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Anorexia

MedGen UID:
743955
Concept ID:
C1971624
Finding
Synonyms: Lack of appetite; Loss of appetite; No appetite; Off food
SNOMED CT: Loss of appetite (79890006); No appetite (79890006); Off food (79890006); Lack of appetite (79890006)
 
HPO: HP:0002039

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews
  • CROGAnorexia

Conditions with this feature

Fabry's disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme a-galactosidase (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesias), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhydrosis, hypohydosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, they may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, males with greater than 1% a-Gal A activity may have either (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, mitral insufficiency and/or cardiomyopathy, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain.
Behcet's syndrome
MedGen UID:
2568
Concept ID:
C0004943
Disease or Syndrome
Behçet disease is an inflammatory condition that affects many parts of the body. The health problems associated with Behçet disease result from widespread inflammation of blood vessels (vasculitis). This inflammation most commonly affects the mouth, genitals, skin, and eyes. Painful mouth sores called aphthous ulcers are usually the first sign of Behçet disease. These sores occur on the lips and tongue and inside the cheeks. The ulcers look like common canker sores, and they typically heal within one to two weeks. About 75 percent of all people with Behçet disease develop similar ulcers on the genitals. These ulcers occur most frequently on the scrotum in men and on the labia in women. Behçet disease can also cause painful bumps and sores on the skin. Most affected individuals develop pus-filled bumps that resemble acne. These bumps can occur anywhere on the body. Some affected people also have red, tender nodules called erythema nodosum. These nodules usually develop on the legs but can also occur on the face, neck, and arms. An inflammation of the eye called uveitis is found in more than half of people with Behçet disease. Eye problems are more common in younger people with the disease and affect men more often than women. Uveitis can result in blurry vision and an extreme sensitivity to light (photophobia). Rarely, inflammation can also cause eye pain and redness. If untreated, the eye problems associated with Behçet disease can lead to blindness. Less commonly, Behçet disease can affect the joints, gastrointestinal tract, large blood vessels, and brain and spinal cord (central nervous system). Central nervous system abnormalities are among the most serious complications of Behçet disease. Related symptoms can include headaches, confusion, personality changes, memory loss, impaired speech, and problems with balance and movement. The signs and symptoms of Behçet disease usually begin in a person's twenties or thirties, although they can appear at any age. Some affected people have relatively mild symptoms that are limited to sores in the mouth and on the genitals. Others have more severe symptoms affecting many parts of the body, including the central nervous system. The features of Behçet disease typically come and go over a period of months or years. In most affected individuals, the health problems associated with this disorder improve with age.
Diaphyseal dysplasia
MedGen UID:
4268
Concept ID:
C0011989
Congenital Abnormality
Camurati-Engelmann disease (CED) is characterized by hyperostosis of the long bones and the skull, proximal muscle weakness, severe limb pain, a wide-based, waddling gait, and joint contractures. Facial features such as frontal bossing, enlargement of the mandible, proptosis, and cranial nerve impingement resulting in facial palsy are seen in severely affected individuals later in life.
Menetrier disease
MedGen UID:
4844
Concept ID:
C0017155
Disease or Syndrome
A condition marked by inflammation and ulcers (breaks on the skin or on the surface of an organ) of the mucosa (inner lining) of the stomach and by overgrowth of the cells that make up the mucosa. Symptoms include vomiting, diarrhea, and weight loss. Patients with giant hypertrophic gastritis may be at a higher risk of stomach cancer.
