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Hypocalcemia

MedGen UID:
5705
Concept ID:
C0020598
Disease or Syndrome
Synonyms: Hypocalcaemia; Low blood calcium levels
SNOMED CT: Hypocalcemia (5291005); Hypocalcemia syndrome (5291005); Calcium deficiency disease (5291005)
 
HPO: HP:0002901

Definition

An abnormally decreased calcium concentration in the blood. [from HPO]

Term Hierarchy

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

Conditions with this feature

Celiac disease
MedGen UID:
3291
Concept ID:
C0007570
Disease or Syndrome
Celiac disease is a systemic autoimmune disease that can be associated with gastrointestinal findings (diarrhea, malabsorption, abdominal pain and distension, bloating, vomiting, and weight loss) and/or highly variable non-gastrointestinal findings (dermatitis herpetiformis, chronic fatigue, joint pain/inflammation, iron deficiency anemia, migraines, depression, attention-deficit disorder, epilepsy, osteoporosis/osteopenia, infertility and/or recurrent fetal loss, vitamin deficiencies, short stature, failure to thrive, delayed puberty, dental enamel defects, and autoimmune disorders). Classic celiac disease, characterized by mild to severe gastrointestinal symptoms, is less common than non-classic celiac disease, characterized by absence of gastrointestinal symptoms.
DiGeorge sequence
MedGen UID:
4297
Concept ID:
C0012236
Disease or Syndrome
Individuals with 22q11.2 deletion syndrome (22q11.2DS) have a range of findings including the following: Congenital heart disease (74% of individuals), particularly conotruncal malformations (tetralogy of Fallot, interrupted aortic arch, ventricular septal defect, and truncus arteriosus). Palatal abnormalities (69%), particularly velopharyngeal incompetence, submucosal cleft palate, bifid uvula, and cleft palate. Characteristic facial features (present in the majority of individuals of northern European heritage). Learning difficulties (70%-90%). An immune deficiency (regardless of the clinical presentation) (77%). Additional findings include the following: Hypocalcemia (50%). Significant feeding and swallowing problems; constipation with or without structural gastrointestinal anomalies (intestinal malrotation, imperforate anus, and Hirschsprung disease). Renal anomalies (31%). Hearing loss (both conductive and sensorineural). Laryngotracheoesophageal anomalies. Growth hormone deficiency. Autoimmune disorders. Seizures (idiopathic or associated with hypocalcemia). CNS anomalies including tethered cord. Skeletal abnormalities (scoliosis with or without vertebral anomalies, clubbed feet, polydactyly, and craniosynostosis). Ophthalmologic abnormalities (strabismus, posterior embryotoxon, tortuous retinal vessels, scleracornea, and anophthalmia). Enamel hypoplasia. Malignancies (rare). Developmental delay (in particular delays in emergence of language), intellectual disability, and learning differences (non-verbal learning disability where the verbal IQ is significantly greater than the performance IQ) are common. Autism or autistic spectrum disorder is found in approximately 20% of children and psychiatric illness (specifically schizophrenia) is present in 25% of adults; however, attention deficit disorder, anxiety, perseveration, and difficulty with social interactions are also common.
Johanson-Blizzard syndrome
MedGen UID:
59798
Concept ID:
C0175692
Disease or Syndrome
Pancreatitis is inflammation of the pancreas that progresses from acute (sudden onset; duration <6 months) to recurrent acute (>1 episode of acute pancreatitis) to chronic (duration >6 months). The range of symptoms and disease course vary from person to person. Familial pancreatitis, defined as pancreatitis from any cause that occurs in a family with an incidence that is greater than would be expected by chance alone, can be non-genetic or genetic, the latter including autosomal dominant hereditary pancreatitis and pancreatitis syndromes characterized by pancreatitis or pancreatic insufficiency. The majority of familial pancreatitis appears to have a complex, multigenic, or gene-environmental etiology with a variable