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Spermatogenesis
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Spermatogenesis
Seminiferous tubule with maturing sperm. H&E stain.
A mature human Spermatozoon
Anatomical terminology
[edit on Wikidata]
Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. This process starts with the mitotic division of the stem cells located close to the basement membrane of the tubules. These cells are called spermatogonial stem cells. The mitotic division of these produces two types of cells. Type A cells replenish the stem cells, and type B cells differentiate into spermatocytes. The primary spermatocyte divides meiotically (Meiosis I) into two secondary spermatocytes; each secondary spermatocyte divides into two equal haploid spermatids by Meiosis II.The spermatids are transformed into spermatozoa(sperm) by the process called Spermiogenesis.These develop into mature spermatozoa, also known as sperm cells.[1] Thus, the primary spermatocyte gives rise to two cells, the secondary spermatocytes, and the two secondary spermatocytes by their subdivision produce four spermatozoa.[2]
Spermatozoa are the mature male gametes in many sexually reproducing organisms. Thus, spermatogenesis is the male version of gametogenesis, of which the female equivalent is oogenesis. In mammals it occurs in the seminiferous tubules of the male testes in a stepwise fashion. Spermatogenesis is highly dependent upon optimal conditions for the process to occur correctly, and is essential for sexual reproduction. DNA methylation and histone modification have been implicated in the regulation of this process.[3] It starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age (see Male infertility).
Contents
1 Purpose
2 Location in humans
3 Duration
4 Stages
4.1 Spermatocytogenesis
4.2 Spermatidogenesis
4.3 Spermiogenesis
5 Role of Sertoli cells
6 Influencing factors
7 Hormonal control
8 See also
9 References
10 Further reading
11 External links
Purpose[edit]
Spermatogenesis produces mature male gametes, commonly called sperm but more specifically known as spermatozoa, which are able to fertilize the counterpart female gamete, the oocyte, during conception to produce a single-celled individual known as a zygote. This is the cornerstone of sexual reproduction and involves the two gametes both contributing half the normal set of chromosomes (haploid) to result in a chromosomally normal (diploid) zygote.
To preserve the number of chromosomes in the offspring – which differs between species – each gamete must have half the usual number of chromosomes present in other body cells. Otherwise, the offspring will have twice the normal number of chromosomes, and serious abnormalities may result. In humans, chromosomal abnormalities arising from incorrect spermatogenesis results in congenital defects and abnormal birth defects (Down syndrome, Klinefelter syndrome) and in most cases, spontaneous abortion of the developing foetus.
Location in humans[edit]
Spermatogenesis takes place within several structures of the male reproductive system. The initial stages occur within the testes and progress to the epididymis where the developing gametes mature and are stored until ejaculation. The seminiferous tubules of the testes are the starting point for the process, where spermatogonial stem cells adjacent to the inner tubule wall divide in a centripetal direction—beginning at the walls and proceeding into the innermost part, or lumen—to produce immature sperm.[1] Maturation occurs in the epididymis. The location [Testes/Scrotum] is specifically important as the process of spermatogenesis requires a lower temperature to produce viable sperm, specifically 1°-8 °C lower than normal body temperature of 37 °C (98.6 °F).[4] Clinically, small fluctuations in temperature such as from an athletic support strap, causes no impairment in sperm viability or count.[5]
Duration[edit]
For humans, the entire process of spermatogenesis is variously estimated as taking 74 days[6][7] (according to tritium-labelled biopsies) and approximately 120 days[8] (according to DNA clock measurements). Including the transport on ductal system, it takes 3 months. Testes produce 200 to 300 million spermatozoa daily.[9] However, only about half or 100 million of these become viable sperm.[10]
Stages[edit]
The entire process of spermatogenesis can be broken up into several distinct stages, each corresponding to a particular type of cell in humans. In the following table, ploidy, copy number and chromosome/chromatid counts are for one cell, generally prior to DNA synthesis and division (in G1 if applicable). The primary spermatocyte is arrested after DNA synthesis and prior to division.
Cell type ploidy/chromosomes in human DNA copy number/chromatids in human Process entered by cell
spermatogonium (types Ad, Ap and B) diploid (2N) / 46 2C / 46 spermatocytogenesis (mitosis)
primary spermatocyte diploid (2N) / 46 4C / 2x46 spermatidogenesis (meiosis I)
two secondary spermatocytes haploid (N) / 23 2C / 2x23 spermatidogenesis (meiosis II)
four spermatids haploid (N) / 23 C / 23 spermiogenesis
four functional spermatozoids haploid (N) / 23 C / 23 spermiation
Spermatocytogenesis[edit]
Main article: Spermatocytogenesis
The process of spermatogenesis as the cells progress from primary spermatocytes, to secondary spermatocytes, to spermatids, to Sperm
Full diagram of human spermatogenesis
Spermatocytogenesis is the male form of gametocytogenesis and results in the formation of spermatocytes possessing half the normal complement of genetic material. In spermatocytogenesis, a diploid spermatogonium, which resides in the basal compartment of the seminiferous tubules, divides mitotically, producing two diploid intermediate cells called primary spermatocytes. Each primary spermatocyte then moves into the adluminal compartment of the seminiferous tubules and duplicates its DNA and subsequently undergoes meiosis I to produce two haploid secondary spermatocytes, which will later divide once more into haploid spermatids. This division implicates sources of genetic variation, such as random inclusion of either parental chromosomes, and chromosomal crossover, to increase the genetic variability of the gamete.
Each cell division from a spermatogonium to a spermatid is incomplete; the cells remain connected to one another by bridges of cytoplasm to allow synchronous development. It should also be noted that not all spermatogonia divide to produce spermatocytes; otherwise, the supply of spermatogonia would run out. Instead, spermatogonial stem cells divide mitotically to produce copies of themselves, ensuring a constant supply of spermatogonia to fuel spermatogenesis.[11]
Spermatidogenesis[edit]
Main article: Spermatidogenesis
Spermatidogenesis is the creation of spermatids from secondary spermatocytes. Secondary spermatocytes produced earlier rapidly enter meiosis II and divide to produce haploid spermatids. The brevity of this stage means that secondary spermatocytes are rarely seen in histological studies.
Spermiogenesis[edit]
Main article: Spermiogenesis
During spermiogenesis, the spermatids begin to form a tail by growing microtubules on one of the centrioles, which turns into basal body. These microtubules form an axoneme. Later the centriole is modified in the process of centrosome reduction.[12] The anterior part of the tail (called midpiece) thickens because mitochondria are arranged around the axoneme to ensure energy supply. Spermatid DNA also undergoes packaging, becoming highly condensed. The DNA is packaged firstly with specific nuclear basic proteins, which are subsequently replaced with protamines during spermatid elongation. The resultant tightly packed chromatin is transcriptionally inactive. The Golgi apparatus surrounds the now condensed nucleus, becoming the acrosome.
