Load FindZebra SummaryDisclaimer: FindZebra Search conducts a search using our specialized medical serach engine. FindZebra Summary uses the GPT-3.5-Turbo API (subject to OpenAI’s API data usage policies) to summarize and reason about the search results. The search is conducted in publicly available information on the Internet that we present “as is”. You should be aware that FindZebra is not supplying any of the content in the search results.
The disease usually occurs from birth to age 15.  Histiocytosis (and malignant histiocytosis ) are both important in veterinary as well as human pathology. Contents 1 Types 2 Diagnosis 2.1 Classification 3 Treatments 4 Society 5 References 6 External links Types [ edit ] Types of LCH have also been known as "eosinophilic granuloma", "Hand-Schuller-Christian disease", "Letterer-Siwe disease", and "histiocytosis X". ... 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
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?
The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile.  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.  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.  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. ... Treatment and control [ edit ] Currently, the most effective treatment is transferring the affected fish to a freshwater bath for a period of 2 to 3 hours. This is achieved by towing the sea cages into fresh water, or pumping the fish from the sea cage to a tarp filled with fresh water.  Mortality rates have been lowered by adding levamisole to the water until the saturation is above 10ppm. ... 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 .
Retiform parapsoriasis Specialty Dermatology Retiform parapsoriasis is a cutaneous condition, considered to be a type of large-plaque parapsoriasis .  It is characterized by widespread, ill-defined plaques on the skin, that have a net-like or zebra-striped pattern.  Skin atrophy , a wasting away of the cutaneous tissue , usually occurs within the area of these plaques.  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 Other names Parapsoriasis variegata  or Parapsoriasis lichenoides  Typical skin changes and discoloration described as poikiloderma vasculare atrophicans Specialty Dermatology Poikiloderma vasculare atrophicans ( PVA ), is a cutaneous condition ( skin disease ) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation , respectively), telangiectasia and skin atrophy .    Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis .  The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906.  PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper".  On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin).   Mycosis fungoides, a type of skin lymphoma , may be a cause of PVA. The condition may also be caused by, associated with or accompany any of the following conditions or disorders: other skin lymphomas, dermatomyositis , lupus erythematosus , Rothmund–Thomson syndrome , Kindler syndrome , dyskeratosis congenita , and chronic radiodermatitis .  Rare causes include arsenic ingestion, and the condition can also be idiopathic .    PVA may be considered a rare variant of cutaneous T-cell lymphoma , a non-Hodgkin's form of lymphoma affecting the skin.  It may also be included among a number of similar conditions that are considered as precursors to mycosis fungoides . PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis ; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis .  Contents 1 Presentation 2 Cause 3 Diagnosis 3.1 Classification 4 Management 5 See also 6 References 7 External links Presentation [ edit ] The layers of the epidermis (left). ... "Les parapsoriasis". Ann Dermatol Syphiligr (Paris) . 3 : 433–468. ^ Sutton RL (1956). Diseases of the skin .
Abnormal depolarizations of cardiac myocytes Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart . ... Early afterdepolarizations [ edit ] Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive action potentials before normal repolarization is completed. Phase 2 may be interrupted due to augmented opening of calcium channels , while phase 3 interruptions are due to the opening of sodium channels . ... They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity.   The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger. This results in a net depolarizing current. The classical feature is Bidirectional ventricular tachycardia .
Human African Trypanosomiasis (HAT), also called sleeping sickness, is a vector-borne parasitic disease caused by a protozoa of the Trypanosoma genus transmitted by the bite of a tsetse fly (genus Glossina ), that is found under its chronic form (average duration of 3 years) in western and central Africa (in case of the T. brucei gambiense sub-species), and under its acute form (lasting from few weeks to 6 months) in eastern and southern Africa (in case of the T. brucei rhodesiense sub-species).
Other probabilities for the other possible allele combinations concerning this gene are: 0% chance of affected offspring if only one parent is a carrier, 0% chance of affected offspring if one parent is affected and the other does not carry the allele, and 50% chance of affected offspring if one parent is affected and the other is a carrier. ... It is not until the baby is born that a diagnosis can be declared.  The diagnosis is declared with the help of several x-rays  and charted bone growth patterns. ... Modification suggestions [ edit ] Height adjustments for goals and volleyball nets. Modified rules to accommodate size and structure. ... "CJO - Abstract - Genetic management of chondrodystrophy in California condors" . Animal Conservation Forum . 3 (2): 145–153 . Retrieved 2007-12-23 . ^ a b "Dwarfism" . ... International Journal of Osteoarchaeology . 17 (3): 318–321. doi : 10.1002/oa.872 . ^ "Dysplasia Epiphysealis Multiplex (DEM) (earlier synonyms: Fairbank's Disease, Ribbing's disease, Epiphyseal dysostosis, Hereditary enchondral dysostosis)" .
