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Hydrocele Testis Wikipedia

. ^ Ku u.a. 2001 KU, J. H.; KIM, M. E.; LEE, N. K.; PARK, Y. H.:The excisional, plication and internal drainage techniques: a comparison of the results for idiopathic hydrocele.In: BJU Int 87 (2001), Nr. 1, S. 82–4 ^ Fracchia, JA; Armenakas, NA; Kohan, AD (1998).

FLT4, AKT1, PEX11B, GJC2, KLHL7, SOX18, PIGN, PIEZO1, ADAMTS3, VEGFC, RPL5, PTEN, PIK3CA, EZH2, MECOM, DIPK1A, CHIT1, TP63, VEGFA, EDN1, CYP4V2
- Hydrocele Mayo Clinic
  
  Overview A hydrocele (HI-droe-seel) is a type of swelling in the scrotum, the pouch of skin that holds the testicles. This swelling happens when fluid collects in the thin sac that surrounds a testicle. Hydroceles are common in newborns. They often go away without treatment by age 1. Older children and adults can get a hydrocele due to an injury within the scrotum or other health problems. A hydrocele often isn't painful or harmful. It might not need any treatment.
- Hydrocele Wikipedia
  
  Hydrocele Other names hydrocoele Scrotal ultrasound of a 10 cm large hydrocele, with anechoic (dark) fluid surrounding the testicle Specialty Urology A hydrocele is an accumulation of serous fluid in a body cavity . A hydrocele testis is the accumulation of fluids around a testicle . It is often caused by peritoneum wrapped around the testicle, called the tunica vaginalis . Provided there is no hernia present, it goes away without treatment in the first year. Primary hydroceles may develop in adulthood, particularly in the elderly and in hot countries, by slow accumulation of serous fluid. This is presumably caused by impaired reabsorption, which appears to be the explanation for most primary hydroceles, although the reason remains obscure. [ citation needed ] A hydrocele can also be the result of a plugged inguinal lymphatic system caused by repeated, chronic infection of Wuchereria bancrofti or Brugia malayi , two mosquito -borne parasites of Africa and Southeast Asia , respectively.
Nevus Flammeus Nuchae Wikipedia

. ^ MedlinePlus Encyclopedia : Stork bite External links [ edit ] Classification D OMIM : 163100 v t e Congenital malformations and deformations of integument / skin disease Genodermatosis Congenital ichthyosis / erythrokeratodermia AD Ichthyosis vulgaris AR Congenital ichthyosiform erythroderma : Epidermolytic hyperkeratosis Lamellar ichthyosis Harlequin-type ichthyosis Netherton syndrome Zunich–Kaye syndrome Sjögren–Larsson syndrome XR X-linked ichthyosis Ungrouped Ichthyosis bullosa of Siemens Ichthyosis follicularis Ichthyosis prematurity syndrome Ichthyosis–sclerosing cholangitis syndrome Nonbullous congenital ichthyosiform erythroderma Ichthyosis linearis circumflexa Ichthyosis hystrix EB and related EBS EBS-K EBS-WC EBS-DM EBS-OG EBS-MD EBS-MP JEB JEB-H Mitis Generalized atrophic JEB-PA DEB DDEB RDEB related: Costello syndrome Kindler syndrome Laryngoonychocutaneous syndrome Skin fragility syndrome Ectodermal dysplasia Naegeli syndrome / Dermatopathia pigmentosa reticularis Hay–Wells syndrome Hypohidrotic ectodermal dysplasia Focal dermal hypoplasia Ellis–van Creveld syndrome Rapp–Hodgkin syndrome / Hay–Wells syndrome Elastic / Connective Ehlers–Danlos syndromes Cutis laxa ( Gerodermia osteodysplastica ) Popliteal pterygium syndrome Pseudoxanthoma elasticum Van der Woude syndrome Hyperkeratosis / keratinopathy PPK diffuse : Diffuse epidermolytic palmoplantar keratoderma Diffuse nonepidermolytic palmoplantar keratoderma Palmoplantar keratoderma of Sybert Meleda disease syndromic connexin Bart–Pumphrey syndrome Clouston's hidrotic ectodermal dysplasia Vohwinkel syndrome Corneodermatoosseous syndrome plakoglobin Naxos syndrome Scleroatrophic syndrome of Huriez Olmsted syndrome Cathepsin C Papillon–Lefèvre syndrome Haim–Munk syndrome Camisa disease focal : Focal palmoplantar keratoderma with oral mucosal hyperkeratosis Focal palmoplantar and gingival keratosis Howel–Evans syndrome Pachyonychia congenita Pachyonychia congenita type I Pachyonychia congenita type II Striate palmoplantar keratoderma Tyrosinemia type II punctate : Acrokeratoelastoidosis of Costa Focal acral hyperkeratosis Keratosis punctata palmaris et plantaris Keratosis punctata of the palmar creases Schöpf–Schulz–Passarge syndrome Porokeratosis plantaris discreta Spiny keratoderma ungrouped: Palmoplantar keratoderma and spastic paraplegia desmoplakin Carvajal syndrome connexin Erythrokeratodermia variabilis HID / KID Other Meleda disease Keratosis pilaris ATP2A2 Darier's disease Dyskeratosis congenita Lelis syndrome Dyskeratosis congenita Keratolytic winter erythema Keratosis follicularis spinulosa decalvans Keratosis linearis with ichthyosis congenita and sclerosing keratoderma syndrome Keratosis pilaris atrophicans faciei Keratosis pilaris Other cadherin EEM syndrome immune system Hereditary lymphedema Mastocytosis / Urticaria pigmentosa Hailey–Hailey see also Template:Congenital malformations and deformations of skin appendages , Template:Phakomatoses , Template:Pigmentation disorders , Template:DNA replication and repair-deficiency disorder Developmental anomalies Midline Dermoid cyst Encephalocele Nasal glioma PHACE association Sinus pericranii Nevus Capillary hemangioma Port-wine stain Nevus flammeus nuchae Other/ungrouped Aplasia cutis congenita Amniotic band syndrome Branchial cyst Cavernous venous malformation Accessory nail of the fifth toe Bronchogenic cyst Congenital cartilaginous rest of the neck Congenital hypertrophy of the lateral fold of the hallux Congenital lip pit Congenital malformations of the dermatoglyphs Congenital preauricular fistula Congenital smooth muscle hamartoma Cystic lymphatic malformation Median raphe cyst Melanotic neuroectodermal tumor of infancy Mongolian spot Nasolacrimal duct cyst Omphalomesenteric duct cyst Poland anomaly Rapidly involuting congenital hemangioma Rosenthal–Kloepfer syndrome Skin dimple Superficial lymphatic malformation Thyroglossal duct cyst Verrucous vascular malformation Birthmark