Maturation then takes place under the influence of testosterone, which removes the remaining unnecessary cytoplasm and organelles. The excess cytoplasm, known as residual bodies, is phagocytosed by surrounding Sertoli cells in the testes. The resulting spermatozoa are now mature but lack motility, rendering them sterile. The mature spermatozoa are released from the protective Sertoli cells into the lumen of the seminiferous tubule in a process called spermiation.
The non-motile spermatozoa are transported to the epididymis in testicular fluid secreted by the Sertoli cells with the aid of peristaltic contraction. While in the epididymis the spermatozoa gain motility and become capable of fertilization. However, transport of the mature spermatozoa through the remainder of the male reproductive system is achieved via muscle contraction rather than the spermatozoon's recently acquired motility.
Role of Sertoli cells[edit]
Labelled diagram of the organisation of Sertoli cells (red) and spermatocytes (blue) in the testis. Spermatids which have not yet undergone spermiation are attached to the lumenal apex of the cell
Main article: Sertoli cell
At all stages of differentiation, the spermatogenic cells are in close contact with Sertoli cells which are thought to provide structural and metabolic support to the developing sperm cells. A single Sertoli cell extends from the basement membrane to the lumen of the seminiferous tubule, although the cytoplasmic processes are difficult to distinguish at the light microscopic level.
Sertoli cells serve a number of functions during spermatogenesis, they support the developing gametes in the following ways:
Maintain the environment necessary for development and maturation, via the blood-testis barrier
Secrete substances initiating meiosis
Secrete supporting testicular fluid
Secrete androgen-binding protein (ABP), which concentrates testosterone in close proximity to the developing gametes
Testosterone is needed in very high quantities for maintenance of the reproductive tract, and ABP allows a much higher level of fertility
Secrete hormones affecting pituitary gland control of spermatogenesis, particularly the polypeptide hormone, inhibin
Phagocytose residual cytoplasm left over from spermiogenesis
Secretion of anti-Müllerian hormone causes deterioration of the Müllerian duct[13]
Protect spermatids from the immune system of the male, via the blood-testis barrier
Contribute to the spermatogonial stem cell niche
The intercellular adhesion molecules ICAM-1 and soluble ICAM-1 have antagonistic effects on the tight junctions forming the blood-testis barrier.[14] ICAM-2 molecules regulate spermatid adhesion on the apical side of the barrier (towards the lumen).[14]
Influencing factors[edit]
The process of spermatogenesis is highly sensitive to fluctuations in the environment, particularly hormones and temperature. Testosterone is required in large local concentrations to maintain the process, which is achieved via the binding of testosterone by androgen binding protein present in the seminiferous tubules. Testosterone is produced by interstitial cells, also known as Leydig cells, which reside adjacent to the seminiferous tubules.
Seminiferous epithelium is sensitive to elevated temperature in humans and some other species, and will be adversely affected by temperatures as high as normal body temperature. Consequently, the testes are located outside the body in a sack of skin called the scrotum. The optimal temperature is maintained at 2 °C (man)–8 °C (mouse) below body temperature. This is achieved by regulation of blood flow[15] and positioning towards and away from the heat of the body by the cremasteric muscle and the dartos smooth muscle in the scrotum.
Dietary deficiencies (such as vitamins B, E and A), anabolic steroids, metals (cadmium and lead), x-ray exposure, dioxin, alcohol, and infectious diseases will also adversely affect the rate of spermatogenesis.[citation needed] In addition, the male germ line is susceptible to DNA damage caused by oxidative stress, and this damage likely has a significant impact on fertilization and pregnancy.[16] Exposure to pesticides also affects spermatogenesis.[17]
Hormonal control[edit]
Hormonal control of spermatogenesis varies among species. In humans the mechanism is not completely understood; however it is known that initiation of spermatogenesis occurs at puberty due to the interaction of the hypothalamus, pituitary gland and Leydig cells. If the pituitary gland is removed, spermatogenesis can still be initiated by follicle stimulating hormone (FSH) and testosterone.[18] In contrast to FSH, LH appears to have little role in spermatogenesis outside of inducing gonadal testosterone production.[18][19]
FSH stimulates both the production of androgen binding protein (ABP) by Sertoli cells, and the formation of the blood-testis barrier. ABP is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis. Intratesticular testosterone levels are 20–100 or 50–200 times higher than the concentration found in blood, although there is variation over a 5- to 10-fold range amongst healthy men.[20][21] FSH may initiate the sequestering of testosterone in the testes, but once developed only testosterone is required to maintain spermatogenesis.[18] However, increasing the levels of FSH will increase the production of spermatozoa by preventing the apoptosis of type A spermatogonia. The hormone inhibin acts to decrease the levels of FSH. Studies from rodent models suggest that gonadotropins (both LH and FSH) support the process of spermatogenesis by suppressing the proapoptotic signals and therefore promote spermatogenic cell survival.[22]
The Sertoli cells themselves mediate parts of spermatogenesis through hormone production. They are capable of producing the hormones estradiol and inhibin. The Leydig cells are also capable of producing estradiol in addition to their main product testosterone. Estrogen has been found to be essential for spermatogenesis in animals.[23][24] However, a man with estrogen insensitivity syndrome (a defective ERα) was found produce sperm with a normal sperm count, albeit abnormally low sperm viability; whether he was sterile or not is unclear.[25] Levels of estrogen that are too high can be detrimental to spermatogenesis due to suppression of gonadotropin secretion and by extension intratesticular testosterone production.[26] Prolactin also appears to be important for spermatogenesis.[19]
See also[edit]
Anisogamy
Evolution of sexual reproduction
Folliculogenesis
Germ cells
Male infertility
Meiosis
Oncofertility
Oogenesis
Origin and function of meiosis
Sertoli cells
Sexual reproduction
Semen analysis
References[edit]
^ Jump up to: a b Sharma S, Hanukoglu A, Hanukoglu I (2018). "Localization of epithelial sodium channel (ENaC) and CFTR in the germinal epithelium of the testis, Sertoli cells, and spermatozoa". Journal of Molecular Histology. 49 (2): 195–208. doi:10.1007/s10735-018-9759-2. PMID 29453757. CS1 maint: Multiple names: authors list (link)
Jump up ^ "The Spermatozoön, in Gray's Anatomy". Retrieved 2010-10-07.
Jump up ^ Song, Ning; Liu, Jie; An, Shucai; Nishino, Tomoya; Hishikawa, Yoshitaka; Koji, Takehiko (2011). "Immunohistochemical Analysis of Histone H3 Modifications in Germ Cells during Mouse Spermatogenesis". Acta Histochemica et Cytochemica. 44 (4): 183–90. doi:10.1267/ahc.11027. PMC 3168764. PMID 21927517.
Jump up ^ "scrotum". Encyclopædia Britannica. Encyclopædia Britannica Online. Encyclopædia Britannica Inc., 2015. Web. 14 Jan. 2015 <http://www.britannica.com/EBchecked/topic/530078/scrotum>.
