Format

Send to:

Choose Destination

Links from PubMed

Diabetes mellitus type 1(IDDM)

MedGen UID:
41522
Concept ID:
C0011854
Disease or Syndrome
Synonyms: Diabetes mellitus, insulin-dependent; DIABETES MELLITUS, INSULIN-DEPENDENT, 1; DIABETES MELLITUS, TYPE I; IDDM
Modes of inheritance:
Heterogeneous
MedGen UID:
67020
Concept ID:
C0242960
Organism Attribute
Source: HPO
The presence of apparently similar characters for which the genetic evidence indicates that different genes or different genetic mechanisms are involved in different pedigrees. In clinical settings genetic heterogeneity refers to the presence of a variety of genetic defects which cause the same disease, often due to mutations at different loci on the same gene, a finding common to many human diseases including ALZHEIMER DISEASE; CYSTIC FIBROSIS; LIPOPROTEIN LIPASE DEFICIENCY, FAMILIAL; and POLYCYSTIC KIDNEY DISEASES. (Rieger, et al., Glossary of Genetics: Classical and Molecular, 5th ed; Segen, Dictionary of Modern Medicine, 1992)
SNOMED CT: Type 1 diabetes mellitus (46635009); Diabetes mellitus type 1 (46635009); Type I diabetes mellitus (46635009); Diabetes mellitus type I (46635009)
 
Genes (locations): FOXP3 (Xp11.23); HNF1A (12q24.31); ITPR3 (6p21.31); OAS1 (12q24.13); PTPN22 (1p13.2)
OMIM®: 222100
HPO: HP:0100651

Definition

The type of diabetes mellitus called IDDM is a disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. It is a genetically heterogeneous autoimmune disease affecting about 0.3% of Caucasian populations (Todd, 1990). Genetic studies of IDDM have focused on the identification of loci associated with increased susceptibility to this multifactorial phenotype. The classical phenotype of diabetes mellitus is polydipsia, polyphagia, and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels. [from OMIM]

Additional description

From GHR
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. In this form of diabetes, specialized cells in the pancreas called beta cells stop producing insulin. Insulin controls how much glucose (a type of sugar) is passed from the blood into cells for conversion to energy. Lack of insulin results in the inability to use glucose for energy or to control the amount of sugar in the blood.Type 1 diabetes can occur at any age; however, it usually develops by early adulthood, most often starting in adolescence. The first signs and symptoms of the disorder are caused by high blood sugar and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, tingling or loss of feeling in the hands and feet, and weight loss. These symptoms may recur during the course of the disorder if blood sugar is not well controlled by insulin replacement therapy. Improper control can also cause blood sugar levels to become too low (hypoglycemia). This may occur when the body's needs change, such as during exercise or if eating is delayed. Hypoglycemia can cause headache, dizziness, hunger, shaking, sweating, weakness, and agitation.Uncontrolled type 1 diabetes can lead to a life-threatening complication called diabetic ketoacidosis. Without insulin, cells cannot take in glucose. A lack of glucose in cells prompts the liver to try to compensate by releasing more glucose into the blood, and blood sugar can become extremely high. The cells, unable to use the glucose in the blood for energy, respond by using fats instead. Breaking down fats to obtain energy produces waste products called ketones, which can build up to toxic levels in people with type 1 diabetes, resulting in diabetic ketoacidosis. Affected individuals may begin breathing rapidly; develop a fruity odor in the breath; and experience nausea, vomiting, facial flushing, stomach pain, and dryness of the mouth (xerostomia). In severe cases, diabetic ketoacidosis can lead to coma and death.Over many years, the chronic high blood sugar associated with diabetes may cause damage to blood vessels and nerves, leading to complications affecting many organs and tissues. The retina, which is the light-sensitive tissue at the back of the eye, can be damaged (diabetic retinopathy), leading to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) may also occur and can lead to kidney failure and end-stage renal disease (ESRD). Pain, tingling, and loss of normal sensation (diabetic neuropathy) often occur, especially in the feet. Impaired circulation and absence of the normal sensations that prompt reaction to injury can result in permanent damage to the feet; in severe cases, the damage can lead to amputation. People with type 1 diabetes are also at increased risk of heart attacks, strokes, and problems with urinary and sexual function.  https://ghr.nlm.nih.gov/condition/type-1-diabetes