MORC2, KCTD7
Carpal Tunnel Syndrome OMIM

Further documentation of the improvement, which may obviate surgery, was presented by Ellis et al. (1982). They concluded that, since K(m) values of EGOT were identical in patients with and without CTS but with identical specific activities, CTS is a primary deficiency of B6, not a dependency state.

TTR, AOC1, ADAMTS10, AEBP1, SMAD6, LTBP1, EFEMP1, HCP5, TTLL5, UMPS, ADAMTS17, B2M, PMP22, CCN2, IL1B, PSMD9, CYP19A1, GSTT1, COL5A1, PGR, SLX1A-SULT1A3, SEMG1, PDGFRB, SULT1A4, MIR106A, MAPK3, PDGFRA, SERPINE1, PTGS2, ROS1, CCL2, DHDDS, SLC6A2, SULT1A3, CHPT1, TGFB1, TGFBR1, GSTK1, NT5E, VDR, VEGFA, HDAC4, ADAMTS5, SLCO6A1, INTU, HPGDS, SEMA5B, OLR1, MMP3, NDUFB2, CECR, ELK3, ACE, CSH2, CSH1, COMT, COL11A1, ERCC8, CASP8, COX2, CALCR, BGN, AMH, ABCD1, ALB, AKT1, ACAN, EPHB1, ESR1, FAP, GHR, MPZ, MMP10, MMP9, MMP1, MIP, IL6R, IL1RN, IGF1, TNC, HSPA9, HLA-DRB3, HLA-DPB1, HLA-DPA1, GSTP1, GSTM1, MTCO2P12
- Carpal Tunnel Syndrome MedlinePlus
  
  Carpal tunnel syndrome is a disorder caused by disturbances in nerve function (neuropathy), leading to pain and numbness or tingling (paresthesia) primarily in the wrist and hand. While carpal tunnel syndrome can occur at any age, it most often affects people between the ages of 40 and 60. In more than half of cases, both hands are affected; however, the severity may vary between hands. When only one hand is affected, it is most often the hand used for writing (the dominant hand). In carpal tunnel syndrome, the pain or paresthesia is usually felt in the wrist, the palm, and the first four fingers of the hand.
- Carpal Tunnel Syndrome Mayo Clinic
  
  Overview Carpal tunnel syndrome is caused by pressure on the median nerve. The carpal tunnel is a narrow passageway surrounded by bones and ligaments on the palm side of the hand. When the median nerve is compressed, symptoms can include numbness, tingling, and weakness in the hand and arm. The anatomy of the wrist, health problems and possibly repetitive hand motions can contribute to carpal tunnel syndrome. Proper treatment usually relieves the tingling and numbness and restores wrist and hand function.
- Carpal Tunnel Syndrome Wikipedia
  
  Retrieved 4 March 2016 . ^ a b c d e f g h i j k l m n o p q r s t American Academy of Orthopaedic Surgeons (February 29, 2016). ... PMID 2348074 . ^ Wiberg, A; Ng, M; Schmid, AB; Smillie, RW; Baskozos, G; Holmes, MV; Künnapuu, K; Mägi, R; Bennett, DL; Furniss, D (4 March 2019). ... ISBN 978-3-319-08140-3 . ^ Kalliainen, Loree K. (2017). "Nonoperative Options for the Management of Carpal Tunnel Syndrome". ... PMID 26303967 . ^ Keith, M. W.; Masear, V.; Chung, K. C.; Amadio, P. C.; Andary, M.; Barth, R. W.; Maupin, K.; Graham, B.; Watters, W. C.; Turkelson, C.
Hyperinsulinemic Hypoglycemia, Familial, 7 OMIM

Quintens et al. (2008) noted that repression of certain ubiquitously expressed housekeeping proteins is necessary in pancreatic beta cells, in order to prevent the insulin toxicity that might result from exocytosis under conditions when circulating insulin is unwanted, citing low-K(m) hexokinases (see HK1, 142600) and monocarboxylic acid transporters (MCTs) as examples.