number of germline pathogenic variants in genes that affect trypsin regulation, including CASR, CTRC, and CLDN2. Hereditary pancreatitis (HP) is defined as either two or more individuals with pancreatitis in two or more generations of a family (i.e., an autosomal dominant pattern of inheritance) or pancreatitis associated with a germline PRSS1 disease-causing gain-of-function variant. The phenotype of hereditary pancreatitis is increased susceptibility to acute pancreatitis, with complications such as chronic inflammation, fibrosis, and chronic pain in some affected individuals. Heterozygous pathogenic variants in PRSS1 are found in 60%-100% of families with hereditary pancreatitis, and most large families with pancreatitis spanning multiple generations; biallelic pathogenic variants in SPINK1 or biallelic pathogenic variants in CFTR result in autosomal recessive pancreatitis. Syndromes in which pancreatitis is a finding include: Pearson marrow pancreas syndrome, CEL maturity-onset diabetes of the young (CEL-MODY), and Johanson-Blizzard syndrome. Shwachman-Diamond syndrome, an autosomal recessive disorder, includes pancreatic exocrine insufficiency as well as other features. Idiopathic sporadic pancreatitis is a single occurrence of pancreatitis in a family for which no etiology is identified.
Shprintzen syndrome
MedGen UID:
65085
Concept ID:
C0220704
Disease or Syndrome
Individuals with 22q11.2 deletion syndrome (22q11.2DS) have a range of findings including the following: Congenital heart disease (74% of individuals), particularly conotruncal malformations (tetralogy of Fallot, interrupted aortic arch, ventricular septal defect, and truncus arteriosus). Palatal abnormalities (69%), particularly velopharyngeal incompetence, submucosal cleft palate, bifid uvula, and cleft palate. Characteristic facial features (present in the majority of individuals of northern European heritage). Learning difficulties (70%-90%). An immune deficiency (regardless of the clinical presentation) (77%). Additional findings include the following: Hypocalcemia (50%). Significant feeding and swallowing problems; constipation with or without structural gastrointestinal anomalies (intestinal malrotation, imperforate anus, and Hirschsprung disease). Renal anomalies (31%). Hearing loss (both conductive and sensorineural). Laryngotracheoesophageal anomalies. Growth hormone deficiency. Autoimmune disorders. Seizures (idiopathic or associated with hypocalcemia). CNS anomalies including tethered cord. Skeletal abnormalities (scoliosis with or without vertebral anomalies, clubbed feet, polydactyly, and craniosynostosis). Ophthalmologic abnormalities (strabismus, posterior embryotoxon, tortuous retinal vessels, scleracornea, and anophthalmia). Enamel hypoplasia. Malignancies (rare). Developmental delay (in particular delays in emergence of language), intellectual disability, and learning differences (non-verbal learning disability where the verbal IQ is significantly greater than the performance IQ) are common. Autism or autistic spectrum disorder is found in approximately 20% of children and psychiatric illness (specifically schizophrenia) is present in 25% of adults; however, attention deficit disorder, anxiety, perseveration, and difficulty with social interactions are also common.
CHARGE association
MedGen UID:
75567
Concept ID:
C0265354
Disease or Syndrome
CHARGE is a mnemonic for coloboma, heart defects, choanal atresia, retarded growth and development, genital abnormalities, and ear anomalies. CHARGE syndrome is characterized by the following: Unilateral or bilateral coloboma of the iris, retina-choroid, and/or disc with or without microphthalmos (80%-90% of individuals). Unilateral or bilateral choanal atresia or stenosis (50%-60%). Cranial nerve dysfunction resulting in hyposmia or anosmia, unilateral or bilateral facial palsy (40%), impaired hearing, and/or swallowing problems (70%-90%). Abnormal outer ears, ossicular malformations, Mondini defect of the cochlea and absent or hypoplastic semicircular canals (>90%). Cryptorchidism in males and hypogonadotropic hypogonadism in both males and females. Developmental delay. Cardiovascular malformations (75%-85%). Growth deficiency (70%-80%). Orofacial clefts (15%-20%). Tracheoesophageal fistula (15%-20%). Neonates with CHARGE syndrome often have multiple life-threatening medical conditions. Feeding difficulties are a major cause of morbidity in all age groups.