Mastocytosis
MedGen UID:
9902
Concept ID:
C0024899
Disease or Syndrome
A clonal myeloproliferative neoplasm characterized by the proliferation and accumulation of neoplastic mast cells in one or multiple organs or organ systems. It is a heterogeneous group of neoplasms, ranging from cutaneous proliferations which may regress spontaneously, to aggressive neoplasms associated with organ failure and short survival.
Takayasu arteritis
MedGen UID:
21458
Concept ID:
C0039263
Disease or Syndrome
A large vessel vasculitis affecting the aorta and its branches. It usually affects young females. It causes vascular obstruction, resulting in asymmetric pulses.
Cyclical vomiting syndrome
MedGen UID:
57509
Concept ID:
C0152164
Disease or Syndrome
Cyclic vomiting syndrome is a disorder that causes recurrent episodes of nausea, vomiting, and tiredness (lethargy). This condition is diagnosed most often in young children, but it can affect people of any age. The episodes of nausea, vomiting, and lethargy last anywhere from an hour to 10 days. An affected person may vomit several times per hour, potentially leading to a dangerous loss of fluids (dehydration). Additional symptoms can include unusually pale skin (pallor), abdominal pain, diarrhea, headache, fever, and an increased sensitivity to light (photophobia) or to sound (phonophobia). In most affected people, the signs and symptoms of each attack are quite similar. These attacks can be debilitating, making it difficult for an affected person to go to work or school. Episodes of nausea, vomiting, and lethargy can occur regularly or apparently at random, or can be triggered by a variety of factors. The most common triggers are emotional excitement and infections. Other triggers can include periods without eating (fasting), temperature extremes, lack of sleep, overexertion, allergies, ingesting certain foods or alcohol, and menstruation. If the condition is not treated, episodes usually occur four to 12 times per year. Between attacks, vomiting is absent, and nausea is either absent or much reduced. However, many affected people experience other symptoms during and between episodes, including pain, lethargy, digestive disorders such as gastroesophageal reflux and irritable bowel syndrome, and fainting spells (syncope). People with cyclic vomiting syndrome are also more likely than people without the disorder to experience depression, anxiety, and panic disorder. It is unclear whether these health conditions are directly related to nausea and vomiting. Cyclic vomiting syndrome is often considered to be a variant of migraines, which are severe headaches often associated with pain, nausea, vomiting, and extreme sensitivity to light and sound. Cyclic vomiting syndrome is likely the same as or closely related to a condition called abdominal migraine, which is characterized by attacks of stomach pain and cramping. Attacks of nausea, vomiting, or abdominal pain in childhood may be replaced by migraine headaches as an affected person gets older. Many people with cyclic vomiting syndrome or abdominal migraine have a family history of migraines. Most people with cyclic vomiting syndrome have normal intelligence, although some affected people have developmental delay or intellectual disability. Autism spectrum disorders, which affect communication and social interaction, have also been associated with cyclic vomiting syndrome. Additionally, muscle weakness (myopathy) and seizures are possible. People with any of these additional features are said to have cyclic vomiting syndrome plus.
Acute intermittent porphyria
MedGen UID:
56452
Concept ID:
C0162565
Disease or Syndrome