SLC16A1
- Exercise-Induced Hyperinsulinism Orphanet
  
  Exercise-induced hyperinsulinism (EIHI) is a form of diazoxide-sensitive diffuse hyperinsulinism (DHI) characterized by episodes of hypoglycemia induced by exercise due to an inappropriate lactate and pyruvate sensitivity in pancreatic beta-cells. Epidemiology Prevalence is estimated at 1/50,000 live births for CHI, EIHI accounts for a very small portion of this group. Clinical description EIHI patients present recurring episodes of hypoglycemia associated with elevated insulin levels, within 30 minutes of a short period of anaerobic exercise. This response may be mimicked by the injection of pyruvate. The degree of hypoglycemia associated with exercise is variable and is only partially responsive to diazoxide. Etiology Mutations in the promoter element of SLC16A1 (SLC16A1, 1p12, solute carrier family 16, member 1) leads to an inappropriate presence of monocarboxylic acid transporter 1(MCT1) .
- Exercise-Induced Hyperinsulinemic Hypoglycemia GARD
  
  Exercise induced hyperinsulinemic hypoglycemia is characterized by a sudden and exaggerated spike in insulin and drop in blood sugar levels. The condition is triggered by vigorous exercise. Signs and symptoms include fainting (syncope), shakiness, nervousness, sweating, dizziness or light-headedness, sleepiness, confusion, difficulty speaking, anxiety, and weakness.
Microvillous Inclusion Disease Wikipedia

. ^ Mueller T; Hess, MW; Schiefermeier, N; Pfaller, K; Ebner, HL; Heinz-Erian, P; Ponstingl, H; Partsch, J; et al. (2008).

MYO5B, STX3, SNHG22, RAB11A, RAB8A, CFTR, SLC26A3, CDC42, PDK1, SLC9A3, AQP7, STXBP2, EZR, VWF, ABCB11, FHL5, IMMT, AICDA, ACTB
- Diarrhea 2, With Microvillus Atrophy OMIM
  
  A number sign (#) is used with this entry because of evidence that microvillus inclusion disease is caused by homozygous or compound heterozygous mutation in the MYO5B (606540) gene on chromosome 18q21. Description Microvillus inclusion disease (MVID) is characterized by onset of intractable life-threatening watery diarrhea during infancy. Two forms are recognized: early-onset MVID with diarrhea beginning in the neonatal period, and late-onset, with first symptoms appearing after 3 or 4 months of life. Definite diagnosis is made by transmission electron microscopy demonstrating shortening or absence of apical microvilli with pathognomonic microvillus inclusions in mature enterocytes and peripheral accumulation of periodic acid-Schiff (PAS)-positive granules or vesicles in immature enterocytes (Muller et al., 2008). The natural course of MVID is often fatal, but partial or total weaning from parenteral nutrition has been described.
- Microvillus Inclusion Disease Orphanet
  
  Microvillus inclusion disease (MVID) is a very rare and severe intestinal disease characterized by intractable neonatal secretory diarrhea persisting at bowel rest and specific histological features of the intestinal epithelium. Epidemiology Prevalence data are not available. Less than 200 cases have been reported to date. There is a male predominance, with a sex ratio of 1.5:1. Clinical description Two clinical forms of MVID have been described: an early-onset form, developing within hours or days of birth, and a late-onset form, occurring in the first months of life. In both, intractable, watery diarrhea is profuse and leads to severe metabolic acidosis, dehydration, malabsorption and failure to thrive. Total parenteral nutrition is necessary, however, in some later-onset cases, partial oral absorption has been described.
- Intractable Diarrhea Of Infancy Orphanet
  
  Intractable diarrhea of infancy (IDI) is a heterogeneous syndrome that includes several diseases with different etiologies. Provisional classification of IDI, according to villous atrophy and based on immunohistological criteria, distinguishes two clearly different groups of IDI: 1) Immune-mediated: characterised by a mononuclear cell infiltration of the lamina propria and considered as being related to T cell activation. 2) The second histological pattern includes early onset severe intractable diarrhea histologically characterised by villous atrophy with low or without mononuclear cell infiltration of the lamina propria but specific histological abnormalities involving the epithelium. Clinical description Based on recent advances in the genetics of autoimmune enteropathy as well as the pathophysiology and clinical presentation, autoimmune enteropathy can be classified into three different types: the classical form of autoimmune enteropathy, identical to the so-called immune dysregulation-polyendocrinopathy-enteropathy-X-linked (IPEX) syndrome (autoimmune enteropathy type 1); autoimmune enteropathy type 2 (without extra-intestinal manifestations) and autoimmune enteropathy type 3 (in girls). Microvillus inclusion disease (MVID) and Intestinal epithelial dysplasia (IED), also known as tufting enteropathy, are congenital enteropathies presenting with villous atrophy and are thought to be related to abnormal enterocytes. Another form of IDI that should be considered in a different way from the two other groups is so-called 'phenotypic diarrhoea'' or 'syndromatic diarrhoea''.
- Microvillus Inclusion Disease GARD
  
  Microvillus inclusion disease is an intestinal disorder characterized by severe, watery diarrhea and an inability of the intestines to absorb nutrients. Symptoms typically develop in the first days (early-onset) or first months (late-onset) of life. Without adequate water and nutrients, children with this condition can become dehydrated, suffer from malnutrition, and fail to grow and develop normally. Management is difficult and relies on total parenteral nutrition . The advent of intestinal transplantation has improved the outlook for these patients. Microvillus inclusion disease is inherited in an autosomal recessive manner.
- Microvillus Inclusion Disease MedlinePlus
  
  Microvillus inclusion disease is a condition characterized by chronic, watery, life-threatening diarrhea typically beginning in the first hours to days of life. Rarely, the diarrhea starts around age 3 or 4 months. Food intake increases the frequency of diarrhea. Microvillus inclusion disease prevents the absorption of nutrients from food during digestion, resulting in malnutrition and dehydration. Affected infants often have difficulty gaining weight and growing at the expected rate (failure to thrive), developmental delay, liver and kidney problems, and thinning of the bones (osteoporosis ). Some affected individuals develop cholestasis, which is a reduced ability to produce and release a digestive fluid called bile.
Pmm2 Deficiency Wikipedia

In Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). GeneReviews® .

