Categories
Herbs & Plants

Convolvulus Scammonia

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Botanical Name: Convolvulus Scammonia
Family: Convolvulaceae
Genus: Convolvulus
Species: C. scammonia
Kingdom: Plantae
Order: Solanales

Common Names: Syrian Bindweed, Scammony

Habitat:Convolvulus Scammonia is native to the countries of the eastern part of the Mediterranean basin; it grows in bushy waste places, from Syria in the south to the Crimea in the north, its range extending westward to the Greek islands, but not to northern Africa or Italy.

Description:
Convolvulus Scammonia is a twining perennial plant,growing to 0.8 m (2ft 7in). It bears flowers like those of Convolvulus arvensis, and having irregularly arrow-shaped leaves and a thick fleshy root. It is in flower in July, and the seeds ripen in September. It has flowers of a very delicate tint of sulphur yellow and leaves of a similar shape to some native species.The flowers are hermaphrodite (have both male and female organs) and are pollinated by Bees, flies, self.The plant is self-fertile.

The roots are 3 to 4 feet long and from 9 to 12 inches in circumference; tapering, covered with a light grey bark and containing a milky juice. Scammony is a gummy resin, obtained from this milky juice of the root by clearing away the earth from the upper part of the root and cutting off the top obliquely, about 2 inches below where the stalks spring. Then a vessel is fixed in such a position as to receive the exuding juice, which gradually hardens and becomes the Scammony of commerce. The best Scammony is black, resinous and shining when in the lump, but of a whitish-ash colour when powdered, with a strong cheesy smell and a somewhat acrid taste, turning milky when touched by the tongue. It occurs in commerce in irregular pieces 1 to 2 inches or more in diameter.
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Cultivation:
Prefers a light basic sharply drained soil of low to medium fertility. Prefers a sunny sheltered position. Thrives in dry soils and succeeds in ordinary garden soils. The root can be up to 1.2 metres long, so for best results a deep soil is required.

Propagation:
Seed – sow spring in a greenhouse. Germination can be slow and erratic, a period of cold stratification might help reduce the germination period. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for their first winter. Plant them out in late spring or early summer, after the last expected frosts. Division in spring. Cuttings of young shoots, August in a frame in sand
Medicinal Uses:
The dried juice, virgin scammony, obtained by incision of the living root, has been used in medicine as scammonium, but the variable quality of the drug has led to the employment of scammoniae resina, which is obtained from the dried root by digestion with alcohol.

It is a drastic cathartic, closely allied in its operation to Jalap; though not so nauseous, it is more active and irritating, and in inflammatory conditions of the alimentary canal should not be used.

The root itself is seldom used: the resin prepared from it is generally combined with other cathartics to diminish its action and prevent griping.

The active principle is the glucoside scammonin or jalapin, C34H114O6. The dose of scammonium is 5 to 10 grains, of scammony resin 3 to 8 grains. Like certain other resins, scammony is inert until it has passed from the stomach into the duodenum, where it meets the bile, a chemical reaction occurring between it and the taurocholate and glycocholate of sodium, whereby it is converted into a powerful purgative. Its action is essentially that of a hydragogue, and is exercised upon practically the entire length of the alimentary canal. The drug is not a cholagogue, nor does it markedly affect the muscular coat of the bowel, but it causes a great increase of secretion from the intestinal glands. It acts in about four hours. In large doses it is a violent gastrointestinal irritant. In consonance with the statement that scammony acts only after admixture with the bile, is the fact that hypodermic or intravenous injection of the drug produces no purgation, or indeed any other result. The drug frequently kills both roundworm and tapeworm, especially the former, and is therefore an anthelmintic. It is not largely used, but is very effective in the treatment of severe constipation, especially in children

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:
https://en.m.wikipedia.org/wiki/Convolvulus_scammonia
http://www.botanical.com/botanical/mgmh/b/binwsy42.html
http://www.pfaf.org/user/Plant.aspx?LatinName=Convolvulus+scammonia

Categories
Therapetic treatment Therapies

PUVA therapy

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Description:
PUVA is an acronym. The P stands for psoralen,(Psoralen is a photosensitizing agent found in plants ) the U for ultra, the V for violet, and the A for that portion of the solar spectrum between 320 and 400 nanometers in wavelength. Psoralens are chemicals found in certain plants that have the ability to absorb ultraviolet light in these wavelengths. Once the light energy is absorbed, these chemicals are energized to interact with DNA, ultimately inhibiting cell multiplication, which is their presumed mode of action.