Jump up ^ Wang C, McDonald V, Leung A, Superlano L, Berman N, Hull L, Swerdloff RS (1997). "Effect of increased scrotal temperature on sperm production in normal men". Fertil. Steril. 68 (2): 334–9. doi:10.1016/s0015-0282(97)81525-7. PMID 9240266.
Jump up ^ Heller CG, Clermont Y (1964). "Kinetics of the germinal epithelium in man". Recent Prog Horm Res. 20: 545–571.
Jump up ^ Amann RP (2008). "The cycle of the seminiferous epithelium in humans: a need to revisit?". J Androl. 29 (5): 469–487. doi:10.2164/jandrol.107.004655. PMID 18497337.
Jump up ^ Forster P, Hohoff C, Dunkelmann B, Schürenkamp M, Pfeiffer H, Neuhuber F, Brinkmann B (2015). "Elevated germline mutation rate in teenage fathers". Proc R Soc B. 282: 20142898. doi:10.1098/rspb.2014.2898. PMC 4345458. PMID 25694621.
Jump up ^ Padubidri, VG; Daftary, SN, eds. (2011). Shaw's Textbook of Gynaecology (15th ed.). p. 201. ISBN 978-81-312-2548-6.
Jump up ^ Johnson L, Petty CS, Neaves WB (1983). "Further quantification of human spermatogenesis: germ cell loss during postprophase of meiosis and its relationship to daily sperm production". Biol. Reprod. 29 (1): 207–15. doi:10.1095/biolreprod29.1.207. PMID 6615966.
Jump up ^ Fishelson, Lev; Gon, Ofer; Holdengreber, Vered; Delarea, Yakob (2007). "Comparative spermatogenesis, spermatocytogenesis, and spermato-zeugmata formation in males of viviparous species of clinid fishes (Teleostei: Clinidae, Blennioidei)". The Anatomical Record. 290 (3): 311–23. doi:10.1002/ar.20412. PMID 17525946.
Jump up ^ Atypical centrioles during sexual reproduction Tomer Avidor-Reiss*, Atul Khire, Emily L. Fishman and Kyoung H. Jo Curr Biol. 2015 Nov 16;25(22):2956-63. doi: 10.1016/j.cub.2015.09.045. Epub 2015 Oct 17. http://journal.frontiersin.org/article/10.3389/fcell.2015.00021/full
Jump up ^ Hadley, Mac E.; Levine, Jon E. (2007). Endocrinology (6th ed.). Upper Saddle River, NJ: Prentice Hall. p. 369. ISBN 0-13-187606-6.
^ Jump up to: a b Xiao, X.; Mruk, D. D.; Cheng, C. Y. (2013). "Intercellular adhesion molecules (ICAMs) and spermatogenesis". Human Reproduction Update. 19 (2): 167–86. doi:10.1093/humupd/dms049. PMC 3576004. PMID 23287428.
Jump up ^ Harrison, RG; Weiner, JS (1949). "Vascular patterns of the mammalian testis and their functional significance". The Journal of Experimental Biology. 26 (3): 304–16, 2 pl. PMID 15407652.
Jump up ^ Lewis, SE; Aitken, RJ (2005). "DNA damage to spermatozoa has impacts on fertilization and pregnancy". Cell and Tissue Research. 322 (1): 33–41. doi:10.1007/s00441-005-1097-5. PMID 15912407.
Jump up ^ Mehrpour, O; Karrari P (2014). "Occupational exposure to pesticides and consequences on male semen and fertility: A review". Toxicol Lett. 230: 146–156. doi:10.1016/j.toxlet.2014.01.029. PMID 24487096.
^ Jump up to: a b c William J. Kraemer; A. D. Rogol (15 April 2008). The Encyclopaedia of Sports Medicine: An IOC Medical Commission Publication, The Endocrine System in Sports and Exercise. John Wiley & Sons. pp. 286–. ISBN 978-0-470-75780-2.
^ Jump up to: a b Fody EP, Walker EM (1985). "Effects of drugs on the male and female reproductive systems". Ann. Clin. Lab. Sci. 15 (6): 451–8. PMID 4062226.
Jump up ^ Wolf-Bernhard Schill; Frank H. Comhaire; Timothy B. Hargreave (26 August 2006). Andrology for the Clinician. Springer Science & Business Media. pp. 76–. ISBN 978-3-540-33713-3.
Jump up ^ Eberhard Nieschlag; Hermann M. Behre; Susan Nieschlag (26 July 2012). Testosterone: Action, Deficiency, Substitution. Cambridge University Press. pp. 130–. ISBN 978-1-107-01290-5.
Jump up ^ Pareek, Tej K.; Joshi, Ayesha R.; Sanyal, Amartya; Dighe, Rajan R. (2007). "Insights into male germ cell apoptosis due to depletion of gonadotropins caused by GnRH antagonists". Apoptosis. 12 (6): 1085–100. doi:10.1007/s10495-006-0039-3. PMID 17268770.
Jump up ^ O'Donnell L, Robertson KM, Jones ME, Simpson ER (2001). "Estrogen and spermatogenesis". Endocr. Rev. 22 (3): 289–318. doi:10.1210/edrv.22.3.0431. PMID 11399746.
Jump up ^ Carreau S, Bouraima-Lelong H, Delalande C (2012). "Role of estrogens in spermatogenesis". Front Biosci. 4: 1–11. PMID 22201851.
Jump up ^ Smith, Eric P.; Boyd, Jeff; Frank, Graeme R.; Takahashi, Hiroyuki; Cohen, Robert M.; Specker, Bonny; Williams, Timothy C.; Lubahn, Dennis B.; Korach, Kenneth S. (1994). "Estrogen Resistance Caused by a Mutation in the Estrogen-Receptor Gene in a Man". New England Journal of Medicine. 331 (16): 1056–1061. doi:10.1056/NEJM199410203311604. ISSN 0028-4793. PMID 8090165.
Jump up ^ Edmund S. Sabanegh, Jr. (20 October 2010). Male Infertility: Problems and Solutions. Springer Science & Business Media. pp. 83–. ISBN 978-1-60761-193-6.
Further reading[edit]
"The testes and spermatogenesis". University of Wisconsin. 1998. Retrieved 2006-11-27. [permanent dead link]
Johnson, L.; Blanchard, T.L.; Varner, D.D.; Scrutchfield, W.L. (1997). "Factors affecting spermatogenesis in the stallion". Theriogenology. 48 (7): 1199–216. doi:10.1016/S0093-691X(97)00353-1. PMID 16728209.
Bardin, C.W. (1991). "Pituitary-testicular axis". In Yen, S.S.C.; Jaffee, R.B. Reproductive Endocrinology (3rd ed.). Philadelphia: WB Saunders. ISBN 0721632068.
Chambers, CV; Shafer, MA; Adger, H; Ohm-Smith, M; Millstein, SG; Irwin Jr, CE; Schachter, J; Sweet, R (1987). "Microflora of the urethra in adolescent boys: Relationships to sexual activity and nongonococcal urethritis". The Journal of Pediatrics. 110 (2): 314–21. doi:10.1016/S0022-3476(87)80180-4. PMID 3100755.