PMM2, PMM1, MPI, LEMD3, AHCY, GYPA, GYPB, GYPE, OGA, ALG6
- Pmm2-Cdg (Cdg-Ia) GeneReviews
  
  Summary Clinical characteristics. PMM2-CDG ( CDG-Ia ) (previously known as congenital disorder of glycosylation type 1a), the most common of a group of disorders of abnormal glycosylation of N-linked oligosaccharides, is divided into three types: infantile multisystem, late-infantile and childhood ataxia-intellectual disability, and adult stable disability. The three types notwithstanding, clinical presentation and course are highly variable, ranging from infants who die in the first year of life to mildly involved adults. Clinical presentations tend to be similar in sibs. In the infantile multisystem type, infants show axial hypotonia, hyporeflexia, esotropia, and developmental delay. Feeding problems, vomiting, failure to thrive, and impaired growth are frequently seen. Subcutaneous fat may be excessive over the buttocks and suprapubic region.
- Congenital Disorder Of Glycosylation, Type Ia OMIM
  
  A number sign (#) is used with this entry because congenital disorder of glycosylation type Ia (CDG Ia, CDG1A) is caused by homozygous or compound heterozygous mutation in the gene encoding phosphomannomutase-2 (PMM2; 601785) on chromosome 16p13. Description Congenital disorders of glycosylation (CDGs) are a genetically heterogeneous group of autosomal recessive disorders caused by enzymatic defects in the synthesis and processing of asparagine (N)-linked glycans or oligosaccharides on glycoproteins. These glycoconjugates play critical roles in metabolism, cell recognition and adhesion, cell migration, protease resistance, host defense, and antigenicity, among others. CDGs are divided into 2 main groups: type I CDGs comprise defects in the assembly of the dolichol lipid-linked oligosaccharide (LLO) chain and its transfer to the nascent protein, whereas type II CDGs (see, e.g., CDG2A, 212066) refer to defects in the trimming and processing of the protein-bound glycans either late in the endoplasmic reticulum or the Golgi compartments. CDG1A is the most common form of CDG and was the first to be characterized at the molecular level (reviews by Marquardt and Denecke, 2003; Grunewald et al., 2002).
- Pmm2-Cdg (Cdg-Ia) GARD
  
  Congenital disorder of glycosylation type Ia (CDG-Ia) is an inherited condition that affects many parts of the body. The type and severity of problems associated with CDG-Ia vary widely among affected individuals, sometimes even among members of the same family. Signs and symptoms are typically evident in infancy and can include hypotonia, inverted nipples, an abnormal distribution of fat, strabismus, developmental delay, failure to thrive , seizures, and distinctive facial features. About 20 percent of affected infants do not survive the first year of life due to multiple organ failure. The most severe cases of CDG-Ia are characterized by hydrops fetalis .
- Pmm2-Cdg Orphanet
  
  PMM2-CDG is the most frequent form of congenital disorder of N-glycosylation and is characterized by cerebellar dysfunction, abnormal fat distribution, inverted nipples, strabismus and hypotonia. 3 forms of PMM2-CDG can be distinguished: the infantile multisystem type, late-infantile and childhood ataxia-intellectual disability type (3-10 yrs old), and the adult stable disability type. Infants usually develop ataxia, psychomotor delay and extraneurological manifestations including failure to thrive, enteropathy, hepatic dysfunction, coagulation abnormalities and cardiac and renal involvement. The phenotype is however highly variable and ranges from infants who die in the first year of life to mildly involved adults.
- Pmm2-Congenital Disorder Of Glycosylation MedlinePlus
  
  PMM2 -congenital disorder of glycosylation ( PMM2 -CDG, also known as congenital disorder of glycosylation type Ia) is an inherited condition that affects many parts of the body. The type and severity of problems associated with PMM2 -CDG vary widely among affected individuals, sometimes even among members of the same family. Individuals with PMM2 -CDG typically develop signs and symptoms of the condition during infancy. Affected infants may have weak muscle tone (hypotonia), retracted (inverted) nipples, an abnormal distribution of fat, eyes that do not look in the same direction (strabismus), developmental delay, and a failure to gain weight and grow at the expected rate (failure to thrive). Infants with PMM2 -CDG also frequently have an underdeveloped cerebellum , which is the part of the brain that coordinates movement.
Anomic Aphasia Wikipedia

.; Cooper-Pye, E.; Hodges, JR.; Patterson, K. (Aug 2008). "Anomia: a doubly typical signature of semantic dementia". ... PMID 3978406 . ^ Miller, N; Willmes, K; De Bleser, R (2000). "The psychometric properties of the English language version of the Aachen Aphasia Test (EAAT)". ... PMID 21636820 . ^ Martin, N; Fink, R; Renvall, K; Laine, M (Nov 12, 2006). "Effectiveness of contextual repetition priming".