Clinical features

Diabetes mellitus
MedGen UID:
8350
Concept ID:
C0011849
Disease or Syndrome
Diabetes is a disease in which your blood glucose, or blood sugar, levels are too high. Glucose comes from the foods you eat. Insulin is a hormone that helps the glucose get into your cells to give them energy. With type 1 diabetes, your body does not make insulin. With type 2 diabetes, the more common type, your body does not make or use insulin well. Without enough insulin, the glucose stays in your blood. You can also have prediabetes. This means that your blood sugar is higher than normal but not high enough to be called diabetes. Having prediabetes puts you at a higher risk of getting type 2 diabetes. Over time, having too much glucose in your blood can cause serious problems. It can damage your eyes, kidneys, and nerves. Diabetes can also cause heart disease, stroke and even the need to remove a limb. Pregnant women can also get diabetes, called gestational diabetes. Blood tests can show if you have diabetes. One type of test, the A1C, can also check on how you are managing your diabetes. Exercise, weight control and sticking to your meal plan can help control your diabetes. You should also monitor your blood glucose level and take medicine if prescribed. . NIH: National Institute of Diabetes and Digestive and Kidney Diseases.
Polyuria
MedGen UID:
19404
Concept ID:
C0032617
Sign or Symptom
An increased rate of urine production.
Polyphagia
MedGen UID:
9369
Concept ID:
C0020505
Finding
A neurological anomaly with gross overeating associated with an abnormally strong desire or need to eat.
Polydipsia
MedGen UID:
43214
Concept ID:
C0085602
Sign or Symptom
Excessive thirst manifested by excessive fluid intake.
Polyuria
MedGen UID:
19404
Concept ID:
C0032617
Sign or Symptom
An increased rate of urine production.
Abnormality of the immune system
MedGen UID:
867388
Concept ID:
C4021753
Anatomical Abnormality
An abnormality of the immune system.
Diabetes mellitus
MedGen UID:
8350
Concept ID:
C0011849
Disease or Syndrome
Diabetes is a disease in which your blood glucose, or blood sugar, levels are too high. Glucose comes from the foods you eat. Insulin is a hormone that helps the glucose get into your cells to give them energy. With type 1 diabetes, your body does not make insulin. With type 2 diabetes, the more common type, your body does not make or use insulin well. Without enough insulin, the glucose stays in your blood. You can also have prediabetes. This means that your blood sugar is higher than normal but not high enough to be called diabetes. Having prediabetes puts you at a higher risk of getting type 2 diabetes. Over time, having too much glucose in your blood can cause serious problems. It can damage your eyes, kidneys, and nerves. Diabetes can also cause heart disease, stroke and even the need to remove a limb. Pregnant women can also get diabetes, called gestational diabetes. Blood tests can show if you have diabetes. One type of test, the A1C, can also check on how you are managing your diabetes. Exercise, weight control and sticking to your meal plan can help control your diabetes. You should also monitor your blood glucose level and take medicine if prescribed. . NIH: National Institute of Diabetes and Digestive and Kidney Diseases.
Hyperglycemia
MedGen UID:
5689
Concept ID:
C0020456
Disease or Syndrome
Hyperglycemia means high blood sugar or glucose. Glucose comes from the foods you eat. Insulin is a hormone that moves glucose into your cells to give them energy. Hyperglycemia happens when your body doesn't make enough insulin or can't use it the right way. People with diabetes can get hyperglycemia from not eating the right foods or not taking medicines correctly. Other problems that can raise blood sugar include infections, certain medicines, hormone imbalances, or severe illnesses.
Ketoacidosis
MedGen UID:
67434
Concept ID:
C0220982
Pathologic Function
Acidosis resulting from accumulation of ketone bodies.
Diabetes mellitus
MedGen UID:
8350
Concept ID:
C0011849
Disease or Syndrome
Diabetes is a disease in which your blood glucose, or blood sugar, levels are too high. Glucose comes from the foods you eat. Insulin is a hormone that helps the glucose get into your cells to give them energy. With type 1 diabetes, your body does not make insulin. With type 2 diabetes, the more common type, your body does not make or use insulin well. Without enough insulin, the glucose stays in your blood. You can also have prediabetes. This means that your blood sugar is higher than normal but not high enough to be called diabetes. Having prediabetes puts you at a higher risk of getting type 2 diabetes. Over time, having too much glucose in your blood can cause serious problems. It can damage your eyes, kidneys, and nerves. Diabetes can also cause heart disease, stroke and even the need to remove a limb. Pregnant women can also get diabetes, called gestational diabetes. Blood tests can show if you have diabetes. One type of test, the A1C, can also check on how you are managing your diabetes. Exercise, weight control and sticking to your meal plan can help control your diabetes. You should also monitor your blood glucose level and take medicine if prescribed. . NIH: National Institute of Diabetes and Digestive and Kidney Diseases.