Glycogen storage disease type 0 Glycogen storage disease type 0 has defect in glycogen synthase Specialty Medical genetics Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GSY). ... Contents 1 Signs and symptoms 2 Causes 3 Pathophysiology 4 Diagnostic 4.1 Laboratory Studies 4.2 Imaging Studies 4.3 Other Tests 4.4 Procedures 4.5 Histologic Findings 4.6 Differential Diagnoses 4.7 Types 5 Treatment 6 Epidemiology 6.1 Mortality/Morbidity 6.2 Sex 6.3 Age 7 References 8 External links Signs and symptoms [ edit ] The most common clinical history in patients with glycogen-storage disease type 0 (GSD-0) is that of an infant or child with symptomatic hypoglycemia or seizures that occur before breakfast or after an inadvertent fast. ... Serum electrolytes calculate the anion gap to determine presence of metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an anion gap in the reference range and no acidosis. ... Types [ edit ] There are two types of this\\e condition glycogen storage disease type 0 to be considered, they are:   Glycogen storage disease due to liver glycogen synthase deficiency Glycogenosis due to muscle and heart glycogen synthase deficiency Treatment [ edit ] The goal for treatment of Glycogen-storage disease type 0 is to avoid hypoglycemia. ... "Mutations in the liver glycogen synthase gene in children with hypoglycemia due to glycogen storage disease type 0" . J. Clin. Invest . 102 (3): 507–15. doi : 10.1172/JCI2890 .
Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired. The signs and symptoms of muscle GSD 0 typically begin in early childhood. ... Because some people with muscle GSD 0 die from sudden cardiac arrest early in life before a diagnosis is made and many with liver GSD 0 have mild signs and symptoms, it is thought that GSD 0 may be underdiagnosed. Causes Mutations in the GYS1 gene cause muscle GSD 0, and mutations in the GYS2 gene cause liver GSD 0.
A number sign (#) is used with this entry because of evidence that liver glycogen storage disease-0 (GSD0A) is caused by homozygous or compound heterozygous mutation in the GYS2 gene (138571), which encodes glycogen synthase-2, on chromosome 12p12. ... Gitzelmann et al. (1996) described 3 children with liver glycogen synthase deficiency from 2 German families and compared the observations with the previously published 3 families comprising 8 patients. ... In the first year of life she ate every 3 to 4 hours and never slept through the night, awakening spontaneously to feed. ... Mapping Orho et al. (1998) established linkage of glycogen storage disease 0 to intragenic and flanking polymorphic markers of the GYS2 gene on chromosome 12p12.2. Molecular Genetics In affected members of 5 families with liver glycogen storage disease 0, Orho et al. (1998) identified homozygous or compound heterozygous mutations in the GYS2 gene (138571.0001-138571.0008) Inheritance - Autosomal recessive Neuro - Seizures Lab - Glycogen synthetase deficiency Metabolic - Neonatal hypoglycemia - Fasting hypoglycemia - Fasting hyperketonemia - Hyperglycemia and hyperlactatemia with feeding ▲ Close
A genetically inherited anomaly of glycogen metabolism and a form of glycogen storage disease (GSD) characterized by fasting hypoglycemia. This is not a glycogenosis, strictly speaking, as the enzyme deficiency decreases glycogen reserves. Epidemiology It is an extremely rare disease; about 20 cases have been reported in the literature so far. Clinical description It commonly appears in infancy or in early childhood. Patients present with morning fatigue and fasting hypoglycemia (without hepatomegaly) associated with hyperketonemia but without hyperalaninemia or hyperlactacidemia.
Glycogen storage disease type 0, liver (liver GSD 0), a form of glycogen storage disease (GSD), is a rare abnormality of glycogen metabolism (how the body uses and stores glycogen, the storage form of glucose). Unlike other types of GSD, liver GSD 0 does not involve excessive or abnormal glycogen storage, and causes moderately decreased glycogen stores in the liver. ... This condition differs from another form of GSD 0 which chiefly affects the muscles and heart ( Glycogen storage disease type 0, muscle ) and is thought to be caused by mutations in the GYS1 gene.
