��888-��888-(��52bet.net��)-��888-��888-(��bet25.net��)-��888-��888-��888-��900bet.net��

Advanced

FindZebra Summary is loading...

Limbal Nodule Wikipedia

Lippincott Williams & Wilkins. p. 42. ISBN 1-60547-888-1 .
Stress Shielding Wikipedia

Materials Science and Engineering: C . 70 (1): 870–888. doi : 10.1016/j.msec.2016.09.069 .
Ras-Associated Autoimmune Leukoproliferative Disorder Wikipedia

"Three-dimensional structure of an oncogene protein: catalytic domain of human c-H-ras p21". Science . 239 (888–893): 888–93. Bibcode : 1988Sci...239..888D . doi : 10.1126/science.2448879 .

NRAS, KRAS, FAS, FASLG, CASP10, MME
- Ras-Associated Autoimmune Leukoproliferative Disease Orphanet
  
  RAS-associated autoimmune leukoproliferative disease (RALD) is a rare genetic disorder characterized by monocytosis, autoimmune cytopenias, lymphoproliferation, hepatosplenomegaly, and hypergammaglobulinemia. Epidemiology Prevalence of this disorder is not known. It is extremely rare with fewer than 20 patients reported to date. Clinical description Age of onset of the clinical signs is invariably in infancy or early childhood. Most patients have atypical features such as elevated counts for cells of myeloid origin (monocytosis and granulocytosis) making their clinical presentation indistinguishable from juvenile myelomonocytic leukemia (JMML; see this term). Many patients undergo repeated bone marrow assessments showing normal cytogenetics despite dysplastic marrow morphology.
- Ras-Associated Autoimmune Leukoproliferative Disorder OMIM
  
  A number sign (#) is used with this entry because of evidence that RAS-associated autoimmune leukoproliferative disorder (RALD) is caused by somatic mutation in the NRAS gene (164790) or the KRAS gene (190070) on chromosome 12p12. One patient with somatic mutation in the NRAS gene has been reported. Description RAS-associated leukoproliferative disorder is characterized by lymphadenopathy, splenomegaly, and variable autoimmune phenomena, including autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, and neutropenia. Laboratory studies show an expansion of lymphocytes due to defective apoptosis, as well as significant autoantibodies. Some patients have recurrent infections, and there may be an increased risk of hematologic malignancy (summary by Oliveira, 2013 and Niemela et al., 2010).
Fetal Valproate Syndrome GARD

A pregnant woman taking anti-seizure medication can enroll in this registry by calling 1-888-233-2334. You can read more about the registry on the North American AED (Antiepileptic Drug) Pregnancy Registry website .
- Valproate Embryopathy, Susceptibility To OMIM
  
  All antiepileptic drugs are potential teratogens. Anticonvulsant treatment during pregnancy presents the challenge of balancing between optimal treatment for seizure control and possible harmful fetal effects. One of the best delineated examples of harmful fetal effects is the fetal valproate syndrome (FVS), comprising typical facial features, developmental delay, and a variety of malformations such as neural tube defects, cardiac and gastrourinary malformations, and limb defects (Winter et al., 1987; Ardinger et al., 1988; Clayton-Smith and Donnai, 1995). Malm et al. (2002) described 3 families in which all offspring, 3 children in 1 family and 2 in each of the other 2 families, were affected by FVS. Malm et al. (2002) published pictures illustrating the facial features of FVS: trigonocephaly, medial deficiency of eyebrows, broad nasal root, anteverted nares, shallow philtrum, and long and thin upper lip. In males with ornithine transcarbamylase (OTC) deficiency (311250), sodium valproate may precipitate acute liver failure (Tripp et al., 1981).
- Fetal Valproate Spectrum Disorder Orphanet
  
  A rare teratogenic disease due to embryo/fetal exposure to valproic acid (VPA) and subsequently characterized by a distinct facial dysmorphism, congenital anomalies and developmental delay (especially in language and communication). Epidemiology Prevalence of fetal valproate syndrome (FVS) is unknown. An incidence of neural tube defects (NTDs) of 1-2% has been associated with the use of VPA during the first trimester of pregnancy (10-20 times the rate seen in the general population) while the incidence of congenital heart disease, neurodevelopmental delay and autism spectrum disorder (ASD) are estimated to be around 4 to 5 times higher than in the general population. Clinical description The majority of infants exposed to VPA in utero are born healthy. Intrauterine growth retardation is present in 10% of cases but postnatal growth is usually normal and general health is good.
Pelvis Syndrome Wikipedia

