Telangiectasias, also known as spider veins, are small dilated blood vessels[1] that can occur near the surface of the skin or mucous membranes, measuring between 0.5 and 1 millimeter in diameter.[2] These dilated blood vessels can develop anywhere on the body, but are commonly seen on the face around the nose, cheeks and chin. Dilated blood vessels can also develop on the legs, although when they occur on the legs, they often have underlying venous reflux or "hidden varicose veins" (see Venous hypertension section below). When found on the legs, they are found specifically on the upper thigh, below the knee joint and around the ankles.

Many patients with spider veins seek the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians are called vascular surgeons or phlebologists. More recently, interventional radiologists have started treating venous problems.

Some telangiectasias are due to developmental abnormalities that can closely mimic the behaviour of benign vascular neoplasms. They may be composed of abnormal aggregations of arteriolescapillaries or venules. Because telangiectasias are vascular lesions, they blanch when tested with diascopy.

Telangiectasias, aside from presenting in many other conditions, are one of the features of the acronymically named CREST syndrome, a form of systemic scleroderma. The syndrome recognises the significantly co-presenting symptoms of calcinosisRaynaud's phenomenonesophageal dysmotilitysclerodactyly and telangiectasia.


The causes of telangiectasia can be divided into congenital and acquired factors.


Goldman states that "numerous inherited or congenital conditions display cutaneous telangiectasia".[2] These include:

Venous hypertension[edit]

In the past, it was believed that leg varicose veins or telangectasia were caused by high venous pressure or "venous hypertension". However it is now understood that venous reflux disease is usually the cause of these problems.[4][full citation needed]

Telangiectasia in the legs is often related to the presence of venous reflux within underlying varicose veins. Flow abnormalities in smaller veins known as reticular veins or feeder veins under the skin can also cause the spider veins to form, thereby making a recurrence of the spider veins in the treated area less likely.

Factors that predispose to the development of varicose and telangiectatic leg veins include

  • Age
  • Sex: It used to be thought that females were affected far more than males. However, research has shown 79% of adult males and 88% of adult females have leg telangiectasia (spider veins).[5]
  • Pregnancy: Pregnancy is a key factor contributing to the formation of varicose and spider veins. Changes in hormone levels are one of the most important reasons women are more likely to develop varicose veins during pregnancy. There is an increase in progesterone, which causes the veins to relax and potentially swell more easily.[6] There's also a significant increase in the blood volume during pregnancy, which tends to distend veins, causing valve dysfunction which leads to blood pooling in the veins. Moreover, later in pregnancy, the enlarged uterus can compress veins, causing higher vein pressure leading to dilated veins. Varicose veins that form during pregnancy may spontaneously improve or even disappear a few months after delivery.[7]
  • Life-style/occupation: Those who are involved with prolonged sitting or standing in their daily activities have an increased risk of developing varicose veins. The weight of the blood continuously pressing against the closed valves causes them to fail, leading to vein distention.[8]

Other acquired causes[edit]

Acquired telangiectasia, not related to other venous abnormalities, for example on the face and trunk, can be caused by factors such as


Before any treatment of leg telangectasia (spider veins) is considered, it is essential to have duplex ultrasonography, the test that has replaced Doppler ultrasound. The reason for this is that there is a clear association between leg telangectasia (spider veins) and underlying venous reflux.[12] Research has shown that 88% to 89% of women with telangectasia (spider veins) have refluxing reticular veins close,[13] and 15% have incompetent perforator veins nearby.[14] As such, it is essential to both find and treat underlying venous reflux before considering any treatment at all.

Sclerotherapy is the "gold standard" and is preferred over laser for eliminating telangiectasiae and smaller varicose leg veins.[15] A sclerosant medication is injected into the diseased vein so it hardens and eventually shrinks away. Recent evidence with foam sclerotherapy shows that the foam containing the irritating sclerosant quickly appears in the patient's heart and lungs, and then in some cases travels through a patent foramen ovale to the brain.[16] This has led to concerns about the safety of sclerotherapy for telangectasias and spider veins.

