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Pediculosis Corporis Wikipedia

A pediculicide should be applied exactly as directed on the bottle or by a physician. [ citation needed ] Delousing can also be practically achieved by boiling all clothes and bedding, or washing them at a high temperature. [3] A temperature of 130 °F or 54 °C for 5 minutes will kill most of the adults and prevent eggs from hatching. [4] Leaving the clothes unwashed, but unworn for a full week, also results in the death of lice and eggs. [3] Where this is not practical or possible, powder dusting with 10% DDT , 1% malathion or 1% permethrin is also effective. [3] Oral ivermectin at a dose of 12 mg on days 0, 7 and 14 has been used in a small trial of 33 people in Marseilles , but did not result in complete eradication, although there was a significant fall in the number of parasites and proportion of people infected. [5] At the moment, ivermectin cannot be routinely recommended for the treatment of body lice. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Global Health - Division of Parasitic Diseases and Malaria (24 September 2013). ... 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.
Limbal Nodule Wikipedia

Lippincott Williams & Wilkins. p. 42. ISBN 1-60547-888-1 .
Lymphatic Filariasis Wikipedia

Avoiding mosquito bites, such as by using insecticide -treated mosquito bed nets , also reduces the transmission of lymphatic filariasis. [19] [22] The Carter Center 's International Task Force for Disease Eradication declared lymphatic filariasis one of six potentially eradicable diseases. [19] According to medical experts, the worldwide effort to eliminate lymphatic filariasis is on track to potentially succeed by 2020. [23] For similar-looking but causally unrelated podoconiosis , international awareness of the disease will have to increase before elimination is possible. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ a b Pfarr KM, Debrah AY, Specht S, Hoerauf A (November 2009). ... Anatomy & Physiology: The Unity of Form and Function . McGraw-Hill. ISBN 978-0-07-287506-5 . ^ a b c "Parasites - Lymphatic Filariasis" . cdc.gov . ... Wallingford: CAB International. pp. 1–848. ISBN 0-85198-689-7 . ^ Grove, David I (2014). ... Oxford: Oxford University Press. pp. 1–602. ISBN 978-0-19-964102-4 . ^ Burma D.P. (2010).

GPT2, THAS, IL10, HSPD1, TLR9, TLR2, LMLN, GGTLC1, TMPRSS13, NARS2, RBM33, TLR1, HSPA14, NBEAL2, HERPUD1, NR0B2, VEGFA, TXN, TNFRSF1B, TLR4, CISH, CTLA4, MSMB, EDN1, FOXC2, FLT4, HGF, IGHG3, IL3, MST1, TGFB1, NARS1, PRL, PTEN, PTPN6, SLA, SMS, LOC102724197
- Lymphatic Filariasis Gard
  
  Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms that only live in the human lymph system , which maintains the body's fluid balance and fights infections. It is spread from person to person by mosquitoes. Most infected people are asymptomatic and never develop clinical symptoms. A small percentage of people develop lymphedema , which may affect the legs, arms, breasts, and genitalia; bacterial infections that cause hardening and thickening of the skin, called elephantiasis; hydrocele (swelling of the scrotum) in men; and pulmonary tropical eosinophilia syndrome . Treatment may include a yearly dose of medicine, called diethylcarbamazine (DEC); while this drug does not kill all of the adult worms, it prevents infected people from giving the disease to someone else.
- Lymphatic Filariasis Orphanet
  
  Lymphatic filariasis (LF) is a severe form of filariasis (see this term), caused by the parasitic worms Wuchereria bancrofti , Brugia malayi and Brugia timori , and the most common cause of acquired lymphedema worldwide. LF is endemic to tropical and subtropical regions. The vast majority of infected patients are asymptomatic but it can also cause a variety of clinical manifestations, including limb lymphedema, genital anomalies (hydrocele, chylocele), elephantiasis in later stages of the disease (frequently in the lower extremities), and tropical pulmonary eosinophilia (nocturnal paroxysmal cough and wheezing, weight loss, low-grade fever, adenopathy, and pronounced blood eosinophilia). Renal involvement (hematuria, proteinuria, nephritic syndrome, glomerulonephritis), and mono-arthritis of the knee or ankle joint have also been reported.
Stress Shielding Wikipedia

Materials Science and Engineering: C . 70 (1): 870–888. doi : 10.1016/j.msec.2016.09.069 .
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. ... Chichester, West Sussex: Blackwell Pub. pp. 2774–2784. ISBN 978-1-4051-6911-0 . ^ "Esophagus Disorders" . Medline Plus . ... Edinburgh: Churchill Livingstone/Elsevier. ISBN 978-0-7020-3085-7 . ^ Ali Nawaz Khan. "Small-Bowel Obstruction Imaging" .

