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.
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).
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 .
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.
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.
As a result of quarantine procedures, some of the post-SARS patients have been documented as suffering from post-traumatic stress disorder (PTSD) and major depressive disorder .   Epidemiology [ edit ] Main article: 2002–2004 SARS outbreak SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%.  The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient.  Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%).  As with MERS and COVID-19 , SARS resulted in significantly more deaths of males than females. 2003 Probable cases of SARS – worldwide Probable cases of SARS by country or region, 1 November 2002 – 31 July 2003  Country or region Cases Deaths Fatality (%) China [a] 5,327 349 6.6 Hong Kong 1,755 299 17.0 Taiwan [b] 346 73   21.1 Canada 251 43 17.1 Singapore 238 33 13.9 Vietnam 63 5 7.9 United States 27 00 Philippines 14 2 14.3 Thailand 9 2 22.2 Germany 9 00 Mongolia 9 00 France 7 1 14.3 Australia 6 00 Malaysia 5 2 40.0 Sweden 5 00 United Kingdom 4 00 Italy 4 00 Brazil 300 India 300 South Korea 300 Indonesia 2 00 South Africa 1 1 100.0 Colombia 1 00 Kuwait 1 00 Ireland 1 00 Macao 1 00 New Zealand 1 00 Romania 1 00 Russia 1 00 Spain 1 00 Switzerland 1 00 Total excluding China [a] 2,769 454 16.4 Total (29 territories) 8,096 774 9.6 ^ a b Figures for China exclude Hong Kong and Macau, which are reported separately by the WHO . ^ After 11 July 2003, 325 Taiwanese cases were 'discarded'. ... NHS Choices . UK National Health Service . 3 October 2014. Archived from the original on 11 March 2016 . ... Archived from the original on 26 January 2013 . Retrieved 3 August 2013 . ^ Monaghan KJ (2004). ... Archived from the original on 14 June 2007 . Retrieved 3 May 2013 . ^ "SARS death leads to China dispute" . ... Archived from the original on 28 November 2007 . Retrieved 3 April 2007 . ^ Fong K (16 August 2013).
Overview Severe acute respiratory syndrome (SARS) is a contagious and sometimes fatal respiratory illness. severe acute respiratory syndrome (SARS) first appeared in China in November 2002. Within a few months, SARS spread worldwide, carried by unsuspecting travelers. SARS showed how quickly infection can spread in a highly mobile and interconnected world. On the other hand, a collaborative international effort allowed health experts to quickly contain the spread of the disease. There has been no known transmission of SARS anywhere in the world since 2004.
A rare pulmonary disease induced by SARS-CoV coronavirus infection, with a reported incubation period varying from 2 to 7 days. Patients present flu-like symptoms, including fever, malaise, myalgia, headache, diarrhoea, and rigors. Dry, nonproductive, cough and dyspnea are frequently reported. Severe cases evolve rapidly, progressing to respiratory distress and failure, requiring intensive care. Mortality rate is 10%. The disease appeared in 2002 in southern China, subsequently spreading in 2003 to 26 countries. Reported human-to-human transmission occurred in Toronto (Canada), Hong Kong Special Administrative Region of China, Chinese Taipei, Singapore, and Hanoi (Viet Nam).
Cambridge University Press. pp. 214 ff . ISBN 0-521-39514-3 . ^ a b Alan Felthous, Henning Sass (2008). ... John Wiley & Sons. p. 11. ISBN 978-0-470-06638-6 . ^ Ann-Louise Shapiro (1996). ... Stanford University Press. p. 100. ISBN 0-8047-2693-0 . ^ Daniel Hack Tuke (1892). ... University of Chicago Press. p. 155. ISBN 0-226-30161-3 . ^ a b Lennard J. Davis (2008). ... McGraw-Hill Professional. p. 226. ISBN 0-8442-8393-2 . ^ Susan Bordo (1996).
Laryngo-tracheo-esophageal cleft (LC) type 0 is a congenital respiratory tract anomaly characterized by a submucosal laryngo-tracheo-esophageal cleft with minor symptoms or an asymptomatic course. ... Clinical description Subjects with type 0 LC may have no obvious symptoms or mild symptoms such as occasional aspirations.
Pterygium inversum unguis Other names Pterygium inversus unguis,  and Ventral pterygium  : 660 Specialty Dermatology Pterygium inversum unguis is characterized by the adherence of the distal portion of the nailbed to the ventral surface of the nail plate.  : 788 The condition may be present at birth or acquired, and may cause pain with manipulation of small objects, typing, and close manicuring of the nail.  : 788 secondary due to connective tissue disorders See also [ edit ] Pterygium unguis Nail Anatomy List of cutaneous conditions References [ edit ] ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ a b James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. ISBN 0-7216-2921-0 . This condition of the skin appendages article is a stub .