GRN, MAPT, PSEN1, CHMP2B, TREM2, TMEM106B, C9orf72, APOE
Paraphilic Infantilism Wikipedia

Retrieved 2006-03-07 . ^ a b Kise, K.; Nguyen, M. (2011). "Adult Baby Syndrome and Gender Identity Disorder". ... ISBN 978-0-313-32968-5 . ^ a b c d Stekel 1952 , pp. 143–144. ^ a b Hawkinson, K., & Zamboni, B. D. (2014). "Adult Baby/Diaper Lovers: An Exploratory Study of an Online Community Sample". ... Continuum International Publishing Group . p. 255. ISBN 978-0-8264-1026-9 . ^ Freund K; Blanchard R (1993). "Erotic target location errors in male gender dysphorics, paedophiles, and fetishists".
Antenatal Depression Wikipedia

Retrieved 2019-10-24 . ^ a b c Kroenke K, Spitzer RL, Williams JB (September 2001). ... S2CID 24565503 . ^ Misri S, Kendrick K, Oberlander TF, Norris S, Tomfohr L, Zhang H, Grunau RE (April 2010). ... PMID 20416145 . ^ Gress-Smith JL, Luecken LJ, Lemery-Chalfant K, Howe R (May 2012). "Postpartum depression prevalence and impact on infant health, weight, and sleep in low-income and ethnic minority women and infants".
Encephalitis Lethargica Wikipedia

At the time, doctors attributed her encephalitis to having contracted influenza during the 1918 pandemic. [38] References [ edit ] ^ Economo's disease at Who Named It? ^ von Economo, K. (May 10, 1917). "Die Encephalitis lethargica". ... S2CID 45138249 . ^ a b McCall, Sherman; Vilensky, Joel A; Gilman, Sid; Taubenberger, Jeffery K (May 2008). "The relationship between encephalitis lethargica and influenza: A critical analysis" . ... PMID 18569452 . ^ a b Haeman, Jang; Boltz, D.; Sturm-Ramirez, K.; Shepherd, K.R.; Jiao, Y.; Webster, R.; Smeyne, Richard J. (2009).

ACTB, HLA-A, POTEF
- Encephalitis Lethargica Orphanet
  
  A rare brain inflammatory disease characterized by acute or subacute encephalitis with involvement of the midbrain and basal ganglia occurring in children as well as adults. Initial symptoms are pharyngitis and fever, followed by progressive lethargy, sleep disturbances, extrapyramidal symptoms (parkinsonism, chorea, dystonia), neuropsychiatric manifestations (obsessive-compulsive behavior, mutism, catatonia), and ocular features (oculogyric crises). Autoantibodies against human basal ganglia are often positive. Survivors may develop post-encephalitic syndromes, most prominently parkinsonism.
- Encephalitis Lethargica GARD
  
  Encephalitis lethargica (EL) is a disease characterized by high fever, headache, double vision, delayed physical and mental response, extreme tiredness ( lethargy ), and sometimes coma . Patients may also experience abnormal eye movements, upper body weakness, muscle pain, tremors , neck rigidity, and behavioral changes including psychosis . A worldwide epidemic of EL occurred from 1917 to 1928 with more than one million reported cases. Although occasional cases are reported with similar symptoms, EL epidemics have not recurred. The cause of this condition is unknown, but a viral origin is suspected.
Streptococcal Pharyngitis Wikipedia

It is, however, the leading cause of acquired heart disease in India, sub-Saharan Africa, and some parts of Australia. [8] Complications arising from streptococcal throat infections include: Acute rheumatic fever [11] Scarlet fever [36] Streptococcal toxic shock syndrome [36] [37] Glomerulonephritis [38] PANDAS syndrome [39] [40] [41] Peritonsillar abscess [8] Cervical lymphadenitis [8] Mastoiditis [8] The economic cost of the disease in the United States in children is approximately $350 million annually. [8] Epidemiology Pharyngitis , the broader category into which Streptococcal pharyngitis falls, is diagnosed in 11 million people annually in the United States. [10] It is the cause of 15–40% of sore throats among children [7] [10] and 5–15% in adults. [8] Cases usually occur in late winter and early spring. [10] References ^ a b c d e f g h i j k l m n o p "Is It Strep Throat?" . ... S2CID 8625679 . ^ a b c d e f g h i j k l m n o p q r Shulman, ST; Bisno, AL; Clegg, HW; Gerber, MA; Kaplan, EL; Lee, G; Martin, JM; Van Beneden, C (Sep 9, 2012). ... PMID 26785402 . ^ a b c d e f g h i j k l m n o p q r s t u v w x Choby BA (March 2009).

MYOM2, GAST, GALNS, HLA-DRB1, TRBV20OR9-2, PAGR1
- Strep Throat Mayo Clinic
  
  Overview Strep throat is a bacterial infection that can make your throat feel sore and scratchy. Strep throat accounts for only a small portion of sore throats. If untreated, strep throat can cause complications, such as kidney inflammation or rheumatic fever. Rheumatic fever can lead to painful and inflamed joints, a specific type of rash, or heart valve damage. Strep throat is most common in children, but it affects people of all ages. If you or your child has signs or symptoms of strep throat, see your doctor for prompt testing and treatment.
Neurofibroma Wikipedia

. ^ a b "Case Based Pediatrics For Medical Students and Residents: Chapter XVIII.11. Neurofibromatosis", by Vince K. Yamashiroya, MD. August, 2002. Department of Pediatrics, University of Hawaii John A. ... Archives of Orthopaedic and Trauma Surgery . 127 (8): 709–12. doi : 10.1007/s00402-007-0303-1 . PMID 17377797 . ^ Iino K, Matsumoto Y, Endo M, et al. (2006). ... PMID 21319287 . ^ Yamamoto M, Yamauchi T, Okano K, Takahashi M, Watabe S, Yamamoto Y (March 2009).

