An anthracene derivative that disrupts MITOCHONDRIA function and structure and is used for the treatment of DERMATOSES, especially PSORIASIS. It may cause FOLLICULITIS.
Loss of scalp and body hair involving microscopically inflammatory patchy areas.
The application of drug preparations to the surfaces of the body, especially the skin (ADMINISTRATION, CUTANEOUS) or mucous membranes. This method of treatment is used to avoid systemic side effects when high doses are required at a localized area or as an alternative systemic administration route, to avoid hepatic processing for example.
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Value of all final goods and services produced in a country in one year.
Drugs used to treat or prevent skin disorders or for the routine care of skin.
Antigen-type substances that produce immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin.
A medical specialty concerned with the skin, its structure, functions, diseases, and treatment.
Granulated cells that are found in almost all tissues, most abundantly in the skin and the gastrointestinal tract. Like the BASOPHILS, mast cells contain large amounts of HISTAMINE and HEPARIN. Unlike basophils, mast cells normally remain in the tissues and do not circulate in the blood. Mast cells, derived from the bone marrow stem cells, are regulated by the STEM CELL FACTOR.
An aromatic perennial plant species that has been used to treat migraines, arthritis, and as a febrifuge. It contains TANNINS, volatile oils (OILS, ESSENTIAL), and sesquiterpene lactones, especially parthenolide.
Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability.

Topical psoriasis therapy. (1/36)

Psoriasis is a common dermatosis, affecting from 1 to 3 percent of the population. Until recently, the mainstays of topical therapy have been corticosteroids, tars, anthralins and keratolytics. Recently, however, vitamin D analogs, a new anthralin preparation and topical retinoids have expanded physicians' therapeutic armamentarium. These new topical therapies offer increased hope and convenience to the large patient population with psoriasis.  (+info)

Anti-psoriatic drug anthralin activates JNK via lipid peroxidation: mononuclear cells are more sensitive than keratinocytes. (2/36)

Anthralin is a widely used, topical therapy for psoriasis. Anti-proliferative and anti-inflammatory properties of anthralin have been identified. Little is known, however, about differential sensitivities of targeted cell types and specific mechanisms of signaling pathway activation. We demonstrate that anthralin exerts potent effects on keratinocytes and mononuclear cells through strong induction of lipid peroxidation and JNK activation, a stress-induced signal transduction pathway. Lipid peroxidation was observed rapidly and half-maximal levels of lipid peroxidation were reached at a 10-fold lower concentration of anthralin for peripheral blood mononuclear cells vs normal keratinocytes. JNK activation was detected in peripheral blood mononuclear cells at a 40-fold lower anthralin dose compared with keratinocytes. For both cell types, selected inhibitors of lipid peroxidation prevented JNK activation. This study demonstrates that mononuclear leukocytes are markedly more sensitive than keratinocytes to anthralin-induced lipid peroxidation and JNK activation. We identify anthralin as a novel and potent inducer of JNK activation and demonstrate that this process is mediated, at least in part, by lipid peroxidation which is among the earliest and most proximate, membrane-related responses to anthralin yet described.  (+info)

Nonspecific inhibition of DNA repair synthesis by tumor promoters in human diploid fibroblasts damaged with N-acetoxy-2-acetylaminofluorene. (3/36)