In some cases stroke and transient ischemic attacks have occurred after sclerotherapy.[17] Varicose veins and reticular veins are often treated before treating telangiectasia, although treatment of these larger veins in advance of sclerotherapy for telangiectasia may not guarantee better results.[18][19][20] Varicose veins can be treated with foam sclerotherapy, endovenous laser treatmentradiofrequency ablation, or open surgery. The biggest risk, however, seems to occur with sclerotherapy, especially in terms of systemic risk of DVTpulmonary embolism, and stroke.[21]

Other issues which arise with the use of sclerotherapy to treat spider veins are staining, shadowing, telangetatic matting, and ulceration. In addition, incompleteness of therapy is common, requiring multiple treatment sessions.[22]

Telangiectasias on the face are often treated with a laser. Laser therapy uses a light beam that is pulsed onto the veins in order to seal them off, causing them to dissolve. These light-based treatments require adequate heating of the veins. These treatments can result in the destruction of sweat glands, and the risk increases with the number of treatments.[citation needed]


  1. ^ "telangiectasia" at Dorland's Medical Dictionary
  2. Jump up to:a b Goldman, Mitchel P (1995). Sclerotherapy treatment of varicose and telangiectatic leg veins (2nd ed.). St. Louis: Mosby. ISBN 0-8151-4011-8.[page needed]
  3. ^ Irrthum, Alexandre; Devriendt, Koenraad; Chitayat, David; Matthijs, Gert; Glade, Conrad; Steijlen, Peter M.; Fryns, Jean-Pierre; Van Steensel, Maurice A. M.; Vikkula, Miikka (2003). "Mutations in the Transcription Factor Gene SOX18 Underlie Recessive and Dominant Forms of Hypotrichosis-Lymphedema-Telangiectasia"The American Journal of Human Genetics72 (6): 1470–8. doi:10.1086/375614PMC 1180307PMID 12740761.
  4. ^ Whiteley (2011). "Understanding Venous Reflux – the cause of varicose veins and venous leg ulcers".
  5. ^ Ruckley, C.V.; Evans, C.J.; Allan, P.L.; Lee, A.J.; Fowkes, F.G.R. (2008). "Telangiectasia in the Edinburgh Vein Study: Epidemiology and Association with Trunk Varices and Symptoms"European Journal of Vascular and Endovascular Surgery36 (6): 719–24. doi:10.1016/j.ejvs.2008.08.012PMID 18848475.
  6. ^ Ismail, Lars; Normahani, Pasha; Standfield, Nigel J.; Jaffer, Usman (2016). "A systematic review and meta-analysis of the risk for development of varicose veins in women with a history of pregnancy". Journal of Vascular Surgery. Venous and Lymphatic Disorders. Elsevier BV. 4 (4): 518–524.e1. doi:10.1016/j.jvsv.2016.06.003ISSN 2213-333XPMID 27639009.
  7. ^ Smyth, Rebecca MD; Aflaifel, Nasreen; Bamigboye, Anthony A; Pregnancy, Cochrane; Group, Childbirth (2021-06-02). "Interventions for varicose veins and leg oedema in pregnancy"The Cochrane Database of Systematic Reviews2015 (10): CD001066. doi:10.1002/14651858.CD001066.pub3PMC 7050615PMID 26477632.
  8. ^ "Varicose veins - Symptoms and causes"Mayo Clinic. Retrieved 2020-08-11.
