurodevelopmental or neuropsychiatric disorders (e.g., developmental delay, intellectual disability, autism spectrum disorder, schizophrenia, anxiety, and bipolar disorder). Using a method of data analysis that avoids ascertainment bias, the authors determined that multicystic kidneys and other structural and functional kidney anomalies occur in 85% to 90% of affected individuals, MODY5 in approximately 40%, and some degree of developmental delay or learning disability in approximately 50%. MODY5 is most often diagnosed before age 25 years (range: age 10-50 years).
Familial partial lipodystrophy 3
MedGen UID:
328393
Concept ID:
C1720861
Disease or Syndrome
Researchers have described at least six forms of familial partial lipodystrophy, which are distinguished by their genetic cause. The most common form of familial partial lipodystrophy is type 2, also called Dunnigan disease. In addition to the signs and symptoms described above, some people with this type of the disorder develop muscle weakness (myopathy), abnormalities of the heart muscle (cardiomyopathy), a form of heart disease called coronary artery disease, and problems with the electrical system that coordinates the heartbeat (the conduction system).\n\nMost people with familial partial lipodystrophy also have high levels of fats called triglycerides circulating in the bloodstream (hypertriglyceridemia), which can lead to inflammation of the pancreas (pancreatitis). Familial partial lipodystrophy can also cause an abnormal buildup of fats in the liver (hepatic steatosis), which can result in an enlarged liver (hepatomegaly) and abnormal liver function. After puberty, some affected females develop multiple cysts on the ovaries, an increased amount of body hair (hirsutism), and an inability to conceive (infertility), which are likely related to hormonal changes.\n\nAbnormal storage of fat in the body can lead to health problems in adulthood. Many people with familial partial lipodystrophy develop insulin resistance, a condition in which the body's tissues cannot adequately respond to insulin, which is a hormone that normally helps to regulate blood sugar levels. Insulin resistance may worsen to become a more serious disease called diabetes mellitus. Some people with familial partial lipodystrophy develop acanthosis nigricans, a skin condition related to high levels of insulin in the bloodstream. Acanthosis nigricans causes the skin in body folds and creases to become thick, dark, and velvety.\n\nFamilial partial lipodystrophy is a rare condition characterized by an abnormal distribution of fatty (adipose) tissue. Adipose tissue is normally found in many parts of the body, including beneath the skin and surrounding the internal organs. It stores fat as a source of energy and also provides cushioning. In people with familial partial lipodystrophy, adipose tissue is lost from the arms, legs, and hips, giving these parts of the body a very muscular appearance. The fat that cannot be stored in the limbs builds up around the face and neck, and inside the abdomen. Excess fat in these areas gives individuals an appearance described as "cushingoid," because it resembles the physical features associated with a hormonal disorder called Cushing disease. This abnormal fat distribution can begin anytime from childhood to adulthood.
Lactic acidosis, chronic adult form
MedGen UID:
320642
Concept ID:
C1835591
Disease or Syndrome
Glomerulocystic kidney disease with hyperuricemia and isosthenuria
MedGen UID:
372162
Concept ID:
C1835934
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease – UMOD (ADTKD-UMOD) is characterized by normal urinalysis and slowly progressive chronic kidney disease (CKD), usually first noted in the teen years and progressing to end-stage renal disease (ESRD) between the third and seventh decades. Hyperuricemia is often present from an early age, and gout (resulting from reduced kidney excretion of uric acid) occurs in the teenage years in about 8% of affected individuals and develops in 55% of affected individuals over time.
Lesch-nyhan phenotype with normal hgprt
MedGen UID:
374332
Concept ID:
C1839883
Finding
Hyperuricemia, infantile, with abnormal behavior and normal hypoxanthine guanine phosphoribosyltransferase
MedGen UID:
383794
Concept ID:
C1855884
Disease or Syndrome
Autosomal dominant medullary cystic kidney disease with hyperuricemia
MedGen UID:
349081
Concept ID:
C1859040
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease – UMOD (ADTKD-UMOD) is characterized by normal urinalysis and slowly progressive chronic kidney disease (CKD), usually first noted in the teen years and progressing to end-stage renal disease (ESRD) between the third and seventh decades. Hyperuricemia is often present from an early age, and gout (resulting from reduced kidney excretion of uric acid) occurs in the teenage years in about 8% of affected individuals and develops in 55% of affected individuals over time.
Adenosine deaminase, elevated, hemolytic anemia due to
MedGen UID:
400240
Concept ID:
C1863235
Disease or Syndrome
Hemolytic anemia due to erythrocyte adenosine deaminase overproduction is a rare, genetic, hematologic disease characterized by mild, chronic hemolytic anemia (due to highly elevated adenosine deaminase activity in red blood cells resulting in their premature destruction), elevated reticulocyte count, splenomegaly and mild hyperbilirubinemia. Other cells and tissues are not affected.
Medullary cystic kidney disease 1
MedGen UID:
358137
Concept ID:
C1868139
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease, MUC1-related (ADTKD-MUC1) was previously known as medullary cystic kidney disease type 1. It is characterized by slowly progressive tubulointerstitial disease that leads to end-stage renal disease (ESRD) and the need for dialysis or kidney transplantation. ESRD typically occurs in adulthood but is extremely variable, occurring at any age between 20 and 70 years. There are no other systemic manifestations.