Acute intermittent porphyria (referred to as AIP in this GeneReview) results from half-normal activity of the enzyme hydroxymethylbilane synthase (HMBS). It is characterized clinically by life-threatening acute neurovisceral attacks of severe abdominal pain without peritoneal signs, often accompanied by nausea, vomiting, tachycardia, and hypertension. Attacks may be complicated by neurologic findings (mental changes, convulsions, and peripheral neuropathy that may progress to respiratory paralysis), and hyponatremia. Acute attacks, which may be provoked by certain drugs, alcoholic beverages, endocrine factors, calorie restriction, stress, and infections, usually resolve within two weeks. Most individuals with AIP have one or a few attacks; about 5% (mainly women) have recurrent attacks (defined as >4 attacks/year) that may persist for years. Other long-term complications are chronic renal failure, hepatocellular carcinoma (HCC), and hypertension. Attacks, which are very rare before puberty, are more common in women than men. All individuals with a genetic change in the gene HMBS that predisposes to AIP are at risk of developing acute attacks; however, most never have symptoms and are said to have latent (or presymptomatic) AIP.
Juvenile myopathy, encephalopathy, lactic acidosis AND stroke
MedGen UID:
56485
Concept ID:
C0162671
Disease or Syndrome
MELAS syndrome, comprising mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, is a genetically heterogeneous mitochondrial disorder with a variable clinical phenotype. The disorder is accompanied by features of central nervous system involvement, including seizures, hemiparesis, hemianopsia, cortical blindness, and episodic vomiting (Pavlakis et al., 1984; Montagna et al., 1988). Other mitochondrial encephalomyopathies include Leigh syndrome (LS; 256000), Kearns-Sayre syndrome (KSS; 530000), MERRF syndrome (545000), and Leber optic atrophy (535000).
Hereditary acrodermatitis enteropathica
MedGen UID:
66355
Concept ID:
C0221036
Disease or Syndrome
severe human skin and gastrointestinal disease inherited as a recessive autosomal trait that is characterized by the symptoms of zinc deficiency and clears up when zinc is added to the diet.
Infantile hypophosphatasia
MedGen UID:
75677
Concept ID:
C0268412
Disease or Syndrome
Hypophosphatasia is characterized by defective mineralization of bone and/or teeth in the presence of low activity of serum and bone alkaline phosphatase. Clinical features range from stillbirth without mineralized bone at the severe end to pathologic fractures of the lower extremities in later adulthood at the mild end. At least six clinical forms are currently recognized based on age at diagnosis and severity of features: Perinatal (lethal) hypophosphatasia characterized by respiratory insufficiency and hypercalcemia. Perinatal (benign) hypophosphatasia with prenatal skeletal manifestations that slowly resolve into the milder childhood or adult form. Infantile hypophosphatasia with onset between birth and age six months of rickets without elevated serum alkaline phosphatase activity. Childhood hypophosphatasia that ranges from low bone mineral density for age with unexplained fractures to rickets. Adult hypophosphatasia characterized by early loss of adult dentition and stress fractures and pseudofractures of the lower extremities in middle age. Odontohypophosphatasia characterized by premature exfoliation of primary teeth and/or severe dental caries as an isolated finding or as part of the above forms of hypophosphatasia.
Arginase deficiency
MedGen UID:
78688
Concept ID:
C0268548
Disease or Syndrome
Arginase deficiency in untreated individuals is characterized by episodic hyperammonemia of variable degree that is infrequently severe enough to be life threatening or to cause death. Most commonly, birth and early childhood are normal. Untreated individuals have slowing of linear growth at age one to three years, followed by development of spasticity, plateauing of cognitive development, and subsequent loss of developmental milestones. If untreated, arginase deficiency usually progresses to severe spasticity, loss of ambulation, complete loss of bowel and bladder control, and severe intellectual disability. Seizures are common and are usually controlled easily.
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).
Congenital defect of folate absorption
MedGen UID:
83348
Concept ID:
C0342705
Disease or Syndrome
Hereditary folate malabsorption (HFM) is characterized by folate deficiency with impaired intestinal folate absorption and impaired folate transport into the central nervous system (CNS). Findings include poor feeding and failure to thrive, anemia often accompanied by leukopenia and/or thrombocytopenia, diarrhea and/or oral mucositis, hypoimmunoglobulinemia, and other immunologic dysfunction resulting in infections with unusual organisms. Neurologic manifestations include developmental delays, cognitive and motor impairment, behavioral disorders and, frequently, seizures.
