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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.
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. ... She was found at 6 o'clock the following morning in a generalized tonic-clonic seizure. Blood glucose was 27 mg/dL, and urinary ketones were present. ... 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.
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.
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) .
London: Churchill Livingstone. pp. 533–53. ISBN 978-0-443-04706-0 . ^ a b Carson, Sandra A.; Simpson, Joe Leigh (1983). ... Boston: John Wright PSG Inc. pp. 177–188. ISBN 978-0-7236-7045-2 . ^ a b Jaffe, Robert B. (2004). ... Philadelphia: Elsevier Saunders. pp. 464–491. ISBN 978-0-7216-9546-4 . ^ a b Forest, Maguelone G. (2006). ... Philadelphia: Elsevier Saunders. pp. 2779–829 . ISBN 978-0-7216-0376-6 . ^ a b c Schardein JL (1980). ... New York: McGraw-Hill. pp. 1541–71. ISBN 978-0-07-142280-2 . ^ a b c Schardein, James L. (2000).
It is not limited to hand contact, but can also be induced, with different symptoms, by inhaling garlic dust or ingesting raw garlic, though the latter cases are relatively rare. [3] DADS penetrates through most types of commercial gloves, and thus wearing gloves while handling garlic has proven inefficient against the allergy. [4] Treatment includes avoiding any contact with garlic oil or vapours, as well as medication, such as administering acitretin (25 mg/day, orally) or applying psoralen and ultraviolet light to the affected skin area over a period of 12 weeks ( PUVA therapy ). [5] See also [ edit ] List of allergies References [ edit ] ^ Lasse Kanerva; Peter Elsner; Jan E. ... Elsevier Health Sciences. p. 305. ISBN 0-323-02578-1 . ^ a b Eric Block (2009). ... Royal Society of Chemistry. p. 228. ISBN 978-0-85404-190-9 . ^ Moyle, M; Frowen, K; Nixon, R (2004). ... PMPH-USA. p. 723. ISBN 978-1-55009-378-0 .
For example, Gilbert's syndrome is associated with severe diarrhea and neutropenia in patients who are treated with irinotecan , which is metabolized by UGT1A1. [13] While paracetamol (acetaminophen) is not metabolized by UGT1A1, [14] it is metabolized by one of the other enzymes also deficient in some people with GS. [15] [16] A subset of people with GS may have an increased risk of paracetamol toxicity. [16] [17] Cardiovascular effects [ edit ] Several analyses have found a significantly decreased risk of coronary artery disease (CAD) in individuals with GS. [18] [19] Specifically, people with mildly elevated levels of bilirubin (1.1 mg/dl to 2.7 mg/dl) were at lower risk for CAD and at lower risk for future heart disease. [20] These researchers went on to perform a meta-analysis of data available up to 2002, and confirmed the incidence of atherosclerotic disease (hardening of the arteries) in subjects with GS had a close and inverse relationship to the serum bilirubin. [18] This beneficial effect was attributed to bilirubin IXα which is recognized as a potent antioxidant, rather than confounding factors such as high-density lipoprotein levels. [20] This association was also seen in long-term data from the Framingham Heart Study . [21] [22] [ non-primary source needed ] Moderately elevated levels of bilirubin in people with GS and the (TA) 7 /(TA) 7 genotype were associated with one-third the risk for both coronary heart disease and cardiovascular disease as compared to those with the (TA) 6 /(TA) 6 genotype (i.e. a normal, nonmutated gene locus). [ citation needed ] Platelet counts and MPV are decreased in patients with Gilbert's syndrome. ... Levels of bilirubin in GS patients are reported to be from 20 μM to 90 μM (1.2 to 5.3 mg/dl) [31] compared to the normal amount of < 20 μM. ... Journal of Hepatology . 33 (3): 348–351. doi : 10.1016/S0168-8278(00)80268-8 . PMID 11019988 . ^ a b Bosma PJ; Chowdhury JR; Bakker C; Gantla S; de Boer A; Oostra BA; Lindhout D; Tytgat GN; Jansen PL; Oude Elferink RP; et al. (1995). ... Greenwood Publishing Group. pp. 175 . ISBN 978-0-313-33528-0 . ^ "Wire preaches delights of three cliffs". ... "Illness that 'shut down' Tech3 MotoGP rookie Jonas Folger diagnosed" . Autosport .com . Motorsport Network . Retrieved 2017-11-09 .
