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Ependymoma Wikipedia

.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). "Ch. 28 The central nervous system".

RELA, C11orf95, EPHB2, GDNF, RTBDN, BCL7C, RAB3A, ZNF668, TP53, NF2, IDH1, APC, TSC2, ERBB2, MSH2, MSH6, IFNG, MLH1, SETBP1, TSC1, PMS2, CDKN2A, YAP1, EGFR, MME, VEGFA, OLIG2, MKI67, MGMT, MDM2, MIB1, TP73, TTR, PTEN, MYCN, TNC, MAMLD1, L1CAM, EPB41L3, MEN1, FGFR1, NOTCH1, H3P10, EZHIP, NCL, ANXA1, CD274, ATRX, SST, CCND1, DAPK1, RASSF1, MIR17, NES, CDKN2B, MUC1, CD44, TNFRSF10C, PROM1, ABCB1, PDGFRA, SLC9A3R1, IL6, KIT, CASP8, FGFR3, DCX, HIC1, SOX10, SMARCB1, ARHGAP24, ETFA, GFAP, TNFSF10, SYP, GATD3A, LINC00899, MIR146B, IL18R1, ABCC8, ZNF148, KRT75, MIR449A, STC1, PSCA, CLDN5, TRERNA1, TERT, LOC110806263, TPR, TIMP3, LINC02210-CRHR1, THBS1, ABCG2, SIK1B, TSPAN4, TWIST1, UBE2N, GATD3B, TDG, VEGFB, ZEB1, SYT1, AZIN2, MVP, MIR10B, DNAJC15, ZMYND10, SHC3, TET2, FBXW7, BEX1, MIR10A, MIR100, LINC01194, HES4, GADL1, ZFHX4, SIK1, ARMC9, ESX1, C1orf194, TP53INP1, GLS2, CBY1, MIR330, KIF4A, EBI3, MIR135B, AKR1A1, MIR34C, TUBB3, MIR29A, LRIG3, HOXB13, MIR24-1, IPO7, MIR221, MIR19A, MXD4, MIR181C, MIR15A, DICER1, HEY2, STAT3, JAG1, SPINK1, EPO, MECOM, EZH2, FCGR1A, FHIT, FOXJ1, FLT1, GH1, GNAO1, HOXA9, HES1, HTC2, HTR1B, IDH2, IGF2, IGFBP2, IGFBP3, IGFBP5, IL1R1, CXCL8, JAG2, JAK2, ERCC1, EPB41, SOX11, S1PR3, AQP1, ASAH1, BDNF, BRAF, CALCA, CALCR, CALR, CAPS, CAV1, RUNX1, CD34, CD38, CD151, CDK6, CHI3L1, CCR7, CRHR1, CTNNB1, DAXX, DRD1, DRD2, KDR, LAMA2, RPSA, STMN1, PTPRS, RAC2, RAD51, ALK, RBL2, RFX3, RRM1, S100A1, S100A2, S100A4, S100A6, S100A12, S100B, SHH, SLC6A8, SMN1, SMN2, SNCA, SNCG, SOX4, SOX9, PTPRA, PTGS2, PLG, NFIC, LRP1, MAP2, MDM4, MET, CD99, ABCC1, MSH3, NELL2, NF1, NFKB1, PIK3CG, NGF, OTX2, PAX5, PAX6, PCNA, PDGFRB, PIK3CA, PIK3CB, PIK3CD, RARB
- Ependymoma Orphanet
  
  Ependymoma is the most frequent intramedullary tumor in adults (but accounts for only 10-12% of pediatric central nervous system tumors), and can be benign or anaplastic. Ependymoma arise from the ependymal cells of the cerebral ventricles, corticle rests and central canal of the spinal cord, and manifest with variable symptoms such headache, vomiting, seizures, focal neurological signs and loss of vision and can cause obstructive hydrocephalus in some cases.
- Ependymal Tumor Orphanet
  
  A tumor of neurectodermal origin arising from ependymal cells that line the ventricles and central canal of the spinal cord, that can occur in both children and adults, and that is characterized by wide a range of clinical manifestations depending on the location of the tumor, such as intracranial hypertension for tumors originating in the posterior fossa, behavioural changes and pyramidal signs for supratentorial tumors, and dysesthesia for tumors of the spinal cord. They can be classified as myxopapillary ependymoma, subependymoma, ependymoma (low grade tumors) or anaplastic ependymoma (grade III tumors).
Caudal Regression Syndrome Wikipedia