  9. ^ Lindsley, Kristina; Matsumura, Sueko; Hatef, Elham; Akpek, Esen K (2012). "Interventions for chronic blepharitis"Cochrane Database of Systematic Reviews5 (5): CD005556. doi:10.1002/14651858.CD005556.pub2PMC 4270370PMID 22592706.
  10. Jump up to:a b c Kennedy, Cornelis; Bastiaens, Maarten T.; Willemze, Rein; Bouwes Bavinck, Jan N.; Bajdik, Chris D.; Westendorp, Rudi G.J. (April 2003). "Effect of Smoking and Sun on the Aging Skin"Journal of Investigative Dermatology120 (4): 548–554. doi:10.1046/j.1523-1747.2003.12092.xPMID 12648216.
  11. ^ Johnson, B. A.; Nunley, J. R. (2000). "Treatment of seborrheic dermatitis"American Family Physician61 (9): 2703–10, 2713–4. PMID 10821151.
  12. ^ Ruckley, C. V.; Allan, P. L.; Evans, C. J.; Lee, A. J.; Fowkes, F. G. R. (2011). "Telangiectasia and venous reflux in the Edinburgh Vein Study". Phlebology27 (6): 297–302. doi:10.1258/phleb.2011.011007PMID 22106449S2CID 29067831.
  13. ^ Weiss, Robert A.; Weiss, Margaret A. (1993). "Doppler Ultrasound Findings in Reticular Veins of the Thigh Subdermic Lateral Venous System and Implications for Sclerotherapy". The Journal of Dermatologic Surgery and Oncology19 (10): 947–51. doi:10.1111/j.1524-4725.1993.tb00983.xPMID 8408914.
  14. ^ Somjen, George M.; Ziegenbein, Robert; Johnston, Andrew H.; Royle, John P. (1993). "Anatomical Examination of Leg Telangiectases with Duplex Scanning". The Journal of Dermatologic Surgery and Oncology19 (10): 940–5. doi:10.1111/j.1524-4725.1993.tb00982.xPMID 8408913.
  15. ^ Sadick N, Sorhaindo L (2007). "16. Laser Treatment of Telangiectatic and Reticular Veins". In Bergan, John J. (ed.). The Vein Book. Amsterdam: Elsevier Academic Press. p. 157. ISBN 978-0-12-369515-4.
  16. ^ Ceulen, Roeland P.M.; Sommer, Anja; Vernooy, Kevin (2008). "Microembolism during Foam Sclerotherapy of Varicose Veins". New England Journal of Medicine358 (14): 1525–6. doi:10.1056/NEJMc0707265PMID 18385510.
  17. ^ Forlee, Martin V.; Grouden, Maria; Moore, Dermot J.; Shanik, Gregor (2006). "Stroke after varicose vein foam injection sclerotherapy"Journal of Vascular Surgery43 (1): 162–4. doi:10.1016/j.jvs.2005.09.032PMID 16414404.
  18. ^ Duffy, David M. (2012). "Sclerotherapy for Telangiectasia – The impact of small changes in vessel size on treatment outcomes" (PDF)Cosmetic Dermatology25 (3): 126–33. Archived from the original (PDF) on 2019-12-15.
  19. ^ Treatment of Leg Veins. Procedures in Cosmetic Dermatology Series. Editors Murad Alam, Sirunya Silapunt. Second Edition Saunders Elsevier Inc. 2011[page needed]
  20. ^ Schuller-Petrovic, S.; Pavlovic, M. D.; Schuller, S.; Schuller-Lukic, B.; Adamic, M. (2012). "Telangiectasias resistant to sclerotherapy are commonly connected to a perforating vessel". Phlebology28 (6): 320–3. doi:10.1258/phleb.2012.012019PMID 22865418S2CID 36994668.
  21. ^ "Varicose Veins Symptoms Available Treatments and Cost to Fix | CMW"Complete Medical Wellness. 2020-07-27. Retrieved 2020-08-11.
  22. ^ Goldman, Mitchel P.; Bennett, Richard G. (1987-08-01). "Treatment of telangiectasia: A review". Journal of the American Academy of Dermatology17 (2): 167–182. doi:10.1016/s0190-9622(87)70187-xISSN 0190-9622PMID 3305603.