Overview Gilbert (zheel-BAYR) syndrome is a common, harmless liver condition in which the liver doesn't properly process bilirubin. Bilirubin is produced by the breakdown of red blood cells. The liver The liver is your largest internal organ. About the size of a football, it's located mainly in the upper right portion of your abdomen, beneath the diaphragm and above your stomach. Gilbert syndrome is an inherited genetic condition. You might not know you have Gilbert syndrome until it's discovered by accident, such as when a blood test shows raised bilirubin levels. Gilbert syndrome requires no treatment. Symptoms The most frequent sign of Gilbert syndrome is an occasional yellowish tinge of the skin and the whites of the eyes as a result of slightly higher levels of bilirubin in the blood.
Gilbert syndrome is a relatively mild condition characterized by periods of elevated levels of a toxic substance called bilirubin in the blood (hyperbilirubinemia). Bilirubin, which has an orange-yellow tint, is produced when red blood cells are broken down. This substance is removed from the body only after it undergoes a chemical reaction in the liver, which converts the toxic form of bilirubin (unconjugated bilirubin) to a nontoxic form called conjugated bilirubin. People with Gilbert syndrome have a buildup of unconjugated bilirubin in their blood (unconjugated hyperbilirubinemia). In affected individuals, bilirubin levels fluctuate and very rarely increase to levels that cause jaundice, which is yellowing of the skin and whites of the eyes.
Arias (1962) demonstrated glucuronyltransferase deficiency in 8 patients with chronic nonhemolytic jaundice and serum unconjugated bilirubin levels of 6.2 to 18.8 mg percent. Arias et al. (1969) concluded that this disorder is distinct from Crigler-Najjar syndrome type I (218800), which also has deficiency of hepatic glucuronyltransferase activity. In Crigler-Najjar syndrome type I, hyperbilirubinemia is severe, with total serum bilirubin levels ranging from 20 to 45 mg/dL, and is frequently accompanied by kernicterus. ... Differential Diagnosis Patients with Gilbert syndrome tend to have total serum bilirubin levels from 1-6 mg/dL. This is distinguished from Crigler-Najjar syndrome type II, in which patients have total serum bilirubin levels between 6 and 20 mg/dL, and Crigler-Najjar syndrome type I, in which patients have total serum bilirubin levels from 20 to 45 mg/dL.
. ^ "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 .
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.
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).
It consists chiefly of a variable mixture of sodium salts of fatty acids , such as oleic and palmitic . [4] Contents 1 Composition 2 Uses 2.1 Soap 2.1.1 Shaving soap 2.2 Food 2.2.1 Greaves 2.3 Fuel 2.3.1 Biodiesel 2.3.2 Aviation fuel 2.4 Printing 2.5 Candles 2.6 Lubrication 2.7 Medicinal 2.8 Industrial 3 References Composition [ edit ] Beef Tallow Nutritional value per 100 g (3.5 oz) Energy 3,774 kJ (902 kcal) Carbohydrates 0 g Fat 100 g Saturated 42 g Monounsaturated 50 g Polyunsaturated 4 g Protein 0 g Other constituents Quantity Cholesterol 109 mg Selenium 0.2 mg Fat percentage can vary. Units μg = micrograms • mg = milligrams IU = International units † Percentages are roughly approximated using US recommendations for adults. Source: USDA FoodData Central The composition of the fatty acids is typically as follows: [5] Saturated fatty acids: Palmitic acid (C16:0): 26% Stearic acid (C18:0): 14% Myristic acid (C14:0): 3% Monounsaturated fatty acids: Oleic acid (C18-1, ω-9): 47% Palmitoleic acid (C16:1): 3% Polyunsaturated fatty acids: Linoleic acid : 3% Linolenic acid : 1% Uses [ edit ] Tallow is used mainly in producing soap and animal feed. [6] Soap [ edit ] Shaving soap [ edit ] An 1883 ad soliciting tallow from butchers and graziers for soap production in the Hawaii newspaper The Daily Bulletin Many items of traditional goods are produced from tallow, which was widely available domestically. ... ISBN 9781462065783 ^ National Research Council, 1976, Fat Content and Composition of Animal Products , Printing and Publishing Office, National Academy of Science, Washington, D.C., ISBN 0-309-02440-4 ; p. 203, online edition ^ Alfred Thomas (2002). ... Fast Food Nation: The Dark Side of All-American Meal . Houghton Mifflin. ISBN 0-395-97789-4 ^ Irvin Molotsky (November 15, 1985).