Archives of Dermatology . 142 (7): 884–888. doi : 10.1001/archderm.142.7.884 .
Mycotic Aneurysm Wikipedia

Philadelphia: Churchill Livingstone; 2000:888-892. ^ Jarrett F, Darling RC, Mundth ED, Austen WG.
List Of Fibrinogen Disorders Wikipedia

Journal of Thrombosis and Haemostasis . 15 (5): 876–888. doi : 10.1111/jth.13655 . PMID 28211264 . ^ Caimi G, Canino B, Lo Presti R, Urso C, Hopps E (2017).
Antisynthetase Syndrome Wikipedia

"Heterogeneity of precipitating antibodies in polymyositis and dermatomyositis". Arthritis Rheum . 23 (8): 881–888. doi : 10.1002/art.1780230802 . PMID 7406938 . ^ Lazarou IN, Guerne PA.

TRIM21, CD40LG, COL4A5, HARS1, IFN1@, PRTN3, HARS2, SLC2A10, NCR3
- Antisynthetase Syndrome Orphanet
  
  A clinically heterogeneous form of idiopathic inflammatory myopathy characterized by myositis, arthralgia, Raynaud phenomenon, mechanic hands, interstitial lung disease (ILD), and serum autoantibodies to aminoacyl transfer RNA synthetases (anti-ARS). Epidemiology Prevalence and annual incidence are not known. AS syndrome represents a subset of polymyositis and dermatomyositis (PM, DM, see these terms), disorders which have estimated prevalence of about 1/4,650. About a quarter of these patients may have AS syndrome, providing a prevalence estimate of 1/25,000 - 1/33,000 worldwide. The disorder affects females twice as often as males. Clinical description The age of onset is highly variable with a mean of 50 years (range 19 to 82). ILD is one of the clinical hallmarks. Respiratory symptoms (shortness of breath, coughing, dysphagia) are found in 40-60% of patients at disease onset.
- Antisynthetase Syndrome GARD
  
  Antisynthetase syndrome is a chronic autoimmune condition that affects the muscles and various other parts of the body. The signs and symptoms can vary but may include muscle inflammation (myositis), polyarthritis (inflammation of many joints), interstitial lung disease , thickening and cracking of the hands, and Raynaud phenomenon . The exact underlying cause is unknown; however, the production of autoantibodies (antibodies that attack normal cells) that attack certain enzymes in the body called 'aminoacyl-tRNA synthetases' appears to be linked to the cause of the syndrome. These autoantibodies may arise after viral infections, or patients may have a genetic predisposition. Treatment is based on the signs and symptoms present in each person but may include corticosteroids, immunosuppressive medications, and/or physical therapy.
Aberrant Subclavian Artery Wikipedia

The Journal of Thoracic and Cardiovascular Surgery . 133 (4): 888–92. doi : 10.1016/j.jtcvs.2006.12.005 .
- Aberrant Subclavian Artery GARD
  
  Aberrant subclavian artery is a rare vascular anomaly that is present from birth. It usually causes no symptoms and is often discovered as an incidental finding (such as through a barium swallow or echocardiogram ). Occasionally the anomaly causes swallowing difficulty (dysphagia lusoria). Swallowing symptoms in children may present as feeding difficulty and/or recurrent respiratory tract infection. When aberrant subclavian artery causes no symptoms, treatment is not needed.
Factor I Deficiency Wikipedia

Journal of Thrombosis and Haemostasis . 15 (5): 876–888. doi : 10.1111/jth.13655 . PMID 28211264 . ^ a b Neerman-Arbez M, de Moerloose P, Casini A (2016).