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 Flavonoids usa diosmin hesperidin

Flavonoids on wikipedia

Flavonoids usa diosmin hesperidin dietary capsules

Flavonoids (or bioflavonoids; from the Latin word flavus, meaning yellow, their color in nature) are a class of polyphenolic secondary metabolites found in plants, and thus commonly consumed in the diets of humans.[1]

Chemically, flavonoids have the general structure of a 15-carbon skeleton, which consists of two phenyl rings (A and B) and a heterocyclic ring (C, the ring containing the embedded oxygen).[1][2] This carbon structure can be abbreviated C6-C3-C6. According to the IUPAC nomenclature,[3][4] they can be classified into:

The three flavonoid classes above are all ketone-containing compounds and as such, anthoxanthins (flavones and flavonols).[1] This class was the first to be termed bioflavonoids. The terms flavonoid and bioflavonoid have also been more loosely used to describe non-ketone polyhydroxy polyphenol compounds, which are more specifically termed flavanoids. The three cycles or heterocycles in the flavonoid backbone are generally called ring A, B, and C.[2] Ring A usually shows a phloroglucinol substitution pattern.


In the 1930s, Albert Szent-Györgyi and other scientists discovered that Vitamin C alone was not as effective at preventing scurvy as the crude yellow extract from oranges, lemons or paprika. They attributed the increased activity of this extract to the other substances in this mixture, which they referred to as "citrin" (referring to citrus) or "Vitamin P" (a reference to its effect on reducing the permeability of capillaries). The substances in question (hesperidin, eriodictyol, hesperidin methyl chalcone and neohesperidin) were however later shown not to fulfil the criteria of a vitamin,[5] so that this term is now obsolete.[6]


Flavonoids are secondary metabolites synthesized mainly by plants. The general structure of flavonoids is a 15-carbon skeleton, containing 2 benzene rings connected by a 3-carbon linking chain.[1] Therefore, they are depicted as C6-C3-C6 compounds. Depending on the chemical structure, degree of oxidation, and unsaturation of the linking chain (C3), flavonoids can be classified into different groups, such as anthocyanidins, chalcones, flavonols, flavanones, flavan-3-ols, flavanonols, flavones, and isoflavonoids.[1] Furthermore, flavonoids can be found in plants in glycoside-bound and free aglycone forms. The glycoside-bound form is the most common flavone and flavonol form consumed in the diet.[1]

A biochemical diagram showing the class of flavonoids and their source in nature through various inter-related plant species.


Functions of flavonoids in plants

Flavonoids are widely distributed in plants, fulfilling many functions.[1] They are the most important plant pigments for flower coloration, producing yellow or red/blue pigmentation in petals designed to attract pollinator animals. In higher plants, they are involved in UV filtration, symbiotic nitrogen fixation, and floral pigmentation. They may also act as chemical messengers, physiological regulators, and cell cycle inhibitors. Flavonoids secreted by the root of their host plant help Rhizobia in the infection stage of their symbiotic relationship with legumes like peas, beans, clover, and soy. Rhizobia living in soil are able to sense the flavonoids and this triggers the secretion of Nod factors, which in turn are recognized by the host plant and can lead to root hair deformation and several cellular responses such as ion fluxes and the formation of a root nodule. In addition, some flavonoids have inhibitory activity against organisms that cause plant diseases, e.g. Fusarium oxysporum.[7]


Over 5000 naturally occurring flavonoids have been characterized from various plants. They have been classified according to their chemical structure, and are usually subdivided into the following subgroups (for further reading see[8]):




Flavylium skeleton of anthocyanidins

Anthocyanidins are the aglycones of anthocyanins; they use the flavylium (2-phenylchromenylium) ion skeleton.[1]


Anthoxanthins are divided into two groups:[9]

DescriptionFunctional groupsStructural formula
Flavone 2-phenylchromen-4-one Flavone skeleton colored.svg Luteolin, Apigenin, Tangeritin
3-hydroxy-2-phenylchromen-4-one Flavonol skeleton colored.svg Quercetin, Kaempferol, Myricetin, Fisetin, Galangin, Isorhamnetin, Pachypodol, Rhamnazin, Pyranoflavonols, Furanoflavonols,



DescriptionFunctional groupsStructural formula
Flavanone 2,3-dihydro-2-phenylchromen-4-one Flavanone skeleton colored.svg Hesperetin, Naringenin, Eriodictyol, Homoeriodictyol



DescriptionFunctional groupsStructural formula
3-hydroxy-2,3-dihydro-2-phenylchromen-4-one Flavanonol skeleton colored.svg Taxifolin (or Dihydroquercetin), Dihydrokaempferol


Flavan structure

Include flavan-3-ols (flavanols), flavan-4-ols and flavan-3,4-diols.