Neonatal Skin: Structure and Function . CRC Press. pp. 67–. ISBN 978-0-8247-0887-0 . ^ Mariagrazia Stracquadanio; Lilliana Ciotta (20 April 2015). ... A Woman Doctor's Guide to Skin Care: Essential Facts and Information on Keeping Skin Healthy . Hyperion. ISBN 978-0-7868-8100-0 . ^ Sarah Bekaert (2007). ... Lippincott Williams & Wilkins. pp. 328–. ISBN 978-0-7817-4059-3 . ^ Newsletter . The Academy. 1986. ^ Adrian Raine (2006). ... CUP Archive. pp. 321–. ISBN 978-0-521-22673-8 . ^ Raphael Rubin; David S. ... Academic Press. 3 October 1994. pp. 1994–. ISBN 978-0-08-058373-0 .
The Hormone Decision . Contemporary Books. ISBN 978-0-07-141615-3 . ^ Maria Siemionow; Marita Eisenmann-Klein (13 January 2010). ... Rowman & Littlefield Publishers. pp. 73–. ISBN 978-0-7591-2332-8 . ^ Vasan; R.S. (1 January 1998). ... Biochemistry and Function of Sterols . CRC Press. pp. 26–27. ISBN 978-0-8493-7674-0 . ^ Michael Crocetti; Michael A. ... Lippincott Williams & Wilkins. pp. 564–. ISBN 978-0-7817-3770-8 . ^ W. Steven Pray (2006). ... Elsevier Health Sciences. pp. 1281–. ISBN 978-0-323-08678-3 . ^ Guy I. Benrubi (28 March 2012).
Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... Neurological disease and therapy. 85 . Informa Health Care. p. 204. ISBN 0-8493-3695-3 . ^ Greenberg, Mark S. (2006). ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007). ... Diagnosis and management in vision care . Butterworths. p. 16. ISBN 0-409-95082-3 . ^ a b Lee, David A.; Eve J. ... Springer. pp. 107–108. ISBN 1-84628-643-3 .
Dermatology . Upjohn Co. ISBN 0-89501-004-6 . ^ a b c d Lynch, Peter J. (1994). Dermatology . Williams & Wilkins. ISBN 0-683-05252-7 . ^ Tilles G, Wallach D (1989). ... McGraw-Hill Medical Pub. Division. ISBN 0-07-144019-4 . ^ Werner B (August 2009). ... Biochemistry and physiology of the skin . Oxford University Press. ISBN 0-19-261253-0 . ^ Fuchs E (February 2007). ... Retrieved 3 June 2013 . ^ Bolognia, Jean L.; et al. (2007).
Genodermatosis is a hereditary disease, knowing as much as possible about a detailed and complete family history helps in screening and diagnosis; 3. People can do a detailed physical examination to observe the special features and manifestations of other organs besides skin. ... Genodermatosis is a kind of skin disease, it affects the texture, color and structure of the cuticle and connective tissue of the skin, some of which can cause abnormalities in other organs.  On the social side, because the genodermatosis makes the patients’ skin and appearance different from the ordinary people and makes them have limitations in some activities, they more or less encounter obstacles in the process of making friends, seeking a mate, going to school and entering the workplace.   Difficulties in communicating with others as well as worldly prejudice may affect their mental health. ... Avery's Diseases of the Newborn . pp. 1475–1494.e1. doi : 10.1016/B978-0-323-40139-5.00104-2 . ISBN 978-0-323-40139-5 . ^ a b Tantcheva-Poór, Iliana; Oji, Vinzenz; Has, Cristina (October 2016). ... Journal of Cosmetic Dermatology . 16 (3): 402–406. doi : 10.1111/jocd.12263 . ... Indian Dermatology Online Journal . 4 (3): 225–7. doi : 10.4103/2229-5178.115527 .
Nevus comedonicus (also known as a " comedo nevus "  ) is characterized by closely arranged, grouped, often linear, slightly elevated papules that have at their center keratinous plugs resembling comedones .  : 634  : 774 See also [ edit ] Nevus comedonicus syndrome Skin lesion List of cutaneous conditions References [ edit ] ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... Louis: Mosby. p. 1673. ISBN 1-4160-2999-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . This Epidermal nevi, neoplasms, cysts article is a stub .
