Tuesday, March 13, 2012

How to Tell the Difference between Scalp Psoriasis and Dandruff



Ayushya Varsha is offering a Psoriasis treatment kit which is a combination of brands available in the market packaged  into one based on experiences through patients.

How to Tell the Difference between Scalp Psoriasis and Dandruff

Two flaky heads are never the same – especially when one is caused by psoriasis and the other is dandruff. It is often difficult to tell them apart as they both share the same visible symptoms of white and grey flakes of dead skin and they both itch. However, make no mistake about it, they are two different scalp problems and require their own treatment approach. So, do you have scalp psoriasis or dandruff? Here are the key things you should know and look for to know the difference.

Difference I: They have different root causes
Whilst scalp psoriasis and dandruff are both caused by a high skin turnover rate, they have different underlying causes. In both conditions, the replacement process by which dead skin cells are shed to make room for new cells is sped up, and so they clump together to form big clusters. However, whilst the scales produced by psoriasis are reminiscent of dandruff flakes, that is the only similarity between them.
Scalp psoriasis is first and foremost a genetic condition that is deeply rooted in the immune system. Sometimes it is inherited from your parents – one naughty little gene can start the trouble – and at other times it can appear out of nowhere. If you have existing psoriasis on other body parts, you are even predisposed to having an outbreak of scalp psoriasis if you hurt your head. This process is known as the Koebner phenomenon, and it describes how psoriasis can spread to an area of skin injury – for example, if your cat scratches your forehead, if your head gets sunburnt on the beach or if you knock it on the doorframe.
However, the shedding of dead skin cells that is at the heart of dandruff is reported to have altogether different causes. Some dermatologists point their fingers at a little fungus called Malassezia. Everybody has minute amounts of this yeast, particularly in greasy areas where skin oils build up (on the scalp and the upper torso), but for some individuals it develops into dandruff. This yeast feeds off the skin oils and secretes oleic acid, which triggers the scalp to bump up its production of skin cells, which leads to dandruff. Other reasons that have been listed include hormonal imbalances (as it normally starts after puberty, when hormones are going haywire), irregular hair brushing, infrequent shampooing, dry skin and stress.

Difference II: They look different
The second major difference between the two conditions is their appearance and the locations where they surface. You don’t need to have a trained eye to see the dissimilarity!
Firstly, whilst dandruff normally appears where the hair grows, scalp psoriasis has no bounds. It can extend beyond the hairline and into the forehead, as well as onto the back of the neck and around the ears.
Secondly, the actually flakes are different. The scales that are produced by scalp psoriasis are generally small and may even look powdery with a silvery sheen. However, dandruff flakes are usually bigger and more “built up”, like a section of roof tiling. There might be a degree of overlapping, particularly in cases of severe scalp psoriasis when the scales are thicker and form “crusts”, but usually this key visual difference between the two is present.
Thirdly, scalp psoriasis is characterized by inflammation and redness, whereas dandruff is not. Sometimes the itchiness that dandruff causes makes some people scratch their heads until their scalps glow red, but its not the same as the inherent red patches with psoriasis.

Difference III: They (might) need different treatment
Since the symptoms are alike, the first line of treatments for scalp psoriasis and dandruff are sometimes similar. However, if the cases are particularly stubborn, they require different approaches. Psoriasis in particular may be resistant to regular treatments due to its genetic nature.
Both scalp conditions normally respond well to certain medicated shampoos which contain coal tar and salicylic acid. This type of acid is great for de-scaling and smoothing over patches of skin. They are also normally available over-the-counter.
For severe dandruff, you might be prescribed an anti-yeast shampoo containing either selenium sulphide, or ketoconazole. Both of them are natural born killers when it comes to the tiny fungus living on your head.
However, anti-yeast shampoos will do nothing for your psoriasis (unless you have an existing yeast condition that is exacerbating your psoriasis!). For severe cases of scalp psoriasis, you might be prescribed a topical steroidal ointment or a few sessions of phototherapy with ultraviolet (UV) light.
Having either scalp psoriasis or dandruff can be very embarrassing, especially when you’re wearing dark clothing and the flakes stand out like little stars at night. However, it’s not the end of the world. By diagnosing your condition properly, you can determine which products to use and which approach works best. Don’t forget to browse our site for psoriasis treatment ideas.