Phosphoribosylpyrophosphate synthetase superactivity
MedGen UID:
370358
Concept ID:
C1970827
Disease or Syndrome
Phosphoribosylpyrophosphate synthetase (PRS) superactivity is characterized by hyperuricemia and hyperuricosuria and is divided into a severe phenotype with infantile or early-childhood onset and a milder phenotype with late-juvenile or early-adult onset. Variable combinations of sensorineural hearing loss, hypotonia, and ataxia observed in the severe type are not usually present in the mild type. In the mild type, uric acid crystalluria or a urinary stone is commonly the first clinical finding, followed later by gouty arthritis if serum urate concentration is not controlled.
Hyperuricemic nephropathy, familial juvenile, 2
MedGen UID:
414347
Concept ID:
C2751310
Disease or Syndrome
The two clinical presentations observed in autosomal dominant tubulointerstitial kidney disease – REN (ADTKD-REN) correlate with the renin protein domains affected by the causative REN variants. Childhood/adolescent onset, the more common presentation (caused by REN variants encoding the signal peptide or prosegment domains), is characterized by decreased estimated glomerular filtration rate, acidosis, hyperkalemia, and anemia early in life, followed by slowly progressive chronic kidney disease (CKD) and gout. Adult onset, the less common presentation (caused by REN variants encoding the mature renin peptide), is characterized by gout or mild slowly progressive CKD, beginning in the third decade. Anemia, hyperkalemia, and acidemia do not occur.
Glycogen storage disease due to glucose-6-phosphatase deficiency type IA
MedGen UID:
415885
Concept ID:
C2919796
Disease or Syndrome
Glycogen storage disease type I (GSDI) is characterized by accumulation of glycogen and fat in the liver and kidneys, resulting in hepatomegaly and renomegaly. The two subtypes (GSDIa and GSDIb) are clinically indistinguishable. Some untreated neonates present with severe hypoglycemia; more commonly, however, untreated infants present at age three to four months with hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia, hypertriglyceridemia, and/or hypoglycemic seizures. Affected children typically have doll-like faces with fat cheeks, relatively thin extremities, short stature, and protuberant abdomen. Xanthoma and diarrhea may be present. Impaired platelet function can lead to a bleeding tendency with frequent epistaxis. Untreated GSDIb is associated with impaired neutrophil and monocyte function as well as chronic neutropenia after the first few years of life, all of which result in recurrent bacterial infections and oral and intestinal mucosal ulcers. Long-term complications of untreated GSDI include growth retardation resulting in short stature, osteoporosis, delayed puberty, gout, renal disease, pulmonary hypertension, hepatic adenomas with potential for malignant transformation, polycystic ovaries, pancreatitis, and changes in brain function. Normal growth and puberty is expected in treated children. Most affected individuals live into adulthood.
Hirsutism-skeletal dysplasia-intellectual disability syndrome
MedGen UID:
460802
Concept ID:
C3149452
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).
Hyperuricemic nephropathy, familial juvenile, 4
MedGen UID:
934708
Concept ID:
C4310741
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease-5 (ADTKD5) is characterized by the onset of progressive chronic renal disease in the first decades of life. Mild hyperuricemia may be present, but gout, hypertension, and proteinuria are usually absent. The disease may be associated with anemia or neutropenia. Some patients may have additional findings, including poor overall growth and impaired cognitive function. Renal biopsy shows tubulointerstitial abnormalities with atrophic tubules and fibrosis; secondary glomerular abnormalities and simple cysts may also be present (summary by Bolar et al., 2016). For a discussion of genetic heterogeneity and revised nomenclature of ADTKD, see ADTKD1 (162000).
Familial juvenile hyperuricemic nephropathy type 1
MedGen UID:
1645893
Concept ID:
C4551496
Disease or Syndrome
Autosomal dominant tubulointerstitial kidney disease – UMOD (ADTKD-UMOD) is characterized by normal urinalysis and slowly progressive chronic kidney disease (CKD), usually first noted in the teen years and progressing to end-stage renal disease (ESRD) between the third and seventh decades. Hyperuricemia is often present from an early age, and gout (resulting from reduced kidney excretion of uric acid) occurs in the teenage years in about 8% of affected individuals and develops in 55% of affected individuals over time.
Glycogen storage disease, type VI
MedGen UID:
6643
Concept ID:
C0017925
Disease or Syndrome
Glycogen storage disease type VI (GSD VI) is a disorder of glycogenolysis caused by deficiency of hepatic glycogen phosphorylase. This critical enzyme catalyzes the rate-limiting step in glycogen degradation, and deficiency of the enzyme in the untreated child is characterized by hepatomegaly, poor growth, ketotic hypoglycemia, elevated hepatic transaminases, hyperlipidemia, and low prealbumin level. GSD VI is usually a relatively mild disorder that presents in infancy and childhood; rare cases of more severe disease manifesting with recurrent hypoglycemia and marked hepatomegaly have been described. More common complications in the setting of suboptimal metabolic control include short stature, delayed puberty, osteopenia, and osteoporosis. Hepatic fibrosis commonly develops in GSD VI, but cirrhosis and hypertrophic cardiomyopathy are rare. Clinical and biochemical abnormalities may decrease with age, but ketosis and hypoglycemia can continue to occur.
Urolithiasis, uric acid, autosomal dominant
MedGen UID:
393068
Concept ID:
C2674049
Finding