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Certain skin diseases are characterized by cells that are rapidly multiplying. Inhibiting this unrestrained multiplication can be useful in treating these diseases. So PUVA is a combination of an oral drug and subsequent ultraviolet light exposure. The treatment may affect certain blood cells and skin cells so that the skin disease improves.

It is a treatment for eczema, psoriasis, graft-versus-host disease, vitiligo, mycosis fungoides, large-plaque parapsoriasis and cutaneous T-cell lymphoma using the sensitizing effects of the drug psoralen. The psoralen is applied or taken orally to sensitize the skin, then the skin is exposed to UVA.

Photodynamic therapy is the general use of nontoxic light-sensitive compounds that are exposed selectively to light, whereupon they become toxic to targeted malignant and other diseased cells. Still, PUVA therapy is often classified as a separate technique from photodynamic therapy.

Plant sources   from where  we get psoralens:
Ficus carica (fig) is probably the most abundant source of psoralens. They are also found in small quantities in Ammi visnaga (bisnaga), Pastinaca sativa (parsnip), Petroselinum crispum (parsley), Levisticum officinale (lovage), Foeniculum vulgare (fruit, i.e., fennel seeds), Daucus carota (carrot), Psoralea corylifolia (babchi), and Apium graveolens (celery).

Types of PUVA therapy:
The most common form of therapy combines 8-methoxypsoralen taken by mouth followed 45-60 minutes later by exposure of the skin to UVA. Less commonly the drug is applied topically (the medication is occasionally diluted in bathtub water in which the patient is immersed) and then after a few minutes the ultraviolet exposure occurs.

Procedure:
Psoralens are taken systemically or can be applied directly to the skin. The psoralens allow a relatively lower dose of UVA to be used. When they are combined with exposure to UVA in PUVA, they are highly effective at clearing psoriasis and vitiligo. Like UVB light treatments, the reason remains unclear, though investigators speculate there may be similar effects on cell turnover and the skin’s immune response.

Choosing the proper dose for PUVA is similar to the procedure followed with UVB. The physician can choose a dose based on the patient’s skin type. The dose will increase in every treatment until the skin starts to respond.

Some clinics test the skin before the treatments, by exposing a small area of the patient’s skin to UVA, after ingestion of psoralen. The dose of UVA that produces uniform redness 72 hours later, called the minimum phototoxic dose (MPD), becomes the starting dose for treatment.

At the very least for vitiligo, narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA since it does not require the use of the Psoralen. As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen.

Narrowband UVB does not cure the legs and hands, compared to the face and neck. To the hands and legs PUVA may be more effective. The reason can be because UVA penetrates deeper in the skin, and the melanocytes in the skin of the hands and legs is deeper in the skin. The Narrowband UVB does not reach the melanocytes.

How maney PUVA  therapy is required:
There ought to be a significant improvement in the patient’s skin disease after about 15 treatments. Treatments are given no sooner than 48 hours apart because the burn induced by PUVA is often delayed for as long as two days (unlike ordinary sunburns). Unless there is a problem, the amount of energy administered to the patient is increased appropriately at each visit depending on the patient’s coloration. After about 30 treatments, a decision is made as to whether to continue treatments. PUVA is not always effective. If there is no improvement after these treatments, it is probably unlikely that continuing this form of treatment is worthwhile. On the other hand, if significant clearing has occurred, it is probably prudent to decrease the frequency of treatments in order to maintain the improvement. Since there is a relationship between the amount of light energy administered and the degree of photo-aging and the induction of skin cancers, it is wise to limit the light exposures as appropriate.

Advantages:
The major advantage to PUVA is that it is an effective therapy that becomes active only at the site of the disease, the skin. It can be used to treat large areas of skin, and the fact that the drug is only activated in the presence of UV light implies that it may be less toxic than other therapies that require systemic administration and whose effects are not localized to just the skin.

PUVA must be administered in a physician’s office under the control of a medical professional so it requires repeated visits to the office. PUVA may not cure psoriasis permanently so treatment can be required indefinitely.

Side effects and complications:
Some patients experience nausea and itching after ingesting the psoralen compound. For these patients PUVA bath therapy may be a good option.

Long term use of PUVA therapy has been associated with higher rates of skin cancer.