Clinical Features Levinsohn et al. (2016) studied 3 unrelated patients with nevus comedonicus. The first was a 43-year-old woman with a 6 cm by 3 cm linear lesion on the back consisting of grouped comedones, with a history of inflammatory cysts within the lesion. ... Molecular Genetics By whole-exome sequencing on DNA from blood and tissue samples from 3 unrelated patients with nevus comedonicus, Levinsohn et al. (2016) identified heterozygous somatic mutations in NC lesions from all 3 patients (see 609798.0003-609798.0005).
A rare, syndromic nevus characterized by the association of typically unilateral, closely arranged, linear, slightly elevated, multiple, nevus comedonicus lesions located usually on the face, neck, trunk or limbs (with or without a central, dark, firm, hyperkeratotic plug and secondary acneiform lesions) with extracutaneous ocular, skeletal, and/or central nervous system abnormalities, such as ipsilateral cataract, corneal erosion, poly-/syndactyly, absent fifth finger, scoliosis, vertebral defects, corpus callosum agenesis, seizures, interhemispheric cyst, intellectual deficiency, and/or developmental delay.
Please note that phase 0 leads to a net gain of Na + , while phases 1-3 lead to a net loss of K + . ... Repolarization of the cardiomyocytes occurs in phases 1-3, and is caused predominantly by the outward movement of potassium ions. ... Sanoski, Cynthia A.,, Deglin, Judith Hopfer, 1950- (Fourteenth ed.). Philadelphia. ISBN 978-0-8036-4085-6 . OCLC 881473728 . ^ Lenz T. ... United Kingdom: Elsevier. p. 568. ISBN 978-0-7020-3084-0 . ^ a b Yap, Yee Guan; Camm, A John (2017-01-17). ... British Journal of Clinical Pharmacology . 81 (3): 420–427. doi : 10.1111/bcp.12726 .
Nevus lipomatosus (cutaneous) superficialis ( NLS or NLCS , also known as "Nevus lipomatosis of Hoffman and Zurhelle"  ) is characterized by soft, yellowish papules or cerebriform plaques , usually of the buttock or thigh, less often of the ear or scalp, with a wrinkled rather than warty surface.   : 625 It is usually congenital in origin or appears within the first three decades.  A pedunculated lipofibroma is a solitary variant of nevus lipomatosus superficialis .  It usually appears in adult life, and usually on the axilla, knee, ear, arm, scalp and the lower trunk.  Pedunculated lipofibroma, gross pathology Micrograph of pedunculated lipofibroma, low magnification, with dermal expansion of fatty tissue. ... The main differential diagnoses are acrochordon , seborrheic keratosis , intradermal melanocytic nevi , neurofibromas , verrucae and fibroepithelioma of Pinkus.  See also [ edit ] Skin lesion List of cutaneous conditions References [ edit ] ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ a b c d Das, Anupam; Chandra, Somodyuti; Mohanty, Swosti; Gharami, RameshC; Podder, Indrashis (2015). ... Indian Journal of Paediatric Dermatology . 0 (0): 0. doi : 10.4103/2319-7250.165641 .
Pili annulati Specialty Medical genetics Pili annulati (also known as " ringed hair "  ) is a genetic trait in which the hair seems ‘banded‘ by alternating segments of light and dark color when seen in reflected light.   : 767  : 640  See also [ edit ] Pili pseudoannulati List of cutaneous conditions References [ edit ] ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ http://www.omim.org/entry/180600 External links [ edit ] Hair Transplant Classification D ICD - 10 : Q84.1 ( ILDS Q84.110) ICD - 9-CM : 757.4 MeSH : C537187 v t e Congenital malformations and deformations of skin appendages Nail disease Anonychia Leukonychia Pachyonychia congenita / Onychauxis Koilonychia Hair disease hypotrichosis /abnormalities: keratin disease Monilethrix IBIDS syndrome Sabinas brittle hair syndrome Pili annulati Pili torti Uncombable hair syndrome Björnstad syndrome Giant axonal neuropathy with curly hair hypertrichosis : Zimmermann–Laband syndrome This condition of the skin appendages article is a stub .
