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.
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 (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 (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.
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
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.
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.
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.
Lippincott Williams & Wilkins. p. 1152. ISBN 0-7817-7513-2 . ^ Pryse-Phillips, William (2003). ... Oxford University Press US. p. 587. ISBN 0-19-515938-1 . ^ Bradley, Walter George (2004). ... Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... Lippincott Williams & Wilkins. p. 1289. ISBN 0-7817-4811-9 . ^ a b Loder, Elizabeth; Dawn A. ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007).
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). ... Cutaneous Lymphomas . Informa Health Care. pp. 365–. ISBN 978-0-8247-2997-4 . Retrieved 30 May 2010 .
Eosinophilic pustular folliculitis (EPF) affects the skin causing itchy, red or skin-colored bumps and pustules (bumps containing pus). The papules mostly appear on the face, scalp, neck and trunk and may last for weeks or months. EPF affects males more than females. There are several forms of EPF. Classic eosinophilic pustular folliculitis mainly occurs in Japan. Immunosuppression-associated EPF is mainly associated with HIV infection, but has also been associated with certain cancers and medications. The infantile form of EPF is seen in infants from birth or within the first year of life. The underlying cause of EFP is unknown. All of these forms have similar skin findings.
Garrod's pads (also known as violinist's pads  ) are a cutaneous condition characterized by calluses on the dorsal aspect of the interphalangeal joints ,  i.e. the back side of the finger joints. They are often seen in violin , viola , and cello players, along with fiddler's neck and other dermatologic conditions peculiar to string musicians.  Although Garrod's pads are conventionally described as appearing on the proximal interphalangeal joint, distal interphalangeal joint involvement has also been described.  Garrod's pads are named after Archibald Garrod who first documented them in 1904 in association with Dupuytren's contracture .  H.A. Bird described them as an incidental finding in a professional violinist and proposed that they arise in such cases due to repeated extreme tension of the extensor tendons over the interphalangeal joints.  Bird noted that violin players use the left hand for a markedly different task than the right hand, with the extensor tendons in the left hand subjected to considerable tension, and that Garrod's pads only arise on the left hand in such cases. This unilateral finding differentiates the occupational hazard of Garrod's pads from more significant disorders. Among violinists and violists, Garrod's pads apparently arise as a protective mechanism for the skin and subcutaneous tissues above the tendons; Bird notes that they do not protect against external trauma unlike most calluses.  Patients with Dupuytren's contracture are four times more likely to have coexisting Garrod's pads.   See also [ edit ] Knuckle pads Harpist's finger Fiddler's neck Cellist's chest Cello scrotum Paget-Schroetter syndrome List of cutaneous conditions List of eponymously named medical signs References [ edit ] ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007).
A number sign (#) is used with this entry because knuckle pads are associated with certain genetic disorders such as epidermolytis palmoplantar keratoderma (144200) or Dupuytren contractures (126900), both of which are autosomal dominant. Knuckle pads are sometimes associated with Dupuytren contractures and it is not completely certain that a different gene is involved. Camptodactyly (114200) also has an uncertain relationship. Skoog (1948) defined knuckle pads as 'subcutaneous nodules on the dorsal aspect of the proximal interphalangeal joints.' Lu et al. (2003) reported association of knuckle pads with epidermolytic palmoplantar keratoderma in a Chinese family and identified a novel leu160-to-phe mutation in the keratin-9 gene (L160F; 607606.0012) as the presumed cause. They presented evidence that both the hyperkeratosis and the knuckle pads were friction-related.
. ^ "Deaths in the district of Inveresk and Musselburgh in the County of Edinburgh" . Statutory Deaths 689/00 0032 . ScotlandsPeople . Retrieved 11 April 2015 . External links [ edit ] Classification D ICD-O : 8011/0, 8011/3 Wikimedia Commons has media related to Epithelioma .