Term Hierarchy

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, weight loss, abdominal pain, anorexia, lactose intolerance, abdominal distention, and irritability) and/or highly variable non-gastrointestinal findings (iron deficiency anemia, dermatitis herpetiformis, chronic fatigue, joint pain/inflammation, 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.
Polyglandular autoimmune syndrome, type 1
MedGen UID:
39125
Concept ID:
C0085859
Disease or Syndrome
Autoimmune polyglandular syndrome type I is characterized by the presence of 2 of 3 major clinical symptoms: Addison disease, and/or hypoparathyroidism, and/or chronic mucocutaneous candidiasis (Neufeld et al., 1981).
Insulin-dependent diabetes mellitus secretory diarrhea syndrome
MedGen UID:
83339
Concept ID:
C0342288
Disease or Syndrome
IPEX (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked) syndrome is characterized by systemic autoimmunity, typically beginning in the first year of life. Presentation is most commonly the clinical triad of watery diarrhea, eczematous dermatitis, and endocrinopathy (most commonly insulin-dependent diabetes mellitus). Most children have other autoimmune phenomena including Coombs-positive anemia, autoimmune thrombocytopenia, autoimmune neutropenia, and tubular nephropathy. Without aggressive immunosuppression or bone marrow transplantation, the majority of affected males die within the first one to two years of life from metabolic derangements or sepsis; a few with a milder phenotype have survived into the second or third decade of life.
Pearson marrow-pancreas syndrome
MedGen UID:
90997
Concept ID:
C0342773
Mitochondrial DNA (mtDNA) deletion syndromes predominantly comprise three overlapping phenotypes that are usually simplex (i.e., a single occurrence in a family), but rarely may be observed in different members of the same family or may evolve in a given individual over time. The three phenotypes are Kearns-Sayre syndrome (KSS), Pearson syndrome, and progressive external ophthalmoplegia (PEO). Rarely Leigh syndrome can be a manifestation of a mtDNA deletion. KSS is a multisystem disorder defined by the triad of onset before age 20 years, pigmentary retinopathy, and PEO. In addition, affected individuals have at least one of the following: cardiac conduction block, cerebrospinal fluid protein concentration greater than 100 mg/dL, or cerebellar ataxia. Onset is usually in childhood. Pearson syndrome is characterized by sideroblastic anemia and exocrine pancreas dysfunction and is usually fatal in infancy. PEO, characterized by ptosis, paralysis of the extraocular muscles (ophthalmoplegia), oropharyngeal weakness, and variably severe proximal limb weakness, is relatively benign.
Wolcott-Rallison dysplasia
MedGen UID:
140926
Concept ID:
C0432217
Disease or Syndrome
Wolcott-Rallison syndrome is a rare autosomal recessive disorder characterized by permanent neonatal or early infancy insulin-dependent diabetes. Epiphyseal dysplasia, osteoporosis, and growth retardation develop at a later age. Other frequent multisystem manifestations include hepatic and renal dysfunction, mental retardation, and cardiovascular abnormalities (summary by Delepine et al., 2000).
Diabetes mellitus, insulin-dependent, 2
MedGen UID:
377588
Concept ID:
C1852092
Disease or Syndrome
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. In this form of diabetes, specialized cells in the pancreas called beta cells stop producing insulin. Insulin controls how much glucose (a type of sugar) is passed from the blood into cells for conversion to energy. Lack of insulin results in the inability to use glucose for energy or to control the amount of sugar in the blood.Type 1 diabetes can occur at any age; however, it usually develops by early adulthood, most often starting in adolescence. The first signs and symptoms of the disorder are caused by high blood sugar and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, tingling or loss of feeling in the hands and feet, and weight loss. These symptoms may recur during the course of the disorder if blood sugar is not well controlled by insulin replacement therapy. Improper control can also cause blood sugar levels to become too low (hypoglycemia). This may occur