In 2012, Spencer West, a man with sacral agenesis and both legs amputated, climbed Mount Kilimanjaro using only his hands. [6] Society [ edit ] Notable cases [ edit ] Johnny Eck , American freak show performer Kenny Easterday , played a fictionalized version of himself in the film Kenny Kurt Fearnley , Australian wheelchair racer Bobby Martin , American footballer Jessica Rogers , American wheelchair racer and swimmer, founder and President of iSACRA (International Caudal Regression Syndrome Association) Rose Siggins , actress ( American Horror Story: Freak Show ) [7] Victoria Pendergast , first female Australian sit-skier at Winter Paralympics Rebecca Dubber , New Zealand para-swimmer and Rio 2016 Paralympic bronze medalist Kevin McKee , two-times olympic champion and two-times world champion in sledge hockey References [ edit ] ^ Sonek JD, Gabbe SG, Landon MB, Stempel LE, Foley MR, Shubert-Moell K (March 1990). "Antenatal diagnosis of sacral agenesis syndrome in a pregnancy complicated by diabetes mellitus".

VANGL1, FUZ, TBXT, ZIC3, VANGL2, PCSK5, GDF6, FANCB, PTH1R, RYR1, CCL2, HAAO, MNX1, SHH, TBX1
Strain (Injury) Wikipedia

PMID 26618057 . ^ a b Mulcahey, Mary K. (June 2020). "Sprains, Strains and Other Soft-Tissue Injuries" .
- Muscle Strains Mayo Clinic
  
  Overview A muscle strain is an injury to a muscle or a tendon — the fibrous tissue that connects muscles to bones. Minor injuries may only overstretch a muscle or tendon, while more severe injuries may involve partial or complete tears in these tissues. Sometimes called pulled muscles, strains commonly occur in the lower back and in the muscles at the back of the thigh (hamstrings). The difference between a strain and a sprain is that a strain involves an injury to a muscle or to the band of tissue that attaches a muscle to a bone, while a sprain injures the bands of tissue that connect two bones together. Initial treatment includes rest, ice, compression and elevation. Mild strains can be successfully treated at home.
Exanthem Wikipedia

PMID 11214144 . ^ Altman, Lawrence K (November 30, 1982). "THE DOCTOR'S WORLD" .

HLA-B, MVK, C1QA, IL1RN, NOD2, GJA1, NLRP3, HLA-DRB1, CTLA4, PIK3R1, APOA1, SDHB, KRT5, TRPS1, KDSR, FGA, FBN1, NAXD, MEFV, EGFR, ERCC5, ERCC4, ERCC3, ERCC2, TNFRSF1B, TNFRSF1A, ENPP1, LBR, GJB3, GLUL, IL17RA, IGLL1, IGHM, PTPN22, IL6, RFXANK, CIITA, IKBKG, BLNK, SPINK5, POMP, ZAP70, HLCS, HLA-DPB1, HLA-DPA1, DNASE1L3, PDGFRA, LMBRD1, SMARCAD1, LRRC8A, MIF, CD28, RFX5, GJB4, BTK, BTD, RFXAP, KIT, LACC1, B2M, TEK, TCF3, ABCC6, SLC6A19, STAT3, SDHA, AK2, SDHC, RAG2, IL2RG, IL17F, LYZ, NLRC4, PRTN3, DCLRE1C, CLEC7A, PSMB4, PSMB8, PSMB9, COX4I2, IL17RC, TRAF3IP2, JAK3, CD79B, CD79A, NLRP12, RAG1, TP53, GPT, HLA-A, PTH1R, RUNX2, EGF, IFNG, NAT2, PIK3CA, CCR4, PTHLH, BRAF, TNFRSF11A, TNFSF11, PTH, PAEP, CD274, KRAS, IL5, CARD14, FAM20A, CSF3, GH1, HPGDS, TNFRSF8, AREG, ADNP, SYP, TSLP, TRIM21, SST, STAT1, SPRTN, TNF, CDAGS, HAVCR2, TGFB1, IL33, MIR126, MUC16, MIR31, MIR146A, TGFA, IL21, TIRAP, RBM45, UNC13D, IFIH1, ASPN, ENOSF1, ODAM, PGRMC1, GNLY, MRPL28, SUB1, SAE1, ADAMTS1, SDS, SATB2, RECQL4, DIRAS3, NAE1, IL1RL2, SMUG1, ABCB11, NXT1, SMN2, IL22, SIRT6, ARID4B, XRCC1, UBASH3A, TPI1, CCL27, SOD1, A1BG, SMN1, SMARCB1, CYBB, CYP2C9, CYP2E1, CYP27B1, NQO1, DLX4, DMP1, DSG1, EEC1, EIF4EBP1, ENO1, EREG, ESAT, GATA1, GNRH1, HMGB1, HSPA8, IAPP, IDH1, CTSK, CSTA, MAPK14, SERPING1, ACTB, AKT1, ALPP, AMBN, AR, RHOH, BCL6, BST2, CASP3, CRYZ, CD1A, CD34, CD44, CD68, CDKN2B, CFTR, CKB, CPA1, IDH2, IFNA1, IFNA13, PTEN, TNFRSF11B, PDCD1, CFP, ABCB1, PHB, PIK3CB, PIK3CD, PIK3CG, PTGS2, NPHS1, PLAAT4, SERPINB4, CCL11, CCL17, CCL22, SDHD, SLC1A3, SLC22A1, OPA1, NM, CCN1, LDHB, IL1B, IL2, IL4, CXCL8, IL9, IL10, IL17A, CXCL10, LGALS3, MTRR, LGALS9, LHCGR, ADAM11, MECP2, KMT2A, MMP2, MMP9, MPO, H3P9
- Rash Wikipedia
  