Enteropathy, familial, with villous edema and immunoglobulin g2 deficiency
MedGen UID:
324980
Concept ID:
C1838238
Disease or Syndrome
Methylmalonic acidemia with homocystinuria cblD
MedGen UID:
341253
Concept ID:
C1848552
Disease or Syndrome
The clinical manifestations of disorders of intracellular cobalamin metabolism can be highly variable even within a single complementation group. The prototype and best understood is cblC; it is also the most common of these disorders. The age of initial presentation of cblC spans a wide range, including: Newborns, who can have intrauterine growth retardation (IUGR) and microcephaly; Infants, who can have poor feeding, failure to thrive, pallor, and neurologic signs, and occasionally hemolytic uremic syndrome (HUS) and/or seizures including infantile spasms; Toddlers, who can have failure to thrive, poor head growth, cytopenias (including megaloblastic anemia), global developmental delay, encephalopathy, and neurologic signs such as hypotonia and seizures; and Adolescents and adults, who can have neuropsychiatric symptoms, progressive cognitive decline, and/or subacute combined degeneration of the spinal cord.
Methylmalonic acidemia with homocystinuria
MedGen UID:
341256
Concept ID:
C1848561
Disease or Syndrome
The clinical manifestations of disorders of intracellular cobalamin metabolism can be highly variable even within a single complementation group. The prototype and best understood is cblC; it is also the most common of these disorders. The age of initial presentation of cblC spans a wide range, including: Newborns, who can have intrauterine growth retardation (IUGR) and microcephaly; Infants, who can have poor feeding, failure to thrive, pallor, and neurologic signs, and occasionally hemolytic uremic syndrome (HUS) and/or seizures including infantile spasms; Toddlers, who can have failure to thrive, poor head growth, cytopenias (including megaloblastic anemia), global developmental delay, encephalopathy, and neurologic signs such as hypotonia and seizures; and Adolescents and adults, who can have neuropsychiatric symptoms, progressive cognitive decline, and/or subacute combined degeneration of the spinal cord.
Susceptibility to acute rheumatic fever
MedGen UID:
376575
Concept ID:
C1849384
Finding
Methylmalonic aciduria due to methylmalonyl-CoA mutase deficiency
MedGen UID:
344424
Concept ID:
C1855114
Disease or Syndrome
Isolated methylmalonic acidemia/aciduria is caused by complete or partial deficiency of the enzyme methylmalonyl-CoA mutase (mut(0) enzymatic subtype or mut(–) enzymatic subtype, respectively), a defect in the transport or synthesis of its cofactor, adenosyl-cobalamin (cblA, cblB, or cblD variant 2 type), or deficiency of the enzyme methylmalonyl-CoA epimerase. Onset of the manifestations of isolated methylmalonic acidemia/aciduria ranges from the neonatal period to adulthood. All phenotypes demonstrate periods of relative health and intermittent metabolic decompensation, usually associated with intercurrent infections and stress. In the neonatal period the disease can present with lethargy, vomiting, hypotonia, hypothermia, respiratory distress, severe ketoacidosis, hyperammonemia, neutropenia, and thrombocytopenia and can result in death. In the infantile/non-B12-responsive phenotype, the most common form, infants are normal at birth but develop lethargy, vomiting, dehydration, hepatomegaly, hypotonia, and encephalopathy. An intermediate B12-responsive phenotype can occasionally present in neonates, but usually presents in the first months or years of life; affected children exhibit anorexia, failure to thrive, hypotonia, and developmental delay, and sometimes have protein aversion and/or vomiting and lethargy after protein intake. Atypical and "benign"/adult methylmalonic acidemia are associated with increased, albeit mild, urinary excretion of methylmalonate; however, it is uncertain if some of these individuals will develop symptoms. Major secondary complications of methylmalonic acidemia include developmental delay (variable); tubulointerstitial nephritis with progressive renal failure; “metabolic stroke” (acute and chronic basal ganglia involvement); disabling movement disorder with choreoathetosis, dystonia, and para/quadriparesis; pancreatitis; growth failure; functional immune impairment; and optic nerve atrophy.