when the body's needs change, such as during exercise or if eating is delayed. Hypoglycemia can cause headache, dizziness, hunger, shaking, sweating, weakness, and agitation.Uncontrolled type 1 diabetes can lead to a life-threatening complication called diabetic ketoacidosis. Without insulin, cells cannot take in glucose. A lack of glucose in cells prompts the liver to try to compensate by releasing more glucose into the blood, and blood sugar can become extremely high. The cells, unable to use the glucose in the blood for energy, respond by using fats instead. Breaking down fats to obtain energy produces waste products called ketones, which can build up to toxic levels in people with type 1 diabetes, resulting in diabetic ketoacidosis. Affected individuals may begin breathing rapidly; develop a fruity odor in the breath; and experience nausea, vomiting, facial flushing, stomach pain, and dryness of the mouth (xerostomia). In severe cases, diabetic ketoacidosis can lead to coma and death.Over many years, the chronic high blood sugar associated with diabetes may cause damage to blood vessels and nerves, leading to complications affecting many organs and tissues. The retina, which is the light-sensitive tissue at the back of the eye, can be damaged (diabetic retinopathy), leading to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) may also occur and can lead to kidney failure and end-stage renal disease (ESRD). Pain, tingling, and loss of normal sensation (diabetic neuropathy) often occur, especially in the feet. Impaired circulation and absence of the normal sensations that prompt reaction to injury can result in permanent damage to the feet; in severe cases, the damage can lead to amputation. People with type 1 diabetes are also at increased risk of heart attacks, strokes, and problems with urinary and sexual function.
Diabetes mellitus, insulin-dependent, 15
MedGen UID:
401019
Concept ID:
C1866519
Disease or Syndrome
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. In this form of diabetes, specialized cells in the pancreas called beta cells stop producing insulin. Insulin controls how much glucose (a type of sugar) is passed from the blood into cells for conversion to energy. Lack of insulin results in the inability to use glucose for energy or to control the amount of sugar in the blood.Type 1 diabetes can occur at any age; however, it usually develops by early adulthood, most often starting in adolescence. The first signs and symptoms of the disorder are caused by high blood sugar and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, tingling or loss of feeling in the hands and feet, and weight loss. These symptoms may recur during the course of the disorder if blood sugar is not well controlled by insulin replacement therapy. Improper control can also cause blood sugar levels to become too low (hypoglycemia). This may occur when the body's needs change, such as during exercise or if eating is delayed. Hypoglycemia can cause headache, dizziness, hunger, shaking, sweating, weakness, and agitation.Uncontrolled type 1 diabetes can lead to a life-threatening complication called diabetic ketoacidosis. Without insulin, cells cannot take in glucose. A lack of glucose in cells prompts the liver to try to compensate by releasing more glucose into the blood, and blood sugar can become extremely high. The cells, unable to use the glucose in the blood for energy, respond by using fats instead. Breaking down fats to obtain energy produces waste products called ketones, which can build up to toxic levels in people with type 1 diabetes, resulting in diabetic ketoacidosis. Affected individuals may begin breathing rapidly; develop a fruity odor in the breath; and experience nausea, vomiting, facial flushing, stomach pain, and dryness of the mouth (xerostomia). In severe cases, diabetic ketoacidosis can lead to coma and death.Over many years, the chronic high blood sugar associated with diabetes may cause damage to blood vessels and nerves, leading to complications affecting many organs and tissues. The retina, which is the light-sensitive tissue at the back of the eye, can be damaged (diabetic retinopathy), leading to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) may also occur and can lead to kidney failure and end-stage renal disease (ESRD). Pain, tingling, and loss of normal sensation (diabetic neuropathy) often occur, especially in the feet. Impaired circulation and absence of the normal sensations that prompt reaction to injury can result in permanent damage to the feet; in severe cases, the damage can lead to amputation. People with type 1 diabetes are also at increased risk of heart attacks, strokes, and problems with urinary and sexual function.