The most significant complication of PUVA therapy for psoriasis is squamous cell skin cancer. Two carcinogenic components of the therapy include the nonionizing radiation of UVA light as well as the psoralen intercalation with DNA. Both processes negatively contribute to genome instability.
History  :  Psoralens have been known since ancient Egypt but have only been available in a chemically synthesized form since the 1970s.

Resources:
http://en.wikipedia.org/wiki/PUVA_therapy
http://www.medicinenet.com/puva_therapy_photochemotherapy/article.htm

Categories
Therapies

Photodynamic therapy

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Description:
Photodynamic therapy (PDT), sometimes called photochemotherapy, is a form of phototherapy using nontoxic light-sensitive compounds that are exposed selectively to light, whereupon they become toxic to targeted malignant and other diseased cells (phototoxicity). PDT has proven ability to kill microbial cells, including bacteria, fungi and viruses. PDT is popularly used in treating acne. It is used clinically to treat a wide range of medical conditions, including wet age-related macular degeneration and malignant cancers, and is recognised as a treatment strategy which is both minimally invasive and minimally toxic.

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Most modern PDT applications involve three key components: a photosensitizer, a light source and tissue oxygen. The combination of these three components leads to the chemical destruction of any tissues which have either selectively taken up the photosensitizer or have been locally exposed to light. The wavelength of the light source needs to be appropriate for exciting the photosensitizer to produce reactive oxygen species. These reactive oxygen species generated through PDT are free radicals (Type I PDT) generated through electron abstraction or transfer from a substrate molecule and highly reactive state of oxygen known as singlet oxygen (Type II PDT). In understanding the mechanism of PDT it is important to distinguish it from other light-based and laser therapies such as laser wound healing and rejuvenation, or intense pulsed light hair removal, which do not require a photosensitizer.

Why it is done:
Photodynamic therapy (PDT) was first used in 1905 for the treatment of skin cancers. Since then, it has been further developed and used for the treatment of many kinds of cancers (lung, colon, etc.) as well as certain kinds of blindness. PDT combines a drug (called a photosensitizer) that is preferentially absorbed by certain kinds of cells and a special light source. When used together, the photosensitizer and the light destroy the targeted cells. More recently, however, PDT has been used for photorejuvenation, wrinkles, discoloration, visible veins, and acne. When used for these conditions, the photosensitizer is applied to the face and then the skin is exposed to a light source. Rapidly growing cells, oil glands, and other structures in the skin absorb the photosensitizer and are destroyed by a reaction caused by the light. Cosmetic improvement in wrinkling, age spots, and visible veins has been documented after PDT treatment.

It is a new advance in facial rejuvenation and there are currently different methods in use. For example some physicians use blue light, red light, or intense pulse light. The photosensitizer is applied to the skin and is left on for a variable period of time. The skin is then exposed to the light source and the photosensitizer is then removed. Reported side effects include transient burning, stinging, swelling, and redness. Side effects are variable depending on what is being treated, how long the photosensitizer is left on, and which light source is used. No long-term studies have been performed to evaluate long term side effects.
Procedure:
In order to achieve the selective destruction of the target area using PDT while leaving normal tissues untouched, either the photosensitizer can be applied locally to the target area, or photosensitive targets can be locally excited with light. For instance, in the treatment of skin conditions, including acne, psoriasis, and also skin cancers, the photosensitizer can be applied topically and locally excited by a light source. In the local treatment of internal tissues and cancers, after photosensitizers have been administered intravenously, light can be delivered to the target area using endoscopes and fiber optic catheters....CLICK & SEE

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Photosensitizers can also target many viral and microbial species, including HIV and MRSA. Using PDT, pathogens present in samples of blood and bone marrow can be decontaminated before the samples are used further for transfusions or transplants. PDT can also eradicate a wide variety of pathogens of the skin and of the oral cavities. Given the seriousness that drug resistant pathogens have now become, there is increasing research into PDT as a new antimicrobial therapy.

Photosensitizers:
In air and tissue, molecular oxygen occurs in a triplet state, whereas almost all other molecules are in a singlet state. Reactions between these are forbidden by quantum mechanics, thus oxygen is relatively non-reactive at physiological conditions. A photosensitizer is a chemical compound that can be promoted to an excited state upon absorption light and undergo intersystem crossing with oxygen to produce singlet oxygen. This species rapidly attacks any organic compounds it encounters, thus being highly cytotoxic. It is rapidly eliminated: in cells, the average lifetime is 3 µs.[5]

A wide array of photosensitizers for PDT exist. They can be divided into porphyrins, chlorophylls and dyes. Some examples include aminolevulinic acid (ALA), Silicon Phthalocyanine Pc 4, m-tetrahydroxyphenylchlorin (mTHPC), and mono-L-aspartyl chlorin e6 (NPe6).