  For other uses, see Rash (disambiguation) . This article needs additional citations for verification . Please help improve this article by adding citations to reliable sources . Unsourced material may be challenged and removed. Find sources: "Rash" – news · newspapers · books · scholar · JSTOR ( January 2008 ) ( Learn how and when to remove this template message ) Rash A diffuse rash on the back of a male Specialty Dermatology A rash is a change of the human skin which affects its color, appearance, or texture. A rash may be localized in one part of the body, or affect all the skin. Rashes may cause the skin to change color, itch , become warm, bumpy, chapped , dry, cracked or blistered , swell, and may be painful.
Thunderstorm Asthma Wikipedia

PMID 18587040 ^ Forouzan A, Masoumi K, Haddadzadeh Shoushtari M, Idani E, Tirandaz F, Feli M, Assarehzadegan MA, Asgari Darian A.
Flock Worker's Lung Wikipedia

. ^ a b c d Eschenbacher, W. L.; Kreiss, K.; Lougheed, M. D.; Pransky, G. S.; Day, B.; Castellan, R.
Paget–schroetter Disease Wikipedia

.; Wells, Philip S.; Gould, Michael K. (2012-02-01). "Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines" .
Hypertensive Retinopathy Wikipedia

See also [ edit ] Hypertensive crisis List of systemic diseases with ocular manifestations Ophthalmology Optometry References [ edit ] ^ a b Bhargava, M; Ikram, M K; Wong, T Y (2011). "How does hypertension affect your eyes?"

TMEM127, MDH2, SDHB, SDHA, RET, VHL, SLC25A11, KIF1B, MAX, SDHD, SDHAF2, HSD11B2, GDNF, FH, DLST, SDHC, ANO1, CTRL, DLD, PSMD9, PSMB10, IKBKB, EDN1, RAC1
Hidradenitis Wikipedia

McGraw-Hill. ISBN 0-07-138076-0 . ^ Sellheyer K, Krahl D (July 2005). " " Hidradenitis suppurativa" is acne inversa!