Lippincott Williams & Wilkins. pp. 254–256. ISBN 0-7817-3905-5 . ^ a b c d e f g h i Smith, Melanie N. (2006-05-10). ... Cambridge University Press . p. 77. ISBN 1-900151-51-0 . ^ Papadakis, Maxine A.; Stephen J. ... McGraw-Hill Professional. p. 60. ISBN 0-07-145892-1 . ^ a b Bosze, Peter; David M. ... Informa Health Care. p. 66. ISBN 963-00-7356-0 . ^ "Cervical Polyps" (PDF) .
Clin Dermatol . 19 (1): 69–71. doi : 10.1016/S0738-081X(00)00215-7 . PMID 11369491 . ^ "Drugs that call for extra caution. ... New York: Simon Schuster. p. 56. ISBN 978-0-684-87309-1 . ^ M.d. Kamath, Bob (30 May 2007). ... Kendall Hunt Publishing. p. 25. ISBN 978-0-7872-8701-6 . ^ Ashton CH (2002).
Mark; Tiwari, Hemant K. (2013), "Multifactorial Inheritance and Complex Diseases", Emery and Rimoin's Principles and Practice of Medical Genetics , Elsevier, pp. 1–15, doi : 10.1016/b978-0-12-383834-6.00014-8 , ISBN 978-0-12-383834-6 ^ Plomin, Robert; Haworth, Claire M. ... Retrieved 2020-04-01 . ^ Korf, Bruce R.; Sathienkijkanchai, Achara (2009), "Introduction to Human Genetics", Clinical and Translational Science , Elsevier, pp. 265–287, doi : 10.1016/b978-0-12-373639-0.00019-4 , ISBN 978-0-12-373639-0 ^ Sayed-Tabatabaei, F.A.; Oostra, B.A.; Isaacs, A.; van Duijn, C.M.; Witteman, J.C.M. (2006-05-12). ... "Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis". The Lancet . 365 (9453): 36–42. doi : 10.1016/s0140-6736(04)17663-0 .
A rare photodermatosis characterized by the development of pruritic or painful vesicles in a photodistributed pattern in response to sunlight exposure. The lesions heal with permanent varioliform scarring. Ocular involvement, deformities of ears and nose, or contractures of the fingers may occasionally be observed. Systemic signs and symptoms are absent. The condition typically occurs in childhood and regresses spontaneously in adolescence or young adulthood.
Greenwood Publishing Group. ISBN 978-0-313-31520-6 , p. 402. ^ Miller, Laura. (2006). ... University of California Press. ISBN 978-0-520-24509-9 ^ Latteier 1998 ^ Buss, David (2019). ... El Rio, TX: Hauck Pub Co. ISBN 978-0-9621797-2-3 . ^ McDonough, Jimmy (2005). ... University of California Press. ISBN 978-0-520-24509-9 ^ Latteier 1998 Further reading [ edit ] Block, Susan (2004). ... The Breast Fetish (pg. 29). Palgrave Macmillan. ISBN 0-312-22129-0 . Glazier, Stephen D. ; Flowerday, Charles (2003).
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). HAT comprises an initial hemo-lymphatic stage characterized by fever, weakness, musculoskeletal pain, anemia, and lymphadenopathy, along with dermatologic, cardiac and endocrine complications or hepatosplenomegaly, followed by a meningo-encephalitic stage characterized by neurologic involvement (sleep disturbances, psychiatric disorders, seizures) that progresses, in the absence of treatment, towards a fatal meningoencephalitis.
Clinical Features Lisch et al. (1992) described 5 family members and 3 unrelated patients (4 males, 4 females), aged 23 to 71 years, with bilateral or unilateral, gray, band-shaped, and feathery opacities that sometimes appeared in whorled patterns. Retroillumination showed that the opacities consisted of intraepithelial, densely crowded, clear microcysts. Light and electron microscopy disclosed diffuse vacuolization of the cytoplasm of epithelial cells in the affected area. Visual acuity was so reduced in 3 patients that abrasion of the corneal epithelium was performed. The corneal abnormalities recurred within months, with the same reduction in visual acuity as before.