Czyba, J.C.; Girod, C. (1980). "Development of normal testis". In Hafez, E.S.E. Descended and Cryptorchid Testis. The Hague: Martinus Nijhoff. ISBN 9024723337.
Whitmore Wf, 3rd; Karsh, L; Gittes, RF (1985). "The role of germinal epithelium and spermatogenesis in the privileged survival of intratesticular grafts". The Journal of Urology. 134 (4): 782–6. PMID 2863395.
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Hives
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see Hive (disambiguation).
Hives
Synonyms
Urticaria
Hives on the arm
Specialty
Dermatology
Symptoms
Red, raised, itchy bumps[1]
Duration
Few days[1]
Causes
Following an infection, result of an allergic reaction[2]
Risk factors
Hay fever, asthma[3]
Diagnostic method
Based on symptoms, patch testing[2]
Treatment
Antihistamines, corticosteroids, leukotriene inhibitors[2]
Frequency
~20%[2]
[edit on Wikidata]
Hives, also known as urticaria, is a kind of skin rash with red, raised, itchy bumps.[1] They may also burn or sting.[2] Often the patches of rash move around.[2] Typically they last a few days and do not leave any long-lasting skin changes.[2] Fewer than 5% of cases last for more than six weeks.[2] The condition frequently recurs.[2]
Hives frequently occur following an infection or as a result of an allergic reaction such as to medication, insect bites, or food.[2] Psychological stress, cold temperature, or vibration may also be a trigger.[1][2] In half of cases the cause remains unknown.[2] Risk factors include having conditions such as hay fever or asthma.[3] Diagnosis is typically based on the appearance. Patch testing may be useful to determine the allergy.[2]
Prevention is by avoiding whatever it is that causes the condition.[2] Treatment is typically with antihistamines such as diphenhydramine and ranitidine.[2] In severe cases, corticosteroids or leukotriene inhibitors may also be used.[2] Keeping the environmental temperature cool is also useful.[2] For cases that last more than six weeks immunosuppressants such as ciclosporin may be used.[2]
About 20% of people are affected.[2] Cases of short duration occur equally in males and females while cases of long duration are more common in females.[4] Cases of short duration are more common among children while cases of long duration are more common among those who are middle aged.[4] Hives have been described at least since the time of Hippocrates.[4] The term urticaria is from the Latin urtica meaning "nettle".[5]
Contents
[hide]
1 Signs and symptoms
2 Cause
2.1 Medications
2.2 Food
2.3 Infection or environmental agent
2.4 Dermatographic urticaria
2.5 Pressure or delayed pressure
2.6 Cholinergic or stress
2.7 Cold-induced
2.8 Solar urticaria
2.9 Water-induced
2.10 Exercise
3 Pathophysiology
3.1 Allergic urticaria
3.2 Autoimmune urticaria
3.3 Infections
3.4 Nonallergic urticaria
3.5 Dietary histamine poisoning
3.6 Stress and chronic idiopathic urticaria
4 Diagnosis
4.1 Acute versus chronic
4.2 Related conditions
4.2.1 Angioedema
4.2.2 Vibratory angioedema
5 Management
5.1 Antihistamines
5.2 Systemic steroids
5.3 Leukotriene-receptor antagonists
5.4 Other
6 Research
7 See also
8 References
9 External links
Signs and symptoms[edit]
Hives on the left chest wall. Notice that they are slightly raised.
Drawing of hives
Welts (raised areas surrounded by a red base) from urticaria can appear anywhere on the surface of the skin. Whether the trigger is allergic or not, a complex release of inflammatory mediators, including histamine from cutaneous mast cells, results in fluid leakage from superficial blood vessels. Welts may be pinpoint in size, or several inches in diameter.
Angioedema is a related condition (also from allergic and nonallergic causes), though fluid leakage is from much deeper blood vessels in the subcutaneous or submucosal layers. Individual hives that are painful, last more than 24 hours, or leave a bruise as they heal are more likely to be a more serious condition called urticarial vasculitis. Hives caused by stroking the skin (often linear in appearance) are due to a benign condition called dermatographic urticaria.
Cause[edit]
Urticaria can also be classified by the purported causative agent. Many different substances in the environment may cause urticaria, including medications, food and physical agents. In perhaps more than 50% of people with chronic urticaria of unknown cause, it is due to an autoimmune reaction.[6]
Medications[edit]
Drugs that have caused allergic reactions evidenced as urticaria include codeine, dextroamphetamine,[7] aspirin, ibuprofen, penicillin, clotrimazole, trichazole, sulfonamides, anticonvulsants, cefaclor, piracetam, vaccines, and antidiabetic drugs. The antidiabetic sulphonylurea glimepiride, in particular, has been documented to induce allergic reactions manifesting as urticaria. Drug-induced urticaria has been known to have an effect on severe cardiorespiratory failure.[medical citation needed]
Food[edit]
The most common food allergies in adults are shellfish and nuts. The most common food allergies in children are shellfish, nuts, eggs, wheat, and soy. One study showed Balsam of Peru, which is in many processed foods, to be the most common cause of immediate contact urticaria.[8] A less common cause is exposure to certain bacteria, such as Streptococcus species or possibly Helicobacter pylori.[9]
Infection or environmental agent[edit]
Urticaria including chronic spontaneous urticaria can be a complication and symptom of a parasitic infection, such as blastocystosis and strongyloidiasis among others.[10]
The rash that develops from poison ivy, poison oak, and poison sumac contact is commonly mistaken for urticaria. This rash is caused by contact with urushiol and results in a form of contact dermatitis called urushiol-induced contact dermatitis. Urushiol is spread by contact, but can be washed off with a strong grease- or oil-dissolving detergent and cool water and rubbing ointments.