MC5R
Ulnar Collateral Ligament Injury Of The Thumb Wikipedia

Sports injuries accounted for most of the remaining injuries, with only 2.4% acquired as a result of skiing injuries. [6] Treatment [ edit ] A post-operative photo of repair of a complete rupture of the ulnar collateral ligament. Note the K-wire to brace the joint. The ulnar collateral ligament is an important stabilizer of the thumb.
Argininemia Wikipedia

External links [ edit ] Classification D ICD - 10 : E72.2 ICD - 10-CM : E72.21 OMIM : 207800 MeSH : D020162 DiseasesDB : 29677 External resources eMedicine : ped/132 GeneReviews : Arginase Deficiency Orphanet : 90 Scholia has a topic profile for Argininemia . v t e Inborn error of amino acid metabolism K → acetyl-CoA Lysine /straight chain Glutaric acidemia type 1 type 2 Hyperlysinemia Pipecolic acidemia Saccharopinuria Leucine 3-hydroxy-3-methylglutaryl-CoA lyase deficiency 3-Methylcrotonyl-CoA carboxylase deficiency 3-Methylglutaconic aciduria 1 Isovaleric acidemia Maple syrup urine disease Tryptophan Hypertryptophanemia G G→ pyruvate → citrate Glycine D-Glyceric acidemia Glutathione synthetase deficiency Sarcosinemia Glycine → Creatine : GAMT deficiency Glycine encephalopathy G→ glutamate → α-ketoglutarate Histidine Carnosinemia Histidinemia Urocanic aciduria Proline Hyperprolinemia Prolidase deficiency Glutamate / glutamine SSADHD G→ propionyl-CoA → succinyl-CoA Valine Hypervalinemia Isobutyryl-CoA dehydrogenase deficiency Maple syrup urine disease Isoleucine 2-Methylbutyryl-CoA dehydrogenase deficiency Beta-ketothiolase deficiency Maple syrup urine disease Methionine Cystathioninuria Homocystinuria Hypermethioninemia General BC / OA Methylmalonic acidemia Methylmalonyl-CoA mutase deficiency Propionic acidemia G→ fumarate Phenylalanine / tyrosine Phenylketonuria 6-Pyruvoyltetrahydropterin synthase deficiency Tetrahydrobiopterin deficiency Tyrosinemia Alkaptonuria / Ochronosis Tyrosinemia type I Tyrosinemia type II Tyrosinemia type III / Hawkinsinuria Tyrosine → Melanin Albinism : Ocular albinism ( 1 ) Oculocutaneous albinism ( Hermansky–Pudlak syndrome ) Waardenburg syndrome Tyrosine → Norepinephrine Dopamine beta hydroxylase deficiency reverse: Brunner syndrome G→ oxaloacetate Urea cycle / Hyperammonemia ( arginine aspartate ) Argininemia Argininosuccinic aciduria Carbamoyl phosphate synthetase I deficiency Citrullinemia N-Acetylglutamate synthase deficiency Ornithine transcarbamylase deficiency / translocase deficiency Transport / IE of RTT Solute carrier family : Cystinuria Hartnup disease Iminoglycinuria Lysinuric protein intolerance Fanconi syndrome : Oculocerebrorenal syndrome Cystinosis Other 2-Hydroxyglutaric aciduria Aminoacylase 1 deficiency Ethylmalonic encephalopathy Fumarase deficiency Trimethylaminuria v t e Medicine Specialties and subspecialties Surgery Cardiac surgery Cardiothoracic surgery Colorectal surgery Eye surgery General surgery Neurosurgery Oral and maxillofacial surgery Orthopedic surgery Hand surgery Otolaryngology ENT Pediatric surgery Plastic surgery Reproductive surgery Surgical oncology Transplant surgery Trauma surgery Urology Andrology Vascular surgery Internal medicine Allergy / Immunology Angiology Cardiology Endocrinology Gastroenterology Hepatology Geriatrics Hematology Hospital medicine Infectious disease Nephrology Oncology Pulmonology Rheumatology Obstetrics and gynaecology Gynaecology Gynecologic oncology Maternal–fetal medicine Obstetrics Reproductive endocrinology and infertility Urogynecology Diagnostic Radiology Interventional radiology Nuclear medicine Pathology Anatomical Clinical pathology Clinical chemistry Cytopathology Medical microbiology Transfusion medicine Other Addiction medicine Adolescent medicine Anesthesiology Dermatology Disaster medicine Diving medicine Emergency medicine Mass gathering medicine Family medicine General practice Hospital medicine Intensive care medicine Medical genetics Narcology Neurology Clinical neurophysiology Occupational medicine Ophthalmology Oral medicine Pain management Palliative care Pediatrics Neonatology Physical medicine and rehabilitation PM&R Preventive medicine Psychiatry Addiction psychiatry Radiation oncology Reproductive medicine Sexual medicine Sleep medicine Sports medicine Transplantation medicine Tropical medicine Travel medicine Venereology Medical education Medical school Bachelor of Medicine, Bachelor of Surgery Bachelor of Medical Sciences Master of Medicine Master of Surgery Doctor of Medicine Doctor of Osteopathic Medicine MD–PhD Related topics Alternative medicine Allied health Dentistry Podiatry Pharmacy Physiotherapy Molecular oncology Nanomedicine Personalized medicine Public health Rural health Therapy Traditional medicine Veterinary medicine Physician Chief physician History of medicine Book Category Commons Wikiproject Portal Outline