Lisch epithelial corneal dystrophy (LECD) is a very rare form of superficial corneal dystrophy characterized by feather-shaped opacities and microcysts in the corneal epithelium arranged in a band-shaped and sometimes whorled pattern, occasionally with impaired vision. Epidemiology Exact prevalence of this form of corneal dystrophy is not known but very few cases have been reported to date. LECD has been documented in one German family and in rare sporadic cases in Germany and the USA. Clinical description Lesions generally develop in childhood. Epithelial opacities are slowly progressive and painless blurred vision sometimes occurs after 60 years of age. Etiology The exact cause is unknown but appears to be genetic. The gene related to Lisch epithelial corneal dystrophy has been mapped to the short arm of the X chromosome (Xp22.3).
The Lancet . 156 (4011): 89–95. doi : 10.1016/S0140-6736(00)65681-7 . ^ Weisse, Martin E (31 December 2000). ... The Lancet . 357 (9252): 299–301. doi : 10.1016/S0140-6736(00)03623-0 . PMID 11214144 . S2CID 35896288 . ^ Powell, KR (January 1979). ... The Journal of Pediatrics . 78 (6): 958–67. doi : 10.1016/S0022-3476(71)80425-0 . PMID 4252715 . ^ Morens, David M; Katz, Alan R; Melish, Marian E (31 May 2001). ... The Lancet . 357 (9273): 2059. doi : 10.1016/S0140-6736(00)05151-5 . PMID 11441870 . S2CID 35925579 .
A rare staphylococcal toxemia caused by epidermolytic toxins of Staphylococcus aureus and characterized by the appearance of widespread erythematous patches, on which large blisters develop. Upon rupture of these blisters, the skin appears reddish and scalded. The lesions typically begin in the face and rapidly expand to other parts of the body. The disease may be complicated by pneumonia and sepsis. It most commonly affects newborns and infants.
Random House, Inc. 2001. p. 1101. ISBN 0-375-72026-X . ^ a b Robbins and Cotran Pathologic Basis of Disease Elsevier. 2005. p. 1232. ISBN 0-8089-2302-1 . ^ William D. James; Timothy G. ... Saunders Elsevier. pp. 686–87. ISBN 0-7216-2921-0 . ^ a b "Lentigo simplex | DermNet New Zealand" . www.dermnetnz.org . ... "An open-label study of the efficacy and tolerability of microencapsulated hydroquinone 4% and retinol 0.15% with antioxidants for the treatment of hyperpigmentation". Cutis . 81 (4): 365–71. ISSN 0011-4162 . PMID 18491487 . ^ Mansouri, P.; Farshi, S.; Hashemi, Z.; Kasraee, B. (2015-07-01).
Lentiginosis Specialty Dermatology Lentiginosis refers to the presence of lentigines in large numbers or in a distinctive configuration.  These are spotted areas created by accumulation on the skin due to sun exposure. Due to a high irregularity any distinction from randomness defines lentiginosis. Although lentigines are benign, they be the signal of an underlying problem such as progressive cardiomyopathic lentiginosis which can cause retardation in children.  See also [ edit ] Lentigines Skin cancer List of cutaneous conditions References [ edit ] ^ http://cancerweb.ncl.ac.uk/cgi-bin/omd?lentiginosis ^ "Lentigines - American Osteopathic College of Dermatology (AOCD)" . www.aocd.org . External links [ edit ] Classification D ICD - 10 : L81.4 ( ILDS L81.402, L81.404, L81.406) MeSH : D007911 DiseasesDB : 34325 SNOMED CT : 402624000 v t e Skin cancer of nevi and melanomas Melanoma Mucosal melanoma Superficial spreading melanoma Nodular melanoma lentigo Lentigo maligna / Lentigo maligna melanoma Acral lentiginous melanoma Amelanotic melanoma Desmoplastic melanoma Melanoma with features of a Spitz nevus Melanoma with small nevus-like cells Polypoid melanoma Nevoid melanoma Melanocytic tumors of uncertain malignant potential Nevus / melanocytic nevus Nevus of Ito / Nevus