CFI, FGA, FGB, FGG, CFH, CD46
- Complement Factor I Deficiency MedlinePlus
  
  Complement factor I deficiency is a disorder that affects the immune system. People with this condition are prone to recurrent infections, including infections of the upper respiratory tract, ears, skin, and urinary tract. They may also contract more serious infections such as pneumonia, meningitis, and sepsis , which may be life-threatening. Some people with complement factor I deficiency have a kidney disorder called glomerulonephritis with isolated C3 deposits. Complement factor I deficiency can also be associated with autoimmune disorders such as rheumatoid arthritis or systemic lupus erythematosus (SLE).
- Complement Factor I Deficiency OMIM
  
  A number sign (#) is used with this entry because complement factor I ('eye') deficiency (CFID) is caused by homozygous or compound heterozygous mutation in the gene encoding complement factor I (CFI; 217030) on chromosome 4q25. Description Hereditary deficiency of complement factor I is associated with a propensity to pyogenic infection and follows an autosomal recessive pattern of inheritance (Vyse et al., 1996). See also complement factor H deficiency (609814), which shows overlapping clinical features. Clinical Features Alper et al. (1970, 1970) and Abramson et al. (1971) reported a patient with increased susceptibility to infection and accelerated catabolism of C3 due to deficiency of the C3 inactivator. Alper et al. (1972) demonstrated that the C3 inactivator also acts as an inhibitor in the alternative complement pathway.
- Immunodeficiency With Factor I Anomaly Orphanet
  
  Immunodeficiency with factor I anomaly is a rare, genetic, primary immunodeficiency disease characterized by increased susceptibility to recurrent, usually severe, infections (particularly by Neisseria meningitidis , Haemophilus influenzae and Streptococcus pneumonia ), typically manifesting as otitis, sinusitis, bronchitis, pneumonia, and/or meningitis. Autoimmune disease (e.g. systemic lupus erythematosus, glomerulonephritis) and atypical hemolytic uremic syndrome may be associated. Laboratory serum analysis reveals, in addition to diminished or undetectable complement factor I, variably decreased complement C3, complement factor B and complement factor H.
Pediculosis Corporis Wikipedia

Clinical Infectious Diseases . 29 (4): 888–911. doi : 10.1086/520454 . PMID 10589908 . ^ a b Page on website of CIGNA ^ Foucault C, Ranque S, Badiaga S (2006).
- Body Lice Mayo Clinic
  
  Overview Body lice are tiny insects, about the size of a sesame seed. Body lice live in your clothing and bedding and travel to your skin several times a day to feed on blood. The most common sites for bites are around the neck, shoulders, armpits, waist and groin — places where clothing seams are most likely to touch skin. Body lice are most common in crowded and unhygienic living conditions, such as refugee camps and shelters for homeless people. They can also spread from contact with an infected person's clothes. Body lice bites can spread certain types of diseases and can even cause epidemics.
Gastrointestinal Disease Wikipedia

Other rarer diseases affecting the pancreas may include pancreatic pseudocysts , exocrine pancreatic insufficiency , and pancreatic fistulas . [3] : 888–891 Pancreatic disease may present with or without symptoms. ... Pancreatic disease might be investigated using abdominal x-rays , MRCP or ERCP , CT scans , and through blood tests such as measurement of the amylase and lipase enzymes. [3] : 888–894 Gallbladder and biliary tract [ edit ] Diseases of the hepatobiliary system affect the biliary tract (also known as the biliary tree ), which secretes bile in order to aid digestion of fats.

ALDH1A2, BARX1, LRRC8D, CRTC1, CFTR, NR1H4, HOTAIR, HULC, MIR369, OLFM4, CASR, STK11, CCL7, PPARG, MUTYH, SMAD7, DEFB1, DBN1, CCAT1
Hypodysfibrinogenemia Wikipedia

Journal of Thrombosis and Haemostasis . 15 (5): 876–888. doi : 10.1111/jth.13655 . PMID 28211264 . ^ a b c d e f g h Casini A, de Moerloose P, Neerman-Arbez M (2016).

FGA, FGB, FGG, F2, F13A1, PLG
- Familial Dysfibrinogenemia Orphanet
  
  Familial dysfibrinogenemia is a coagulation disorder characterized by a bleeding tendency due to a functional anomaly of circulating fibrinogen. Epidemiology Prevalence is unknown but dysfibrinogenemia is more frequent than afibrinogenemia which has a prevalence of 1/1,000,000. Clinical description Most patients with dysfibrinogenemia are asymptomatic. The others may have mild bleeding symptoms or even thrombosis. Etiology The deficiency is due to various mutations in the FGA , FGB , or FGG genes. Genetic counseling Transmission is mainly autosomal dominant.
- Dysfibrinogenemia GARD
  