Flavan-3ol Flavan-3-ol (flavanol)
Flavan-4ol Flavan-4-ol
Flavan-3,4-diol Flavan-3,4-diol (leucoanthocyanidin)


Dietary sources

Blueberries are a source of dietary anthocyanidins

Parsley is a source of flavones
A variety of flavonoids are found in citrus fruits, including grapefruit

Flavonoids (specifically flavanoids such as the catechins) are "the most common group of polyphenolic compounds in the human diet and are found ubiquitously in plants".[1][10] Flavonols, the original bioflavonoids such as quercetin, are also found ubiquitously, but in lesser quantities. The widespread distribution of flavonoids, their variety and their relatively low toxicity compared to other active plant compounds (for instance alkaloids) mean that many animals, including humans, ingest significant quantities in their diet.[1] Foods with a high flavonoid content include parsley,[11] onions,[11] blueberries and other berries,[11] black tea,[11] green tea and oolong tea,[11] bananas, all citrus fruits, Ginkgo biloba, red wine, sea-buckthorns, buckwheat,[12] and dark chocolate with a cocoa content of 70% or greater.


Parsley, both fresh and dried, contains flavones.[11]


Blueberries are a dietary source of anthocyanidins.[11][13]

Black tea

Black tea is a rich source of dietary flavan-3-ols.[11]


The citrus flavonoids include hesperidin (a glycoside of the flavanone hesperetin), quercitrin, rutin (two glycosides of the flavonol quercetin), and the flavone tangeritin. The flavonoids are much less concentrated in the pulp than in the peels (for example, 165 vs. 1156 mg/100g in pulp vs. peel of satsuma mandarin, and 164 vis-à-vis 804 mg/100g in pulp vs. peel of clementine).[14]



Flavonoids exist naturally in cocoa, but because they can be bitter, they are often removed from chocolate, even dark chocolate.[15] Although flavonoids are present in milk chocolate, milk may interfere with their absorption;[16] however this conclusion has been questioned.[17]


Peanut (red) skin contains significant polyphenol content, including flavonoids.[18][19]

Food sourceFlavonesFlavonolsFlavanones
Red onion 0 4 - 100 0
Parsley, fresh 24 - 634 8 - 10 0
Thyme, fresh 56 0 0
Lemon juice, fresh 0 0 - 2 2 - 175

Unit: mg/100g[1]

Dietary intake

Mean flavonoid intake in mg/d per country, the pie charts show the relative contribution of different types of flavonoids.[20]

Food composition data for flavonoids were provided by the USDA database on flavonoids.[11] In the United States NHANES survey, mean flavonoid intake was 190 mg/d in adults, with flavan-3-ols as the main contributor.[21] In the European Union, based on data from EFSA, mean flavonoid intake was 140 mg/d, although there were considerable differences among individual countries.[20] The main type of flavonoids consumed in the EU and USA were flavan-3-ols (80% for USA adults), mainly from tea or cocoa in chocolate, while intake of other flavonoids was considerably lower.[1][20][21]

Data are based on mean flavonoid intake of all countries included in the 2011 EFSA Comprehensive European Food Consumption Database.[20]


Neither the United States Food and Drug Administration (FDA) nor the European Food Safety Authority (EFSA) has approved any health claim for flavonoids or approved any flavonoids as prescription drugs.[1][22][23][24] The U.S. FDA has warned numerous dietary supplement companies about illegal advertising and misleading health claims.[25][26]

Metabolism and excretion

Flavonoids are poorly absorbed in the human body (less than 5%), then are quickly metabolized into smaller fragments with unknown properties, and rapidly excreted.[1][24][27][28] Flavonoids have negligible antioxidant activity in the body, and the increase in antioxidant capacity of blood seen after consumption of flavonoid-rich foods is not caused directly by flavonoids, but by production of uric acid resulting from flavonoid depolymerization and excretion.[1] Microbial metabolism is a major contributor to the overall metabolism of dietary flavonoids.[1][29] The effect of habitual flavonoid intake on the human gut microbiome is unknown.[1][30]


