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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.
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). ... Uncoordinated eye movements, disorientation, seizures, and coma may accompany severe episodes. [2] Glycogen-storage disease type 0 affects only the liver. ... Patients with glycogen-storage disease type 0 have normal-to-increased response to glucagon in the fed state, with hyperglycemia and lactic acidemia. [2] Laboratory Studies [ edit ] Serum glucose levels are measured to document the degree of hypoglycemia. ... The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [2] Mortality/Morbidity [ edit ] The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency. Major long-term concerns include growth delay, osteopenia, and neurologic damage resulting in developmental delay, intellectual deficits, and personality changes. [2] Sex [ edit ] No sexual predilection is observed because the deficiency of glycogen synthetase activity is inherited as an autosomal recessive trait. [2] Age [ edit ] Glycogen-storage disease type 0 is most commonly diagnosed during infancy and early childhood. [2] References [ edit ] ^ Orho M, Bosshard NU, Buist NR, et al.
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. The 2 index cases presented with morning fatigue, had ketotic hypoglycemia when fasting which rapidly disappeared after eating, and hepatic glycogen deficiency with absent or very low hepatic glycogen synthase activity. ... Gitzelmann (1996) stated that he is aware of 2 additional families with affected members. ... 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.
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). ... CUP Archive. pp. 321–. ISBN 978-0-521-22673-8 . ^ Raphael Rubin; David S. ... Lippincott Williams & Wilkins. pp. 1195–. ISBN 978-0-7817-1750-2 . ^ Annual Reports in Medicinal Chemistry . Academic Press. 3 October 1994. pp. 1994–. ISBN 978-0-08-058373-0 . Further reading [ edit ] Shukla, G.
Jaypee Brothers Publishers. 2007. pp. 347–. ISBN 978-81-8061-996-0 . ^ Leonard J. Deftos (1 January 1998). ... 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).
Nevus comedonicus (also known as a " comedo nevus " [1] ) is characterized by closely arranged, grouped, often linear, slightly elevated papules that have at their center keratinous plugs resembling comedones . [2] : 634 [3] : 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). Dermatology: 2-Volume Set . St. 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 .
By 10 years of age, his lesion extended inferiorly to the posteromedial right thigh, and consisted of a 10 cm by 2 cm plaque composed of several atrophic cribiform scars and scattered pink comedones, with another smaller plaque below it.
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 comedonicus syndrome Specialty Dermatology Nevus comedonicus syndrome is a skin condition characterized by a nevus comedonicus associated with cataracts , scoliosis , and neurologic abnormalities. [1] : 635 [2] : 776 [3] : 849 See also [ edit ] Epidermal nevus syndrome Cutaneous conditions References [ edit ] ^ 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 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . St. Louis: Mosby. ISBN 1-4160-2999-0 .
Lippincott Williams & Wilkins. p. 1152. ISBN 0-7817-7513-2 . ^ Pryse-Phillips, William (2003). ... Neurology in clinical practice . 2 (4th ed.). Taylor & Francis. p. 2074. ISBN 0-7506-7469-5 . ^ Bernstein, Carolyn; Elaine McArdle (2009). ... Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007).
Pili annulati Specialty Medical genetics Pili annulati (also known as " ringed hair " [1] ) is a genetic trait in which the hair seems ‘banded‘ by alternating segments of light and dark color when seen in reflected light. [1] [2] : 767 [3] : 640 [4] See also [ edit ] Pili pseudoannulati List of cutaneous conditions References [ edit ] ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . 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 .
Snell and Foley (1932) described 9 affected persons in 4 generations with an instance of male-to-male transmission, consistent with autosomal dominant inheritance. Mapping By linkage analysis of 2 unrelated families with autosomal dominant inheritance of pili annulati, Green et al. (2004) found significant linkage to a 9.2-cM region on chromosome 12q between D12S367 and D12S1723 (maximum combined lod score of 4.78 at D12S1723).
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.
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. [1] : 638 [2] : 764 [3] 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). Dermatology: 2-Volume Set . St. Louis: Mosby. ISBN 1-4160-2999-0 .
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).
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.' ... Gedda and Cavalieri (1963) reported 6 families; in 2 families, the parents were related, and in 2 others, 2 sibs were affected.
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. ... 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. ISBN 0-312-32501-0 . External links [ edit ] Classification D ICD - 10 : F40 - F40.8 Library resources about Neurosis Resources in your library Resources in other libraries Janov, Arthur (1991).
Pili pseudoannulati Other names Pseudo pili annulati [1] : 640 Specialty Dermatology Pili pseudoannulati is an anomaly of human hair that mimics pili annulati ; however, the two differ in that the light bands of pili annulati are caused by internal effects, whereas the bright segments of pili pseudoannulati are caused by reflection and refraction of light by flattened, twisted surfaces of hair. [2] : 767 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 . This condition of the skin appendages article is a stub .