Diabetes mellitus, insulin-dependent, 20
MedGen UID:
382706
Concept ID:
C2675866
Disease or Syndrome
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. In this form of diabetes, specialized cells in the pancreas called beta cells stop producing insulin. Insulin controls how much glucose (a type of sugar) is passed from the blood into cells for conversion to energy. Lack of insulin results in the inability to use glucose for energy or to control the amount of sugar in the blood.Type 1 diabetes can occur at any age; however, it usually develops by early adulthood, most often starting in adolescence. The first signs and symptoms of the disorder are caused by high blood sugar and may include frequent urination (polyuria), excessive thirst (polydipsia), fatigue, blurred vision, tingling or loss of feeling in the hands and feet, and weight loss. These symptoms may recur during the course of the disorder if blood sugar is not well controlled by insulin replacement therapy. Improper control can also cause blood sugar levels to become too low (hypoglycemia). This may occur when the body's needs change, such as during exercise or if eating is delayed. Hypoglycemia can cause headache, dizziness, hunger, shaking, sweating, weakness, and agitation.Uncontrolled type 1 diabetes can lead to a life-threatening complication called diabetic ketoacidosis. Without insulin, cells cannot take in glucose. A lack of glucose in cells prompts the liver to try to compensate by releasing more glucose into the blood, and blood sugar can become extremely high. The cells, unable to use the glucose in the blood for energy, respond by using fats instead. Breaking down fats to obtain energy produces waste products called ketones, which can build up to toxic levels in people with type 1 diabetes, resulting in diabetic ketoacidosis. Affected individuals may begin breathing rapidly; develop a fruity odor in the breath; and experience nausea, vomiting, facial flushing, stomach pain, and dryness of the mouth (xerostomia). In severe cases, diabetic ketoacidosis can lead to coma and death.Over many years, the chronic high blood sugar associated with diabetes may cause damage to blood vessels and nerves, leading to complications affecting many organs and tissues. The retina, which is the light-sensitive tissue at the back of the eye, can be damaged (diabetic retinopathy), leading to vision loss and eventual blindness. Kidney damage (diabetic nephropathy) may also occur and can lead to kidney failure and end-stage renal disease (ESRD). Pain, tingling, and loss of normal sensation (diabetic neuropathy) often occur, especially in the feet. Impaired circulation and absence of the normal sensations that prompt reaction to injury can result in permanent damage to the feet; in severe cases, the damage can lead to amputation. People with type 1 diabetes are also at increased risk of heart attacks, strokes, and problems with urinary and sexual function.
Renal tubulopathy, diabetes mellitus, and cerebellar ataxia
MedGen UID:
463309
Concept ID:
C3151959
Disease or Syndrome
Ataxia, combined cerebellar and peripheral, with hearing loss and diabetes mellitus
MedGen UID:
863873
Concept ID:
C4015436
Disease or Syndrome
Coronary artery disease, autosomal dominant, 1
MedGen UID:
330802
Concept ID:
C1842247
Disease or Syndrome
Coronary artery disease (CAD) and its most important complication, acute myocardial infarction (MI), are leading causes of death and disability in the developed world. Multiple risk factors for CAD/MI have been identified, including family history, hypertension, hypercholesterolemia, obesity, smoking, and diabetes. Several genomewide scans of affected sib pairs have identified susceptibility loci for CAD, e.g., 607339 and 300464.