Cronkhite-Canada syndrome
MedGen UID:
129128
Concept ID:
C0282207
Disease or Syndrome
Cronkhite-Canada syndrome is characterized by gastrointestinal hamartomatous polyposis, alopecia, onychodystrophy, skin hyperpigmentation, and diarrhea. It is associated with high morbidity (summary by Sweetser et al., 2012).
Visceral steatosis
MedGen UID:
90962
Concept ID:
C0341447
Pathologic Function
Hypocalcemia, autosomal dominant 1
MedGen UID:
87438
Concept ID:
C0342345
Disease or Syndrome
Autosomal dominant hypocalcemia-1 is associated with low or normal serum parathyroid hormone concentrations (PTH). Approximately 50% of patients have mild or asymptomatic hypocalcemia; about 50% have paresthesias, carpopedal spasm, and seizures; about 10% have hypercalciuria with nephrocalcinosis or kidney stones; and more than 35% have ectopic and basal ganglia calcifications (summary by Nesbit et al., 2013). Thakker (2001) noted that patients with gain-of-function mutations in the CASR gene, resulting in generally asymptomatic hypocalcemia with hypercalciuria, have low-normal serum PTH concentrations and have often been diagnosed with hypoparathyroidism because of the insensitivity of earlier PTH assays. Because treatment with vitamin D to correct the hypocalcemia in these patients causes hypercalciuria, nephrocalcinosis, and renal impairment, these patients need to be distinguished from those with other forms of hypoparathyroidism (see 146200). Thakker (2001) suggested the designation 'autosomal dominant hypocalcemic hypercalciuria' for this CASR-related disorder. Genetic Heterogeneity of Autosomal Dominant Hypocalcemia Autosomal dominant hypocalcemia-2 (HYPOC2; 615361) is caused by mutation in the GNA11 gene (139313) on chromosome 19p13.
Cranioectodermal dysplasia 1
MedGen UID:
96586
Concept ID:
C0432235
Disease or Syndrome
Cranioectodermal dysplasia (CED), a ciliopathy also known as Sensenbrenner syndrome, is a multisystem disorder with skeletal involvement (narrow thorax, shortened proximal limbs, and brachydactyly), ectodermal features (widely-spaced hypoplastic teeth, hypodontia, sparse hair, skin laxity, abnormal nails), joint laxity, growth retardation, and characteristic facial features (frontal bossing, low-set simple ears, high forehead, telecanthus/epicanthus, full cheeks, everted lower lip). Most affected children develop nephronophthisis that often leads to end-stage renal disease (ESRD) in infancy or childhood, a major cause of morbidity and mortality. Hepatic fibrosis and retinal dystrophy, other manifestations of ciliopathies, are also observed. Dolichocephaly, often secondary to sagittal craniosynostosis, is a primary manifestation that distinguishes CED from most other ciliopathies. Brain malformations and developmental delay may also occur.
Hypoparathyroidism familial isolated
MedGen UID:
322005
Concept ID:
C1832648
Disease or Syndrome
Garfield and Karaplis (2001) reviewed the various causes and clinical forms of hypoparathyroidism. They noted that hypoparathyroidism is a clinical disorder characterized by hypocalcemia and hyperphosphatemia. It manifests when parathyroid hormone (PTH; 168450) secreted from the parathyroid glands is insufficient to maintain normal extracellular fluid calcium concentrations or, less commonly, when PTH is unable to function optimally in target tissues, despite adequate circulating levels. Congenital absence of the parathyroid and thymus glands (III and IV pharyngeal pouch syndrome, or DiGeorge syndrome, 188400) is usually a sporadic condition (Taitz et al., 1966).
Timothy syndrome
MedGen UID:
331395
Concept ID:
C1832916
Disease or Syndrome