Clinical Features Cady and Trotter (1920) reported 3 unrelated families with ringed hair. ... In addition, individuals with pili annulati usually have normal growth of hair, whereas those with monilethrix have alopecia as well as associated follicular keratosis. Inheritance In 3 families with ringed hair reported by Cady and Trotter (1920), the transmission pattern was consistent with autosomal dominant inheritance.
Pili annulati is a hair disorder. In pili annulati, affected hair has a pattern of light and dark banding. People with pili annulati may describe their hair as "striped" or as having silvery beads. Pili annulati typically involves 20-80% of scalp hair, however it can involve facial and body hair as well. Affected hairs may be more prone to breakage. Pili annulati can present in infancy, childhood, or later in life. It can be seen with the naked eye, however it may be more difficult to see in people with dark hair.
Pili annulati is an isolated, benign hair shaft abnormality, usually presenting after the age of 2 and affecting the hair of the scalp or very rarely beard, axillary, or pubic hair, that is characterized by a banded or speckled appearance due to alternating light bands (corresponding to air-filled cavities within the cortex of the affected hair shafts) and dark bands. The bands have a lifelong duration, may only be detectable under light microscopy, are more apparent in fair-colored hair or with age-related graying, and have no effect on hair growth or fragility in the vast majority of cases.
Pili torti Menkes disease Specialty Medical genetics Pili torti (also known as "Twisted hairs") is characterized by short and brittle hairs that appear flattened and twisted when viewed through a microscope.  : 638  : 764  This phenotype is noted in Menkes disease , and Lichen Planopilaris Pili torti can also occur after use of retinoids, such as isotretinoin See also [ edit ] List of cutaneous conditions Crandall syndrome References [ edit ] ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). 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 . External links [ edit ] Classification D ICD - 10 : Q84.1 ( ILDS Q84.120) MeSH : C562485 C562485, C562485 DiseasesDB : 29682 v t e Congenital malformations and deformations of skin appendages Nail disease Anonychia Leukonychia Pachyonychia congenita / Onychauxis Koilonychia Hair disease hypotrichosis /abnormalities: keratin disease Monilethrix IBIDS syndrome Sabinas brittle hair syndrome Pili annulati Pili torti Uncombable hair syndrome Björnstad syndrome Giant axonal neuropathy with curly hair hypertrichosis : Zimmermann–Laband syndrome This condition of the skin appendages article is a stub .
Pili torti is a hair shaft abnormality characterized by flat hair that is twisted at irregular intervals. Hair is normal at birth but progressively stops growing long and becomes fragile. Pili torti can be isolated or occur in association with syndromes such as Menkes disease or Bazex syndrome (see these terms).
Description Pili torti, or twisted hair, is a condition in which the hair shafts are flattened and rotated along their long axis. Hairs are fragile and break at short length. Some patients may have associated dental or nail findings, and many have resolution of the fragile hair at puberty (review by Dawber, 1996). Pili torti is also a feature in several disorders, including Bjornstad syndrome (BJS; 262000), Bazex syndrome (BZX; 301845), and Menkes disease (309400). Clinical Features Pili torti was first described and named by Ronchese (1932), who observed 2 affected Italian sisters. The proband had dull blonde scalp hair that was 'lank and frizzy, with a wild, bushy appearance.'
Pili torti is a rare hair condition characterized by fragile hair. In pili torti hair has a flattened shaft with clusters of narrow twists at irregular intervals. Some cases may be inherited in autosomal dominant or autosomal recessive patterns, while others are acquired. In the inherited form, symptoms tend to be present from early childhood. It can occur alone or as part of other diseases like ectodermal dysplasias , Menke disease , Bjornstand syndrome , or Bazex syndrome . Acquired cases of pili torti may be associated with anorexia nervosa , malnutrition, oral retinoid treatment, or inflammatory scalp conditions (e.g., cutaneous lupus erythematousus ).
State University of New York Press. ISBN 0-7914-5754-0 . ^ Jacobson, Kirsten. 2006. ... The Loss of Sadness . Oxford. ISBN 978-0-19-531304-8 . ^ Wilson, Mitchell. 1993. ... Houghton Mifflin. 2007. ISBN 978-0-618-82435-9 . ^ a b Boeree, C. George (2002). ... New York: Anchor Books / Doubleday . ISBN 0-385-05221-9 . Ladell, R. M., and T. ... Albany: State University of New York Press. ISBN 0-7914-5754-0 Winokur, Jon . 2005. Encyclopedia Neurotica.