Recent clinical studies

Etiology

Lee JS, Kim TJ, Hong SK, Min C, Yoo DM, Wee JH, Choi HG
Int J Environ Res Public Health 2021 Jul 8;18(14) doi: 10.3390/ijerph18147299. PMID: 34299750Free PMC Article
Yu X, Gong S, Chen J, Zhang H, Shen Z, Gu Y, Lv S, Zhang D, Wang Y, Ding X, Zhang X
Sleep Med 2021 Aug;84:40-45. Epub 2021 May 21 doi: 10.1016/j.sleep.2021.05.014. PMID: 34091320
Sun P, Chen M, Guo X, Li Z, Zhou Y, Yu S, Yang H, Sun G, Zheng L, Sun Y
BMC Public Health 2021 Apr 23;21(1):776. doi: 10.1186/s12889-021-10858-x. PMID: 33892657Free PMC Article
Gu Y, Meng G, Zhang Q, Liu L, Wu H, Zhang S, Wang Y, Zhang T, Wang X, Sun S, Wang X, Zhou M, Jia Q, Song K, Wu X, Niu K
Endocr Pract 2021 Apr;27(4):291-297. Epub 2021 Jan 30 doi: 10.1016/j.eprac.2020.10.009. PMID: 33524634
Dong X, Liu X, Zhang L, Li R, Tu R, Hou J, Mao Z, Huo W, Guo Y, Li S, Chen G, Wang C
Sci Total Environ 2021 May 20;770:145300. Epub 2021 Jan 21 doi: 10.1016/j.scitotenv.2021.145300. PMID: 33517006