Timothy syndrome is a multisystem disorder characterized by cardiac, hand/foot, facial, and neurodevelopmental features. Typical cardiac findings include a rate-corrected QT interval >480 ms, functional 2:1 AV block with bradycardia, tachyarrhythmias, and congenital heart defects (patent ductus arteriosus, patent foramen ovale, ventricular septal defect, tetralogy of Fallot, hypertrophic cardiomyopathy). The diagnosis of Timothy syndrome is generally made within the first few days of life although it may be suspected prenatally due to 2:1 AV block or bradycardia in the fetus. Hand/foot findings are unilateral or bilateral cutaneous syndactyly variably involving fingers two (index), three (middle), four (ring), and five (little) and bilateral cutaneous syndactyly of toes two and three. Facial findings include depressed nasal bridge, low-set ears, thin vermilion border of the upper lip, and round face. Neuropsychiatric involvement includes global developmental delays and autism spectrum disorders. Ventricular tachyarrhythmia is the leading cause of death, followed by infection and complications of intractable hypoglycemia. Average age of death is 2.5 years.
Kenny-Caffey syndrome type 1
MedGen UID:
340923
Concept ID:
C1855648
Disease or Syndrome
An autosomal recessive form of Kenny-Caffey syndrome due to mutation(s) in the TBCE gene, encoding tubulin-specific chaperone E. This condition is characterized by hypoparathyroidism with hypocalcemia, marked growth retardation, craniofacial anomalies, absent diploic space in the skull, cortical thickening of long bones with medullary stenosis, and small hands and feet.
Hypoparathyroidism retardation dysmorphism syndrome
MedGen UID:
340984
Concept ID:
C1855840
Disease or Syndrome
HRDS is an autosomal recessive multisystem disorder characterized by intrauterine and postnatal growth retardation, infantile-onset hypoparathyroidism that can result in severe hypocalcemic seizures, dysmorphic facial features, and developmental delay (summary by Padidela et al., 2009 and Ratbi et al., 2015).
Urioste Martinez-Frias syndrome
MedGen UID:
343489
Concept ID:
C1856159
Disease or Syndrome
Pseudohypoparathyroidism type 1B
MedGen UID:
350343
Concept ID:
C1864100
Disease or Syndrome
Disorders of GNAS inactivation include the phenotypes pseudohypoparathyroidism Ia, Ib, and Ic (PHP-Ia, -Ib, -Ic), pseudopseudohypoparathyroidism (PPHP), progressive osseous heteroplasia (POH), and osteoma cutis (OC). PHP-Ia and PHP-Ic are characterized by: End-organ resistance to endocrine hormones including parathyroid hormone (PTH), thyroid-stimulating hormone (TSH), gonadotropins (LH and FSH), growth hormone-releasing hormone (GHRH), and CNS neurotransmitters (leading to obesity and variable degrees of intellectual disability and developmental delay); and The Albright hereditary osteodystrophy (AHO) phenotype (short stature, round facies, and subcutaneous ossifications) and brachydactyly type E (shortening mainly of the 4th and/or 5th metacarpals and metatarsals and distal phalanx of the thumb). Although PHP-Ib is characterized principally by PTH resistance, some individuals also have partial TSH resistance and mild features of AHO (e.g., brachydactyly). PPHP, a more limited form of PHP-Ia, is characterized by various manifestations of the AHO phenotype without the hormone resistance or obesity. POH and OC are even more restricted variants of PPHP: POH consists of dermal ossification beginning in infancy, followed by increasing and extensive bone formation in deep muscle and fascia. OC consists of extra-skeletal ossification that is limited to the dermis and subcutaneous tissues.
Gracile bone dysplasia
MedGen UID:
356331
Concept ID:
C1865639
Disease or Syndrome
Gracile bone dysplasia is a perinatally lethal condition characterized by gracile bones with thin diaphyses, premature closure of basal cranial sutures, and microphthalmia (summary by Unger et al., 2013).
Hypomagnesemia 1, intestinal
MedGen UID:
355596
Concept ID:
C1865974
Disease or Syndrome