NF1, SUZ12, KIT, NF2, SPRED1, CDKN2A, PDGFB, TP53, SUFU, SMARCB1, SDHC, SDHB, EGFR, S100B, PDGFRA, S100A1, MDK, NRG1, EGF, SMUG1, VEGFA, FGF2, MDM2, SOX9, PDGFRB, CCND1, FN1, TOP2A, BRAF, CDKN2B-AS1, STAT3, CTNNB1, SST, EED, HMGA2, SYK, CNTN2, FGF23, VDR, TGFA, AURKA, NKX2-1, CXCR4, WT1, TLE1, TGFB1, ALDH1A1, RGS6, SPRY1, H3P23, TMED7-TICAM2, CCR2, MIR339, MIR34A, MIR210, MIR21, MIR10B, TICAM2, GADL1, THSD7A, AZIN2, ARID1B, ADAP2, TMED7, CD274, PDCD4, BRD4, KANK1, SNF8, DCTN6, ZNRD2, CIB1, NES, PTN, SOAT1, DCX, GHSR, GEM, FOLH1, MLANA, EZH2, EVI2B, ERBB2, EPHB2, EFNA3, DUSP5, CSF1, GSTP1, COL3A1, CNP, CDKN2B, CDKN1B, CDK4, CD44, CD38, RUNX1, ATRX, ATM, CXCR3, HGF, SMARCA2, PPARD, CXCL12, CCL2, RASA1, PTPN11, AR, PTEN, PSMD9, MAPK3, MAPK1, PRKAR1A, PMP22, IFI27, PLG, PGR, PDGFA, SERPINE1, NGF, MVD, MMP13, LEP, CXCL10, IFNA2, H3P10
- Neurofibroma Orphanet
  
  A rare benign peripheral nerve sheath tumor characterized by a well-demarcated intraneural or diffusely infiltrative extraneural space-occupying lesion consisting of Schwann cells, perineurial-like cells, and fibroblasts. It presents as a cutaneous nodule, a circumscribed mass in a peripheral nerve, a plexiform enlargement of a major nerve trunk, or with diffuse but localized involvement of skin and subcutaneous tissue. Multiple neurofibromas are typically associated with neurofibromatosis 1. Malignant transformation occurs almost exclusively in plexiform neurofibromas and neurofibromas of major nerves.
- Neurofibroma GARD
  
  A neurofibroma is a non-cancerous (benign) tumor that develops from the cells and tissues that cover nerves. Some people who develop neurofibromas have a genetic condition known as neurofibromatosis (NF). There are different types of NF, but type 1 is the most common.
Periventricular Leukomalacia Wikipedia

Robbin's Review of Pathology. 2nd ed. pp. 116, 121 ^ Tsukimori, K; Komatsu, H; Yoshimura, T; Hikino, S; Hara, T; Wake, N; Nakano, H (August 2007). ... ISSN 0022-3565 . PMID 10027860 . ^ Yokochi, K (March 2001). "Gait patterns in children with spastic diplegia and periventricular leukomalacia". ... Accessed November 27, 2008 External links [ edit ] Classification D ICD - 10 : P91.2 ICD - 9-CM : 779.7 MeSH : D007969 DiseasesDB : 9868 External resources MedlinePlus : 007232 eMedicine : ped/1773 v t e Conditions originating in the perinatal period / fetal disease Maternal factors complicating pregnancy, labour or delivery placenta Placenta praevia Placental insufficiency Twin-to-twin transfusion syndrome chorion / amnion Chorioamnionitis umbilical cord Umbilical cord prolapse Nuchal cord Single umbilical artery presentation Breech birth Asynclitism Shoulder presentation Growth Small for gestational age / Large for gestational age Preterm birth / Postterm pregnancy Intrauterine growth restriction Birth trauma scalp Cephalohematoma Chignon Caput succedaneum Subgaleal hemorrhage Brachial plexus injury Erb's palsy Klumpke paralysis Affected systems Respiratory Intrauterine hypoxia Infant respiratory distress syndrome Transient tachypnea of the newborn Meconium aspiration syndrome Pleural disease Pneumothorax Pneumomediastinum Wilson–Mikity syndrome Bronchopulmonary dysplasia Cardiovascular Pneumopericardium Persistent fetal circulation Bleeding and hematologic disease Vitamin K deficiency bleeding HDN ABO Anti-Kell Rh c Rh D Rh E Hydrops fetalis Hyperbilirubinemia Kernicterus Neonatal jaundice Velamentous cord insertion Intraventricular hemorrhage Germinal matrix hemorrhage Anemia of prematurity Gastrointestinal Ileus Necrotizing enterocolitis Meconium peritonitis Integument and thermoregulation Erythema toxicum Sclerema neonatorum Nervous system Perinatal asphyxia Periventricular leukomalacia Musculoskeletal Gray baby syndrome muscle tone Congenital hypertonia Congenital hypotonia Infections Vertically transmitted infection Neonatal infection rubella herpes simplex mycoplasma hominis ureaplasma urealyticum Omphalitis Neonatal sepsis Group B streptococcal infection Neonatal conjunctivitis Other Miscarriage Perinatal mortality Stillbirth Infant mortality Neonatal withdrawal