Diagnosis

Eckenstaler R, Benndorf RA
Int J Mol Sci 2021 Jun 22;22(13) doi: 10.3390/ijms22136678. PMID: 34206432Free PMC Article
Shan R, Ning Y, Ma Y, Gao X, Zhou Z, Jin C, Wu J, Lv J, Li L
Int J Environ Res Public Health 2021 Feb 28;18(5) doi: 10.3390/ijerph18052360. PMID: 33671018Free PMC Article
Chen MQ, Wang HY, Shi WR, Sun YX
Postgrad Med 2021 Mar;133(2):242-249. Epub 2020 Sep 14 doi: 10.1080/00325481.2020.1809870. PMID: 32921215
Koto R, Nakajima A, Horiuchi H, Yamanaka H
Mod Rheumatol 2021 Jan;31(1):261-269. Epub 2020 Jul 20 doi: 10.1080/14397595.2020.1784556. PMID: 32552370
Balakumar P, Alqahtani A, Khan NA, Mahadevan N, Dhanaraj SA
Pharmacol Res 2020 Nov;161:105209. Epub 2020 Sep 23 doi: 10.1016/j.phrs.2020.105209. PMID: 32979505

Therapy

Lee JS, Kim TJ, Hong SK, Min C, Yoo DM, Wee JH, Choi HG
Int J Environ Res Public Health 2021 Jul 8;18(14) doi: 10.3390/ijerph18147299. PMID: 34299750Free PMC Article
Winder M, Owczarek AJ, Mossakowska M, Broczek K, Grodzicki T, Wierucki Ł, Chudek J
Int J Environ Res Public Health 2021 Jan 6;18(2) doi: 10.3390/ijerph18020387. PMID: 33419128Free PMC Article
Wei Y, Zhu J, Wetzstein SA
Ecotoxicol Environ Saf 2021 Jan 15;208:111670. Epub 2020 Nov 20 doi: 10.1016/j.ecoenv.2020.111670. PMID: 33396180
Koto R, Nakajima A, Horiuchi H, Yamanaka H
Mod Rheumatol 2021 Jan;31(1):261-269. Epub 2020 Jul 20 doi: 10.1080/14397595.2020.1784556. PMID: 32552370
Aihemaitijiang S, Zhang Y, Zhang L, Yang J, Ye C, Halimulati M, Zhang W, Zhang Z
Nutrients 2020 Dec 15;12(12) doi: 10.3390/nu12123835. PMID: 33334038Free PMC Article