Polarizing light indicated variability in the thickness of the hair shaft, and illuminating light did not show bands, 2 additional features that distinguished it from pili annulati. Further examination of the hair shaft showed that the pseudopili annulati hairs had periodic widening and narrowing, that the fiber cross-section was roughly elliptical, and that a periodic twisting of the hair (30 to 40 degrees in 2 alternating directions) was superimposed on the ellipticity. ... INHERITANCE - Isolated cases SKIN, NAILS, & HAIR Hair - Scalp hair appears banded, with alternating light and dark segments (0.5 to 1.5 mm) - Hair may appear alternating shiny and dull - Hairs have elliptical diameter with flattened surface - Hair shaft shows partial twisting on its axis (periodicity of 1 to 2 mm) - Reflected light shows bright and dark bands - Transmitted light shows no banding or inhomogeneities MISCELLANEOUS - Onset in infancy or early childhood - No increased fragility of hair - Considered a normal variant - Distinct from pili annulati ( 180600 ) ▲ Close
Pigmented hairy epidermal nevus syndrome is a cutaneous condition characterized by a Becker nevus , ipsilateral hypoplasia of the breast , and skeletal defects such as scoliosis . [1] : 635 [2] : 776 See also [ edit ] Epidermal nevus syndrome Skin lesion List of cutaneous conditions References [ edit ] ^ 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 .
Cutaneous diphtheria infection Specialty Infectious disease Cutaneous diphtheria is an infection of the skin by Corynebacterium diphtheriae . [1] : 265 It is also known as "desert sore". [2] See also [ edit ] Diphtheria Skin lesion References [ edit ] ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 0-7216-2921-0 . ^ Geoffrey V. Gill; Nick Beeching (1 March 2004). ... Wiley-Blackwell. pp. 33–. ISBN 978-0-632-06496-0 . Retrieved 14 May 2010 .
Pterygium unguis (also known as "Dorsal pterygium" [1] : 660 ) forms as a result of scarring between the proximal nailfold and matrix, with the classic example being lichen planus , though it has been reported to occur as a result of sarcoidosis and Hansen's disease . [2] See also [ edit ] Pterygium inversum unguis Nail anatomy 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 . This condition of the skin appendages article is a stub .
Ichthyosis linearis circumflexa Specialty Dermatology Ichthyosis linearis circumflexa is a distinctive skin condition of generalized hyperkeratosis and polycyclic and serpiginous erythematous plaques with a characteristic, migratory, double-edged scale at the margins, and is the typical cutaneous manifestation of Netherton's syndrome . [1] : 496 [2] : 563 See also [ edit ] Ichthyosis prematurity syndrome 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 . This Genodermatoses article is a stub .
Netherton disease is a rare disorder affecting the skin, hair and immune system. Symptoms are present at birth and include red, scaly skin. Other symptoms include outbreaks of red, circular scaly rashes, thin, fragile hair (bamboo hair), and immune reactions such as hay fever, asthma, itchy skin, and eczema. Dehydration and infection are common and can be serious. Babies tend to grow slowly and have poor weight gain. Netherton syndrome is caused by the SPINK5 gene not working correctly. It is inherited in an autosomal recessive pattern. Netherton syndrome is diagnosed based on clinical examination, the symptoms, and genetic testing.
Netherton syndrome (NS) is a skin disorder characterized by congenital ichthyosiform erythroderma (CIE), a distinctive hair shaft defect (trichorrhexis invaginata; TI) and atopic manifestations. Epidemiology Incidence is estimated at 1/200,000 births. Clinical description Patients generally present at birth with generalized erythroderma and scaling, and failure to thrive. Frequent complications include hypernatremic dehydration, recurrent infections, and diarrhea and intestinal malabsorption. The disease course is heterogeneous: the generalized erythroderma may persist in some patients, but more frequently it evolves during childhood into ichthyosis linearis circumflexa (ILC). ILC is a milder and highly characteristic skin disorder marked by migratory erythematous plaques with a double-edged scale.
In Netherton syndrome, and often in the other 2 conditions, the stratum corneum layer was largely replaced by parakeratotic cells. ... Marked growth retardation was noted at the age of 2 years. Papillomatous skin lesions developed in the groin at the age of 15 years. ... Nevet et al. (2017) reported a Muslim Arab female infant with Netherton syndrome, who at the age of 2 days underwent partial resection of the small intestine for 'apple peel' intestinal atresia. ... Inheritance In a review of 44 cases of Netherton syndrome, Smith et al. (1995) found at least 6 reports of affected sibs and 2 reports of parental consanguinity, suggesting autosomal recessive inheritance. ... However, in all 9 patients, LEKTI protein expression was absent or present as small immunoreactive foci in fewer than 2% of epithelial cells from skin biopsies and/or buccal mucosa.