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

Cutaneous symptoms include one or more of the following: cold contact-induced urticarial (which may be the first sign of the disease); painful episodes of finger and/or toe arterial spasms termed Raynaud phenomena ; cyanosis , a palpable purpura termed cryofibrinogenemic purpura ), and a lace-like purplish discoloration termed livedo reticularis all of which occur primarily in the lower extremities but some of which may occur in the nose, ears, and buttocks; non-healing painful ulcerations and gangrene of the areas impacted by the cited symptoms. [2] Patients also have a history of cold sensitivity (~25% of cases), arthralgia (14-58%), neuritis (7-19%), myalgia (0-14%); and overt thrombosis of arteries and veins (25-40%) which may on rare occasions involve major arteries such of those of the brain and kidney. [5] [6] [7] Signs of renal involvement ( proteinuria , hematuria , decreased glomerular filtration rate , and/or, rarely, renal failure ) occur in 4-25% of cases. [5] [8] Compared to secondary cryofibrinogemia, primary crygofibrinogenemia has a higher incidence of cutaneous lesions, arthralgia, and cold sensitivity while having a far lower incidence of renal involvement. [5] Patients with secondary cryofibrinogenemia also exhibit signs and symptoms specific to the infectious, malignant, premalignant vasculitis, and autoimmune disorders associated with their disease. [2] While rare, individuals with cryofibrinogenemic disease may experience pathological bleeding due to the consumption of blood clotting factors consequential to the formation of cryofibrinogen precipitates. [2] [5] Diagnosis [ edit ] Suggested diagnostic criteria for cryoglobulinemic disease fall into the following obligatory and additional categories: [5] Obligatory criteria: 1) cold sensitivity; 2) cutaneous symptoms (i.e. urticaria, purpura, Raynaud phenomenon, ulceration/necrosis/gangrene, and/or livedo reticularis); 3) arterial and/or venous thrombotic events; fever; 4) arthralgia/myalgia; 5) neuritis in >1 site; and 6) renal disorder. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . : 822 ^ a b c d e f g h i j k l m Grada A, Falanga V (2017). ... Journal of Thrombosis and Haemostasis . 15 (5): 876–888. doi : 10.1111/jth.13655 . PMID 28211264 . ^ Casini A, Sokollik C, Lukowski SW, Lurz E, Rieubland C, de Moerloose P, Neerman-Arbez M (2015).