Several photosensitizers are commercially available for clinical use, such as Allumera, Photofrin, Visudyne, Levulan, Foscan, Metvix, Hexvix, Cysview, and Laserphyrin, with others in development, e.g. Antrin, Photochlor, Photosens, Photrex, Lumacan, Cevira, Visonac, BF-200 ALA. Amphinex. Also Azadipyrromethenes.

Although these photosensitizers can be used for wildly different treatments, they all aim to achieve certain characteristics:

*High absorption at long wavelengths

*Tissue is much more transparent at longer wavelengths (~700–850 nm). Absorbing at longer wavelengths would allow the light to penetrate deeper,[8] and allow the treatment of larger tumors.

*High singlet oxygen quantum yield

*Low photobleaching to prevent degradation of the photosensitizer

*Natural fluorescence

*Many optical dosimetry techniques, such as fluorescence spectroscopy, depend on the drug being naturally fluorescent[10]

*High chemical stability

*Low dark toxicity

*The photosensitizer should not be harmful to the target tissue until the treatment beam is applied.

*Preferential uptake in target tissue

The major difference between different types of photosensitizers is in the parts of the cell that they target. Unlike in radiation therapy, where damage is done by targeting cell DNA, most photosensitizers target other cell structures. For example, mTHPC has been shown to localize in the nuclear envelope and do its damage there. In contrast, ALA has been found to localize in the mitochondria and Methylene Blue in the lysosomes.

To allow treatment of deeper tumours some researchers are using internal chemiluminescence to activate the photosensitiser.

PUVA therapy is using psoralen as photosensitiser and UVA ultraviolet as light source, but this form of therapy is usually classified as a separate form of therapy from photodynamic therapy.

Targeted PDT:
Some photosensitisers naturally accumulate in the endothelial cells of vascular tissue allowing ‘vascular targeted’ PDT, but there is also research to target the photosensitiser to the tumour (usually by linking it to antibodies or antibody fragments). It is currently only in pre-clinical studies.

Applications:
Compared to normal tissues, most types of cancers are especially active in both the uptake and accumulation of photosensitizers agents, which makes cancers especially vulnerable to PDT. Since photosensitizers can also have a high affinity for vascular endothelial cells.

Usage in acne:
PDT is currently in clinical trials to be used as a treatment for severe acne. Initial results have shown for it to be effective as a treatment only for severe acne, though some question whether it is better than existing acne treatments. The treatment causes severe redness and moderate to severe pain and burning sensation. A phase II trial, while it showed improvement occurred, failed to show improved response compared to the blue/violet light alone
Advantages:
There are several advantages of photodynamic therapy over other forms of facial rejuvenation. For example, PDT is less destructive (and therefore less painful) than many of the deeper peels and lasers. There is also minimal recovery time. It is also a proven technique for the treatment of precancerous lesions. Thus, depending on the technique used, there may be an additional benefit of preventing skin cancer.

Disadvantages:
The disadvantage of photodynamic therapy is that it is new. Long-term side effects are unknown, and the benefits are not as well studied. For example, PDT is not known how long the benefits last.

Although PDT is a promising new therapy, you need to discuss the risks, benefits, and alternatives with your physician to decide if PDT is right for you.
Modern development of PDT in Russia:
Of all the nations beginning to use PDT in the late 20th century, the Russians were the quickest to advance its use clinically and to make many developments. One early Russian development was a new photosensitizer called Photogem which, like HpD, was derived from haematoporphyrin in 1990 by Professor Andrey F. Mironov and coworkers in Moscow. Photogem was approved by the Ministry of Health of Russia and tested clinically from February 1992 to 1996. A pronounced therapeutic effect was observed in 91 percent of the 1500 patients that underwent PDT using Photogem, with 62 percent having a total tumor resolution. Of the remaining patients, a further 29 percent had a partial tumor resolution, where the tumour at least halved in size. In those patients that had been diagnosed early, 92 percent of the patients showed complete resolution of the tumour.