The effects of selected tumor-promoting agents and their nonpromoting analogs on DNA repair synthesis were examined in human diploid fibroblasts (WI-38) damaged with N-acetoxy-2-acetylaminofluorene. Over a range of doses, three promoters (croton oil, 12-O-tetradecanoylphorbol-13-acetate, and anthralin) were found to inhibit DNA repair synthesis while their nonpromoting analogs (phorbol and 1,8-dihydroxyanthraquinone) had little effect. Another tumor promoter, phenol, inhibited DNA repair synthesis only at very high concentrations while an analog, 4-nitrophenol, produced inhibition of DNA repair synthesis at molar concentrations at which phenol had no effect. To investigate the specificity of this phenomenon, the effects of these agents on DNA-replicative synthesis, RNA synthesis, protein synthesis, and cell morphology were evaluated. At equimolar concentrations, tumor promoters were found to inhibit DNA-replicative synthesis as effectively as repair synthesis. RNA and protein synthesis were similarly inhibited over the same range of concentrations. Extensive morphological changes, interpreted as evidence of toxicity, were seen at concentrations of promoters that inhibited the macromolecular syntheses studied. The nonpromoting analogs, with the exception of nitrophenol, had little effect on these processes and showed only slight morphological damage. Thus tumor-promoting agents appeared to inhibit a number of macromolecular synthetic events, including DNA repair synthesis. It is suggested that the effect of tumor promoters on DNA repair synthesis is part of a general response to cellular injury rather than a selective response involving a single metabolic pathway. Furthermore, it is unlikely that the inhibition of repair synthesis represents the major mode of action of promoting agents in the carcinogenic process.  (+info)

A highly decreased binding of cyclic adenosine monophosphate to protein kinase A in erythrocyte membranes is specific for active psoriasis. (4/36)

A cyclic adenosine monophosphate binding abnormality in psoriatic erythrocytes that could be corrected by retinoid treatment has been reported. It was tested whether this binding abnormality is specific for psoriasis and the effects of treatment were compared with etretinate, cyclosporine A, or anthralin on 2-(3)H-8-N(3)-cyclic adenosine monophosphate binding to the regulatory subunit of protein kinase A in erythrocyte membranes. One hundred and fifteen individuals were evaluated, including: (i) 34 healthy persons; (ii) 15 patients with nonatopic inflammatory skin diseases (eczema, erythroderma, tinea, Grover's disease, erysipelas, urticaria); (iii) eight with other dermatoses mediated by immune mechanisms (systemic lupus erythematosus, lichen planus, necrotizing vasculitis, erythema nodosum, systemic sclerosis); (iv) 14 with generalized atopic dermatitis; and (v) 44 with psoriasis vulgaris clinically assessed by Psoriasis Area and Severity Index. In psoriasis, the course of the binding of 2-(3)H-8-N(3)-cyclic adenosine monophosphate to erythrocytes was measured in nine patients during a 10 wk treatment with etretinate, in 21 patients during a 10 wk treatment with cyclosporine A, and one patient under topical treatment with anthralin for 4 wk. We found the following femtomolar binding per mg protein: (i) healthy persons (1064 +/- 124, mean +/- SD); (ii) nonatopic inflammatory skin diseases (995 +/- 103); (iii) immune dermatoses (961 +/- 92); (iv) atopic dermatitis (960 +/- 110); and (v) psoriasis (645 +/- 159; p < 0.0001 compared with nonpsoriatics, Mann-Whitney U test). Treatment of psoriasis with etretinate, cyclosporine A, or anthralin normalized the binding of cyclic adenosine monophosphate, which was inversely correlated to the Psoriasis Area and Severity Index score. It was concluded that the decreased binding of cyclic adenosine monophosphate to protein kinase A in erythrocytes is specific for psoriasis and normalizes after successful treatment.  (+info)

A systematic review of adverse effects associated with topical treatments for psoriasis. (5/36)

Mild to moderate psoriasis is a disease that can often be treated with topical medications. The diversity of topical therapies and their disparate side effects complicates treatment planning. Our purpose is to compare the rates of adverse events associated with different topical psoriasis treatments. A review of medical literature from 1996 to March, 2002 was conducted using guidelines set by QUORUM statement criteria. In monotherapy studies, corticosteriods caused fewer adverse reactions compared to vitamin D analogues and tazarotene. In combination studies adverse event rates were higher than in monotherapy studies, except for the combination of topical steroid and calcipotriene which decreased irritation. Irritant contact dermatitis was the main side effect with vitamin D analogues, tazarotene, dithranol or coal tar, while side effects of topical corticosteriods included headache, viral infection and skin atrophy. Topical agents for psoriasis are usually well-tolerated without severe side effects. Formulating a patient's medication regimen should take into account the needs for short-term management and long-term control of psoriasis. Since clearance is not a realistic expectation, reasonable goals should be set as excessive use of topical treatments may increase the risk of both cutaneous and systemic side effects.  (+info)