TREX1
Lichen Spinulosus Wikipedia

Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . References [ edit ] Friedman S (1990). ... PMID 2179296 . External links [ edit ] Derm Net NZ Emedicine Thehinhso v t e Diseases of the skin and appendages by morphology Growths Epidermal Wart Callus Seborrheic keratosis Acrochordon Molluscum contagiosum Actinic keratosis Squamous-cell carcinoma Basal-cell carcinoma Merkel-cell carcinoma Nevus sebaceous Trichoepithelioma Pigmented Freckles Lentigo Melasma Nevus Melanoma Dermal and subcutaneous Epidermal inclusion cyst Hemangioma Dermatofibroma (benign fibrous histiocytoma) Keloid Lipoma Neurofibroma Xanthoma Kaposi's sarcoma Infantile digital fibromatosis Granular cell tumor Leiomyoma Lymphangioma circumscriptum Myxoid cyst Rashes With epidermal involvement Eczematous Contact dermatitis Atopic dermatitis Seborrheic dermatitis Stasis dermatitis Lichen simplex chronicus Darier's disease Glucagonoma syndrome Langerhans cell histiocytosis Lichen sclerosus Pemphigus foliaceus Wiskott–Aldrich syndrome Zinc deficiency Scaling Psoriasis Tinea ( Corporis Cruris Pedis Manuum Faciei ) Pityriasis rosea Secondary syphilis Mycosis fungoides Systemic lupus erythematosus Pityriasis rubra pilaris Parapsoriasis Ichthyosis Blistering Herpes simplex Herpes zoster Varicella Bullous impetigo Acute contact dermatitis Pemphigus vulgaris Bullous pemphigoid Dermatitis herpetiformis Porphyria cutanea tarda Epidermolysis bullosa simplex Papular Scabies Insect bite reactions Lichen planus Miliaria Keratosis pilaris Lichen spinulosus Transient acantholytic dermatosis Lichen nitidus Pityriasis lichenoides et varioliformis acuta Pustular Acne vulgaris Acne rosacea Folliculitis Impetigo Candidiasis Gonococcemia Dermatophyte Coccidioidomycosis Subcorneal pustular dermatosis Hypopigmented Tinea versicolor Vitiligo Pityriasis alba Postinflammatory hyperpigmentation Tuberous sclerosis Idiopathic guttate hypomelanosis Leprosy Hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized Drug eruptions Viral exanthems Toxic erythema Systemic lupus erythematosus Localized Cellulitis Abscess Boil Erythema nodosum Carcinoid syndrome Fixed drug eruption Specialized Urticaria Erythema ( Multiforme Migrans Gyratum repens Annulare centrifugum Ab igne ) Nonblanchable Purpura Macular Thrombocytopenic purpura Actinic/solar purpura Papular Disseminated intravascular coagulation Vasculitis Indurated Scleroderma / morphea Granuloma annulare Lichen sclerosis et atrophicus Necrobiosis lipoidica Miscellaneous disorders Ulcers Hair Telogen effluvium Androgenic alopecia Alopecia areata Systemic lupus erythematosus Tinea capitis Loose anagen syndrome Lichen planopilaris Folliculitis decalvans Acne keloidalis nuchae Nail Onychomycosis Psoriasis Paronychia Ingrown nail Mucous membrane Aphthous stomatitis Oral candidiasis Lichen planus Leukoplakia Pemphigus vulgaris Mucous membrane pemphigoid Cicatricial pemphigoid Herpesvirus Coxsackievirus Syphilis Systemic histoplasmosis Squamous-cell carcinoma This condition of the skin appendages article is a stub .
Pachyonychia Congenita Gene_reviews