Around this time, Russian scientists also collaborated with NASA medical scientists who were looking at the use of LEDs as more suitable light sources, compared to lasers, for PDT applications.

Modern development of PDT in Asia:
PDT has also seen considerably development in Asia. Since 1990, the Chinese have been developing specialist clinical expertise with PDT using their own domestically produced photosensitizers, derived from Haematoporphyrin, and light sources. PDT in China is especially notable for the technical skill of specialists in effecting resolution of difficult to reach tumours
Resources:
http://en.wikipedia.org/wiki/Photodynamic_therapy
http://www.dermanetwork.org/information/pdt.asp

Categories
News on Health & Science

Which Sunscreens are the Safest?

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The Environmental Working Group‘s 2011 sunscreen guide can help you determine which sunscreens are unsafe. The group recommends just 20 percent of the 600-plus sport sunscreens it evaluated.

For a product to score high marks, it needed to be free of potentially harmful chemicals. Not surprisingly, their list of products to avoid list contains some popular brands.

According to Yahoo News, companies with sunscreens that scored poorly include Aveeno, Banana Boat, CVS, and Neutrogena. For more information, and to see which products EWG approved, you can click on the Yahoo link below.

Time Magazine also recounts some of the Environmental Working Group‘s advice:
“Avoid oxybenzone and retinyl palmitate. Many effective products contain one or both compounds — oxybenzone and retinyl palmitate — that the EWG specifically suggests avoiding. Oxybenzone is an endocrine disrupter, the EWG says, and retinyl palmitate is a form of topical vitamin A that some animal studies suggest may be linked to an increased risk of skin cancer.”

Resources:
Yahoo Shine May 24, 2011

Time Magazine May 24, 2011

Environmental Working Group 2011 Sunscreen Guide

Posted By Dr. Mercola | June 06 2011

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Categories
Ailmemts & Remedies

Gorlin syndrome

Alternative Names:Nevoid basal cell carcinoma syndrome (NBCCS),basal cell nevus syndrome, multiple basal cell carcinoma syndrome and Gorlin–Goltz syndrome

Definition:
Gorlin syndrome is an inherited medical condition involving defects within multiple body systems such as the skin, nervous system, eyes, endocrine system, and bones. People with this syndrome are particularly prone to developing a common and usually non-life-threatening form of non-melanoma skin cancers.

You may click to see more pictures of  Gorlin syndrome

People with the syndrome have a predisposition to multiple basal cell carcinomas (a form of skin cancer), jaw cysts and other generally harmless abnormalities in the bone. The severity of the disease can be wide-ranging.

About 10% of people with the condition do not develop basal cell carcinomas (BCCs). the name Gorlin syndrome refers to researcher Robert J. Gorlin (1923–2006).

First described in 1960, NBCCS is an autosomal dominant condition that can cause unusual facial appearances and a predisposition for basal cell carcinoma, a malignant type of skin cancer. The prevalence is reported to be 1 case per 56,000-164,000 population. Recent work in molecular genetics has shown NBCCS to be caused by mutations in the PTCH (Patched) gene found on chromosome arm 9q. If a child inherits the defective gene from either parent, he or she will have the disorder

Incidence:
About 750,000 new cases of sporadic basal cell carcinomas (BCCs) occur each year in the United States. Ultraviolet (UV) radiation from the sun is the main trigger of these cancers, and people with fair skin are especially at risk. Most sporadic BCCs arise in small numbers on sun-exposed skin of people over age 50, although younger people may also be affected. By comparison, NBCCS has an incidence of 1 in 50,000 to 150,000 with higher incidence in Australia. One aspect of NBCCS is that basal cell carcinomas will occur on areas of the body which are not generally exposed to sunlight, such as the palms and soles of the feet and lesions may develop at the base of palmer and plantar pits. One of the prime features of NBCCS is development of multiple BCCs at an early age, often in the teen years. Each person who has this syndrome is affected to a different degree, some having many more characteristics of the condition than others.