Prognosis

Shan R, Ning Y, Ma Y, Gao X, Zhou Z, Jin C, Wu J, Lv J, Li L
Int J Environ Res Public Health 2021 Feb 28;18(5) doi: 10.3390/ijerph18052360. PMID: 33671018Free PMC Article
Gu Y, Meng G, Zhang Q, Liu L, Wu H, Zhang S, Wang Y, Zhang T, Wang X, Sun S, Wang X, Zhou M, Jia Q, Song K, Wu X, Niu K
Endocr Pract 2021 Apr;27(4):291-297. Epub 2021 Jan 30 doi: 10.1016/j.eprac.2020.10.009. PMID: 33524634
Balakumar P, Alqahtani A, Khan NA, Mahadevan N, Dhanaraj SA
Pharmacol Res 2020 Nov;161:105209. Epub 2020 Sep 23 doi: 10.1016/j.phrs.2020.105209. PMID: 32979505
Hashimoto S, Nagai M, Ohira T, Fukuma S, Hosoya M, Yasumura S, Satoh H, Suzuki H, Sakai A, Ohtsuru A, Kawasaki Y, Takahashi A, Okazaki K, Kobashi G, Kamiya K, Yamashita S, Fukuhara SI, Ohto H; Fukushima Health Management Survey Group.
Clin Exp Nephrol 2020 Nov;24(11):1025-1032. Epub 2020 Jul 26 doi: 10.1007/s10157-020-01924-6. PMID: 32715354Free PMC Article
An P, Chen K, Wang A, Jin X, Chen Y, Gu W, Yan W, Zang L, Dou J, Mu Y, Lv Z
Clin Rheumatol 2020 Dec;39(12):3757-3767. Epub 2020 May 26 doi: 10.1007/s10067-020-05095-3. PMID: 32458241

Clinical prediction guides

Yu X, Gong S, Chen J, Zhang H, Shen Z, Gu Y, Lv S, Zhang D, Wang Y, Ding X, Zhang X
Sleep Med 2021 Aug;84:40-45. Epub 2021 May 21 doi: 10.1016/j.sleep.2021.05.014. PMID: 34091320
Shan R, Ning Y, Ma Y, Gao X, Zhou Z, Jin C, Wu J, Lv J, Li L
Int J Environ Res Public Health 2021 Feb 28;18(5) doi: 10.3390/ijerph18052360. PMID: 33671018Free PMC Article
Gu Y, Meng G, Zhang Q, Liu L, Wu H, Zhang S, Wang Y, Zhang T, Wang X, Sun S, Wang X, Zhou M, Jia Q, Song K, Wu X, Niu K
Endocr Pract 2021 Apr;27(4):291-297. Epub 2021 Jan 30 doi: 10.1016/j.eprac.2020.10.009. PMID: 33524634
Dong X, Liu X, Zhang L, Li R, Tu R, Hou J, Mao Z, Huo W, Guo Y, Li S, Chen G, Wang C
Sci Total Environ 2021 May 20;770:145300. Epub 2021 Jan 21 doi: 10.1016/j.scitotenv.2021.145300. PMID: 33517006
Wei Y, Zhu J, Wetzstein SA
Ecotoxicol Environ Saf 2021 Jan 15;208:111670. Epub 2020 Nov 20 doi: 10.1016/j.ecoenv.2020.111670. PMID: 33396180

Recent systematic reviews

Huang J, Ma ZF, Zhang Y, Wan Z, Li Y, Zhou H, Chu A, Lee YY
Glob Health Res Policy 2020 Nov 30;5(1):52. doi: 10.1186/s41256-020-00178-9. PMID: 33292806Free PMC Article
Hu AM, Brown JN
Clin Rheumatol 2020 Nov;39(11):3287-3294. Epub 2020 May 16 doi: 10.1007/s10067-020-05079-3. PMID: 32418037
Pan Z, Huang M, Fang M, Xie X, Huang Z
Endocrine 2020 Aug;69(2):286-293. Epub 2020 Apr 13 doi: 10.1007/s12020-020-02281-w. PMID: 32285287
Ebrahimpour-Koujan S, Saneei P, Larijani B, Esmaillzadeh A
Crit Rev Food Sci Nutr 2020;60(1):1-10. Epub 2018 Oct 2 doi: 10.1080/10408398.2018.1503155. PMID: 30277800
Uk Kang T, Park KY, Kim HJ, Ahn HS, Yim SY, Jun JB
Mod Rheumatol 2019 Nov;29(6):1031-1041. Epub 2018 Dec 14 doi: 10.1080/14397595.2018.1537555. PMID: 30334638

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