International Pachyonychia Congenita Research Registry (IPCRR) Data Summary (as of 10 May 2017) View in own window Gene in Which Pathogenic Variants Were Confirmed KRT6A KRT6B KRT6C KRT16 KRT17 TOTAL Number evaluated for finding 1 304 71 22 247 130 774 Toenails thickened 10 toenails 286 (94%) 26 (37%) 0 (00%) 99 (40%) 100 (77%) 511 (66%) 7-9 toenails 9 (03%) 14 (20%) 0 (00%) 52 (21%) 11 (08%) 86 (11%) 4-6 toenails 2 (01%) 21 (30%) 3 (14%) 63 (26%) 7 (05%) 96 (12%) 1-3 toenails 4 (01%) 9 (13%) 10 (45%) 44 (18%) 8 (06%) 75 (10%) Total w/toenails thickened 301 (99%) 70 (99%) 13 (59%) 238 (96%) 126 (97%) 748 (97%) Age at onset Birth - <1 yr 264 (88%) 10 (14%) 1 (08%) 45 (19%) 92 (73%) 412 (54%) 1-4 yrs 33 (11%) 19 (27%) 6 (46%) 78 (33%) 24 (19%) 160 (21%) 5-14 yrs 4 (01%) 34 (49%) 4 (31%) 74 (31%) 10 (08%) 126 (17%) ≥15 yrs 0 (00%) 7 (10%) 2 (15%) 43 (18%) 1 (01%) 53 (07%) Fingernails thickened 10 fingernails 271 (89%) 4 (06%) 0 (00%) 73 (30%) 62 (48%) 410 (53%) 7-9 fingernails 10 (03%) 4 (06%) 0 (00%) 11 (04%) 13 (10%) 38 (05%) 4-6 fingernails 14 (05%) 17 (24%) 0 (00%) 30 (12%) 28 (22%) 89 (11%) 1-3 fingernails 6 (02%) 7 (10%) 0 (00%) 28 (11%) 9 (07%) 50 (06%) Total w/fingernails thickened 301 (99%) 32 (45%) 0 (00%) 142 (57%) 112 (86%) 587 (76%) Age at onset Birth - <1 yr 267 (89%) 4 (13%) 0 (00%) 33 (23%) 85 (76%) 389 (66%) 1-4 yrs 30 (10%) 8 (25%) 0 (00%) 42 (30%) 19 (17%) 99 (17%) 5-14 yrs 3 (01%) 11 (34%) 0 (00%) 34 (24%) 6 (05%) 54 (09%) ≥15 yrs 1 (00%) 10 (31%) 0 (00%) 34 (24%) 3 (03%) 48 (08%) Plantar keratoderma Always (never completely goes away) 254 (84%) 67 (94%) 19 (86%) 240 (97%) 86 (66%) 666 (86%) Sometimes (feet clear up completely at times) 7 (02%) 1 (01%) 0 (00%) 1 (00%) 14 (11%) 23 (03%) Seldom (feet usually clear of symptoms) 5 (02%) 0 (00%) 0 (00%) 0 (00%) 4 (03%) 9 (01%) Total w/plantar keratoderma 266 (88%) 68 (96%) 19 (86%) 241 (98%) 104 (80%) 698 (90%) Age at onset Birth - <1 yr 39 (15%) 2 (03%) 1 (05%) 23 (10%) 12 (12%) 77 (11%) 1-4 yrs 152 (57%) 23 (34%) 9 (47%) 130 (54%) 35 (34%) 349 (50%) 5-14 yrs 70 (26%) 42 (62%) 9 (47%) 82 (34%) 43 (41%) 246 (35%) ≥15 yrs 5 (02%) 1 (01%) 0 (00%) 8 (03%) 15 (14%) 29 (04%) Plantar pain w/plantar keratoderma 2 Often require medication for pain 65 (24%) 12 (18%) 5 (26%) 74 (31%) 19 (18%) 175 (25%) Very painful, but do not use medication 114 (43%) 32 (47%) 11 (58%) 111 (46%) 34 (33%) 302 (43%) Somewhat painful 77 (29%) 24 (35%) 3 (16%) 50 (21%) 36 (35%) 190 (27%) Total w/plantar keratoderma/pain 256 (96%) 68 (100%) 19 (100%) 235 (98%) 89 (86%) 667 (96%) Palmar keratoderma Always (never completely goes away) 86 (28%) 11 (15%) 2 (09%) 148 (60%) 21 (16%) 268 (35%) Sometimes (hands clear up completely at times) 32 (11%) 7 (10%) 1 (05%) 15 (06%) 22 (17%) 77 (10%) Seldom (hands usually clear of symptoms) 49 (16%) 13 (18%) 3 (14%) 22 (09%) 27 (21%) 114 (15%) Total w/palmar keratoderma 167 (55%) 31 (44%) 6 (27%) 185 (75%) 70 (54%) 459 (59%) Additional findings Oral leukokeratosis 269 (88%) 18 (25%) 4 (18%) 88 (36%) 34 (26%) 413 (53%) Cysts 188 (62%) 49 (69%) 4 (18%) 64 (26%) 121 (93%) 426 (55%) Follicular hyperkeratosis 162 (53%) 30 (42%) 0 (00%) 30 (12%) 86 (66%) 308 (40%) Natal or prenatal teeth 12 (04%) 0 (00%) 0 (00%) 0 (00%) 99 (76%) 111 (14%) 1.