Familial hypomagnesemia with secondary hypocalcemia is a rare autosomal recessive disorder characterized by very low serum magnesium levels. Hypocalcemia is a secondary consequence of parathyroid failure and parathyroid hormone resistance as a result of severe magnesium deficiency. The disease typically manifests during the first months of life with generalized convulsions or signs of increased neuromuscular excitability, such as muscle spasms or tetany. Untreated, the disease may be fatal or lead to severe neurologic damage. Treatment includes immediate administration of magnesium, usually intravenously, followed by life-long high-dose oral magnesium (review by Knoers, 2009). Genetic Heterogeneity of Hypomagnesemia A form of hypomagnesemia due to kidney defects and high urinary magnesium excretion associated with hypocalciuria (HOMG2; 154020) is caused by mutation in the FXYD2 gene (601814). Renal hypomagnesemia-3 (HOMG3; 248250), associated with hypercalciuria and nephrocalcinosis, is caused by mutation in the CLDN16 gene (603959). Renal hypomagnesemia-4 (HOMG4; 611718), which is normocalciuric, is caused by mutation in the EGF gene (131530). Renal hypomagnesemia-5 (HOMG5; 248190), associated with hypercalciuria, nephrocalcinosis, and severe ocular involvement, is caused by mutation in the CLDN19 gene (610036). Renal hypomagnesemia-6 (HOMG6; 613882) is caused by mutation in the CNNM2 gene (607803). Patients with Gitelman syndrome (263800) and Bartter syndrome (see 241200) also show hypomagnesemia, and steatorrhea and severe chronic diarrhea states, such as Crohn disease (see 226600) and Whipple disease, that can result in severe hypomagnesemia.
Lipodystrophy, congenital generalized, type 3
MedGen UID:
436541
Concept ID:
C2675861
Disease or Syndrome
Congenital generalized lipodystrophy, also known as Berardinelli-Seip syndrome, is an autosomal recessive disorder characterized by marked paucity of adipose tissue, extreme insulin resistance, hypertriglyceridemia, hepatic steatosis, and early onset of diabetes (Garg, 2004). For a general description and a discussion of genetic heterogeneity of congenital generalized lipodystrophy, see CGL1 (608594).
Craniofacioskeletal syndrome
MedGen UID:
394716
Concept ID:
C2678036
Disease or Syndrome
ALG12-congenital disorder of glycosylation
MedGen UID:
443954
Concept ID:
C2931001
Disease or Syndrome
Congenital disorders of glycosylation (CDG), previously called carbohydrate-deficient glycoprotein syndromes (CDGSs), are a group of hereditary multisystem disorders first recognized by Jaeken et al. (1980). The characteristic biochemical abnormality of CDGs is the hypoglycosylation of glycoproteins, which is routinely determined by isoelectric focusing (IEF) of serum transferrin. Type I CDG comprises those disorders in which there is a defect in the assembly of lipid-linked oligosaccharides or their transfer onto nascent glycoproteins, whereas type II CDG comprises defects of trimming, elongation, and processing of protein-bound glycans. For a general discussion of CDGs, see CDG1A (212065) and CDG1B (602579).
Pseudohypoparathyroidism type II
MedGen UID:
444371
Concept ID:
C2932717
Disease or Syndrome
Pseudohypoparathyroidism (PHP) is a term applied to a heterogeneous group of disorders whose common feature is resistance to parathyroid hormone (PTH; 168450). PHP type II is characterized by a normal cAMP response to PTH infusion, but a deficient phosphaturic response, indicating a defect distal to cAMP generation in renal cells. The clinical features of Albright hereditary osteodystrophy (AHO; see 103580) are not present in PHP II (Mantovani and Spada, 2006). For a general phenotypic description, classification, and a discussion of molecular genetics of pseudohypoparathyroidism, see PHP1A (103580).
Hypocalcemia, autosomal dominant 2
MedGen UID:
815573
Concept ID:
C3809243
Disease or Syndrome
Myopathy, tubular aggregate, 2
MedGen UID:
862994
Concept ID:
C4014557
Disease or Syndrome
Kenny-Caffey syndrome type 2
MedGen UID:
1373312
Concept ID:
C4316787
Disease or Syndrome
An autosomal dominant form of Kenny-Caffey Syndrome due to mutation(s) in the FAM111A gene, encoding protein FAM111A. This condition is characterized by transient hypocalcemia, delayed closure of the anterior fontanel, eye anomalies, including microphthalmia, proportionate short stature, and cortical thickening and medullary stenosis of the tubular bones.