Carney triad
MedGen UID:
388099
Concept ID:
C1858592
Disease or Syndrome
A very rare disorder marked by tumors of the gastrointestinal tract (usually the stomach), tumors that form in embryonic nervous tissue in the head, neck, and torso, and tumors that form in cartilage in the lungs. Sometimes tumors also form in the adrenal glands and esophagus. Carney triad is most common in young females.
Temporal arteritis
MedGen UID:
365495
Concept ID:
C1956391
Disease or Syndrome
An autoimmune, systemic, giant cell granulomatous arteritis predominantly involving the arteries that supply blood to the central nervous system, head and eyes. Superficial arteries of the scalp that are involved tend to be enlarged and tender. Signs and symptoms include headaches, myalgias, visual disturbances, and skin necrosis.
Sarcoidosis 1
MedGen UID:
394568
Concept ID:
C2697310
Finding
Sarcoidosis is a granulomatous disorder associated with an accumulation of CD4+ T cells and a Th1 immune response. In childhood, 2 distinct types of sarcoidosis have been described (Shetty and Gedalia, 1998). Usually the disease is detected in older children by chest radiography, and the clinical manifestations are characterized by a classic triad of lung, lymph node, and eye involvement, similar to those in adults. In contrast, early-onset sarcoidosis (EOS; 609464), which usually appears in those younger than 4 years of age, is rare and has a distinct triad of skin, joint, and eye disorders, without apparent pulmonary involvement. Compared with an asymptomatic and sometimes naturally disappearing course of the disease in older children, EOS is progressive and in many cases causes severe complications, such as blindness, joint destruction, and visceral involvement.
Homocystinuria due to CBS deficiency
MedGen UID:
461694
Concept ID:
C3150344
Disease or Syndrome
Homocystinuria caused by cystathionine ß-synthase (CBS) deficiency is characterized by developmental delay/intellectual disability, ectopia lentis and/or severe myopia, skeletal abnormalities (excessive height and length of the limbs), and thromboembolism. Expressivity is variable for all of the clinical signs. Two phenotypic variants are recognized, B6-responsive homocystinuria and B6-non-responsive homocystinuria. B6-responsive homocystinuria is typically, but not always, milder than the non-responsive variant. In the majority of untreated affected individuals, ectopia lentis occurs by age eight years. Individuals are often tall and slender with an asthenic (‘marfanoid’) habitus and are prone to osteoporosis. Thromboembolism is the major cause of early death and morbidity. IQ in individuals with untreated homocystinuria ranges widely, from 10 to 138. In B6-responsive individuals the mean IQ is 79 versus 57 for those who are B6 non-responsive. Other features that may occur include: seizures, psychiatric problems, extrapyramidal signs (e.g., dystonia), hypopigmentation, malar flush, livedo reticularis, and pancreatitis.
Cholangiocarcinoma, susceptibility to
MedGen UID:
816486
Concept ID:
C3810156
Neoplastic Process
Carcinomas of the biliary tract are aggressive malignancies, with 5-year survival of less than 10%. These carcinomas arise throughout the biliary tree and are anatomically classified as either intrahepatic or extrahepatic cholangiocarcinomas. Gallbladder carcinomas also arise from the biliary tree but have distinct natural histories compared to cholangiocarcinomas, suggesting different underlying tumor biology. Cholangiocarcinoma incidence varies widely between geographic regions, reflecting the impact of different underlying etiologies. In endemic areas, liver fluke infections by O. viverrini and Clonorchis sinensis, both group I carcinogens, represent the major risk factor for cholangiocarcinomas. In nonendemic regions, other risk factors, including choledochal cysts (603003), hepatolithiasis, and primary sclerosing cholangitis (613806), are likely contributors (summary by Chan-on et al., 2013). Overall, the majority of patients lack such identifiable risk factors (summary by Jiao et al., 2013).