Bifid penis A bifid penis (or double penis ) is a rare congenital defect where two genital tubercles develop.   Many male marsupials such as the kangaroo naturally have a bifid penis, with left and right prongs that they insert into multiple vaginal canals simultaneously.  See also [ edit ] Diphallia Meatotomy Penile subincision References [ edit ] ^ Lewis, Keeta D. & Bear, Bonnie (2002). ... Elsevier Health Sciences. p. 161. ISBN 978-0-7216-8521-2 . CS1 maint: uses authors parameter ( link ) ^ Jones, Richard E. & López, Kristin H. (2006). Human reproductive biology (3rd ed.). Academic Press. p. 145 . ISBN 978-0-12-088465-0 . CS1 maint: uses authors parameter ( link ) ^ Vaughan, Terry A.; et al. (2010). ... Jones & Bartlett. p. 389. ISBN 978-0-7637-6299-5 . This genetic disorder article is a stub .
A rare, non-syndromic, urogenital tract malformation characterized by complete or partial penile duplication, ranging from only glans duplication to the presence of two penis shafts with either one (i.e. bifid phallus) or two (i.e. true diphallia) corpora cavernosum in each. Additional anomalies, such as urethra duplication, an abnormal voiding pattern, hypo- or epispadias, bifid/ectopic scrotum, bladder exstrophy or duplication, are frequently associated, but it may also present as an isolated anomaly. In severe cases, pubic symphysis diastasis, imperforate or duplicated anus, colon/ rectosigmoidal duplication, inguinal hernia and vertebral anomalies may be observed.
Iranian Journal of Pediatrics . 20 (3): 353–7. PMC 3446048 . PMID 23056729 . ^ "Indian man wants op to remove extra organ" . ... Iranian Journal of Pediatrics . 20 (3): 353–357. PMID 23056729 . ^ a b Karabagli, Murat (2017). ... Revista Médica del Instituto Mexicano del Seguro Social . 54 (3): 401–3. PMID 27100989 – via PubMed. ^ a b c Karagöz, Yeşim (2014). ... "Normal development of the male anterior urethra" (PDF) . Teratology . 61 (3): 172–83. doi : 10.1002/(SICI)1096-9926(200003)61:3<172::AID-TERA4>3.0.CO;2-B . ... International Journal of Morphology . 30 (3): 791–796. doi : 10.4067/S0717-95022012000300003 .
Bubble hair deformity Specialty Dermatology Bubble hair deformity is an abnormality of the hair shaft.  It is characterized by rows of bubbles seen microscopically within localized areas of brittle hair.  : 647  : 769 See also [ edit ] List of cutaneous conditions References [ edit ] ^ Detwiler SP, Carson JL, Woosley JT, Gambling TM, Briggaman RA (January 1994). ... 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 . This condition of the skin appendages article is a stub .
Kinking hair , or acquired progressive kinking , is a skin condition primarily reposted in postpubescent males with androgenetic alopecia , presenting with gradual curling and darkening of the frontal, temporal, auricular , and vertex hairs which, under the microscope, show kinks and twists with or without longitudinal grooving.  : 647  : 767  See also [ edit ] List of cutaneous conditions 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 . ^ Tosti A, Piraccini BM, Pazzaglia M, Misciali C (October 1999).
Erosive pustular dermatitis of the scalp Other names Erosive pustular dermatosis of the scalp  Specialty Dermatology Erosive pustular dermatitis of the scalp presents with pustules , erosions, and crusts on the scalp of primarily older Caucasian females, and on biopsy, has a lymphoplasmacytic infiltrate with or without foreign body giant cells and pilosebaceous atrophy.  : 650  : 761 See also [ edit ] Skin lesion Cicatricial alopecia List of cutaneous conditions References [ edit ] ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... 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 . This condition of the skin appendages article is a stub .
Erosive pustular dermatosis of the scalp is a rare chronic inflammation of the scalp usually occurring in elderly women (>70 years old) and characterized by the development of painful pustules, shallow erosions, and crusting on atrophic skin that eventually result in cicatricial alopecia.
Sex Crimes and Paraphilia . Prentice Hall . p. 91. ISBN 0-13-170350-1 . ^ Thompson, Steven L. ... Westport, Connecticut: Praeger . p. 446. ISBN 978-0-313-30503-0 . ^ Kolocotroni, Vassiliki; Goldman, Jane ; Taxidou, Olga (1998). ... Waterloo, Ontario: Wilfrid Laurier University Press . ISBN 978-0-88920-512-3 . ^ Miller, Alan (1999). ... New York City: Springer . ISBN 978-0-387-98499-5 . ^ McDonagh, Deana; et al. (2004). ... London: Taylor & Francis . ISBN 978-0-415-30363-7 . ^ Heller, Steven ; Meggs, Philip B. (2001).