Cytokines and signal transduction pathways mediated by anthralin in alopecia areata-affected Dundee experimental balding rats. (6/36)

Although many therapeutic modalities have been tested on alopecia areata, patient outcomes have been disappointing. Use of animal models would help to develop more efficient therapies as well as understanding therapeutic mechanisms. We have demonstrated that 0.1% topical anthralin ointment is 100% effective in restoring follicular activity in Dundee experimental balding rats. This is the most promising topical treatment for Dundee experimental balding rats among the therapeutic agents tested on this model. Various cytokines have been shown to be associated with the pathogenesis of alopecia areata. To test whether any of these cytokines might be modulated by anthralin, an RNase protection assay and the real-time polymerase chain reaction were performed to compare their expression between anthralin-treated and control skins. These experiments showed that expression of tumor necrosis factor-alpha and interferon-gamma was inhibited by anthralin, whereas expression of interleukin-1alpha/beta and their receptor antagonist, interleukin-1Ra, and interleukin-10 was stimulated by anthralin. In addition, using an antibody-based multi-immunoblotting technique, we found that certain signaling regulatory proteins were modulated by anthralin. Their potential roles in reversing the autoimmune-arrested follicular activity in Dundee experimental balding rats are discussed.  (+info)

Old wine in new bottles: reviving old therapies for alopecia areata using rodent models. (7/36)

Alopecia areata is regarded as a tissue-restricted autoimmune disease of hair follicles in which follicular activity is arrested because of the continued activity of lymphocytic infiltrates. Actual loss of hair follicles does not occur, even in hairless lesions. A variety of immunomodulating therapies, including contact sensitizers and immunomodulators, are part of the usual armamentarium for this disorder. None of these treatments have been consistent in their efficacy, and many have untoward side effects. Nevertheless, their uses in valid animal models provide a tool to dissect out molecular mechanisms of therapeutic effects. For several decades, both mechlorethamine (for the treatment of cutaneous T cell lymphoma) and anthralin (for the treatment of psoriasis) have been used successfully. When these therapies were tested in rat and mouse alopecia areata models, we found anthralin and mechlorethamine to be the most effective topical modalities, respectively. The underlying cellular mechanisms may act through targeting infiltrative lymphocytes, and the molecular mechanisms may involve specific cytokine expression changes. These visible, accessible, and unilaterally treated animal model systems are ideal for studying novel alopecia areata therapies, particularly in terms of their in vivo molecular mechanisms of action.  (+info)

Anthralin, a non-TPA type tumor promoter, synergistically enhances phorbol ester-caused prostaglandin E2 release from primary cultured mouse epidermal cells. (8/36)

Primary cultures of mouse epidermal cells (i.e., target cells of skin tumor promotion) stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) release prostaglandin E2 within 30 min. Anthralin, a non-TPA type tumor promoter, also stimulated PGE2 release; however, no release was detectable at least up to 4 hr after the addition of anthralin. When the cells were incubated with TPA plus anthralin, both PGE2 and arachidonic acid release were synergistically enhanced. Other non-TPA type tumor promoters, i.e., chrysarobin, 7-bromomethylbenz[a]anthracene, benzoylperoxide, okadaic acid and palytoxin, did not potentiate the TPA-caused PGE2 release. In protein kinase C-down regulated cells, the synergistic stimulation of PGE2 and arachidonic acid release by TPA plus anthralin were not detected. Anthralin plus TPA did not alter the incorporation of arachidonic acid into cellular phospholipids. Cellular cyclooxygenase activity was increased 2 hr after TPA stimulation. Anthralin-caused increase in cyclooxygenase activity was detected at 6 hr after the addition of anthralin. Cyclooxygenase activity was synergistically increased by treating the cells with TPA plus anthralin. Cycloheximide and actinomycin D inhibited the increase in cyclooxygenase activity caused by anthralin or TPA plus anthralin. These results indicate that anthralin synergistically stimulates TPA-caused PGE2 release by synergistically increasing arachidonic acid release and cellular cyclooxygenase activity.  (+info)