Recent clinical studies

Etiology

Eismontas V, Slepavicius A, Janusonis V, Zeromskas P, Beisa V, Strupas K, Dambrauskas Z, Gulbinas A, Martinkenas A
BMC Surg 2018 Aug 9;18(1):55. doi: 10.1186/s12893-018-0387-2. PMID: 30092793Free PMC Article
Falch C, Hornig J, Senne M, Braun M, Konigsrainer A, Kirschniak A, Muller S
Int J Surg 2018 Jul;55:46-50. Epub 2018 May 16 doi: 10.1016/j.ijsu.2018.05.014. PMID: 29777882
Filho EBY, Machry RV, Mesquita R, Scheffel RS, Maia AL
Endocrine 2018 Aug;61(2):224-231. Epub 2018 May 2 doi: 10.1007/s12020-018-1601-9. PMID: 29721800
Floege J, Tsirtsonis K, Iles J, Drueke TB, Chertow GM, Parfrey P
Kidney Int 2018 Jun;93(6):1475-1482. Epub 2018 Mar 7 doi: 10.1016/j.kint.2017.12.014. PMID: 29525393
Yılmaz B, Aygün C, Çetinoğlu E
J Matern Fetal Neonatal Med 2018 Jul;31(14):1889-1893. Epub 2017 Jun 14 doi: 10.1080/14767058.2017.1331430. PMID: 28610460

Diagnosis

Eismontas V, Slepavicius A, Janusonis V, Zeromskas P, Beisa V, Strupas K, Dambrauskas Z, Gulbinas A, Martinkenas A
BMC Surg 2018 Aug 9;18(1):55. doi: 10.1186/s12893-018-0387-2. PMID: 30092793Free PMC Article
Filho EBY, Machry RV, Mesquita R, Scheffel RS, Maia AL
Endocrine 2018 Aug;61(2):224-231. Epub 2018 May 2 doi: 10.1007/s12020-018-1601-9. PMID: 29721800
Floege J, Tsirtsonis K, Iles J, Drueke TB, Chertow GM, Parfrey P
Kidney Int 2018 Jun;93(6):1475-1482. Epub 2018 Mar 7 doi: 10.1016/j.kint.2017.12.014. PMID: 29525393
Castro A, Del Rio L, Gavilan J
Otolaryngol Head Neck Surg 2018 Jan;158(1):76-82. Epub 2017 Sep 12 doi: 10.1177/0194599817730334. PMID: 28895449
Al Khadem MG, Rettig EM, Dhillon VK, Russell JO, Tufano RP
Laryngoscope 2018 Mar;128(3):769-774. Epub 2017 Aug 26 doi: 10.1002/lary.26805. PMID: 28842998

Therapy

Eismontas V, Slepavicius A, Janusonis V, Zeromskas P, Beisa V, Strupas K, Dambrauskas Z, Gulbinas A, Martinkenas A
BMC Surg 2018 Aug 9;18(1):55. doi: 10.1186/s12893-018-0387-2. PMID: 30092793Free PMC Article
Falch C, Hornig J, Senne M, Braun M, Konigsrainer A, Kirschniak A, Muller S
Int J Surg 2018 Jul;55:46-50. Epub 2018 May 16 doi: 10.1016/j.ijsu.2018.05.014. PMID: 29777882
Filho EBY, Machry RV, Mesquita R, Scheffel RS, Maia AL
Endocrine 2018 Aug;61(2):224-231. Epub 2018 May 2 doi: 10.1007/s12020-018-1601-9. PMID: 29721800
Floege J, Tsirtsonis K, Iles J, Drueke TB, Chertow GM, Parfrey P
Kidney Int 2018 Jun;93(6):1475-1482. Epub 2018 Mar 7 doi: 10.1016/j.kint.2017.12.014. PMID: 29525393
Al Khadem MG, Rettig EM, Dhillon VK, Russell JO, Tufano RP
Laryngoscope 2018 Mar;128(3):769-774. Epub 2017 Aug 26 doi: 10.1002/lary.26805. PMID: 28842998