  Dysfibrinogenemia is a coagulation (clotting) disorder characterized by having an abnormal form of fibrinogen. Fibrinogen is a protein produced by the liver which helps control bleeding by helping blood clots to form. Having abnormal fibrinogen results in defective clot formation and can cause an increased or decreased ability to clot. Dysfibrinogenemias may be inherited (congenital) or acquired. Congenital dysfibrinogenemia is rare. About 40% of people with this form have no symptoms. About 50% have a bleeding disorder , and the remaining 10% have either a thrombotic disorder (excessive clotting) or both bleeding and thrombotic disorders.
- Dysfibrinogenemia, Congenital OMIM
  
  A number sign (#) is used with this entry because congenital dysfibrinogenemia is caused by mutation in one of the fibrinogen genes: alpha (FGA; 134820), beta (FGB; 134830), or gamma (FGG; 134850). It is most often caused by heterozygous mutation, but can also be caused by homozygous or compound heterozygous mutation. Congenital hypodysfibrinogenemia is caused by heterozygous, homozygous, or compound heterozygous mutation in one of the fibrinogen genes. Description Inherited disorders of fibrinogen affect either the quantity (afibrinogenemia and hypofibrinogenemia; 202400) or the quality (dysfibrinogenemia) of the circulating fibrinogen, or both (hypodysfibrinogenemia). Patients with dysfibrinogenemia are frequently asymptomatic, but some patients have bleeding diathesis, thromboembolic complications, or both (summary by de Moerloose and Neerman-Arbez, 2009).
Chemotherapy-Induced Peripheral Neuropathy Wikipedia

"Nutraceuticals and chemotherapy induced peripheral neuropathy (CIPN): A systematic review". Clin Nutr . 32 (6): 888–93. doi : 10.1016/j.clnu.2013.04.007 .

MMP9, HDAC6, HMGB1, TLR4, HSPB1, HSPB2, ARHGEF10, TNF, SARM1, HSPB3, NGF, BDNF, SRI, CX3CL1, TNS1, TP53, TYROBP, SRL, RPS6KB2, RAG2, VEGFA, AKT1, TRPV1, TLR9, HCN1, EPHA6, SPNS1, PRX, CEP72, TREM2, NCS1, NR1I2, RAPGEF3, SIGMAR1, ABCC4, NAMPT, TRPA1, PIK3CG, PTGS2, PIK3CA, PIK3CD, PIK3CB, BPI, CALCA, CASP3, TNFRSF8, CHRNA4, MAPK14, CX3CR1, DDIT3, SARDH, EPHA5, EPHA8, ERBB2, F3, FAAH, PTK2B, GPX7, GSK3B, HCRT, HIF1A, HSPA4, IL1B, IL6, IL17A, MAPT, NARS1, NEFL, OPRM1, P2RX3, ANK1, MIR338
Post-Transplant Lymphoproliferative Disorder Wikipedia

"Epstein-Barr Virus-related post-transplant lymphoproliferative disorders: pathogenetic insights for targeted therapy" (PDF) . Am J Transplant . 11 (5): 888–95. doi : 10.1111/j.1600-6143.2011.03499.x .

KRT20, MS4A1, ABO, PIK3CB, RTEL1, PDLIM7, TP53, TNF, TGFB1, PIK3CG, PIK3CD, PIK3CA, XIAP, NCAM1, IL10, HLA-B, FCGR3B, FCGR3A, CRP, CDKN2A, CD19, H3P10
- Post-Transplant Lymphoproliferative Disease Orphanet
  
  A group of rare immunodeficiency-associated lymphoproliferative disorders characterized by lymphoid or plasmacytic proliferations developing in the context of immunosuppression in a recipient of a solid organ or stem cell allograft. The group includes non-destructive post-transplant lymphoproliferative disorders (PTLDs), polymorphic PTLD, monomorphic PTLDs, and classic Hodgkin lymphoma PTLD. Patients may have more than one type of PTLD in a single or in different locations. The most commonly involved sites are lymph nodes, gastrointestinal tract, lungs, and liver, although the disease may occur almost anywhere in the body. In solid organ transplant recipients, PTLD may also involve the allograft.
Adjustment Disorders Mayo Clinic

The Suicide & Crisis Lifeline in the U.S. has a Spanish-language phone line at 1-888-628-9454 (toll-free). Causes Adjustment disorders are caused by major changes or stressors in your life.