of Ota Spitz nevus Pigmented spindle cell nevus Halo nevus Pseudomelanoma Blue nevus of Jadassohn–Tièche Cellular Epithelioid Deep penetrating Amelanotic Malignant Congenital melanocytic nevus ( Giant Medium-sized Small-sized ) Balloon cell nevus Dysplastic nevus / Dysplastic nevus syndrome Acral nevus Becker's nevus Benign melanocytic nevus Nevus spilus v t e Pigmentation disorders / Dyschromia Hypo- / leucism Loss of melanocytes Vitiligo Quadrichrome vitiligo Vitiligo ponctué Syndromic Alezzandrini syndrome Vogt–Koyanagi–Harada syndrome Melanocyte development Piebaldism Waardenburg syndrome Tietz syndrome Loss of melanin / amelanism Albinism Oculocutaneous albinism Ocular albinism Melanosome transfer Hermansky–Pudlak syndrome Chédiak–Higashi syndrome Griscelli syndrome Elejalde syndrome Griscelli syndrome type 2 Griscelli syndrome type 3 Other Cross syndrome ABCD syndrome Albinism–deafness syndrome Idiopathic guttate hypomelanosis Phylloid hypomelanosis Progressive macular hypomelanosis Leukoderma w/o hypomelanosis Vasospastic macule Woronoff's ring Nevus anemicus Ungrouped Nevus depigmentosus Postinflammatory hypopigmentation Pityriasis alba Vagabond's leukomelanoderma Yemenite deaf-blind hypopigmentation syndrome Wende–Bauckus syndrome Hyper- Melanin / Melanosis / Melanism Reticulated Dermatopathia pigmentosa reticularis Pigmentatio reticularis faciei et colli Reticulate acropigmentation of Kitamura Reticular pigmented anomaly of the flexures Naegeli–Franceschetti–Jadassohn syndrome Dyskeratosis congenita X-linked reticulate pigmentary disorder Galli–Galli disease Revesz syndrome Diffuse/ circumscribed Lentigo / Lentiginosis : Lentigo simplex Liver spot Centrofacial lentiginosis Generalized lentiginosis Inherited patterned lentiginosis in black persons Ink spot lentigo Lentigo maligna Mucosal lentigines Partial unilateral lentiginosis PUVA lentigines Melasma Erythema dyschromicum perstans Lichen planus pigmentosus Café au lait spot Poikiloderma ( Poikiloderma of Civatte Poikiloderma vasculare atrophicans ) Riehl melanosis Linear Incontinentia pigmenti Scratch dermatitis Shiitake mushroom dermatitis Other/ ungrouped Acanthosis nigricans Freckle Familial progressive hyperpigmentation Pallister–Killian syndrome Periorbital hyperpigmentation Photoleukomelanodermatitis of Kobori Postinflammatory hyperpigmentation Transient neonatal pustular melanosis Other pigments Iron Hemochromatosis Iron metallic discoloration Pigmented purpuric dermatosis Schamberg disease Majocchi's disease Gougerot–Blum syndrome Doucas and Kapetanakis pigmented purpura / Eczematid-like purpura of Doucas and Kapetanakis Lichen aureus Angioma serpiginosum Hemosiderin hyperpigmentation Other metals Argyria Chrysiasis Arsenic poisoning Lead poisoning Titanium metallic discoloration Other Carotenosis Tar melanosis Dyschromia Dyschromatosis symmetrica hereditaria Dyschromatosis universalis hereditaria See also Skin color Skin whitening Tanning Sunless Tattoo removal Depigmentation This Genodermatoses article is a stub .
With giant hemangiomas in small children, thrombocytopenia and red cell changes compatible with trauma ('microangiopathic hemolytic anemia') have been observed. The mechanism of the hematologic changes is obscure. No evidence of a simple genetic basis has been discovered. Propp and Scharfman (1966) reported a male infant with thrombocytopenia associated with a large hemangioma of the right arm and axilla. The patient had low platelet counts with a markedly diminished platelet survival time and an absence of platelet agglutinin or complement-fixing antibody. Radiochromate-tagged platelet studies suggested sequestration in the hemangioma, liver, and spleen.