KRT17, KRT16, KRT6A, KRT6B, KRT10, KRT6C, KRT80, SLURP1, PNOC, NFE2L2, AQP5, FLG, KRT1, KLKB1, GJB2, GABPA, MTOR, KRT9
- Pachyonychia Congenita 4 Omim
  
  A number sign (#) is used with this entry because pachyonychia congenita-4 (PC4) is caused by heterozygous mutation in the KRT6B gene (148042) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
- Pachyonychia Congenita Orphanet
  
  Pachyonychia congenita (PC) is a rare genodermatosis predominantly featuring painful palmoplantar keratoderma, thickened nails, cysts and whitish oral mucosa. Epidemiology The prevalence is not known but approximately 1000 patients have been registered to date worldwide. Clinical description PC presents clinically as a spectrum of conditions. PC onset is variable with most cases manifesting soon after birth, others becoming clinically apparent only in late childhood and rarely in adulthood. The first signs of the disease usually are thickened nails or neonatal teeth.
- Pachyonychia Congenita Gard
  
  Pachyonychia congenita (PC) is a rare inherited condition that primarily affects the nails and skin. The fingernails and toenails may be thickened and abnormally shaped . Affected people can also develop painful calluses and blisters on the soles of their feet and less frequently on the palms of their hands ( palmoplantar keratoderma ). Additional features include white patches on the tongue and inside of the mouth (leukokeratosis); bumps around the elbows, knees, and waistline (follicular hyperkeratosis); and cysts of various types including steatocystoma. Features may vary among affected people depending on their specific mutation.
- Pachyonychia Congenita, Autosomal Recessive Omim
  
  For a phenotypic description and a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Inheritance Chong-Hai and Rajagopalan (1977) suggested autosomal recessive inheritance of pachyonychia congenita in a 4-year-old Malaysian girl with first-cousin parents, although they recognized new dominant mutation as a possibility. See also Sivasundram et al. (1985). INHERITANCE - Autosomal recessive HEAD & NECK Mouth - No oral leukoplakia SKIN, NAILS, & HAIR Skin - Horny papules (face, leg, buttocks) - No palmoplantar hyperkeratosis - No hyperhidrosis Nails - Episodic inflammatory swelling of nail bed - Recurrent shedding of nails - Hard,thickened nails (pachyonychia) - Subungual hyperkeratosis MISCELLANEOUS - See also pachyonychia congenita, type 3 (PC1, 167200 ) ▲ Close
- Pachyonychia Congenita 3 Omim
  
  A number sign (#) is used with this entry because pachyonychia congenita-3 (PC3) is caused by heterozygous mutation in the keratin-6a gene (KRT6A; 148041) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
- Pachyonychia Congenita 2 Omim
  
  A number sign (#) is used with this entry because of evidence that pachyonychia congenita-2 (PC2) is caused by heterozygous mutation in the KRT17 gene (148069) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
- Pachyonychia Congenita 1 Omim
  
  A number sign (#) is used with this entry because pachyonychia congenita-1 (PC1) is caused by heterozygous mutation in the keratin-16 gene (KRT16; 148067) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita. PC type 1, the Jadassohn-Lewandowsky type, shows oral leukokeratosis.
Histiocytosis Wikipedia

Information concerning histiocytosis and clinicians located in European countries may be found in many languages at the web portal of Euro Histio Net (EHN). This is a project funded by the European Union, coordinated by Jean Donadieu, APHP , Paris, France. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Goldberg, J; Nezelof, C (1986), "Lymphohistiocytosis: a multi-factorial syndrome of macrophagic activation clinico-pathological study of 38 cases", Hematol Oncol , 4 (4): 275–289, PMID 3557322 . ^ Egan, Caoimhe; Jaffe, Elaine S. (2018). ... Springer Science & Business Media. p. 383. ISBN 978-0-387-73743-0 . External links [ edit ] Classification D ICD - 10 : C96.1 , D76.0 ICD - 9-CM : 202.3 , 277.89 MeSH : D015614 SNOMED CT : 60657004 External resources MedlinePlus : 000068 eMedicine : ped/1997 v t e Histiocytosis WHO-I/ Langerhans cell histiocytosis / X-type histiocytosis Letterer–Siwe disease Hand–Schüller–Christian disease Eosinophilic granuloma Congenital self-healing reticulohistiocytosis WHO-II/ non-Langerhans cell histiocytosis / Non-X histiocytosis Juvenile xanthogranuloma Hemophagocytic lymphohistiocytosis Erdheim-Chester disease Niemann–Pick disease Sea-blue histiocyte Benign cephalic histiocytosis Generalized eruptive histiocytoma Xanthoma disseminatum Progressive nodular histiocytosis Papular xanthoma Hereditary progressive mucinous histiocytosis Reticulohistiocytosis ( Multicentric reticulohistiocytosis , Reticulohistiocytoma ) Indeterminate cell histiocytosis WHO-III/ malignant histiocytosis Histiocytic sarcoma Langerhans cell sarcoma Interdigitating dendritic cell sarcoma Follicular dendritic cell sarcoma Ungrouped Rosai–Dorfman disease