HDAC5, OPN1SW, BDNF, BRAF, JAK2, MIF, MVD, TH, MIR451A
Gunther Disease Wikipedia

The British Journal of Dermatology . 167 (4): 888–900. doi : 10.1111/j.1365-2133.2012.11154.x .

UROS, GATA1, HMBS
Van Der Woude Syndrome Wikipedia

External links [ edit ] Classification D ICD - 10 : Q38.0 OMIM : 119300 606713 MeSH : C563529 C536528, C563529 DiseasesDB : 31926 External resources eMedicine : ped/2753 Orphanet : 888 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

IRF6, GRHL3, TNF, IL6, IL1B, TLR4, IL10, ACTB, IL17A, IFNG, CXCL8, COX2, HMGB1, NHLH1, PPARG, PTGS2, STAT3, HSPA4, MTCO2P12, AKT1, CYBB, AIF1, AHR, DCDC2, NOX4, AGO2, SIRT1, TNFSF13, UMOD, TRPC3, TP53, ETV6, TH, TGFB2, TFDP1, TFAP2A, CNTN2, SYT1, ARG1, SLC22A4, CCL21, CCL5, RIPK4, GORASP1, ROCK1, WNK1, THRIL, NCF1, MIR211, MIR206, MIR195, MIR183, MIR17, MIR15B, MIR132, MIR122, MALAT1, CFAP57, TICAM1, TRIM69, CPO, TIRAP, NLRP3, WDR26, WNK2, RORA, REN, F3, DNTT, CCK, IRF3, IRF2, IDO1, CDH2, CNR2, CXCR1, IL7R, CYP2E1, DRD2, RELA, IFNA13, IFNA1, HSP90AA1, EPHB2, FOXA1, ERN1, CXCL2, GPT, GLI2, KISS1, LAMB2, MAP3K3, MST1, NECTIN1, PVR, CCND1, MAPK1, PRKAB1, PRKAA2, PRKAA1, BCL2, AP2A1, PIK3CG, PIK3CD, PIK3CB, PIK3CA, NRF1, NME2, NME1, CASP3, NFATC1, CAV1, PKM
- Van Der Woude Syndrome Orphanet
  
  Van der Woude syndrome (VWS) is a rare congenital genetic dysmorphic syndrome characterized by paramedian lower-lip fistulae, cleft lip with or without cleft palate, or isolated cleft palate. Epidemiology The disorder represents the most common single-gene cause of cleft lip/cleft palate, i.e. 2% of all individuals with cleft lip/palate. Estimated incidence at birth is between 1/35,000 and 1/100,000 in European and Asian populations. Males and females are affected equally. Clinical description At birth, patients with VWS have one or more of the following dysmorphic features: paramedian lower-lip pits (fistulae, usually bilateral), small mounds with a sinus tract leading from a mucous gland of the lip, or cleft lip/cleft palate. Lip pits are the most common sign (>80%) and are mostly asymptomatic although dribbling and infection is possible.
- Van Der Woude Syndrome 1, Modifier Of OMIM
  
  Mapping Van der Woude syndrome-1 (VWS1; 119300), which maps to 1q32, is characterized by pits and/or sinuses of the lower lip, cleft lip/palate (CL/P), cleft palate (CP), bifid uvula, and hypodontia. The expression of VWS1, which has incomplete penetrance, is highly variable. Both the occurrence of CL/P and CP within the same kindred and a recurrence risk of less than 40% for CP among descendants with VWS suggested that the development of clefts in this syndrome is influenced by modifying genes at other loci. To test this hypothesis, Sertie et al. (1999) conducted linkage analysis in a large Brazilian kindred with VWS, considering as affected the individuals with CP, regardless of whether it was associated with other signs of VWS. The results suggested that a gene at chromosome 17p11.2-p11.1, together with the causative VWS1 gene at chromosome 1q32, enhances the probability of CP in an individual carrying the 2 at-risk genes.
- Van Der Woude Syndrome GARD
  