There are several types of alopecia areata, including:

1. Alopecia areata patchy - This is the most common form of the disease, where hair loss occurs in patches on the scalp or other parts of the body.
2. Alopecia totalis - Hair loss occurs over the entire scalp.
3. Alopecia universalis - Hair loss occurs over the entire body, including the scalp, eyebrows, and eyelashes.
4. Alopecia areata barbae - Hair loss occurs in the beard area.
5. Alopecia areata traction - Hair loss occurs due to pulling or tension on the hair shaft, often seen in children who pull their own hair.

The symptoms of alopecia areata may include:

1. Patchy hair loss
2. Thinning of hair
3. Redness and scalp inflammation
4. Itching or burning sensation on the scalp
5. Nail changes such as ridging, thinning, or pitting

Alopecia areata can be diagnosed through a physical examination and medical history. A skin scraping or biopsy may be performed to confirm the diagnosis.

Treatment for alopecia areata depends on the severity and location of hair loss, as well as the individual's overall health. Options may include:

1. Topical corticosteroids - Medicated creams or ointments applied directly to the affected area to reduce inflammation and promote hair growth.
2. Oral corticosteroids - Medications taken by mouth to reduce inflammation and suppress the immune system.
3. Anthralin - A medication that is applied to the skin to reduce inflammation and promote hair growth.
4. Immunotherapy - Injections or tablets that stimulate the immune system to attack cancer cells, but also can cause hair loss.
5. Wigs, hats, or other hairpieces - Used to cover up patchy hair loss.
6. Counseling or therapy - To help cope with the emotional impact of hair loss.
7. Hair transplantation - A surgical procedure that involves moving healthy hair follicles from one part of the scalp to another.

It is important to note that these treatments may not work for everyone and may have side effects. It's important to talk to a doctor or dermatologist to determine the best course of treatment for alopecia areata.

In addition to medical treatment, there are also some natural remedies that can help with alopecia areata such as:

1. Diet and nutrition - Eating a balanced diet rich in vitamins and minerals can promote hair growth.
2. Stress management - High stress levels have been linked to alopecia areata, so finding ways to manage stress, such as through exercise or meditation, may help.
3. Saw palmetto - A herb that has been shown to promote hair growth and slow down hair loss.
4. Fish oil - Omega-3 fatty acids found in fish oil have been shown to promote hair growth.
5. Coconut oil - Applying coconut oil to the scalp may help to stimulate hair growth.
6. Henna - A natural dye that can be used to color and strengthen hair, and may also help to promote hair growth.
7. Rosemary essential oil - May help to promote hair growth by increasing blood flow to the scalp.
8. Lavender essential oil - May help to reduce stress and promote relaxation, which can help with alopecia areata.

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

Some common types of skin diseases include:

1. Acne: a condition characterized by oil clogged pores, pimples, and other blemishes on the skin.
2. Eczema: a chronic inflammatory skin condition that causes dry, itchy, and scaly patches on the skin.
3. Psoriasis: a chronic autoimmune skin condition characterized by red, scaly patches on the skin.
4. Dermatitis: a term used to describe inflammation of the skin, often caused by allergies or irritants.
5. Skin cancer: a type of cancer that affects the skin cells, often caused by exposure to UV radiation from the sun or tanning beds.
6. Melanoma: the most serious type of skin cancer, characterized by a mole that changes in size, shape, or color.
7. Vitiligo: a condition in which white patches develop on the skin due to the loss of pigment-producing cells.
8. Alopecia: a condition characterized by hair loss, often caused by autoimmune disorders or genetics.
9. Nail diseases: conditions that affect the nails, such as fungal infections, brittleness, and thickening.
10. Mucous membrane diseases: conditions that affect the mucous membranes, such as ulcers, inflammation, and cancer.

Skin diseases can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment options vary depending on the specific condition and may include topical creams or ointments, oral medications, light therapy, or surgery.