Dermatographic urticaria[edit]
Main article: Dermatographic urticaria
Dermatographic urticaria (also known as dermatographism or "skin writing") is marked by the appearance of weals or welts on the skin as a result of scratching or firm stroking of the skin. Seen in 4–5% of the population, it is one of the most common types of urticaria,[11] in which the skin becomes raised and inflamed when stroked, scratched, rubbed, and sometimes even slapped.[12]
The skin reaction usually becomes evident soon after the scratching, and disappears within 30 minutes. Dermatographism is the most common form of a subset of chronic hives, acknowledged as "physical hives".[citation needed]
It stands in contrast to the linear reddening that does not itch seen in healthy people who are scratched. In most cases, the cause is unknown, although it may be preceded by a viral infection, antibiotic therapy, or emotional upset. Dermographism is diagnosed by taking a tongue blade and drawing it over the skin of the arm or back. The hives should develop within a few minutes. Unless the skin is highly sensitive and reacts continually, treatment is not needed. Taking antihistamines can reduce the response in cases that are annoying to the patient.[citation needed]
Pressure or delayed pressure[edit]
This type of urticaria can occur right away, precisely after a pressure stimulus or as a deferred response to sustained pressure being enforced to the skin. In the deferred form, the hives only appear after about six hours from the initial application of pressure to the skin. Under normal circumstances, these hives are not the same as those witnessed with most urticariae. Instead, the protrusion in the affected areas is typically more spread out. The hives may last from eight hours to three days. The source of the pressure on the skin can happen from tight fitted clothing, belts, clothing with tough straps, walking, leaning against an object, standing, sitting on a hard surface, etc. The areas of the body most commonly affected are the hands, feet, trunk, abdomen, buttocks, legs and face. Although this appears to be very similar to dermatographism, the cardinal difference is that the swelled skin areas do not become visible quickly and tend to last much longer. This form of the skin disease is, however, rare.[citation needed]
Cholinergic or stress[edit]
Main article: Cholinergic urticaria
Cholinergic urticaria (CU) is one of the physical urticaria which is provoked during sweating events such as exercise, bathing, staying in a heated environment, or emotional stress. The hives produced are typically smaller than classic hives and are generally shorter-lasting.[13][14]
Multiple subtypes have been elucidated, each of which require distinct treatment.[15][16]
Cold-induced[edit]
Further information: Chronic cold urticaria
The cold type of urticaria is caused by exposure of the skin to extreme cold, damp and windy conditions; it occurs in two forms. The rare form is hereditary and becomes evident as hives all over the body 9 to 18 hours after cold exposure. The common form of cold urticaria demonstrates itself with the rapid onset of hives on the face, neck, or hands after exposure to cold. Cold urticaria is common and lasts for an average of five to six years. The population most affected is young adults, between 18 and 25 years old. Many people with the condition also suffer from dermographism and cholinergic urticaria.[citation needed]
Severe reactions can be seen with exposure to cold water; swimming in cold water is the most common cause of a severe reaction. This can cause a massive discharge of histamine, resulting in low blood pressure, fainting, shock and even loss of life. Cold urticaria is diagnosed by dabbing an ice cube against the skin of the forearm for 1 to 5 minutes. A distinct hive should develop if a patient suffers cold urticaria. This is different from the normal redness that can be seen in people without cold urticaria. Patients with cold urticaria need to learn to protect themselves from a hasty drop in body temperature. Regular antihistamines are not generally efficacious. One particular antihistamine, cyproheptadine (Periactin), has been found to be useful. The tricyclic antidepressant doxepin has also been found to be an effective blocking agent of histamine discharge. Finally, a medication named ketotifen, which keeps mast cells from discharging histamine, has also been employed with widespread success.[citation needed]
Solar urticaria[edit]
Main article: Solar urticaria
This form of the disease occurs on areas of the skin exposed to the sun; the condition becomes evident within minutes of exposure.[citation needed]
Water-induced[edit]
Main article: Water urticaria
This type of urticaria is also termed rare, and occurs upon contact with water. The response is not temperature-dependent and the skin appears similar to cholinergic form of the disease. The appearance of hives is within one to 15 minutes of contact with the water, and can last from 10 minutes to two hours. This kind of hives do not seem to be stimulated by histamine discharge like the other physical hives. Most researchers believe this condition is actually skin sensitivity to additives in the water, such as chlorine. Water urticaria is diagnosed by dabbing tap water and distilled water to the skin and observing the gradual response. Aquagenic urticaria is treated with capsaicin (Zostrix) administered to the chafed skin. This is the same treatment used for shingles. Antihistamines are of questionable benefit in this instance, since histamine is not the causative factor.[citation needed]
Chizzola maculae is a very specific skin lesion due to fluoride exposure. The size of a coin, these lesions may resemble small blue bruises or be wholly pink. Doctors George Waldbott and V. A. Cecilioni named the lesions after a town in Italy, where they were common in young women and children.[17] According to Waldbott, chizzola maculae are early symptoms of fluoride intoxication.[18][19]
Exercise[edit]
The condition was first distinguished in 1980. People with exercise urticaria (EU) experience hives, itchiness, shortness of breath and low blood pressure five to 30 minutes after beginning exercise. These symptoms can progress to shock and even sudden death. Jogging is the most common exercise to cause EU, but it is not induced by a hot shower, fever, or with fretfulness. This differentiates EU from cholinergic urticaria.[citation needed]
EU sometimes occurs only when someone exercises within 30 minutes of eating particular foods, such as wheat or shellfish. For these individuals, exercising alone or eating the injuring food without exercising produces no symptoms. EU can be diagnosed by having the patient exercise and then observing the symptoms. This method must be used with caution and only with the appropriate resuscitative measures at hand. EU can be differentiated from cholinergic urticaria by the hot water immersion test. In this test, the patient is immersed in water at 43 °C (109.4 °F). Someone with EU will not develop hives, while a person with cholinergic urticaria will develop the characteristic small hives, especially on the neck and chest.[citation needed]
The immediate symptoms of this type are treated with antihistamines, epinephrine and airway support. Taking antihistamines prior to exercise may be effective. Ketotifen is acknowledged to stabilise mast cells and prevent histamine release, and has been effective in treating this hives disorder. Avoiding exercise or foods that cause the mentioned symptoms is very important. In particular circumstances, tolerance can be brought on by regular exercise, but this must be under medical supervision.[citation needed]
Pathophysiology[edit]
See also: List of human leukocyte antigen alleles associated with cutaneous conditions
The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage of capillaries in the dermis, and resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells.[citation needed]
Urticaria is caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin. This process can be the result of an allergic or nonallergic reaction, differing in the eliciting mechanism of histamine release.[20]
Allergic urticaria[edit]
Histamine and other proinflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high-affinity cell surface receptors. Basophils and other inflammatory cells are also seen to release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases.
Autoimmune urticaria[edit]
Over half of all cases of chronic idiopathic urticaria are the result of an autoimmune trigger. Roughly 50% of patients with chronic urticaria spontaneously develop autoantibodies directed at the receptor FcεRI located on skin mast cells. Chronic stimulation of this receptor leads to chronic hives. Patients often have other autoimmune conditions, such as autoimmune thyroiditis, celiac disease, type 1 diabetes, rheumatoid arthritis, Sjögren's syndrome or systemic lupus erythematosus.[6]
Infections[edit]
Hive-like rashes commonly accompany viral illnesses, such as the common cold. They usually appear three to five days after the cold has started, and may even appear a few days after the cold has resolved.
Nonallergic urticaria[edit]
Mechanisms other than allergen-antibody interactions are known to cause histamine release from mast cells. Many drugs, for example morphine, can induce direct histamine release not involving any immunoglobulin molecule. Also, a diverse group of signaling substances, called neuropeptides, have been found to be involved in emotionally induced urticaria. Dominantly inherited cutaneous and neurocutaneous porphyrias (porphyria cutanea tarda, hereditary coproporphyria, variegate porphyria and erythropoietic protoporphyria) have been associated with solar urticaria. The occurrence of drug-induced solar urticaria may be associated with porphyrias. This may be caused by IgG binding, not IgE.