Arbitrarily, the guideline is set at 18 mg, which is the USDA Recommended Dietary Allowance for women aged between 19 and 50. [29] Abstract: richest foods in heme iron Food Serving size Iron % guideline clam [a] 100g 28 mg 155% pork liver 100g 18 mg 100% lamb kidney 100g 12 mg 69% cooked oyster 100g 12 mg 67% cuttlefish 100g 11 mg 60% lamb liver 100g 10 mg 57% octopus 100g 9.5 mg 53% mussel 100g 6.7 mg 37% beef liver 100g 6.5 mg 36% beef heart 100g 6.4 mg 35% Abstract: richest foods in non-heme iron Food Serving size Iron % guideline raw yellow beans 100g 7 mg 35% spirulina 15g 4.3 mg 24% falafel 140g 4.8 mg 24% soybean kernels 125ml=1/2cup 4.6 mg 23% spinach 125g 4.4 mg 22% lentil 125ml=1/2cup 3.5 mg 17.5% treacle (CSR Australia) 20ml=1Tbsp 3.4 mg 17% molasses (Bluelabel Australia) 20ml=1Tbsp 1.8 mg 9% candied ginger root 15g~3p 1.7 mg 8.5% toasted sesame seeds 10g 1.4 mg 7% cocoa (dry powder) 5g~1Tbsp .8 mg 4% Food recommendations for children [ edit ] Children at 6 months should start having solid food that contains enough iron, which could be found in both heme and non-heme iron [33] Heme iron : Red meat (for example, beef, pork, lamb, goat, or venison) Fatty fish Poultry (for example, chicken or turkey) Eggs Non-heme iron : Iron-fortified infant cereals Tofu Beans and lentils Dark green leafy vegetables Iron deficiency can have serious health consequences that diet may not be able to quickly correct; hence, an iron supplement is often necessary if the iron deficiency has become symptomatic. ... Why We Get Sick: The New Science of Darwinian Medicine . New York. page 29 ISBN 0-679-74674-9 . ^ Weinberg, E. D. (1984). ... Oxford University Press . pp. 626–628. ISBN 0-19-852558-3 . ^ Rockey D, Cello J (1993). ... Guidelines for Patient Blood Management and Blood . ISBN 978-1-56395-333-0 . Archived from the original on 15 October 2014 . ... Belmont, California: Wadsworth, Cengage Learning . ISBN 978-0-495-11657-8 . Umbreit, Jay (2005).
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.
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.
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.
Folliculitis decalvans Specialty Dermatology Folliculitis decalvans is an inflammation of the hair follicle that leads to bogginess or induration of involved parts of the scalp along with pustules , erosions, crusts, ulcers, and scale. [1] : 649 [2] : 760–1 It begins at a central point and spreads outward, leaving scarring, sores, and, due to the inflammation, hair loss in its wake. [3] No permanent cure has been found for this condition, but there is promise in a regimen of dual therapy with rifampin 300 mg twice daily and clindamycin 300 mg twice daily. ... 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 . ^ Otberg N, Kang H, Alzolibani AA, Shapiro J (2008).