Recent clinical studies

Etiology

Roy M, Shatenstein B, Gaudreau P, Morais JA, Payette H
J Aging Health 2015 Mar;27(2):220-38. Epub 2014 Aug 12 doi: 10.1177/0898264314546715. [Epub ahead of print] PMID: 25117180
Leroy HA, Baroncini M, Delestret I, Florent V, Vinchon M
Childs Nerv Syst 2014 Dec;30(12):2089-95. Epub 2014 Aug 21 doi: 10.1007/s00381-014-2533-1. [Epub ahead of print] PMID: 25142692
Martone AM, Onder G, Vetrano DL, Ortolani E, Tosato M, Marzetti E, Landi F
Nutrients 2013 Oct 14;5(10):4126-33. doi: 10.3390/nu5104126. PMID: 24128975Free PMC Article
Soenen S, Chapman IM
J Am Med Dir Assoc 2013 Sep;14(9):642-8. Epub 2013 Mar 19 doi: 10.1016/j.jamda.2013.02.004. [Epub ahead of print] PMID: 23522494
Landi F, Liperoti R, Russo A, Giovannini S, Tosato M, Barillaro C, Capoluongo E, Bernabei R, Onder G
Eur J Nutr 2013 Apr;52(3):1261-8. Epub 2012 Aug 25 doi: 10.1007/s00394-012-0437-y. [Epub ahead of print] PMID: 22923016

Diagnosis

Rahmandar MH, Bawcom A, Romano ME, Hamid R
Pediatrics 2014 Dec;134(6):e1709-14. Epub 2014 Nov 3 doi: 10.1542/peds.2013-2711. [Epub ahead of print] PMID: 25367534
Vesoulis ZA, Attarian SJ, Zeller B, Cole FS
Pharmacotherapy 2014 Dec;34(12):e341-4. Epub 2014 Oct 3 doi: 10.1002/phar.1495. [Epub ahead of print] PMID: 25280267
Leroy HA, Baroncini M, Delestret I, Florent V, Vinchon M
Childs Nerv Syst 2014 Dec;30(12):2089-95. Epub 2014 Aug 21 doi: 10.1007/s00381-014-2533-1. [Epub ahead of print] PMID: 25142692
Miller S, McNutt L, McCann MA, McCorry N
J Palliat Med 2014 Apr;17(4):482-5. doi: 10.1089/jpm.2013.0324. PMID: 24702642
Martone AM, Onder G, Vetrano DL, Ortolani E, Tosato M, Marzetti E, Landi F
Nutrients 2013 Oct 14;5(10):4126-33. doi: 10.3390/nu5104126. PMID: 24128975Free PMC Article

Therapy

Rahmandar MH, Bawcom A, Romano ME, Hamid R
Pediatrics 2014 Dec;134(6):e1709-14. Epub 2014 Nov 3 doi: 10.1542/peds.2013-2711. [Epub ahead of print] PMID: 25367534
Vesoulis ZA, Attarian SJ, Zeller B, Cole FS
Pharmacotherapy 2014 Dec;34(12):e341-4. Epub 2014 Oct 3 doi: 10.1002/phar.1495. [Epub ahead of print] PMID: 25280267
Xia QC, Feng ZX, Ping CX
Altern Ther Health Med 2014 Sep-Oct;20(5):45-52. PMID: 25141371
Miller S, McNutt L, McCann MA, McCorry N
J Palliat Med 2014 Apr;17(4):482-5. doi: 10.1089/jpm.2013.0324. PMID: 24702642
Vancampfort D, Vanderlinden J, De Hert M, Soundy A, Adámkova M, Skjaerven LH, Catalán-Matamoros D, Lundvik Gyllensten A, Gómez-Conesa A, Probst M
Disabil Rehabil 2014;36(8):628-34. Epub 2013 Jul 4 doi: 10.3109/09638288.2013.808271. [Epub ahead of print] PMID: 23826882