Dietary histamine poisoning[edit]
This is termed scombroid food poisoning. Ingestion of free histamine released by bacterial decay in fish flesh may result in a rapid-onset, allergic-type symptom complex which includes urticaria. However, the urticaria produced by scombroid is reported not to include wheals.[21]
Stress and chronic idiopathic urticaria[edit]
Chronic idiopathic urticaria has been anecdotally linked to stress since the 1940s.[22] A large body of evidence demonstrates an association between this condition and both poor emotional well-being[23] and reduced health-related quality of life.[24] A link between stress and this condition has also been shown.[25] A recent study has demonstrated an association between stressful life events (e.g. bereavement, divorce, etc.) and chronic idiopathic urticaria[26] and also an association between post-traumatic stress and chronic idiopathic urticaria.[27]
Diagnosis[edit]
The cause of chronic urticaria can rarely be determined.[28] In some cases regular extensive allergy testing over a long period of time is requested in hopes of getting new insight.[29][30] No evidence shows regular allergy testing results in identification of a problem or relief for people with chronic urticaria.[29][30] Regular allergy testing for people with chronic urticaria is not recommended.[28]
Acute versus chronic[edit]
Acute urticaria is defined as the presence of evanescent wheals which completely resolve within six weeks.[31] Acute urticaria becomes evident a few minutes after the person has been exposed to an allergen. The outbreak may last several weeks, but usually the hives are gone in six weeks. Typically, the hives are a reaction to food, but in about half the cases, the trigger is unknown. Common foods may be the cause, as well as bee or wasp stings, or skin contact with certain fragrances. Acute viral infection is another common cause of acute urticaria (viral exanthem). Less common causes of hives include friction, pressure, temperature extremes, exercise, and sunlight.
Chronic urticaria (ordinary urticaria)[32] is defined as the presence of evanescent wheals which persist for greater than six weeks.[31] Some of the more severe chronic cases have lasted more than 20 years. A survey indicated chronic urticaria lasted a year or more in more than 50% of sufferers and 20 years or more in 20% of them.[33]
Acute and chronic urticaria are visually indistinguishable.
Related conditions[edit]
Angioedema[edit]
Angioedema is similar to urticaria,[34] but in angioedema, the swelling occurs in a lower layer of the dermis than in urticaria,[35] as well as in the subcutis. This swelling can occur around the mouth, eyes, in the throat, in the abdomen, or in other locations. Urticaria and angioedema sometimes occur together in response to an allergen, and is a concern in severe cases, as angioedema of the throat can be fatal.
Vibratory angioedema[edit]
This very rare form of angioedema develops in response to contact with vibration. In vibratory angioedema, symptoms develop within two to five minutes after contact with a vibrating object, and abate after about an hour. Patients with this disorder do not suffer from dermographism or pressure urticaria. Vibratory angioedema is diagnosed by holding a vibrating device such as a laboratory vortex machine against the forearm for four minutes. Speedy swelling of the whole forearm extending into the upper arm is also noted later. The principal treatment is avoidance of vibratory stimulants. Antihistamines have also been proven helpful.[citation needed]
Management[edit]
The mainstay of therapy for both acute and chronic urticaria is patient education, avoiding triggers and using antihistamines.
Chronic urticaria can be difficult to treat and lead to significant disability. Unlike the acute form, 50–80% of people with chronic urticaria have no identifiable triggers. Fortunately, 50% of people with chronic urticaria will experience remission within 1 year.[36] Overall, treatment is geared towards symptomatic management. Individuals with chronic urticaria may need other medications in addition to antihistamines to control symptoms. Patients who experience urticaria with angioedema require emergency treatment as this is a life-threatening condition.
Treatment guidelines for the management of chronic urticaria have been published.[37][38] According to the 2014 American practice parameters, treatment involves a step wise approach. Step 1 consists of second generation, H1 receptor blocking antihistamines. Systemic glucocorticoids can also be used for episodes of severe disease but should not be used for long term due to their long list of side effects. Step 2 consists of increasing the dose of the current antihistamine, adding other antihistamines, or adding a leukotriene receptor antagonist such as montelukast. Step 3 consists of adding or replacing the current treatment with hydroxyzine or doxepin. If the individual doesn't respond to steps 1–3 then they are considered to have refractory symptoms. At this point, anti-inflammatory medications (dapsone, sulfasalazine), immunosuppressants (cyclosporin, sirolimus) or other medications like omalizumab can be used. These options are explained in more detail below.
Antihistamines[edit]
Non-sedating antihistamines that block the histamine H1 receptors are the first line of therapy. First generation antihistamines such as diphenhydramine or hydroxyzine block both central and peripheral H1 receptors and can be sedating. Second generation antihistamines such as loratadine, cetirizine, or desloratadine selectively antagonize the peripheral H1 receptors and are less sedating, less anticholinergic, and generally preferred over the first generation antihistamines.[39][40]
People who don’t respond to the maximum dose of H1 antihistamines may benefit from increasing the dose, then to switching to another non-sedating antihistamine, then to adding a leukotriene antagonist, then to using an older antihistamine, then to using systemic steroids and finally to using ciclosporin or omalizumab.[39]
Systemic steroids[edit]
Oral glucocorticoids are effective in controlling symptoms of chronic urticaria however they have an extensive list of adverse effects such as adrenal suppression, weight gain, osteoporosis, hyperglycemia, etc. Therefore, their use should be limited to a couple of weeks. In addition, one study found that systemic glucocorticoids combined with antihistamines did not hasten the time to symptom control compared with antihistamines alone.[41]
Leukotriene-receptor antagonists[edit]
Leukotrienes are released from mast cells along with histamine. The medications, montelukast and zafirlukast block leukotriene receptors and can be used as add on treatment or in isolation for patients with CU. It is important to note that these medications may be more beneficial for patients with NSAID induced CU.[42][43]
Other[edit]
Other options for refractory symptoms of chronic urticaria include anti-inflammatory medications, omalizumab, and immunosuppressants. Potential anti-inflammatory agents include dapsone, sulfasalazine, and hydroxychloroquine. Dapsone is a sulfone antimicrobial agent and is thought to suppress prostaglandin and leukotriene activity. It is helpful in therapy-refractory cases[44] and is contraindicated in patients with G6PD deficiency. Sulfasalazine, a 5-ASA derivative, is thought to alter adenosine release and inhibit IgE mediated mast cell degranulation, Sulfasalazine is a good option for people with anemia who cannot take dapsone. Hydroxychloroquine is an antimalarial agent that suppresses T lymphocytes. It has a low cost however it takes longer than dapsone or sulfasalazine to work.