TNF, MBP, AARS2, TPI1, ARID1A, PLA2G6, SON, DDHD2, RPS6KC1, PMM2, PC, NOTCH1, TMCO1, DLL4, MCOLN1, RNF113A, MPLKIP, ARID2, RBPJ, CLCN4, DOCK6, TBCK, GTF2E2, GTF2H5, ERCC3, EOGT, ERCC2, ARHGAP31, IL6, STIP1, NES, SQSTM1, NOP53, ZNF260, KRT20, ARHGEF5, ANC, SERPINH1, TFPI, VEGFA, IL10, COL4A1, CRP, ACE, ECHS1, EPO, HOXD13, IFIT3, IL2, CXCL8, IL18, TNFRSF1A, MYT1, PEX1, SFTPD, SLC1A2, SOD2, SOD3, SOX2, MS4A1, TLR2, H3P7
- Periventricular Leukomalacia GARD
  
  Periventricular leukomalacia (PVL) is a brain injury disorder characterized by the death of the white matter of the brain due to softening of the brain tissue. It can affect fetuses or newborns, and premature babies are at the greatest risk of the disorder. PVL is caused by a lack of oxygen or blood flow to the area around the ventricles of the brain, which results in the death of brain tissue. Although babies with PVL generally have no apparent signs or symptoms of the disorder at delivery, they are at risk for motor disorders, cerebral palsy , delayed mental development, coordination problems, and vision and hearing impairments.There is no cure for PVL. Treatment is generally supportive. Prognosis is dependent on the extent of damage to the ventricles.
- Periventricular Leukomalacia Orphanet
  
  A rare neurologic condition characterized by focal periventricular necrosis and diffuse cerebral white matter injury. It most commonly occurs in premature infants. Signs of brain damage typically begin to show in early childhood. Long-term outcomes depend on the extent of the white matter injury and include cognitive delay, motor delay, vision and hearing impairment, and cerebral palsy.
Uterine Atony Wikipedia

Most women with mild to moderate anemia, however, resolve the anemia sufficiently rapidly with oral iron alone and do not need parenteral iron. [1] [2] Prognosis [ edit ] Women with a history of PPH have a 2 to 3 times higher risk of PPH in their following pregnancies. [36] [1] [37] References [ edit ] ^ a b c d e f g h i j k l m n o p q r s t u v Gill P, Patel A, Van Hook JW (2020). ... PMC 1298111 . PMID 11089490 . ^ a b Belghiti K, Kayem G, Dupont C, Rudigoz RC, Bouvier-Colle MH, Deneux-Tharaux C (2011-12-21). ... S2CID 2190885 . ^ Oberg AS, Hernandez-Diaz S, Palmsten K, Almqvist C, Bateman BT (2014). "Patterns of recurrence of postpartum hemorrhage in a large population-based cohort" .
Spectrum Disorder Wikipedia

CS1 maint: multiple names: authors list ( link ) ^ Tienari P, Wynne LC, Läksy K, et al. (September 2003). "Genetic boundaries of the schizophrenia spectrum: evidence from the Finnish Adoptive Family Study of Schizophrenia". ... PMID 16960654 . ^ Angst J, Merikangas K (August 1997). "The depressive spectrum: diagnostic classification and course". ... PMID 16330723 . ^ Lara DR, Pinto O, Akiskal K, Akiskal HS (August 2006). "Toward an integrative model of the spectrum of mood, behavioral and personality disorders based on fear and anger traits: I.
Ketosis Wikipedia

Ketosis Other names Ketonemia Ketone bodies : acetone, acetoacetic acid, and beta-hydroxybutyric acid Pronunciation / k ɪ ˈ t oʊ s ɪ s / Specialty Endocrinology Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. [1] Physiologic ketosis is a normal response to low glucose availability, such as low-carbohydrate diets or fasting , that provides an additional energy source for the brain in the form of ketones. ... Retrieved 30 September 2019 . ^ a b c d Mattson MP, Moehl K, Ghena N, Schmaedick M, Cheng A (2018). ... PMID 14769489 . ^ Fukao T, Mitchell G, Sass JO, Hori T, Orii K, Aoyama Y (2014). "Ketone body metabolism and its defects".

ACAT1, PAX4, INS, SLC16A1, GCK, ABCC8, ITPR3, IL6, GYS2, POLG2, GK, GHSR, POLG, HNF1A, MLYCD, FBP1, PTPN22, EIF2AK3, DBT, PDX1, RRM2B, ACSF3, SLC5A2, TWNK, PHKG2, MMAA, ATP5F1D, BCKDHA, BCKDHB, ACADM, PHKA2, CA5A, IVD, MMAB, MCCC2, KCNJ11, SLC25A4, FGF21, GLP1R, SLC30A8, SLC30A10, GCG, LEP, MCTS1, MCAT, CMA1, INSR, SREBF1, SOAT1, SLC2A2, PTEN, MAPK3, PPARD, ACAA1, TNF, CHPT1, ZGLP1, ZFP57, TAS2R12P, NRSN1, RBM45, SOCS4, EHMT1, APOBR, UBL4A, ATG14, CHP1, TPPP, TMED2, ACAA2, RGS6, CD163, POMC, MARK1, PIK3CG, PTK2B, DMD, CYP7A1, CYP2E1, CYC1, CPT2, CPT1A, CORT, CDR2, CD9, CCK, BMP4, BGLAP, APOE, ALDH2, AKT2, AKT1, AHSG, ADH1B, ACP1, DPP4, G6PD, PIK3CD, GAD1, PIK3CB, PIK3CA, PAX6, OXCT1, ORM1, TNFRSF11B, NHS, CD46, LPL, IL1B, IFNG, IDE, HNF4A, HLCS, HLA-DRB1, HIF1A, HADHB, GCLC, GAD2, H3P19
Group A Streptococcal Infection Wikipedia