ARG1, ARNTL, MED23, ABCD1, ARSD, ASL, DECR1, NOS1, NOS2, OTC, PPARG
- Arginase Deficiency GARD
  
  Arginase deficiency is an inherited metabolic disease in which the body is unable to process arginine (a building block of protein). It belongs to a group of disorders known as urea cycle disorders . These occur when the body's process for removing ammonia is disrupted, which can cause ammonia levels in the blood to rise (hyperammonemia). In most cases, symptoms appear between the ages of one and three years. Symptoms may include feeding problems, vomiting, poor growth, seizures, and stiff muscles with increased reflexes (spasticity). People with arginase deficiency may also have developmental delay, loss of developmental milestones, and intellectual disability.
- Argininemia OMIM
  
  A number sign (#) is used with this entry because argininemia is caused by homozygous or compound heterozygous mutation in the arginase-1 gene (ARG1; 608313) on chromosome 6q23. Description Arginase deficiency is an autosomal recessive inborn error of metabolism caused by a defect in the final step in the urea cycle, the hydrolysis of arginine to urea and ornithine. Urea cycle disorders are characterized by the triad of hyperammonemia, encephalopathy, and respiratory alkalosis. Five disorders involving different defects in the biosynthesis of the enzymes of the urea cycle have been described: ornithine transcarbamylase deficiency (311250), carbamyl phosphate synthetase deficiency (237300), argininosuccinate synthetase deficiency, or citrullinemia (215700), argininosuccinate lyase deficiency (207900), and arginase deficiency. Clinical Features Terheggen et al. (1969, 1970) described 2 sisters, aged 18 months and 5 years, with spastic paraplegia, epileptic seizures, and severe mental retardation.
- Arginase Deficiency MedlinePlus
  
  Arginase deficiency is an inherited disorder that causes the amino acid arginine (a building block of proteins) and ammonia to accumulate gradually in the blood. Ammonia, which is formed when proteins are broken down in the body, is toxic if levels become too high. The nervous system is especially sensitive to the effects of excess ammonia. Arginase deficiency usually becomes evident by about the age of 3. It most often appears as stiffness, especially in the legs, caused by abnormal tensing of the muscles (spasticity). Other symptoms may include slower than normal growth, developmental delay and eventual loss of developmental milestones, intellectual disability, seizures, tremor, and difficulty with balance and coordination (ataxia).
- Argininemia Orphanet
  
  A rare autosomal recessive amino acid metabolism disorder characterized clinically by variable degrees of hyperammonemia, developing from about 3 years of age, and leading to progressive loss of developmental milestones and spasticity in the absence of treatment.
- Arginase Deficiency GeneReviews
  
  Summary Clinical characteristics. 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. Individuals treated from birth, either as a result of newborn screening or having an affected older sib, appear to have minimal symptoms. Diagnosis/testing. The diagnosis of arginase deficiency is established in a proband with suggestive clinical and/or biochemical findings and confirmed by identification of biallelic pathogenic variants in ARG1 or, in limited instances, by failure to detect arginase enzyme activity (usually <1% of normal) in red blood cell extracts.
Renal Papillary Necrosis Wikipedia

. ^ Greenberg, Arthur; Cheung, Alfred K. (2005-01-01). Primer on Kidney Diseases .
Rotor Syndrome Wikipedia