Omalizumab was approved by the FDA in 2014 for patients 12 years old and above with chronic urticaria. It is a monoclonal antibody directed against IgE. Significant improvement in pruritus and quality of life was observed in a phase III, multicenter, randomized control trial.[45]
Immunosuppressants used for CU include cyclosporine, tacrolimus, sirolimus, and mycophenolate. Calcineurin inhibitors, such as cyclosporine and tacrolimus, inhibit cell responsiveness to mast cell products and inhibit T cell activity. They are preferred by some experts to treat severe symptoms.[46] Sirolimus and mycophenolate have less evidence for their use in the treatment of chronic urticaria but reports have shown them to be efficacious.[47][48] Immunosuppressants are generally reserved as the last line of therapy for severe cases due to their potential for serious adverse effects.
Research[edit]
Afamelanotide is being studied as an urticaria treatment.[49]
Opioid antagonists such as naltrexone have tentative evidence to support their use.[50]
See also[edit]
Urticarial vasculitis
References[edit]
^ Jump up to: a b c d "Hives". Archived from the original on 19 August 2016. Retrieved 10 August 2016.
^ Jump up to: a b c d e f g h i j k l m n o p q r s Jafilan, L; James, C (December 2015). "Urticaria and Allergy-Mediated Conditions.". Primary care. 42 (4): 473–83. PMID 26612369. doi:10.1016/j.pop.2015.08.002.
^ Jump up to: a b Zuberbier, Torsten; Grattan, Clive; Maurer, Marcus (2010). Urticaria and Angioedema. Springer Science & Business Media. p. 38. ISBN 9783540790488. Archived from the original on 2016-08-21.
^ Jump up to: a b c Griffiths, Christopher; Barker, Jonathan; Bleiker, Tanya; Chalmers, Robert; Creamer, Daniel (2016). Rook's Textbook of Dermatology, 4 Volume Set (9 ed.). John Wiley & Sons. p. Chapter 42.3. ISBN 9781118441176.
Jump up ^ A Dictionary of Entomology. CABI. 2011. p. 1430. ISBN 9781845935429. Archived from the original on 2016-08-21.
^ Jump up to: a b Fraser K, Robertson L (Dec 2013). "Chronic urticaria and autoimmunity". Skin Therapy Lett (Review). 18 (7): 5–9. PMID 24305753. Archived from the original on 2016-01-31.
Jump up ^ "Prescribing Information Dexedrine". GlaxoSmithKline. June 2006.
Jump up ^ Alexander A. Fisher (2008). Fisher's Contact Dermatitis. PMPH-USA. Archived from the original on 2014-07-05. Retrieved 2014-04-24.
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Jump up ^ Hirschmann, J. V.; Lawlor, F; English, JS; Louback, JB; Winkelmann, RK; Greaves, MW (1987). "Cholinergic Urticaria - A Clinical and Histologic Study". Archives of Dermatology. 123 (4): 462–7. PMID 3827277. doi:10.1001/archderm.1987.01660280064024.
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Jump up ^ Chung, Man Cheung; Symons, Christine; Gilliam, Jane; Kaminski, Edward R. (2010). "Stress, psychiatric co-morbidity and coping in patients with chronic idiopathic urticaria". Psychology & Health. 25 (4): 477–90. PMID 20204926. doi:10.1080/08870440802530780.
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Jump up ^ Bernstein, J (2014). "The diagnosis and management of acute and chronic urticaria: 2014 update.". J Allergy Clin Immunol. 133 (5): 1270–1277.e66. doi:10.1016/j.jaci.2014.02.036.
^ Jump up to: a b Zuberbier, T (January 2012). "A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria.". The World Allergy Organization journal. 5 Suppl 1: S1–5. PMID 23282889. doi:10.1097/WOX.0b013e3181f13432.
Jump up ^ Sharma, M; Bennett, C; Cohen, SN; Carter, B (14 November 2014). "H1-antihistamines for chronic spontaneous urticaria.". The Cochrane database of systematic reviews (11): CD006137. PMID 25397904. doi:10.1002/14651858.CD006137.pub2.
Jump up ^ Kim S, Baek S, Shin B, Yoon SY, Park SY, Lee T, Lee YS, Bae YJ, Kwon HS, Cho YS, Moon HB, Kim TB (2013). "Influence of initial treatment modality on long-term control of chronic idiopathic urticaria". PLoS ONE. 8 (7): e69345. PMC 3720657  . PMID 23935990. doi:10.1371/journal.pone.0069345.
Jump up ^ AU Erbagci Z SO (2002). "The leukotriene receptor antagonist montelukast in the treatment of chronic idiopathic urticaria: a single-blind, placebo-controlled, crossover clinical study". J Allergy Clin Immunol. 110 (3): 484–488. PMID 12209099. doi:10.1067/mai.2002.126676.
Jump up ^ Pacor ML, Di Lorenzo G, Corrocher R (2001). "Efficacy of leukotriene receptor antagonist in chronic urticaria. A double-blind, placebo-controlled comparison of treatment with montelukast and cetirizine in patients with chronic urticaria with intolerance to food additive and/or acetylsalicylic acid". Clin Exp Allergy. 31 (10): 1607–1614. PMID 11678862. doi:10.1046/j.1365-2222.2001.01189.x.
Jump up ^ Boehm I, et al. (Jul 1999). "Urticaria treated with dapsone". Allergy. 54 (7): 765–6. PMID 10442538. doi:10.1034/j.1398-9995.1999.00187.x.
Jump up ^ Maurer, Marcus; Rosén, Karin; Hsieh, Hsin-Ju; Saini, Sarbjit; Grattan, Clive; Gimenéz-Arnau, Ana; Agarwal, Sunil; Doyle, Ramona; Canvin, Janice; Kaplan, Allen; Casale, Thomas (2013). "Omalizumab for the Treatment of Chronic Idiopathic or Spontaneous Urticaria". New England Journal of Medicine. 368 (10): 924–35. PMID 23432142. doi:10.1056/NEJMoa1215372.
Jump up ^ Kaplan AP (2009). "What the first 10,000 patients with chronic urticaria have taught me: a personal journey". J Allergy Clin Immunol. 123 (3): 713–717. PMID 19081615. doi:10.1016/j.jaci.2008.10.050.
Jump up ^ Morgan M (2009). "Treatment of refractory chronic urticaria with sirolimus". Arch Dermatol. 145 (6): 637. PMID 19528416. doi:10.1001/archdermatol.2009.13.
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Jump up ^ Phan, NQ; Bernhard, JD; Luger, TA; Ständer, S (October 2010). "Antipruritic treatment with systemic μ-opioid receptor antagonists: a review.". Journal of the American Academy of Dermatology. 63 (4): 680–8. PMID 20462660. doi:10.1016/j.jaad.2009.08.052.