Inflammation has been implicated as a possible origin of numerous local and systemic diseases, such as cancer,[31] cardiovascular disorders,[32] diabetes mellitus,[33] and celiac disease.[34] There is no clinical evidence that dietary flavonoids affect any of these diseases.[1]


Clinical studies investigating the relationship between flavonoid consumption and cancer prevention or development are conflicting for most types of cancer, probably because most human studies have weak designs, such as a small sample size.[1][35] There is little evidence to indicate that dietary flavonoids affect human cancer risk in general, but observational studies and clinical trials on hormone-dependent cancers (breast and prostate) have shown benefits.[1]

A recent review has suggested that dietary intake of flavonoids is associated with a reduced risk of different types of cancer, including gastric, breast, prostate, and colorectal cancer.[36]

Cardiovascular diseases

Although no significant association has been found between flavan-3-ol intake and cardiovascular disease mortality, clinical trials have shown improved endothelial function and reduced blood pressure (with a few studies showing inconsistent results).[1] Reviews of cohort studies in 2013 found that the studies had too many limitations to determine a possible relationship between increased flavonoid intake and decreased risk of cardiovascular disease, although a trend for an inverse relationship existed.[1][37]

In vitro

Laboratory studies on isolated cells or cell cultures in vitro indicate that flavonoids may selectively inhibit kinases, but in vivo results could differ because of low bioavailability.[1]

Synthesis, detection, quantification, and semi-synthetic alterations

Color spectrum

Flavonoid synthesis in plants is induced by light color spectrums at both high and low energy radiations. Low energy radiations are accepted by phytochrome, while high energy radiations are accepted by carotenoids, flavins, cryptochromes in addition to phytochromes. The photomorphogenic process of phytochrome-mediated flavonoid biosynthesis has been observed in Amaranthus, barley, maize, Sorghum and turnip. Red light promotes flavonoid synthesis.[38]

Availability through microorganisms

Several recent research articles have demonstrated the efficient production of flavonoid molecules from genetically engineered microorganisms.[39][40][41] and the project SynBio4Flav[42][43] aims to provide a cost-effective alternative to current flavonoid production breaking down their complex biosynthetic pathways into standardized specific parts, which can be transferred to engineered microorganisms within Synthetic Microbial Consortia to promote flavonoid assembly through distributed catalysis.

Tests for detection

Shinoda test

Four pieces of magnesium filings are added to the ethanolic extract followed by few drops of concentrated hydrochloric acid. A pink or red colour indicates the presence of flavonoid.[44] Colours varying from orange to red indicated flavones, red to crimson indicated flavonoids, crimson to magenta indicated flavonones.

Sodium hydroxide test

About 5 mg of the compound is dissolved in water, warmed, and filtered. 10% aqueous sodium hydroxide is added to 2 ml of this solution. This produces a yellow coloration. A change in color from yellow to colorless on addition of dilute hydrochloric acid is an indication for the presence of flavonoids.[45]

p-Dimethylaminocinnamaldehyde test

A colorimetric assay based upon the reaction of A-rings with the chromogen p-dimethylaminocinnamaldehyde (DMACA) has been developed for flavanoids in beer that can be compared with the vanillin procedure.[46]


Lamaison and Carnet have designed a test for the determination of the total flavonoid content of a sample (AlCI3 method). After proper mixing of the sample and the reagent, the mixture is incubated for ten minutes at ambient temperature and the absorbance of the solution is read at 440 nm. Flavonoid content is expressed in mg/g of quercetin.[47]

Semi-synthetic alterations

Immobilized Candida antarctica lipase can be used to catalyze the regioselective acylation of flavonoids.[48]

See also



Passicos E, Santarelli X, Coulon D (July 2004). "Regioselective acylation of flavonoids catalyzed by immobilized Candida antarctica lipase under reduced pressure". Biotechnology Letters. 26 (13): 1073–6. doi:10.1023/B:BILE.0000032967.23282.15. PMID 15218382. S2CID 26716150.