Genes, SLCO1B1 and SLCO1B3 that result in complete functional deficiencies of both protein products (OATP1B1 and OATP1B3, respectively), are also present. [ citation needed ] Rotor syndrome is largely a diagnosis of exclusion. [2] Serological abnormalities in Rotor syndrome only include elevated total serum bilirubin (typically elevated between 2 to 5 mg/dL but may be as high as 20 mg/dL). [2] Most of the time, alanine aminotransferase , aspartate aminotransferase , gamma-glutamyl transferase , and alkaline phosphatase levels are normal, but mild elevations can be seen. [2] If any of these lab values are markedly elevated, investigation for other, more serious conditions is warranted. [2] Imaging studies cannot diagnose Rotor syndrome but can help rule out other diseases that cause hyperbilirubinemia . [2] For example, ultrasound of the liver and the biliary tree can help investigate the causes of extra-hepatic biliary obstruction . [2] The gallbladder is visualized on oral cholecystography in Rotor syndrome while it is not visualized in Dubin Johnson syndrome. [2] Ultimately, the best method of diagnosing the disease is the analysis of urine coproporphyrin excretion. [2] The total urine coproporphyrin excretion in Rotor syndrome has a 2- to 5-fold elevation, with 65% constituting coproporphyrin I. [2] Treatment [ edit ] To treat the jaundice, phenobarbital is normally used. [ citation needed ] Rotor syndrome is a benign disease requiring no treatment. [2] Jaundice is a lifelong finding, but the disease is not associated with morbidity or mortality, and life expectancy is not affected. [2] Most individuals with Rotor syndrome are born to consanguineous couples and its diagnosis may coincidently identify consanguinity. [2] Distinguishing Rotor syndrome from other more serious disorders is important to avoid unnecessary workup and interventions. [2] It is also critical to reassure and calm patients or family members of patients with Rotors syndrome that the condition is benign. [2] Eponym [ edit ] Rotor syndrome is named after the Filipino internist Arturo Belleza Rotor (1907–1988). [8] See also [ edit ] Jaundice Bilirubin metabolism Gilbert's syndrome Crigler–Najjar syndrome References [ edit ] ^ a b Online Mendelian Inheritance in Man (OMIM): 237450 ^ a b c d e f g h i j k l m n o p q r s t Kumar, A; Mehta, D (2020), "article-36575", Rotor Syndrome , This book is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/ ), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated., Treasure Island (FL): StatPearls Publishing, PMID 30335339 , retrieved 2020-07-17 ^ a b Wolkoff AW, Wolpert E, Pascasio FN, Arias IM (February 1976).

SLCO1B1, SLCO1B3, ABCC2
- Hyperbilirubinemia, Rotor Type OMIM
  
  A number sign (#) is used with this entry because Rotor type hyperbilirubinemia (HBLRR) is caused by digenic inheritance of homozygous mutations in the SLCO1B1 (604843) and SLCO1B3 (605495) genes, which are located near each other on chromosome 12p. Description The Rotor type of hyperbilirubinemia is an autosomal recessive form of primary conjugated hyperbilirubinemia. It is similar to Dubin-Johnson syndrome (DJS; 237500) in that affected individuals develop mild jaundice not associated with hemolysis shortly after birth or in childhood. However, Rotor syndrome can be distinguished from DJS by a lack of hepatocyte pigment deposits, delayed plasma clearance of the unconjugated anionic dye bromsulfthalein, poor hepatic visualization on certain radiographic imaging studies, and prominent urinary excretion of coproporphyrin I (summary by van de Steeg et al., 2012). Clinical Features Because of clinical similarities, the Rotor and Dubin-Johnson syndromes were initially considered to be the same entity.
- Rotor Syndrome Orphanet
  
  A benign, inherited liver disorder characterized by chronic, predominantly conjugated, nonhemolytic hyperbilirubinemia with normal liver histology. Epidemiology Rotor syndrome (RT) is a very rare disorder: the exact prevalence is unknown but over 50 cases have been reported in literature so far. Clinical description It is usually diagnosed in children or adolescents, but mild jaundice is often noted from birth. The main symptom consists of mild-to-moderate, recurrent jaundice without pruritus. Attacks of abdominal pain and low-grade fever can occur but are rare.
- Rotor Syndrome GeneReviews
  