CS1 maint: archived copy as title ( link ) ^ Howard, SJ; Stoker, K; Foster, K (16 June 2015). "Public health management of group A streptococcal infection in mother-baby pairs in England; a case series review" . ... E.; Roberson, A.; Cieslak, P. R.; Lynfield, R.; Gershman, K.; Craig, A.; Albanese, B. A.; Farley, M.
- Streptococcus, Group A, Severity Of Infection By OMIM
  
  Since the early 1980s, a resurgence of severe, invasive infections by group A streptococci (GAS; Streptococcus pyogenes) has occurred. The reemergence of streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF) has been reported in several countries. Both are rapidly progressive invasive diseases that are associated with high mortality rate, ranging from 30 to 80% despite prompt antibiotic therapy and debridement. A particular subclone of the M1 serotype (M1T1) has persisted for more than 20 years as the most prevalent strain isolated from these infections. Release of inflammatory cytokines triggered by streptococcal superantigens has a pivotal role in invasive streptococcal disease.
Drug Interaction Wikipedia

The former acts on cardiac fibres and its effect is increased if there are low levels of potassium (K) in blood plasma. Furosemide is a diuretic that lowers arterial tension but favours the loss of K + . ... PMID 7568331 . ^ Palmer, Adam C.; Sorger, Peter K. (2017-12-14). "Combination Cancer Therapy Can Confer Benefit via Patient-to-Patient Variability without Drug Additivity or Synergy" . ... PMID 19109115 . ^ Haider SI, Johnell K, Thorslund M, Fastbom J (December 2007). ... PMID 18184532 . ^ Haider SI, Johnell K, Weitoft GR, Thorslund M, Fastbom J (January 2009).
Rhinitis Wikipedia

For allergic rhinitis, intranasal corticosteroids are recommended. [45] For severe symptoms intranasal antihistamines may be added. [45] Pronunciation and etymology [ edit ] Rhinitis is pronounced / r aɪ ˈ n aɪ t ɪ s / , [46] while coryza is pronounced / k ə ˈ r aɪ z ə / . [47] Rhinitis comes from the Ancient Greek ῥίς rhis , gen .: ῥινός rhinos "nose". ... PMID 27227021 . ^ Eriksson J, Bjerg A, Lötvall J, Wennergren G, Rönmark E, Torén K, Lundbäck B (November 2011). "Rhinitis phenotypes correlate with different symptom presentation and risk factor patterns of asthma". ... PMID 21764573 . ^ Scherer Hofmeier K, Bircher A, Tamm M, Miedinger D (April 2012).
Lymphatic Filariasis Wikipedia

Archived from the original on 2016-10-12. ^ a b c d e f g h i j k l m n o p q r s t u "Lymphatic filariasis Fact sheet N°102" . ... Univ Puerto Rico Med J . 22 : 187–193. [ verification needed ] ^ Saladin K (2007). Anatomy & Physiology: The Unity of Form and Function . ... Archived from the original on 2017-07-13. ^ Deribe K, Tomczyk S, Tekola-Ayele F (2013).

GPT2, THAS, IL10, HSPD1, TLR9, TLR2, LMLN, GGTLC1, TMPRSS13, NARS2, RBM33, TLR1, HSPA14, NBEAL2, HERPUD1, NR0B2, VEGFA, TXN, TNFRSF1B, TLR4, CISH, CTLA4, MSMB, EDN1, FOXC2, FLT4, HGF, IGHG3, IL3, MST1, TGFB1, NARS1, PRL, PTEN, PTPN6, SLA, SMS, LOC102724197
- Lymphatic Filariasis GARD
  
  Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms that only live in the human lymph system , which maintains the body's fluid balance and fights infections. It is spread from person to person by mosquitoes. Most infected people are asymptomatic and never develop clinical symptoms. A small percentage of people develop lymphedema , which may affect the legs, arms, breasts, and genitalia; bacterial infections that cause hardening and thickening of the skin, called elephantiasis; hydrocele (swelling of the scrotum) in men; and pulmonary tropical eosinophilia syndrome . Treatment may include a yearly dose of medicine, called diethylcarbamazine (DEC); while this drug does not kill all of the adult worms, it prevents infected people from giving the disease to someone else.
- Lymphatic Filariasis Orphanet
  
  Lymphatic filariasis (LF) is a severe form of filariasis (see this term), caused by the parasitic worms Wuchereria bancrofti , Brugia malayi and Brugia timori , and the most common cause of acquired lymphedema worldwide. LF is endemic to tropical and subtropical regions. The vast majority of infected patients are asymptomatic but it can also cause a variety of clinical manifestations, including limb lymphedema, genital anomalies (hydrocele, chylocele), elephantiasis in later stages of the disease (frequently in the lower extremities), and tropical pulmonary eosinophilia (nocturnal paroxysmal cough and wheezing, weight loss, low-grade fever, adenopathy, and pronounced blood eosinophilia). Renal involvement (hematuria, proteinuria, nephritic syndrome, glomerulonephritis), and mono-arthritis of the knee or ankle joint have also been reported.