SLC29A3, IFNGR1, BRAF, ALK, MAP2K7, PTPRC, EPHB2, MAPK1, MAP2K1, MAP2K2, S100A1, ARAF, TLR7, CD274, ZHX2, PPT2, CD163, TP53, TIMP1, S100B, CD68, RET, RAF1, CSF1R, PTGS1, XIAP, POU6F1, KIF5B, IL6, CD1A, HPRT1, SEMA6A
Ascariasis Wikipedia

Advances in Parasitology . 73 : 197–230. doi : 10.1016/s0065-308x(10)73008-6 . ISBN 978-0-12-381514-9 . PMID 20627144 . ^ a b Fenwick A (March 2012). ... Lancet . 380 (9859): 2095–128. doi : 10.1016/S0140-6736(12)61728-0 . hdl : 10536/DRO/DU:30050819 . PMID 23245604 . ... Advances in Parasitology . 66 : 149–91. doi : 10.1016/S0065-308X(08)00203-0 . ISBN 978-0-08-087900-0 . PMID 18486690 . ^ Hall A, Hewitt G, Tuffrey V, de Silva N (April 2008). ... Wallingford: CAB International. pp. 1–848. ISBN 0-85198-689-7 . ^ Mascarini-Serra L (April 2011). ... "The intestinal parasites of King Richard III". Lancet . 382 (9895): 888. doi : 10.1016/S0140-6736(13)61757-2 . hdl : 2381/31491 .

GOT2, IFNG, STAT6
- Ascariasis Mayo_clinic
  
  Overview Ascariasis (as-kuh-RIE-uh-sis) is a type of roundworm infection. These worms are parasites that use your body as a host to mature from larvae or eggs to adult worms. Adult worms, which reproduce, can be more than a foot (30 centimeters) long. Ascariasis worm Ascariasis worms are typically pink or white with tapered ends. Female worms can be more than 15 inches (40 centimeters) long and a little less than a quarter inch (6 millimeters) in diameter.
Affluenza Wikipedia

Affluenza: How to Be Successful and Stay Sane . Vermilion . ISBN 978-0-09-190011-3 . ^ James, Oliver (2008). The Selfish Capitalist . Vermilion . ISBN 978-0-09-192381-5 . ^ James, Oliver (2007). ... London: Vermilion. p. 344 . ISBN 978-0-09-190010-6 . 1. The mean prevalence of emotional distress for the six English-speaking nations combined was 21.6%. ... (Archive is the same work, but on a different website) Further reading [ edit ] The Circle of Simplicity , Cecile Andrews, ISBN 0-06-092872-7 The Golden Ghetto: The Psychology of Affluence , Jessie H. O'Neill, ISBN 978-0-9678554-0-0 Voluntary Simplicity , Duane Elgin, ISBN 0-688-12119-5 Voluntary Simplicity , Daniel Doherty & Amitai Etzioni, ISBN 0-7425-2066-8 How Much Is Too Much?
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.
Amoebic Gill Disease Wikipedia

The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile. [2] It was first diagnosed in the summer of 1984/1985 in populations of Atlantic salmon off the east coast of Tasmania and was found to be caused by N. perurans n.sp. [3] Contents 1 Clinical signs and diagnosis 2 Treatment and control 3 Notes 4 References Clinical signs and diagnosis [ edit ] Symptoms typically begin to appear two months after the fish are transferred from freshwater hatcheries to open net sea cages. [4] Symptoms include mucus build-up on the gills of infected fish and hyper-plastic lesions, causing white spots and eventual deterioration of the gill tissue. ... searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] ^ "Neoparamoeba perurans n. sp., an agent of amoebic gill disease of Atlantic salmon (Salmo salar)". ... searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] ^ https://www.int-res.com/articles/dao/25/d025p023.pdf ^ http://eafp.org/display/Search?searchQuery=amoebic+gill+disease&moduleId=2708303&moduleFilter=&categoryFilter=&startAt=0 [ permanent dead link ] References [ edit ] Amoebic Gill Disease Wikivet .
Posterolateral Corner Injuries Wikipedia