  Van der Woude syndrome is a condition that affects the development of the face. Many people with this disorder are born with a cleft lip and/or a cleft palate . Affected individuals usually have depressions (pits) near the center of the lower lip, which may appear moist due to the presence of salivary and mucous glands in the pits. Small mounds of tissue on the lower lip may also occur. In some cases, people with van der Woude syndrome have missing teeth. Growth and intelligence are usually normal. This condition is caused by mutations in the IRF6 gene and is inherited in a autosomal dominant fashion.
- Van Der Woude Syndrome 2 OMIM
  
  A number sign (#) is used with this entry because of evidence that van der Woude syndrome-2 (VWS2) is caused by heterozygous mutation in the GRHL3 gene (608317) on chromosome 1p36. Description Van der Woude syndrome (VWS) is a dominantly inherited developmental disorder characterized by pits and/or sinuses of the lower lip, and cleft lip and/or cleft palate (CL/P, CP). It is the most common cleft syndrome. For a discussion of genetic heterogeneity of van der Woude syndrome, see VWS1 (119300). Clinical Features Koillinen et al. (2001) studied a large Finnish pedigree with van der Woude syndrome in which the clinical features were typical for VWS with the exception that usually CL/P is twice as common as CP, but in this family, 9 of the 11 affected individuals had CP and only 1 had CL/P. In addition, only 1 affected family member exhibited lip pits, and he did not have clefting anomalies.
- Van Der Woude Syndrome 1 OMIM
  
  A number sign (#) is used with this entry because van der Woude syndrome-1 (VWS1) is caused by heterozygous mutation in the gene encoding interferon regulatory factor-6 (IRF6; 607199) on chromosome 1q32. Description Van der Woude syndrome (VWS) is a dominantly inherited developmental disorder characterized by pits and/or sinuses of the lower lip, and cleft lip and/or cleft palate (CL/P, CP). It is the most common cleft syndrome. Genetic Heterogeneity of van der Woude Syndrome Also see VWS2 (606713), caused by mutation in the GRHL3 gene (608317) on chromosome 1p36. Clinical Features In 3 generations of a family, Levy (1962) found malformations of the lower lip consisting of symmetrical lumps. Two sibs had cleft palate in addition to the lip anomaly. The literature on this syndrome was analyzed by van der Woude (1954), who found confirmation for the autosomal dominant mode of inheritance.
- Van Der Woude Syndrome MedlinePlus
  
  Van der Woude syndrome is a condition that affects the development of the face. Many people with this disorder are born with a cleft lip, a cleft palate (an opening in the upper lip or roof of the mouth), or both. Affected individuals usually have depressions (pits) near the center of the lower lip, which may appear moist due to the presence of salivary and mucous glands in the pits. Small mounds of tissue on the lower lip may also occur. In some cases, people with van der Woude syndrome have missing teeth. People with van der Woude syndrome who have cleft lip and/or palate, like other individuals with these facial conditions, have an increased risk of delayed language development, learning disabilities, or other mild cognitive problems.
Medication Overuse Headaches Mayo Clinic

Or contact the National Headache Foundation at www.headaches.org or 888-643-5552 . Preparing for your appointment You're likely to start by seeing your primary care provider.

CALCA, S100A12, STIN2-VNTR, SLC6A4, DRD2, GOLPH3, SCLY, ITSN2, PYCARD, SCN11A, RAMP1, HDAC3, WFS1, TYMS, TAL1, APOA1, SLC1A2, APOE, PNOC, OTC, MTHFR, KRT7, HTR1F, HTR1A, ACE, COMT, BDNF, SFSWAP
Goodpasture Syndrome Wikipedia