Prognosis

Eismontas V, Slepavicius A, Janusonis V, Zeromskas P, Beisa V, Strupas K, Dambrauskas Z, Gulbinas A, Martinkenas A
BMC Surg 2018 Aug 9;18(1):55. doi: 10.1186/s12893-018-0387-2. PMID: 30092793Free PMC Article
Falch C, Hornig J, Senne M, Braun M, Konigsrainer A, Kirschniak A, Muller S
Int J Surg 2018 Jul;55:46-50. Epub 2018 May 16 doi: 10.1016/j.ijsu.2018.05.014. PMID: 29777882
Filho EBY, Machry RV, Mesquita R, Scheffel RS, Maia AL
Endocrine 2018 Aug;61(2):224-231. Epub 2018 May 2 doi: 10.1007/s12020-018-1601-9. PMID: 29721800
Floege J, Tsirtsonis K, Iles J, Drueke TB, Chertow GM, Parfrey P
Kidney Int 2018 Jun;93(6):1475-1482. Epub 2018 Mar 7 doi: 10.1016/j.kint.2017.12.014. PMID: 29525393
Al Khadem MG, Rettig EM, Dhillon VK, Russell JO, Tufano RP
Laryngoscope 2018 Mar;128(3):769-774. Epub 2017 Aug 26 doi: 10.1002/lary.26805. PMID: 28842998

Clinical prediction guides

Eismontas V, Slepavicius A, Janusonis V, Zeromskas P, Beisa V, Strupas K, Dambrauskas Z, Gulbinas A, Martinkenas A
BMC Surg 2018 Aug 9;18(1):55. doi: 10.1186/s12893-018-0387-2. PMID: 30092793Free PMC Article
Falch C, Hornig J, Senne M, Braun M, Konigsrainer A, Kirschniak A, Muller S
Int J Surg 2018 Jul;55:46-50. Epub 2018 May 16 doi: 10.1016/j.ijsu.2018.05.014. PMID: 29777882
Filho EBY, Machry RV, Mesquita R, Scheffel RS, Maia AL
Endocrine 2018 Aug;61(2):224-231. Epub 2018 May 2 doi: 10.1007/s12020-018-1601-9. PMID: 29721800
Floege J, Tsirtsonis K, Iles J, Drueke TB, Chertow GM, Parfrey P
Kidney Int 2018 Jun;93(6):1475-1482. Epub 2018 Mar 7 doi: 10.1016/j.kint.2017.12.014. PMID: 29525393
Yılmaz B, Aygün C, Çetinoğlu E
J Matern Fetal Neonatal Med 2018 Jul;31(14):1889-1893. Epub 2017 Jun 14 doi: 10.1080/14767058.2017.1331430. PMID: 28610460

Recent systematic reviews

Sanabria A, Kowalski LP, Tartaglia F
Laryngoscope 2018 Feb;128(2):534-541. Epub 2017 May 31 doi: 10.1002/lary.26681. PMID: 28561328
Antakia R, Edafe O, Uttley L, Balasubramanian SP
Thyroid 2015 Jan;25(1):95-106. doi: 10.1089/thy.2014.0101. PMID: 25203484
Newman DB, Fidahussein SS, Kashiwagi DT, Kennel KA, Kashani KB, Wang Z, Altayar O, Murad MH
Heart Fail Rev 2014 Mar;19(2):199-205. doi: 10.1007/s10741-013-9371-1. PMID: 23355181
Qi WX, Lin F, He AN, Tang LN, Shen Z, Yao Y
Curr Med Res Opin 2013 Sep;29(9):1067-73. Epub 2013 Jun 24 doi: 10.1185/03007995.2013.813840. PMID: 23745518
Alhefdhi A, Mazeh H, Chen H
Oncologist 2013;18(5):533-42. Epub 2013 May 1 doi: 10.1634/theoncologist.2012-0283. PMID: 23635556Free PMC Article

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