Increased recurvatum indicates possible combined injuries to the posterolateral corner and cruciate ligaments. [23] [24] The increase on recurvatum is best reported as the heel height off the examining table. Varus stress test at 0° and 30° - Varus stress testing is accomplished while the patient is lying supine on an examination table. The physician supports the thigh against the side of the exam table and applies a varus force to the knee joint while holding the ankle or foot , first at 0°of flexion and then at 30°. As the knee is stressed, the practitioner should feel for increased gapping at the lateral joint space. ... A negative varus stress test shows no difference between either knee at 0° or 30°. Increased gapping at 0° of flexion typically reflects a serious posterolateral injury with a high probability of accompanying cruciate ligament involvement. ... The posterolateral corner of the knee: Repair versus reconstruction. Am J Sports Med. 2005;33(6):881-888 ^ a b c d e f g h i j Cooper JM, McAndrews PT, LaPrade RF. ... The posterolateral corner of the knee: repair versus reconstruction. Am J Sports Med. 2005;33(6):881-888 ^ LaPrade RF, Resig S, Wentorf F, Lewis JL.
Retiform Parapsoriasis Wikipedia

Retiform parapsoriasis Specialty Dermatology Retiform parapsoriasis is a cutaneous condition, considered to be a type of large-plaque parapsoriasis . [1] It is characterized by widespread, ill-defined plaques on the skin, that have a net-like or zebra-striped pattern. [2] Skin atrophy , a wasting away of the cutaneous tissue , usually occurs within the area of these plaques. [1] See also [ edit ] Parapsoriasis Poikiloderma vasculare atrophicans List of cutaneous conditions References [ edit ] ^ a b Lambert WC, Everett MA (Oct 1981). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . External links [ edit ] Classification D ICD - 10 : L41.5 ICD - 9-CM : 696.2 v t e Papulosquamous disorders Psoriasis Pustular Generalized pustular psoriasis ( Impetigo herpetiformis ) Acropustulosis / Pustulosis palmaris et plantaris ( Pustular bacterid ) Annular pustular psoriasis Localized pustular psoriasis Other Guttate psoriasis Psoriatic arthritis Psoriatic erythroderma Drug-induced psoriasis Inverse psoriasis Napkin psoriasis Seborrheic-like psoriasis Parapsoriasis Pityriasis lichenoides ( Pityriasis lichenoides et varioliformis acuta , Pityriasis lichenoides chronica ) Lymphomatoid papulosis Small plaque parapsoriasis ( Digitate dermatosis , Xanthoerythrodermia perstans ) Large plaque parapsoriasis ( Retiform parapsoriasis ) Other pityriasis Pityriasis rosea Pityriasis rubra pilaris Pityriasis rotunda Pityriasis amiantacea Other lichenoid Lichen planus configuration Annular Linear morphology Hypertrophic Atrophic Bullous Ulcerative Actinic Pigmented site Mucosal Nails Peno-ginival Vulvovaginal overlap synromes with lichen sclerosus with lupus erythematosis other: Hepatitis-associated lichen planus Lichen planus pemphigoides Other Lichen nitidus Lichen striatus Lichen ruber moniliformis Gianotti–Crosti syndrome Erythema dyschromicum perstans Idiopathic eruptive macular pigmentation Keratosis lichenoides chronica Kraurosis vulvae Lichen sclerosus Lichenoid dermatitis Lichenoid reaction of graft-versus-host disease This dermatology article is a stub .
- Poikiloderma Vasculare Atrophicans Wikipedia
  
  Seminars in Cutaneous Medicine and Surgery . 19 (2): 91–99. doi : 10.1016/S1085-5629(00)80005-X . PMID 10892710 . ^ Diseases Database (DDB): 10208 ^ a b c d Chapman, R.