External links [ edit ] GBM antibodies: immunofluorescence image Classification D ICD - 10 : M31.0 ( ILDS M31.010) ICD - 9-CM : 446.21 OMIM : 233450 MeSH : D019867 DiseasesDB : 5363 External resources MedlinePlus : 000142 eMedicine : med/923 ped/888 v t e Systemic vasculitis Large vessel Takayasu's arteritis Giant cell arteritis Medium vessel Polyarteritis nodosa Kawasaki disease Thromboangiitis obliterans Small vessel Pauci-immune c-ANCA Granulomatosis with polyangiitis p-ANCA Eosinophilic granulomatosis with polyangiitis Microscopic polyangiitis Type III hypersensitivity Cutaneous small-vessel vasculitis IgA vasculitis Ungrouped Acute hemorrhagic edema of infancy Cryoglobulinemic vasculitis Bullous small vessel vasculitis Cutaneous small-vessel vasculitis Other Goodpasture syndrome Sneddon's syndrome v t e Hypersensitivity and autoimmune diseases Type I / allergy / atopy ( IgE ) Foreign Atopic eczema Allergic urticaria Allergic rhinitis (Hay fever) Allergic asthma Anaphylaxis Food allergy common allergies include: Milk Egg Peanut Tree nut Seafood Soy Wheat Penicillin allergy Autoimmune Eosinophilic esophagitis Type II / ADCC IgM IgG Foreign Hemolytic disease of the newborn Autoimmune Cytotoxic Autoimmune hemolytic anemia Immune thrombocytopenic purpura Bullous pemphigoid Pemphigus vulgaris Rheumatic fever Goodpasture syndrome Guillain–Barré syndrome " Type V "/ receptor Graves' disease Myasthenia gravis Pernicious anemia Type III ( Immune complex ) Foreign Henoch–Schönlein purpura Hypersensitivity vasculitis Reactive arthritis Farmer's lung Post-streptococcal glomerulonephritis Serum sickness Arthus reaction Autoimmune Systemic lupus erythematosus Subacute bacterial endocarditis Rheumatoid arthritis Type IV / cell-mediated ( T cells ) Foreign Allergic contact dermatitis Mantoux test Autoimmune Diabetes mellitus type 1 Hashimoto's thyroiditis Multiple sclerosis Coeliac disease Giant-cell arteritis Postorgasmic illness syndrome Reactive arthritis GVHD Transfusion-associated graft versus host disease Unknown/ multiple Foreign Hypersensitivity pneumonitis Allergic bronchopulmonary aspergillosis Transplant rejection Latex allergy (I+IV) Autoimmune Sjögren syndrome Autoimmune hepatitis Autoimmune polyendocrine syndrome APS1 APS2 Autoimmune adrenalitis Systemic autoimmune disease v t e Diseases of collagen , laminin and other scleroproteins Collagen disease COL1 : Osteogenesis imperfecta Ehlers–Danlos syndrome, types 1, 2, 7 COL2 : Hypochondrogenesis Achondrogenesis type 2 Stickler syndrome Marshall syndrome Spondyloepiphyseal dysplasia congenita Spondyloepimetaphyseal dysplasia, Strudwick type Kniest dysplasia (see also C2/11 ) COL3 : Ehlers–Danlos syndrome, types 3 & 4 Sack–Barabas syndrome COL4 : Alport syndrome COL5 : Ehlers–Danlos syndrome, types 1 & 2 COL6 : Bethlem myopathy Ullrich congenital muscular dystrophy COL7 : Epidermolysis bullosa dystrophica Recessive dystrophic epidermolysis bullosa Bart syndrome Transient bullous dermolysis of the newborn COL8: Fuchs' dystrophy 1 COL9: Multiple epiphyseal dysplasia 2, 3, 6 COL10: Schmid metaphyseal chondrodysplasia COL11: Weissenbacher–Zweymüller syndrome Otospondylomegaepiphyseal dysplasia (see also C2/11 ) COL17: Bullous pemphigoid COL18: Knobloch syndrome Laminin Junctional epidermolysis bullosa Laryngoonychocutaneous syndrome Other Congenital stromal corneal dystrophy Raine syndrome Urbach–Wiethe disease TECTA DFNA8/12, DFNB21 see also fibrous proteins v t e Disease of the kidney glomerules Primarily nephrotic Non-proliferative Minimal change Focal segmental Membranous Proliferative Mesangial proliferative Endocapillary proliferative Membranoproliferative/mesangiocapillary By condition Diabetic Amyloidosis Primarily nephritic , RPG Type I RPG / Type II hypersensitivity Goodpasture syndrome Type II RPG / Type III hypersensitivity Post-streptococcal Lupus diffuse proliferative IgA Type III RPG / Pauci-immune Granulomatosis with polyangiitis Microscopic polyangiitis Eosinophilic granulomatosis with polyangiitis General glomerulonephritis glomerulonephrosis