Hemangioma thrombocytopenia syndrome is characterized by profound thrombocytopenia in association with two rare vascular tumors: kaposiform hemangioendotheliomas and tufted angiomas . The profound thrombocytopenia can cause life threatening bleeding and progress to a disseminated coagulopathy in patients with these tumors. The condition typically occurs in early infancy or childhood, although prenatal cases (diagnosed with the aid of ultrasonography), newborn presentations, and rare adult cases have been reported.
Kasabach-Merritt syndrome (KMS), also known as hemangioma-thrombocytopenia syndrome, is a rare disorder characterized by profound thrombocytopenia, microangiopathic hemolytic anemia, and subsequent consumptive coagulopathy in association with vascular tumors, particularly kaposiform hemangioendothelioma or tufted angioma.
Hagerstown, MD: Lippincott Williams & Wilkins. p. 1150. ISBN 0-7817-2655-7 . Retrieved 2008-06-16 . ^ a b c d e f Scalea TM (2005). ... Boca Raton: CRC. pp. 26–32. ISBN 978-0-8493-8138-6 . Retrieved 2008-07-06 . ^ a b Porth, Carol (2007). ... Hagerstown, MD: Lippincott Williams & Wilkins. p. 838. ISBN 978-0-7817-7087-3 . Retrieved 2008-07-03 . ^ Pitkänen A, McIntosh TK (2006). ... Neurotrauma: New Insights Into Pathology and Treatment . Elsevier. pp. 13–19. ISBN 978-0-444-53017-2 . Retrieved 2008-06-10 . ^ a b Granacher RP (2007). ... Neuroscience . 101 (2): 289–95. doi : 10.1016/S0306-4522(00)00380-8 . PMID 11074152 . S2CID 20457228 . ^ Sauaia A, Moore FA, Moore EE, et al.
Fitzpatrick's Dermatology in General Medicine (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ James W, Berger T, Elston D (2005). Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. ISBN 0-7216-2921-0 . ^ Pardasani AG, Feldman SR, Clark AR (February 2000). ... Journal of the American Academy of Dermatology . 42 (5 Pt 2): 885–7. doi : 10.1016/s0190-9622(00)90263-9 . PMID 10767696 . ^ Mehlis S (2019).
Guttate psoriasis is a skin condition in which small, red, and scaly teardrop-shaped spots appear on the arms, legs, and middle of the body. It is a relatively uncommon form of psoriasis . The condition often develops very suddenly, and is usually triggered by an infection (e.g., strep throat, bacteria infection, upper respiratory infections or other viral infections). Other triggers include injury to the skin, including cuts, burns, and insect bites, certain malarial and heart medications, stress, sunburn, and excessive alcohol consumption. Treatment depends on the severity of the symptoms, ranging from at-home over the counter remedies to medicines that suppress the body's immune system to sunlight and phototherapy.
In earlier tests on tissue and cell samples obtained from patients, ARQ 092 reduced phosphorylation of AKT and downstream targets of AKT in as little as two hours.  The Phase 0 trial opened in November 2015 and recruited patients in a study titled "Dose Finding Trial of ARQ 092 in Children and Adults With Proteus Syndrome"  This trial is based on in vitro data showing inhibition of AKT1 in cell lines from patients with Proteus syndrome.  Notable cases [ edit ] In a 1986 article in the British Medical Journal , Michael Cohen and J.A.R. ... Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. p. 554. ISBN 978-0-7216-2921-6 . ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine . (6th ed.). McGraw-Hill. ISBN 0-07-138076-0 . ^ a b c d El-Sobky, Tamer Ahmed; Elsayed, Solaf M.; El Mikkawy, Dalia M.E. (2015). ... The New England Journal of Medicine . 365 (7): 661–3. doi : 10.1056/NEJMe1107384 . ... "A mosaic activating mutation in AKT1 associated with the Proteus syndrome" . N Engl J Med . 365 (7): 611–9. doi : 10.1056/NEJMoa1104017 .