Prognosis

Roy M, Shatenstein B, Gaudreau P, Morais JA, Payette H
J Aging Health 2015 Mar;27(2):220-38. Epub 2014 Aug 12 doi: 10.1177/0898264314546715. [Epub ahead of print] PMID: 25117180
Leroy HA, Baroncini M, Delestret I, Florent V, Vinchon M
Childs Nerv Syst 2014 Dec;30(12):2089-95. Epub 2014 Aug 21 doi: 10.1007/s00381-014-2533-1. [Epub ahead of print] PMID: 25142692
Miller S, McNutt L, McCann MA, McCorry N
J Palliat Med 2014 Apr;17(4):482-5. doi: 10.1089/jpm.2013.0324. PMID: 24702642
Martone AM, Onder G, Vetrano DL, Ortolani E, Tosato M, Marzetti E, Landi F
Nutrients 2013 Oct 14;5(10):4126-33. doi: 10.3390/nu5104126. PMID: 24128975Free PMC Article
Arezzo di Trifiletti A, Misino P, Giannantoni P, Giannantoni B, Cascino A, Fazi L, Rossi Fanelli F, Laviano A
Clin Nutr 2013 Aug;32(4):527-32. Epub 2012 Nov 20 doi: 10.1016/j.clnu.2012.11.011. [Epub ahead of print] PMID: 23218121

Clinical prediction guides

Roy M, Shatenstein B, Gaudreau P, Morais JA, Payette H
J Aging Health 2015 Mar;27(2):220-38. Epub 2014 Aug 12 doi: 10.1177/0898264314546715. [Epub ahead of print] PMID: 25117180
Vesoulis ZA, Attarian SJ, Zeller B, Cole FS
Pharmacotherapy 2014 Dec;34(12):e341-4. Epub 2014 Oct 3 doi: 10.1002/phar.1495. [Epub ahead of print] PMID: 25280267
Leroy HA, Baroncini M, Delestret I, Florent V, Vinchon M
Childs Nerv Syst 2014 Dec;30(12):2089-95. Epub 2014 Aug 21 doi: 10.1007/s00381-014-2533-1. [Epub ahead of print] PMID: 25142692
Vancampfort D, Vanderlinden J, De Hert M, Soundy A, Adámkova M, Skjaerven LH, Catalán-Matamoros D, Lundvik Gyllensten A, Gómez-Conesa A, Probst M
Disabil Rehabil 2014;36(8):628-34. Epub 2013 Jul 4 doi: 10.3109/09638288.2013.808271. [Epub ahead of print] PMID: 23826882
Martone AM, Onder G, Vetrano DL, Ortolani E, Tosato M, Marzetti E, Landi F
Nutrients 2013 Oct 14;5(10):4126-33. doi: 10.3390/nu5104126. PMID: 24128975Free PMC Article

Recent systematic reviews

Xia QC, Feng ZX, Ping CX
Altern Ther Health Med 2014 Sep-Oct;20(5):45-52. PMID: 25141371
Miller S, McNutt L, McCann MA, McCorry N
J Palliat Med 2014 Apr;17(4):482-5. doi: 10.1089/jpm.2013.0324. PMID: 24702642
Hofer M, Pozzi A, Joray M, Ott R, Hähni F, Leuenberger M, von Känel R, Stanga Z
Nutrition 2014 May;30(5):524-30. Epub 2014 Jan 29 doi: 10.1016/j.nut.2013.09.019. [Epub ahead of print] PMID: 24698345
Vancampfort D, Vanderlinden J, De Hert M, Soundy A, Adámkova M, Skjaerven LH, Catalán-Matamoros D, Lundvik Gyllensten A, Gómez-Conesa A, Probst M
Disabil Rehabil 2014;36(8):628-34. Epub 2013 Jul 4 doi: 10.3109/09638288.2013.808271. [Epub ahead of print] PMID: 23826882
Ruiz Garcia V, López-Briz E, Carbonell Sanchis R, Gonzalvez Perales JL, Bort-Marti S
Cochrane Database Syst Rev 2013 Mar 28;3:CD004310. doi: 10.1002/14651858.CD004310.pub3. PMID: 23543530

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