Preventive measures to reduce the risk of skin diseases include protecting the skin from UV radiation, using sunscreen, wearing protective clothing, and avoiding exposure to known allergens or irritants. Early detection and treatment can help prevent complications and improve outcomes for many skin conditions.

Some of the key features of immediate hypersensitivity include:

1. Rapid onset of symptoms: Symptoms typically occur within minutes to hours of exposure to the allergen.
2. IgE antibodies: Immediate hypersensitivity is caused by the binding of IgE antibodies to surface receptors on mast cells and basophils.
3. Mast cell and basophil activation: The activation of mast cells and basophils leads to the release of histamine and other chemical mediators that cause symptoms.
4. Anaphylaxis: Immediate hypersensitivity can progress to anaphylaxis, a life-threatening allergic reaction that requires immediate medical attention.
5. Specificity: Immediate hypersensitivity is specific to a particular allergen and does not occur with other allergens.
6. Cross-reactivity: There may be cross-reactivity between different allergens, leading to similar symptoms.
7. Prevention: Avoidance of the allergen is the primary prevention strategy for immediate hypersensitivity. Medications such as antihistamines and epinephrine can also be used to treat symptoms.

In particular, 1,8-Dihydroxy-9,10-anthraquinone is the precursor for the important topical antipsoriatic drug anthralin, 1,8- ... "Anthralin: Historical and current perspectives". Journal of the American Academy of Dermatology. 9 (2): 173-192. doi:10.1016/ ...
Recently, anthralin's effectiveness as an anti-psoriatic agent has also been in part attributed to its abilities to induce ... Dithranol (INN) or anthralin (USAN and former BAN) is a hydroxyanthrone, anthracene derivative, medicine applied to the skin of ... The anti-proliferative effects of anthralin appear to result from both an inhibition of DNA synthesis as well as from its ... In addition Dithranol may act by reducing the elevated levels of cGMP that occurs in psoriasis.[citation needed] Anthralin is a ...
... anthralin was derived. Anthralin was found to be an effective treatment for psoriasis by Galewsky in 1916. Busse, Kristine L; ... Anthralin is a synthetic compound derived from chrysarophanic acid, which is an extract of the Vouacopoua araroba tree. Its ... Anthralin can, however, discolor hair, clothing, and surrounding skin and often causes irritant dermatitis when applied at a ... Anthralin is available in multiple formulations, including cream, ointment or paste. Steele, Tace; Rogers, Cindy J.; Jacob, ...
There is some tentative evidence that anthralin may be useful for treating alopecia areata. Hormonal modulators (oral ...
In 1953, John Ingram, an English dermatologist, added topical anthralin paste to his Goeckerman regimen. This is known as the ...
Peptides Anthralin - 16kDa polypeptide, binds to both TSPO receptor and dihydropyridine-sensitive calcium channels with high ...
... anthralin or topical coal tar), and topical immunotherapy ciclosporin, sometimes in different combinations. Topical ...
... anthralin, chrysarobin, glutaraldehyde, or resorcin.: 791 Nail anatomy List of cutaneous conditions James, William; Berger, ...
... or anthralin Hydroxyanthraquinone This set index page lists chemical structure articles associated with the same molecular ...
However, phototherapy can be effective when used in conjunction with certain topical treatments such as anthralin, coal tar, ...
... anthralin) MeSH D04.615.117.159 - anthraquinones MeSH D04.615.117.159.200 - carmine MeSH D04.615.117.159.205 - cascara MeSH ...
Topical application of anthralin, used in the treatment of psoriasis, is often accompanied by severe skin inflammation, ... Anthralin, at concentrations between 5 microM and 25 microM, caused a marked increase in granulocyte macrophage-colony ... Furthermore, anthralin induced chemokine secretion without the need of primary cytokines. Taken together, these studies suggest ... The role of inflammatory cytokines and their induction by anthralin-derived reactive oxygen species were studied in cultures of ...
Creams or ointments that contain coal tar or anthralin. *Creams to remove the scaling (usually salicylic acid or lactic acid) ...