  Summary Clinical characteristics. Rotor syndrome is characterized by mild conjugated and unconjugated hyperbilirubinemia that usually begins shortly after birth or in childhood. Jaundice may be intermittent. Conjunctival icterus may be the only clinical manifestation. Diagnosis/testing. The diagnosis of Rotor syndrome is established in a proband with isolated, predominantly conjugated hyperbilirubinemia without cholestasis or liver injury and typical findings on cholescintigraphy. Identification of biallelic pathogenic variants in SLCO1B1 and SLCO1B3 on molecular genetic testing can confirm the diagnosis when cholescintigraphy is either not available or not recommended due to risks associated with the procedure. Management. Treatment of manifestations: No treatment required. Agents/circumstances to avoid: Although no adverse drug effects have been documented in persons with Rotor syndrome, the absence of the hepatic proteins OATP1B1 and OATP1B3 may have serious consequences for liver uptake – and thus for the toxicity of numerous commonly used drugs and/or their metabolites.
- Rotor Syndrome GARD
  
  Rotor syndrome is an inherited disorder characterized by elevated levels of bilirubin in the blood (hyperbilirubinemia). Bilirubin is produced when red blood cells are broken down, and has an orange-yellow tint. The buildup of bilirubin in the body causes yellowing of the skin or whites of the eyes (jaundice), which is the only symptom of the disorder. Jaundice is usually evident in infancy or early childhood, and it may come and go. Rotor syndrome is caused by having mutations in both the SLCO1B1 and SLCO1B3 genes and is inherited in an autosomal recessive manner.
- Rotor Syndrome MedlinePlus
  
  Rotor syndrome is a relatively mild condition characterized by elevated levels of a substance called bilirubin in the blood (hyperbilirubinemia). Bilirubin is produced when red blood cells are broken down. It has an orange-yellow tint, and buildup of this substance can cause yellowing of the skin or whites of the eyes (jaundice). In people with Rotor syndrome, jaundice is usually evident shortly after birth or in childhood and may come and go; yellowing of the whites of the eyes (also called conjunctival icterus) is often the only symptom. There are two forms of bilirubin in the body: a toxic form called unconjugated bilirubin and a nontoxic form called conjugated bilirubin. People with Rotor syndrome have a buildup of both unconjugated and conjugated bilirubin in their blood, but the majority is conjugated.
Aneurysm Of Sinus Of Valsalva Wikipedia

. ^ Vural KM, Sener E, Taşdemir O, Bayazit K (July 2001). "Approach to sinus of Valsalva aneurysms: a review of 53 cases" .

FLNA
- Aneurysm Of Sinus Of Valsalva Orphanet
  
  Sinus of Valsalva aneurysm (SVA) is a rare congenital heart malformation of one or more of the aortic sinuses, consisting of a dilation that when unruptured is usually asymptomatic but when ruptured presents with progressive exertional dyspnea, fatigue, chest pain and that can lead to congestive heart failure if left untreated.
Transient Hyperammonemia Of The Newborn Wikipedia

Retrieved November 12, 2012 . ^ a b c d e f g h i j k l m n o p Krishnan, L.; Diwakar, K.K.; Patil, P.; Bhaskaranand, N. (1996).
Phosphorus Deficiency Wikipedia

., Bekjarov, G., Dospatliev, L., Ivanov, & K., Zaprjanova, P. (2010). ICP determination of phosphorus in soils and plants.
Stasis Papillomatosis Wikipedia

Obtenido de Clinical Key . [ full citation needed ] ^ a b c d e Sato T, Katagiri K, Itami S, Takayasu S (May 1996). "A case of stasis papillomatosis associated with psoriasis vulgaris".
Epiploic Appendagitis Wikipedia

BMC Surgery 7:11. ^ a b c d e f g h i Singh, Ajay K.; Gervais, Debra A.; Hahn, Peter F.; Sagar, Pallavi; Mueller, Peter R.; Novelline, Robert A. (2005-11-01).
Comedocarcinoma Wikipedia

. ^ a b "Understanding Your Pathology Report: Ductal Carcinoma In Situ (DCIS)" . www.cancer.org . Retrieved 2020-04-23 . ^ Pai, K., Baliga, P., & Shrestha, B. L. (2013).
Phantom Vibration Syndrome Wikipedia

Retrieved 2019-02-11 . ^ a b c d e f g h i j k Deb A (2014). "Phantom vibration and phantom ringing among mobile phone users: A systematic review of literature".