Specialty Medical genetics Netherton syndrome is a severe, autosomal recessive [1] form of ichthyosis associated with mutations in the SPINK5 gene. [2] [3] It is named after Earl W. Netherton (1910–1985), an American dermatologist who discovered it in 1958. [4] Contents 1 Signs and symptoms 2 Cause 3 Diagnosis 4 Treatment 5 See also 6 References 7 External links Signs and symptoms [ edit ] Netherton syndrome is characterized by chronic skin inflammation, universal pruritus (itch), severe dehydration, and stunted growth. ... Cause [ edit ] Netherton syndrome is an autosomal recessive disorder associated with mutations in the SPINK5 gene, which encodes the serine protease inhibitor lympho-epithelial Kazal-type-related inhibitor ( LEKTI ). [2] These mutations result in a dysfunctional protein that has a reduced capacity to inhibit serine proteases expressed in the skin. Potential endogenous targets of LEKTI include KLK5 , KLK7 and KLK14 . [7] These enzymes are involved in various aspects of epidermal remodelling, including desquamation , PAR-2 activation and degradation of lipid hydrolases, suggesting a potential mechanism for the development of atopic manifestations characteristic of Netherton syndrome. [8] Disease severity is determined by the level of LEKTI expression and, consequently, serine protease activity. ... "Mutations in SPINK5, encoding a serine protease inhibitor, cause Netherton syndrome". Nat. Genet . 25 (2): 141–142. doi : 10.1038/75977 . PMID 10835624 . ... Fitzpatrick's Dermatology in General Medicine . (6th ed.). Page 496. McGraw-Hill. ISBN 0-07-138076-0 . ^ Netherton, E. W. A unique case of trichorrhexis nodosa: 'bamboo hairs.'.
Netherton syndrome is a disorder that affects the skin, hair, and immune system. Newborns with Netherton syndrome have skin that is red and scaly (ichthyosiform erythroderma), and the skin may leak fluid. Some affected infants are born with a tight, clear sheath covering their skin called a collodion membrane. This membrane is usually shed during the first few weeks of life. Because newborns with this disorder are missing the protection provided by normal skin, they are at risk of becoming dehydrated and developing infections in the skin or throughout the body (sepsis), which can be life-threatening. Affected babies may also fail to grow and gain weight at the expected rate (failure to thrive).
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.
While diarrhea is common in people with SARS, the fecal–oral route does not appear to be a common mode of transmission. [9] The basic reproduction number of SARS-CoV, R 0 , ranges from 2 to 4 depending on different analyses. ... 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 . [31] [32] 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%. [4] The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient. [9] Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%). [33] 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 [34] Country or region Cases Deaths Fatality (%) China [a] 5,327 349 6.6 Hong Kong 1,755 299 17.0 Taiwan [b] 346 73 [35] [36] 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 3 00 India 3 00 South Korea 3 00 Indonesia 200 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'. ... Journal of Virological Methods . 128 (1–2): 21–8. doi : 10.1016/j.jviromet.2005.03.021 . ... Emerging Infectious Diseases . 10 (2): 173–5. doi : 10.3201/eid1002.031038 . ... American Journal of Biomedical Science & Research . 6 (2): 001017. doi : 10.34297/AJBSR.2019.06.001017 . ^ Senior K (November 2003).
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.
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). ... Stanford University Press. pp. 114 ff . ISBN 0-8047-3860-2 . ^ a b Femi Oyebode (2008). ... Cornell University Press. p. 48. ISBN 0-8014-4410-1 . ^ Anthony J. Close (1990). ... McGraw-Hill Professional. p. 226. ISBN 0-8442-8393-2 . ^ Susan Bordo (1996).
Nevus lipomatosus (cutaneous) superficialis ( NLS or NLCS , also known as "Nevus lipomatosis of Hoffman and Zurhelle" [1] ) 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. [1] [2] : 625 It is usually congenital in origin or appears within the first three decades. [3] A pedunculated lipofibroma is a solitary variant of nevus lipomatosus superficialis . [3] It usually appears in adult life, and usually on the axilla, knee, ear, arm, scalp and the lower trunk. [3] 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. [3] See also [ edit ] Skin lesion List of cutaneous conditions References [ edit ] ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set . St. Louis: Mosby. p. 1840. ... 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 .
Chondrodermatitis nodularis chronica helicis Other names Chondrodermatitis nodularis helicis [1] : 782 Chondrodermatitis helicis nodularis in a 67-year-old man Specialty Dermatology Chondrodermatitis nodularis chronica helicis is a small, nodular, tender, chronic inflammatory lesion occurring on the helix of the ear, most often in men. [2] : 610 Histopathology, showing an ulceration surrounded by acanthosis and parakeratosis, with absence of atypia. ... 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 Dermal and subcutaneous growths article is a stub .