Anthralin. Anthralin is a synthetic tarlike substance that is sometimes used to treat alopecia areata and promote hair growth. ...
Keratolytic agents (eg, anthralin, urea): Use of these medications may facilitate more direct steroid contact with the skin ...
3. Overall, the potential severity of side effects from tars is less than that from anthralin and much less than that from ... 3. Overall, the potential severity of side effects from tars is less than that from anthralin and much less than that from ... Tars and anthralins.. *Coal tar phototherapy for psoriasis reevaluated: erythemogenic versus suberythemogenic ultraviolet with ...
In certain embodiments, the additional therapeutic agent is anthralin. In certain embodiments, the additional therapeutic agent ... anthralin and retinoids. In certain embodiments, the additional therapeutic agent is a corticosteroid. In certain embodiments, ...
A convenient synthesis of 14C-anthralin. Huang, H. S., Mayer, K. K., Muller, K. & Wiegrebe, W., 1994, In: Archiv der Pharmazie. ...
Anthralin - Preferred Concept UI. M0001305. Scope note. An anthracene derivative that disrupts MITOCHONDRIA function and ... Anthralin Entry term(s). 1,8 Dihydroxy 9 anthrone 1,8,9-Anthracenetriol 1,8-Dihydroxy-9(10H)-anthracenone 1,8-Dihydroxy-9- ...
Anthralin. *SADBE. *Minoxidil. Moreover, UVA phototherapy is coming up as a non-invasive way to provide an alternative ...
Allantoin; Alum (medicinal); Alum (medicinal)nonmedicinal (ammonium) (potassium); Anthralin; Antiseborrheics; Bleaching agent ( ...
use anthralin (medication for psoriasis). *use tretinoin (medication for acne and other skin conditions) ...
According to modern medicine, topical corticosteroids, topical retinoids, anthralin, phototherapy, Enbrel injections are ...
Short-contact anthralin therapy (SCAT) was developed to optimize effectiveness and mini- mize staining and irritation. Allowing ...
1,8-Dihydroxy-9(10H)-anthracenone use Anthralin 1,8-Dihydroxy-9-anthrone use Anthralin ...
It was concluded that the performance of azelaic acid is comparable with the results obtained with anthralin for hair (re) ... The results using azelaic acid were compared with the effectiveness of anthralin (1,8-dihydroxy-9- oxoanthracene), a drug ...
CONCLUSION: DPCP and anthralin was as effective as DPCP alone and anthralin did not add to the effect of DPCP in treating AA. ... AIM: To evaluate the safety and efficacy of combined DPCP and anthralin versus standard protocol (DPCP alone). METHODS: A ... A randomized trial of diphenylcyclopropenone (DPCP) combined with anthralin versus DPCP alone for treating moderate to severe ... or in combination with anthralin (group D/A). Percentage of hair regrowth after 6 months of treatment and the incidence of drug ...
... or anthralin. Bath solutions and lubricants may be soothing, but they are seldom strong enough to improve the condition of the ...
The immunostimulation of topical irritants, especially anthralin, or topical immunogens (diphencyprone, squaric acid ... may be a useful drug as a single agent or as an adjuvant with topical anthralin. There is a low incidence of local dryness/ ...
BCC is associated with the induction of the proliferative activity of basal cells with the capacity of local invasion and tissue destruction. Although BCC is locally aggressive, metastatic spread rarely occurs.6,7 Podoplanin is a specific marker to delineate the LECs. The role of podoplanin during lymphangiogenesis was previously explored in different disorders.9,15. The significantly higher number of podoplanin-stained LVs in the BCC group, compared to control group, along with nonsignificant increase in LVA, indicate that the formation of neolymphatic network and lymphangiogenesis in BCC carcinogenesis is more important than LV remodeling. Unlike our results, Neinaa et al16 did not find a statistically significant increase in LV density in BCC samples compared to those of normal skin. A higher count of LVs and lower total LVA in intratumoral tissue, compared to peritumoral stroma, have been noted in previous literature, which described small and collapsed intratumoral LVs.17 This finding has ...
... or anthralin may be used in combination with natural sunlight or another ultraviolet (UV) light treatment.b) Oral or injectable ...