External links[edit]
Classification
V · T · D
ICD-10: L50
ICD-9-CM: 708
MeSH: D014581
DiseasesDB: 13606
External resources
MedlinePlus: 000845
eMedicine: search/Urticaria
Patient UK: Hives

Media related to Hives at Wikimedia Commons
Urticaria photo library at Dermnet
[show]
v
t
e
Diseases of the skin and appendages by morphology
Growths
Epidermal
wart
callus
seborrheic keratosis
acrochordon
molluscum contagiosum
actinic keratosis
squamous-cell carcinoma
basal-cell carcinoma
Merkel-cell carcinoma
nevus sebaceous
trichoepithelioma
Pigmented
Freckles
lentigo
melasma
nevus
melanoma
Dermal and
subcutaneous
epidermal inclusion cyst
hemangioma
dermatofibroma (benign fibrous histiocytoma)
keloid
lipoma
neurofibroma
xanthoma
Kaposi's sarcoma
infantile digital fibromatosis
granular cell tumor
leiomyoma
lymphangioma circumscriptum
myxoid cyst
Rashes
With
epidermal
involvement
Eczematous
contact dermatitis
atopic dermatitis
seborrheic dermatitis
stasis dermatitis
lichen simplex chronicus
Darier's disease
glucagonoma syndrome
langerhans cell histiocytosis
lichen sclerosus
pemphigus foliaceus
Wiskott–Aldrich syndrome
Zinc deficiency
Scaling
psoriasis
tinea (corporis
cruris
pedis
manuum
faciei)
pityriasis rosea
secondary syphilis
mycosis fungoides
systemic lupus erythematosus
pityriasis rubra pilaris
parapsoriasis
ichthyosis
Blistering
herpes simplex
herpes zoster
varicella
bullous impetigo
acute contact dermatitis
pemphigus vulgaris
bullous pemphigoid
dermatitis herpetiformis
porphyria cutanea tarda
epidermolysis bullosa simplex
Papular
scabies
insect bite reactions
lichen planus
miliaria
keratosis pilaris
lichen spinulosus
transient acantholytic dermatosis
lichen nitidus
pityriasis lichenoides et varioliformis acuta
Pustular
acne vulgaris
acne rosacea
folliculitis
impetigo
candidiasis
gonococcemia
dermatophyte
coccidioidomycosis
subcorneal pustular dermatosis
Hypopigmented
tinea versicolor
vitiligo
pityriasis alba
postinflammatory hyperpigmentation
tuberous sclerosis
idiopathic guttate hypomelanosis
leprosy
hypopigmented mycosis fungoides
Without
epidermal
involvement
Red
Blanchable
Erythema
Generalized
drug eruptions
viral exanthems
toxic erythema
systemic lupus erythematosus
Localized
cellulitis
abscess
boil
erythema nodosum
carcinoid syndrome
fixed drug eruption
Specialized
urticaria
erythema (multiforme
migrans
gyratum repens
annulare centrifugum
ab igne)
Nonblanchable
Purpura
Macular
thrombocytopenic purpura
actinic/solar purpura
Papular
disseminated intravascular coagulation
vasculitis
Indurated
scleroderma/morphea
granuloma annulare
lichen sclerosis et atrophicus
necrobiosis lipoidica
Miscellaneous
disorders
Ulcers
Hair
telogen effluvium
androgenic alopecia
alopecia areata
systemic lupus erythematosus
tinea capitis
loose anagen syndrome
lichen planopilaris
folliculitis decalvans
acne keloidalis nuchae
Nail
onychomycosis
psoriasis
paronychia
ingrown nail
Mucous
membrane
Aphthous stomatitis
oral candidiasis
lichen planus
leukoplakia
pemphigus vulgaris
mucous membrane pemphigoid
cicatricial pemphigoid
herpesvirus
coxsackievirus
syphilis
systemic histoplasmosis
squamous-cell carcinoma
[show]
v
t
e
Urticaria and erythema (L50–L54, 695, 708)
Urticaria
(acute/chronic)
Allergic urticaria
Urticarial allergic eruption
Physical urticaria
Cold urticaria
Familial
Primary cold contact urticaria
Secondary cold contact urticaria
Reflex cold urticaria
Heat urticaria
Localized heat contact urticaria
Solar urticaria
Dermatographic urticaria
Vibratory angioedema
Pressure urticaria
Cholinergic urticaria
Aquagenic urticaria
Other urticaria
Acquired C1 esterase inhibitor deficiency
Adrenergic urticaria
Exercise urticaria
Galvanic urticaria
Schnitzler syndrome
Urticaria-like follicular mucinosis
Angioedema
Episodic angioedema with eosinophilia
Hereditary angioedema
Erythema
Erythema multiforme/
drug eruption
Erythema multiforme minor
Erythema multiforme major
Stevens–Johnson syndrome, Toxic epidermal necrolysis
panniculitis (Erythema nodosum)
Acute generalized exanthematous pustulosis
Figurate erythema
Erythema annulare centrifugum
Erythema marginatum
Erythema migrans
Erythema gyratum repens
Other erythema
Necrolytic migratory erythema
Erythema toxicum
Erythroderma
Palmar erythema
Generalized erythema
[show]
v
t
e
Hypersensitivity and autoimmune diseases (279.5–6)
Type I/allergy/atopy
(IgE)
Foreign
Atopic eczema
Allergic urticaria
Allergic rhinitis (Hay fever)
Allergic asthma
Anaphylaxis
Food allergy
common allergies include: Milk
Egg
Peanut
Tree nut
Seafood
Soy
Wheat
Penicillin allergy
Autoimmune
Eosinophilic esophagitis
Type II/ADCC
IgM
IgG
Foreign
Hemolytic disease of the newborn
Autoimmune
Cytotoxic
Autoimmune hemolytic anemia
Immune thrombocytopenic purpura
Bullous pemphigoid
Pemphigus vulgaris
Rheumatic fever
Goodpasture's syndrome
Guillain–Barré syndrome
"Type V"/receptor
Graves' disease
Myasthenia gravis
Pernicious anemia
Type III
(Immune complex)
Foreign
Henoch–Schönlein purpura
Hypersensitivity vasculitis
Reactive arthritis
Farmer's lung
Post-streptococcal glomerulonephritis
Serum sickness
Arthus reaction
Autoimmune
Systemic lupus erythematosus
Subacute bacterial endocarditis
Rheumatoid arthritis
Type IV/cell-mediated
(T cells)
Foreign
Allergic contact dermatitis
Mantoux test
Autoimmune
Diabetes mellitus type 1
Hashimoto's thyroiditis
Multiple sclerosis
Coeliac disease
Giant-cell arteritis
Postorgasmic illness syndrome
Reactive arthritis
GVHD
Transfusion-associated graft versus host disease
Unknown/
multiple
Foreign
Hypersensitivity pneumonitis
Allergic bronchopulmonary aspergillosis
Transplant rejection
Latex allergy (I+IV)
Autoimmune
Sjögren's syndrome
Autoimmune hepatitis
Autoimmune polyendocrine syndrome
APS1
APS2
Autoimmune adrenalitis
Systemic autoimmune disease
Authority control
GND: 4075291-4
NDL: 00574800
Retrieved from "https://en.wikipedia.org/w/index.php?title=Hives&oldid=808130467"
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