HLA-DRB1, RBM45, COL4A3, HLA-DQB1, MPO, FCGR2B, FCGR3A, FCGR3B, FCGR2A, DDR1, IGAN1, B3GAT1, CERT1, PXDN, TNF, TGFB1, SYK, RPS19, PPARA, ABO, MMP12, LAMA5, IL1RN, BTK, HLA-DQB2, HLA-DPB1, HLA-C, CFH, GNAO1, EGFR, ATN1, WG
- Goodpasture Syndrome OMIM
  
  Clinical Features Goodpasture syndrome is an autoimmune disease of lung and kidney. Viral and streptococcal infections and exposure to hydrocarbon fumes have been suggested as possible causes. Three familial instances (Gossain et al., 1972; Maddock et al., 1967), including a pair of identical twins (D'Apice et al., 1978), have been reported. One twin had pumped gasoline in a filling station for 2 weeks before onset; the other twin had, 5 days before onset, started a job spraying ball-bearings with a fine mist of mineral turpentine. The host factor might be immune response genes. Maddock et al. (1967) described the Goodpasture syndrome in 2 male first cousins.
- Anti-Glomerular Basement Membrane Disease Orphanet
  
  A rare, fulminant small vessel vasculitis that affects the capillary beds of the kidneys and lungs and characterized by the presence of anti-glomerular basement membrane (GBM) and, in its full-blown form, anti-alveolar basement membrane (ABM) antibodies. Consequently, it may manifest as a rapidly progressive, isolated glomerulonephritis (anti-GBM nephritis) or as a pulmonary-renal syndrome with severe lung hemorrhage. Epidemiology The incidence of the disease is estimated to be approximately 0.6-1.8 cases per million per year in both Asian and European Caucasian (more frequently affected) populations. Men and women seem equally affected. The disorder is responsible for 1-5% of all cases of glomerulonephritis and is the cause in up to 10-15% of patients with rapidly progressive crescentic glomerulonephritis. Clinical description Anti-GBM disease onset is bimodal, occurring mainly in the third and the seventh decades of life.
- Goodpasture Syndrome GARD
  
  Goodpasture syndrome is an autoimmune disease that affects the lungs and kidneys and is characterized by pulmonary alveolar hemorrhage (bleeding in the lungs) and a kidney disease known as glomerulonephritis . Some use the term "Goodpasture syndrome" for the findings of glomerulonephritis and pulmonary hemorrhage and the term "Goodpasture disease" for those patients with glomerulonephritis, pulmonary hemorrhage, and anti-GBM antibodies . Currently, the preferred term for both conditions is “ anti-GBM antibody disease ”. Circulating antibodies are directed against the collagen of the part of the kidney known as the glomerular basement membrane (GBM), resulting in acute or rapidly progressive glomerulonephritis. Antibodies also attack the collagen of the air sacs of the lung (alveoli) resulting in bleeding of the lung (pulmonary hemorrhage).
- Pulmonary-Renal Syndrome Wikipedia
  
  Pulmonary-renal syndrome (PRS) is a rare medical syndrome in which respiratory failure involving bleeding in the lungs and kidney failure ( glomerulonephritis ) occur. [1] PRS is associated with a high rate of morbidity and death. [1] The term was first used by Goodpasture in 1919 to describe the association of respiratory and kidney failure. [1] Contents 1 Causes 2 Diagnosis 2.1 Differential diagnosis 3 Treatment 4 References Causes [ edit ] Pulmonary-renal syndromes are most commonly caused by an underlying autoimmune disease. PRS is most commonly due to ANCA -associated vasculitides (e.g., granulomatosis with polyangiitis ) or due to anti-basement membrane diseases (e.g., Goodpasture's syndrome ). Granulomatosis with polyangiitis usually presents with nasopharyngeal involvement as well, whereas Goodpasture's will not. Microscopic polyangiitis is the most common cause of pulmonary-renal syndrome. [ citation needed ] Other causes include systemic lupus erythematosus , eosinophilic granulomatosis with polyangiitis , microscopic polyangiitis , dermatomyositis , polymyositis , mixed connective tissue disease , poststreptococcal glomerulonephritis , rheumatoid arthritis , and systemic sclerosis . [1] Less common causes also include IgA vasculitis and cryoglobulinemic vasculitis . Other etiologies include toxic injury such as paraquat poisoning, infection with hantavirus , leptospirosis , or legionella , or vascular, as seen in nephrotic syndrome when a renal vein thrombosis embolizes to the lungs.