Specific disease entities [ edit ] Demographic studies suggest that cholesterol levels form a U-shape curve when plotted against mortality; this suggests that low cholesterol is associated with increased mortality, mainly due to depression , cancer , hemorrhagic stroke , aortic dissection and respiratory diseases. [1] It is possible that whatever causes the low cholesterol level also causes mortality, and that the low cholesterol is simply a marker of poor health. [2] Links with depression have been supported by studies. [3] In contrast, no evidence was found for a link with hemorrhagic stroke (although higher cholesterol levels conferred a relative protection), and neither did statin drugs worsen the risk. [4] The Heart Protection Study found no increase in either respiratory disease or neuropsychiatric illness in a large trial population taking a statin drug. [5] Elderly [ edit ] In the elderly, low cholesterol may confer a health risk that may not be offset by the beneficial effects of cholesterol lowering. [6] Similarly, for elderly patients admitted to hospital, low cholesterol may predict short-term mortality. [7] The prevalence of hypocholesterolemia in the elderly ranges between 2% to 36%, depending on specific cutoff levels and age range investigated. [8] Alerting physicians to hypocholesterolemia may benefit some of their patients who take cholesterol-lowering drugs and decrease the rate of their emergency room visits. [9] Critical illness [ edit ] In the setting of critical illness, low cholesterol levels are predictive of clinical deterioration, and are correlated with altered cytokine levels. [10] Causes [ edit ] Possible causes of low cholesterol are: [ citation needed ] statins hyperthyroidism , or an overactive thyroid gland adrenal insufficiency liver disease malabsorption (inadequate absorption of nutrients from the intestines ), such as in celiac disease malnutrition abetalipoproteinemia - a rare genetic disease that causes cholesterol readings below 50 mg/dl. It is found mostly in Jewish populations. [11] hypobetalipoproteinemia - a genetic disease that causes cholesterol readings below 50 mg/dl [11] manganese deficiency Smith–Lemli–Opitz syndrome Marfan syndrome leukemias and other hematological diseases [12] Diagnosis [ edit ] Classification [ edit ] According to the American Heart Association in 1994, only total cholesterol levels below 160 mg/dL or 4.1 mmol/l are to be classified as "hypocholesterolemia". [2] However, this is not agreed on universally and some put the level lower. ... BMC Health Services Research . 18 (1): 4. doi : 10.1186/s12913-017-2812-0 . ISSN 1472-6963 . PMC 5755463 . PMID 29301522 . ^ Tsabar, Nir; Press, Yan; Rotman, Johanna; Klein, Bracha; Grossman, Yonatan; Vainshtein-Tal, Maya; Eilat-Tsanani, Sophia (2019-10-12). ... Journal of the American Medical Directors Association . 0 (0). doi : 10.1016/j.jamda.2019.08.018 .
Identification criteria [ edit ] According to the World Health Organization, if a woman presents any of the conditions below during pregnancy, childbirth or within 42 days of termination of pregnancy and survives, she is considered as a maternal near miss case. [10] Cardiovascular dysfunction a) Shock b) Cardiac Arrest c) Severe hypoperfusion (lactate >5 mmol/L or >45 mg/dL) d) Severe acidosis (pH<7.1) e) Use of continuous vasoactive drugs f) Cardio-pulmonary resuscitation Respiratory dysfunction g) Acute cyanosis h) Gasping i) Severe tachypnea (respiratory rate>40 breaths per minute) j) Severe bradypnea (respiratory rate<6 breaths per minute) k) Severe hypoxemia (O2 saturation <90% for ≥60min or PAO2/FiO2<200) l) Intubation and ventilation not related to anaesthesia Renal dysfunction m) Oliguria non responsive to fluids or diuretics n) Severe acute azotemia (creatinine >300 μmol/ml or >3.5 mg/dL) o) Dialysis for acute renal failure Coagulation dysfunction p) Failure to form clots q) Severe acute thrombocytopenia (<50,000 platelets/ml) r) Massive transfusion of blood or red cells (≥ 5 units) Hepatic dysfunction s) Jaundice in the presence of pre-eclampsia t) Severe acute hyperbilirubinemia (bilirubin>100 μmol/L or >6.0 mg/dL) Neurologic dysfunction u) Prolonged unconsciousness or coma (lasting >12 hours) v) Stroke w) Uncontrollable fit / status epilepticus x) Global paralysis Uterine dysfunction y) Hysterectomy due to uterine infection or haemorrhage Sources [ edit ] Adisasmita, Asri; et al. (2008). ... Community-based Maternity Care . Oxford University Press. ISBN 0-19-262768-6 . Minkauskienė, Meilė; Rūta Nadišauskienė; Žilvinas Padaiga1; Said Makari (2004). ... Clinical Risk Management in Midwifery . Elsevier Health Sciences. ISBN 0-7506-2851-0 . References [ edit ] ^ Marsh 1998:176 ^ a b Minkauskienė 2004:299 ^ See also the Poisson distribution for a discussion of statistical methodological difficulties when the number of cases is "small" ^ Lewis 2003:31 ^ list is based on Adisasmita 2008 unless otherwise indicated ^ Tingle 2002:3 ^ Lewis 2003:29 ^ Adisasmita 2008 ^ Dott 2005 ^ WHO 2009 External links [ edit ]
Called benign infantile seizures associated with mild gastroenteritis (BIS with MG), the seizures only occur during this illness and no not recur. ... Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2008. ch. 227. ISBN 0-7817-5777-0 ^ Panayiotopoulos CP.
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).