Recent clinical studies

Etiology

Kramer G, Kuniss N, Kloos C, Lehmann T, Müller N, Wolf G, Lorkowski S, Müller UA
Diabetes Res Clin Pract 2016 Jun;116:299-305. Epub 2016 Apr 23 doi: 10.1016/j.diabres.2016.04.025. PMID: 27321348
Kolesnikova LI, Kolesnikov SI, Darenskaya MA, Grebenkina LA, Semenova NV, Osipova EV, Gnusina SV, Bardymova TA
Bull Exp Biol Med 2015 Dec;160(2):278-80. Epub 2015 Dec 8 doi: 10.1007/s10517-015-3149-5. PMID: 26642791
Klamt S, Vogel M, Kapellen TM, Hiemisch A, Prenzel F, Zachariae S, Ceglarek U, Thiery J, Kiess W
Pediatr Diabetes 2015 Nov;16(7):493-503. Epub 2015 Jul 17 doi: 10.1111/pedi.12298. PMID: 26189407
Myśliwska J, Ryba-Stanisławowska M, Smardzewski M, Słomiński B, Myśliwiec M, Siebert J
Mediators Inflamm 2014;2014:946209. Epub 2014 Jun 2 doi: 10.1155/2014/946209. PMID: 25053869Free PMC Article
Hilmi A, Pasternak Y, Friger M, Loewenthal N, Haim A, Hershkovitz E
Isr Med Assoc J 2013 Jun;15(6):267-70. PMID: 23882887

Diagnosis

Pereira KC, Pugliese BS, Guimarães MM, Gama MP
J Pediatr Adolesc Gynecol 2015 Feb;28(1):66-71. PMID: 25705760
Hilmi A, Pasternak Y, Friger M, Loewenthal N, Haim A, Hershkovitz E
Isr Med Assoc J 2013 Jun;15(6):267-70. PMID: 23882887
Dizdarevic-Bostandic A, Burekovic A, Velija-Asimi Z, Godinjak A
Med Arch 2013;67(3):160-1. PMID: 23848031
van Schinkel LD, Auger D, van Elderen SG, Ajmone Marsan N, Delgado V, Lamb HJ, Ng AC, Smit JW, Bax JJ, Westenberg JJ, de Roos A
Int J Cardiovasc Imaging 2013 Mar;29(3):633-41. Epub 2012 Sep 22 doi: 10.1007/s10554-012-0125-2. PMID: 23001157
Matanovic D, Popovic S, Parapid B, Petronic I, Cirovic D, Nikolic D
Arch Ital Biol 2012 Dec;150(4):251-8. PMID: 23479458

Therapy

Kramer G, Kuniss N, Kloos C, Lehmann T, Müller N, Wolf G, Lorkowski S, Müller UA
Diabetes Res Clin Pract 2016 Jun;116:299-305. Epub 2016 Apr 23 doi: 10.1016/j.diabres.2016.04.025. PMID: 27321348
Polizzi S, Ferrara G, Restaino S, Rinaldi S, Tognetto D
J Basic Clin Physiol Pharmacol 2015 Mar;26(2):161-3. doi: 10.1515/jbcpp-2014-0058. PMID: 25153234
Myśliwska J, Ryba-Stanisławowska M, Smardzewski M, Słomiński B, Myśliwiec M, Siebert J
Mediators Inflamm 2014;2014:946209. Epub 2014 Jun 2 doi: 10.1155/2014/946209. PMID: 25053869Free PMC Article
Hilmi A, Pasternak Y, Friger M, Loewenthal N, Haim A, Hershkovitz E
Isr Med Assoc J 2013 Jun;15(6):267-70. PMID: 23882887
Matanovic D, Popovic S, Parapid B, Petronic I, Cirovic D, Nikolic D
Arch Ital Biol 2012 Dec;150(4):251-8. PMID: 23479458