With simultaneous application to the skin of minoxidil and topical preparations containing tretinoin, anthralin / dithranol ( ...
... anthelion anthemene antheming anthemion anthocarp anthodium anthology anthotaxy anthozoan anthozoic anthozoon anthralin ...
","grey",0 24538,"Anthralin","1143-38-0","C1143380","cheminventory_bottle,cheminventory_sample,epa:all_plated,tox21:all_plated, ...
Anthralin Medicated Shampoo Anthralin Topical Cream Antihemophilic Factor VIII, Human Recombinant Residues 743-1636 Deleted ...
Willow Birch Pharma is a leading FDA-Registered / NAPB Accredited supplier of Active Pharmaceutical Ingredients (APIs) to the US Compounding Industry.. ...
  • Irritation may also occur, but this can be minimized by applying the anthralin only to the psoriasis patches and avoiding uninvolved skin. (
  • Topical application of anthralin, used in the treatment of psoriasis, is often accompanied by severe skin inflammation, presumably due to free radical products of the drug. (
  • Anthralin - a topical agent prescribed for the treatment of psoriasis. (
  • The Berlin regime is a well known psoriasis treatment, consisting of selective UVB phototherapy in combination with the local treatment liquor carbonis detergens in the evening and anthralin in the morning. (
  • It may be combined with tar, anthralin and topical corticosteroids. (
  • 3. Overall, the potential severity of side effects from tars is less than that from anthralin and much less than that from topical corticosteroids (atrophy, rebound). (
  • Other treatments that may subdue the immune system are anthralin, minoxidil, and DPCP. (
  • Other topical therapies include vitamin D-based medicines, retinoids (related to vitamin A), coal tar, and anthralin (another tar product). (
  • In addition, NHKs were either treated with neutralizing antibodies to tumor necrosis factor (TNF)-alpha or transfected with a CAT-linked IL-8 promoter to establish the direct effects of anthralin on chemokine synthesis. (
  • Anthralin, at concentrations between 5 microM and 25 microM, caused a marked increase in granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin (IL)-6, IL-8 and TNFalpha synthesis that was selectively inhibited by specific antioxidants. (
  • Anthralin was added to cultures of NHKs in the presence or absence of various antioxidants, including superoxide dismutase, tetramethylthiourea, N-acetylcysteine and vitamin E and relative changes in cytokine secretion and in the number of mRNA transcripts were examined. (
  • Anthralin is a synthetic tarlike substance that is sometimes used to treat alopecia areata and promote hair growth. (
  • 1] If anthralin is used, ensure that the infant's skin does not come into direct contact with the areas of maternal skin that have been treated and the infant does not ingest the product from the mother's skin. (
  • Anthralin slows down the growth of the skin cells and has anti-inflammatory actions. (
  • Anthralin can cause staining (purple/brown color) of your clothes, skin, and hair, which limits its use. (
  • You should not use Anthralin on the face, genitals or in the skin folds. (
  • The role of inflammatory cytokines and their induction by anthralin-derived reactive oxygen species were studied in cultures of normal human keratinocytes (NHKs). (
  • Topical application of anthralin, used in the treatment of psoriasis, is often accompanied by severe skin inflammation, presumably due to free radical products of the drug. (
  • 2. Fluorescence remission spectroscopy of psoriatic lesions and the effect of topical anthralin therapy. (
  • Anthralin, at concentrations between 5 microM and 25 microM, caused a marked increase in granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin (IL)-6, IL-8 and TNFalpha synthesis that was selectively inhibited by specific antioxidants. (
  • In addition, NHKs were either treated with neutralizing antibodies to tumor necrosis factor (TNF)-alpha or transfected with a CAT-linked IL-8 promoter to establish the direct effects of anthralin on chemokine synthesis. (
  • Taken together, these studies suggest that oxygen radicals generated from anthralin are responsible for the induction of inflammatory cytokines which, in turn contributes to their dermal toxicity. (