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Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Prat C, Lemaire O, Bret J, Zabraniecki L, Fournié B (May 2008). ... Archives de Médecine des Infants . Paris. 32 : 129–135. ISSN 0365-4311 . ^ synd/2108 at Who Named It?
Mucopolysaccharidosis type IV (MPS IV), also known as Morquio syndrome, is a progressive condition that mainly affects the skeleton. The rate at which symptoms worsen varies among affected individuals. The first signs and symptoms of MPS IV usually become apparent during early childhood. Affected individuals develop various skeletal abnormalities, including short stature, knock knees , and abnormalities of the ribs, chest, spine, hips, and wrists. People with MPS IV often have joints that are loose and very flexible (hypermobile), but they may also have restricted movement in certain joints. A characteristic feature of this condition is underdevelopment (hypoplasia) of a peg-like bone in the neck called the odontoid process.
Summary Clinical characteristics. The phenotypic spectrum of mucopolysaccharidosis IVA (MPS IVA) is a continuum that ranges from a severe and rapidly progressive early-onset form to a slowly progressive later-onset form. Children with MPS IVA have no distinctive clinical findings at birth. The severe form is usually apparent between ages one and three years, often first manifesting as kyphoscoliosis, knock-knee (genu valgum), and pectus carinatum; the slowly progressive form may not become evident until late childhood or adolescence often first manifesting as hip problems (pain, stiffness, and Legg Perthes disease). Progressive bone and joint involvement leads to short stature, and eventually to disabling pain and arthritis. Involvement of other organ systems can lead to significant morbidity, including respiratory compromise, obstructive sleep apnea, valvular heart disease, hearing impairment, visual impairment from corneal clouding, dental abnormalities, and hepatomegaly.
Mucopolysaccharidosis type IVA (MPS IVA, also called Morquio syndrome, type A) is a metabolic condition that primarily affects the skeleton. The severity, age of onset, and associated symptoms vary significantly from person to person and range from a severe and rapidly progressive, early-onset form to a slowly progressive, later-onset form. The severe form is usually diagnosed between ages 1 and 3, while the milder form may not become evident until late childhood or adolescence. Signs and symptoms include various skeletal abnormalities such as short stature, knock knees, pectus carinatum , and malformations of the spine, hips and wrists. Affected people may also experience involvement of other organ systems such as respiratory problems, valvular heart disease , hearing impairment, corneal clouding , dental abnormalities, hepatomegaly , and spinal cord compression.
.; et al. (2006), Andrews' Diseases of the Skin: clinical Dermatology , Saunders Elsevier, ISBN 0-7216-2921-0 ^ Marques, Silvio Alencar (October 2013). ... Anais Brasileiros de Dermatologia . 88 (5): 700–711. doi : 10.1590/abd1806-4841.20132463 . ISSN 0365-0596 . PMC 3798345 . PMID 24173174 . ^ Queiroz-Telles, Flavio; Fahal, Ahmed Hassan; Falci, Diego R; Caceres, Diego H; Chiller, Tom; Pasqualotto, Alessandro C (November 2017). ... PMID 19879504 . ^ RESTREPO, ANGELA; TOBÓN, ANGELA MARÍA (2010), "Paracoccidioides brasiliensis", Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases , Elsevier, pp. 3357–3363, doi : 10.1016/b978-0-443-06839-3.00268-x , ISBN 9780443068393 ^ Felipe, Maria S.
A rare mycosis characterized by an acute form mostly occurring in children and young adults presenting with fever, weight loss, lymph node enlargement, hepatosplenomegaly, and bone marrow dysfunction, versus a chronic form which usually involves the lungs and mucosae of the upper respiratory tract, skin, lymph nodes, and adrenal glands, but may affect any part of the body. The most common sequelae are chronic respiratory insufficiency and Addison's disease. The infectious agent, Paracoccidioides brasiliensis , is a fungus limited to Latin America.
Archivos de la Sociedad Española de Oftalmología . 77 (11): 597–604. ISSN 0365-6691 . PMID 12410405 . Archived from the original on 7 October 2011. ^ Bennett QM (June 2008). ... Cengage Learning. ISBN 978-1-305-53720-0 . ^ Gregory, Richard Langton (1977). ... Philadelphia: Mosby / Elsevier. ISBN 978-0-323-03599-6 . OCLC 853286620 . ^ Polat U., Schor C., Tong J., Zomet A., Lev M., Yehezkel O., Sterkin A., Levi D.M. (2012).
Overview Presbyopia is the gradual loss of your eyes' ability to focus on nearby objects. It's a natural, often annoying part of aging. Presbyopia usually becomes noticeable in your early to mid-40s and continues to worsen until around age 65. You may become aware of presbyopia when you start holding books and newspapers at arm's length to be able to read them. A basic eye exam can confirm presbyopia. You can correct the condition with eyeglasses or contact lenses. You might also consider surgery. Symptoms Presbyopia develops gradually.