Prognosis

Kolesnikova LI, Kolesnikov SI, Darenskaya MA, Grebenkina LA, Semenova NV, Osipova EV, Gnusina SV, Bardymova TA
Bull Exp Biol Med 2015 Dec;160(2):278-80. Epub 2015 Dec 8 doi: 10.1007/s10517-015-3149-5. PMID: 26642791
Dizdarevic-Bostandic A, Burekovic A, Velija-Asimi Z, Godinjak A
Med Arch 2013;67(3):160-1. PMID: 23848031
van Schinkel LD, Auger D, van Elderen SG, Ajmone Marsan N, Delgado V, Lamb HJ, Ng AC, Smit JW, Bax JJ, Westenberg JJ, de Roos A
Int J Cardiovasc Imaging 2013 Mar;29(3):633-41. Epub 2012 Sep 22 doi: 10.1007/s10554-012-0125-2. PMID: 23001157
Matanovic D, Popovic S, Parapid B, Petronic I, Cirovic D, Nikolic D
Arch Ital Biol 2012 Dec;150(4):251-8. PMID: 23479458
Suláková T, Janda J, Cerná J, Janštová V, Feber J
J Hum Hypertens 2012 Jun;26(6):357-64. Epub 2011 May 5 doi: 10.1038/jhh.2011.38. PMID: 21544085

Clinical prediction guides

Carneiro VL, Fraiz FC, Ferreira Fde M, Pintarelli TP, Oliveira AC, Boguszewski MC
Arch Endocrinol Metab 2015 Dec;59(6):535-40. doi: 10.1590/2359-3997000000117. PMID: 26677088
Polizzi S, Ferrara G, Restaino S, Rinaldi S, Tognetto D
J Basic Clin Physiol Pharmacol 2015 Mar;26(2):161-3. doi: 10.1515/jbcpp-2014-0058. PMID: 25153234
Nobis S, Lehr D, Ebert DD, Berking M, Heber E, Baumeister H, Becker A, Snoek F, Riper H
BMC Psychiatry 2013 Nov 15;13:306. doi: 10.1186/1471-244X-13-306. PMID: 24238346Free PMC Article
van Schinkel LD, Auger D, van Elderen SG, Ajmone Marsan N, Delgado V, Lamb HJ, Ng AC, Smit JW, Bax JJ, Westenberg JJ, de Roos A
Int J Cardiovasc Imaging 2013 Mar;29(3):633-41. Epub 2012 Sep 22 doi: 10.1007/s10554-012-0125-2. PMID: 23001157
Suláková T, Janda J, Cerná J, Janštová V, Feber J
J Hum Hypertens 2012 Jun;26(6):357-64. Epub 2011 May 5 doi: 10.1038/jhh.2011.38. PMID: 21544085

Recent systematic reviews

Dai YN, Yu WL, Zhu HT, Ding JX, Yu CH, Li YM
World J Gastroenterol 2015 May 7;21(17):5407-16. doi: 10.3748/wjg.v21.i17.5407. PMID: 25954115Free PMC Article
Visser J, Snel M, Van Vliet HA
Cochrane Database Syst Rev 2013 Mar 28;(3):CD003990. doi: 10.1002/14651858.CD003990.pub4. PMID: 23543528
Yu ZY, Chen LS, Zhang LC, Zhou TB
Nephrology (Carlton) 2012 Jul;17(5):480-7. doi: 10.1111/j.1440-1797.2012.01592.x. PMID: 22385293
Codner E, Soto N, Merino PM
Pediatr Diabetes 2012 Feb;13(1):108-23. Epub 2011 Oct 13 doi: 10.1111/j.1399-5448.2011.00825.x. PMID: 21995767
Visser J, Snel M, Van Vliet HA
Cochrane Database Syst Rev 2006 Oct 18;(4):CD003990. doi: 10.1002/14651858.CD003990.pub3. PMID: 17054193

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center