Components:-
Some or all of the following may be seen in someone with Gorlin Syndrome:

1.Multiple basal cell carcinomas of the skin
2.Odontogenic keratocyst: Seen in 75% of patients and is the most common finding. There are usually multiple lesions found in the mandible. They occur at a young age (19 yrs average).
3.Rib and vertebrae anomalies
4.Intracranial calcification
5.Skeletal abnormalities: bifid ribs, kyphoscoliosis, early calcification of falx cerebri (diagnosed with AP radiograph)
6.Distinct faces: frontal and temporopariental bossing, hypertelorism, and mandibular prognathism

What genes are related to Gorlin syndrome?
Mutations in the PTCH1 gene cause Gorlin syndrome. This gene provides instructions for making a protein called Patched-1, which functions as a receptor. Receptor proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. Together, ligands and their receptors trigger signals that affect cell development and function. A protein called Sonic Hedgehog is the ligand for the Patched-1 receptor. Patched-1 prevents cell growth and division (proliferation) until Sonic Hedgehog is attached.

The PTCH1 gene is a tumor suppressor gene, which means it keeps cells from proliferating too rapidly or in an uncontrolled way. Mutations in this gene prevent the production of Patched-1 or lead to the production of an abnormal version of the receptor. An altered or missing Patched-1 receptor cannot effectively suppress cell growth and division. As a result, cells proliferate uncontrollably to form the tumors that are characteristic of Gorlin syndrome.

You may click to learn more about the PTCH1 gene.

How do people inherit Gorlin syndrome?
Gorlin syndrome is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the features that are present from birth, such as large head size and skeletal abnormalities. An affected person often inherits a PTCH1 mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family. For tumors to develop, a mutation in the other copy of the PTCH1 gene must occur in certain cells during the person’s lifetime. Most people who are born with one PTCH1 mutation eventually acquire a second mutation in certain cells and develop basal cell carcinomas and other tumors.

Causes:-
Gorlin syndrome is an autosomal dominant condition. The abnormal gene is found on chromosome 9. New mutations (where neither parent carries the gene) are common.

Diagnosis:
Diagnosis of NBCCS is made by having 2 major criteria or 1 major and 2 minor criteria.

The major criteria consist of the following:

1.more than 2 BCCs or 1 BCC in a person younger than 20 years;
2.odontogenic keratocysts of the jaw
3.3 or more palmar or plantar pits
4.ectopic calcification or early (<20 years) calcification of the falx cerebri
5.bifid, fused, or splayed ribs
6.first-degree relative with NBCCS.

.
The minor criteria include the following:

1.macrocephaly.
2.congenital malformations, such as cleft lip or palate, frontal bossing, eye anomaly (cataract, colobma, microphtalmia, nystagmus).
3.other skeletal abnormalities, such as Sprengel deformity, pectus deformity, polydactyly, syndactyly or hypertelorism.
4.radiologic abnormalities, such as bridging of the sella turcica, vertebral anomalies, modeling defects or flame-shaped lucencies of hands and feet.
5.ovarian and cardio fibroma or medulloblastoma (the latter is generally found in children below the age of two).
People with NBCCS need education about the syndrome, and may need counseling and support, as coping with the multiple BCCs and multiple surgeries is often difficult. They should reduce UV light exposure, to minimize the risk of BCCs. They should also be advised that receiving Radiation therapy for their skin cancers may be contraindicated. They should look for symptoms referable to other potentially involved systems: the CNS, the genitourinary system, the cardiovascular system, and dentition.

Genetic counseling is advised for prospective parents, since one parent with NBCCS causes a 50% chance that their child will also be affected.

Treatment:
Although there’s no cure, the carcinomas can be treated by surgery, lasers or photodynamic therapy, which reduces scarring.

If there’s a family history of the syndrome, it’s possible for family members to be tested to see if they carry the faulty gene.

Those with Gorlin syndrome are now advised to avoid – or to take advice before undergoing – any radiation treatment, as it’s thought it may exacerbate the condition.

Treatment is usually supportive treatment, that is, treatment to reduce any symptoms rather than to cure the condition.

*Enucleation of the odontogenic cysts can help but new lesions, infections and jaw deformity are usually a result.
*The severity of the basal cell carcinoma determines the prognosis for most patients. BCCs rarely cause gross disfigurement, disability or death .

*Genetic counseling

Advice and support:-
•Gorlin Syndrome Group
•Tel: 01772 496849
•Email: info@gorlingroup.org
•Website: www.gorlingroup.org

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/gorlinsyndrome1.shtml
http://en.wikipedia.org/wiki/Nevoid_basal_cell_carcinoma_syndrome
http://ghr.nlm.nih.gov/condition/gorlin-syndrome
http://dermnetnz.org/systemic/gorlins.html

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