DD = developmental delay; ID = intellectual disability; OT = occupational therapy; PT = physical therapy Developmental Disability / Intellectual Disability Management Issues The following information represents typical management recommendations for individuals with developmental delay / intellectual disability in the United States; standard recommendations may vary from country to country. Ages 0-3 years. Referral to an early intervention program is recommended for access to occupational, physical, speech, and feeding therapy as well as infant mental health services, special educators, and sensory impairment specialists.
A number sign (#) is used with this entry because 3-methylglutaconic aciduria type III, also known as autosomal recessive optic atrophy-3 or optic atrophy plus syndrome, is caused by mutation in the OPA3 gene (606580). See also autosomal dominant optic atrophy-3 (165300), an allelic disorder with a less severe phenotype. For a phenotypic description and a discussion of genetic heterogeneity of 3-methylglutaconic aciduria, see MGCA type I (250950). Description Type III 3-methylglutaconic aciduria is a neuroophthalmologic syndrome consisting of early-onset bilateral optic atrophy and later-onset spasticity, extrapyramidal dysfunction, and cognitive deficit. Urinary excretion of 3-methylglutaconic acid and of 3-methylglutaric acid is increased (Anikster et al., 2001).
Costeff syndrome is an inherited condition characterized by vision loss, delayed development, and movement problems. Vision loss is primarily caused by degeneration (atrophy) of the optic nerves , which carry information from the eyes to the brain. This optic nerve atrophy often begins in infancy or early childhood and results in vision impairment that worsens over time. Some affected individuals have rapid and involuntary eye movements (nystagmus) or eyes that do not look in the same direction (strabismus). Development of motor skills, such as walking, is often delayed in people with Costeff syndrome.
3-methylglutaconic aciduria type III (MGA III) is an organic aciduria characterised by the association of optic atrophy and choreoathetosis with 3-methylglutaconic aciduria. Epidemiology The vast majority of reported cases involved the Iraqi-Jewish population, in which the prevalence of the disorder has been estimated at around 1 in 10 000. Clinical description Onset of the optic atrophy occurs during infancy with a progressive decrease in visual acuity. The choreoathetoid movement disorder manifests later, usually within the first ten years of life. Other clinical features may include spastic paraparesis, mild ataxia and cognitive deficit, dysarthria, and nystagmus.
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).
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). ... Anais Brasileiros de Dermatologia . 89 (6): 865–877. doi : 10.1590/abd1806-4841.20142966 . ISSN 0365-0596 . PMC 4230654 . PMID 25387490 . ^ Bolotin, Diana; Petronic-Rosic, Vesna (2011). ... Journal of the American Academy of Dermatology . 28 (3): 505–506. doi : 10.1016/S0190-9622(08)81769-0 . ISSN 0190-9622 . PMID 8445075 . ^ Johnson, H.
Dermatitis herpetiformis is a rare, chronic, skin disorder characterized by groups of severely itchy blisters and raised skin lesions. These are more common on the knees, elbows, buttocks and shoulder blades. The slow onset of symptoms usually begins during adulthood, but children can also be affected. Other symptoms may include fluid-filled sores; red lesions that resemble hives; and itchiness, redness and burning. The exact cause of this disease is not known, but it is frequently associated with the inability to digest gluten.
A chronic autoimmune subepidermal bullous disease characterized by grouped pruritic lesions such as papules, urticarial plaques, erythema, and herpetiform vesiculae, with a predominantly symmetrical distribution on extensor surfaces of the elbows (90%), knees (30%), shoulders, buttocks, sacral region, and face of children and adults. Erosions, excoriations and hyperpigmentation usually follow. It may also appear as a consequence of gluten intolerance.
Dermatitis herpetiformis (DH) and celiac disease (CD; 212750) are gluten-sensitive diseases. In classic CD the small intestine is predominantly affected, whereas in DH the skin is also affected, showing typical rash and IgA deposits. Reunala (1996) reported on the familial incidence of DH in a prospective study started in 1969 in Finland. A total of 1,018 patients with DH were diagnosed and questioned for positive family histories. Of the 999 unrelated DH patients, 105 (10.5%) had 1 or several affected first-degree relatives.
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.[16046] 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.
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.
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).
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?
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) .
In Dogger Bank itch, sensitivity is acquired after repeated handling of the sea chervils that become entangled in fishing nets. [ citation needed ] The specific toxin responsible for the rash was determined to be the sulfur -bearing salt (2-hydroxyethyl) dimethylsulfoxonium chloride. [3] This salt is also found in some sea sponges and has potent in vitro activity against leukemia cells. [4] Treatment [ edit ] A study of two cases in 2001 suggests that the rash responds to oral ciclosporin . ... The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Bonnevie, P. (1948). ... Comparative Biochemistry and Physiology B . 128 (1): 27–30. doi : 10.1016/S1096-4959(00)00316-X . CS1 maint: multiple names: authors list ( link ) ^ a b Bowers PW, Julian CG., PW; Julian, CG (2001).
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 .