Sunday, March 11, 2012

MANMATI'S SUCCESS STORY OF INFERTILITY


CLINICAL STUDY on LIV. 52 HB
Summary: In this case a 25 year female who was infertile presented for infertility having married for 9 years. In course of 5 months of treatment which includes 4 months on Liv. 52 HB as in the study the patient turned negative on status of Hepatitis B antigen. The AST and ALT values were reduced to normal values within 2 months of initiation of the treatment. The patient is 5 months through her pregnancy and has tolerated the drug well with no missed abortion or any associated signs of discomfort.
 THE CASE STUDY-
The drug Liv. 52 HB has been successfully evaluated in a study which began  under the guidance of Dr. P. Patki (Head - Medical Services & Clinical Trials - R&D, The Himalaya Drug Company). The following will detail the study as it has progressed to reach its objectives.
The patient (Manmati Shah) a 25 year old Hindu female reported along with her husband (Vijay Kr. Shah), a resident of village Karsua, Post Waidhan, District Singrauli, Madhya Pradesh for infertility. The history of the presenting comlaint was as old as 9 years.
The initial treatment included a mixed approach and used both modern and ayurvedic medicines for treatment. The initial prescription with the treatment starting 12th of February, 2011 and the first follow up on 24th, February, 201 was  as follows –
Rx
Tab Liv. 52 - DS
2 TID x 15 days
Tab PANCH NIMBADI BATI
2 TID x 15 days

Syp. DASHMOOLARISHTHA
15 ML BID WITH 15ML FRESH WATER x 15 days
Cap OXYTARD
1 BID x 15 days
Syp. DASHMOOLARISHTHA
10 ML BID WITH 15ML FRESH WATER x 15 days
PROTEIN POWDER
2 TSP. WITH MILK TWICE DAILY
FOLLOW UP 1  -  (24/02/2011)
Rx
Tab Liv. 52 - DS
2 QID x 50 days
Syp. PUNARNAVARISHTHA
15 ML BID WITH 15ML FRESH WATER  x 50 days
Cap OXYTARD
1 BID x 50 days
Cap MAP-DSR
1 OD x 50 days
Tab. LAMIVIR - HBV
1 OD x 50 days
Tab. BALOX
1 BID X 10 days


Fowllowing this period from 18th of March the treatment was further revised as follows limiting the medications only to Ayurveda –
FOLLOW UP 2 -  (18/03/2011)
Rx
Cap. LIV. 52 HB
2 BID x 30 days
Syp. TRIGUNASAVA
10 ML BID WITH 10ML FRESH WATER  x 30 days
Cap OXYTARD
1 BID x 30 days
FOLLOW UP 3  -  (20/04/2011)
Rx
Cap. LIV. 52 HB
2 BID x 60 days
Syp. TRIGUNASAVA
10 ML BID WITH 10ML FRESH WATER  x 60 days
Cap OXYTARD
1 BID x 60 days




FOLLOW UP 4  -  (25/05/2011)
The treatment was continuing. This included evaluation of confirmation of pregnancy status and AST, ALT, HbsAG and HCV status.
FOLLOW UP 5  -  (19/06/2011)
Rx
Cap. LIV. 52 HB
2 BID x 60 days
Syp. TRIGUNASAVA
10 ML BID WITH 10ML FRESH WATER  x 60 days
Cap OXYTARD
1 BID x 60 days
FOLLOW UP 6  -  (27/07/2011)
The treatment was continuing. This included evaluation of confirmation of pregnancy status and AST, ALT, HbsAG and HCV status.
At this point after having attained the positive turn in AST and ALT values as early as in May following 2 months of use in July a Negative status has also been attained for Hepatitis B.








Future course as adopted -
The patient remains under observation and the new born shall be evaluated at birth for HBsAg Status to confirm safety during pregnancy and also evaluate the prevention of placental transmission of Hepatitis Antigen across to the developing foetus.
Objectives achieved thus far –
1.)    In 4 months of time frame Hepatitis stus has been achieved as Negative.
2.)    AST and ALT values returned to normal in 2 months of time.
3.)    Dependence on a coalesce use of an antiviral drug as lamivudine is not required since the status has been achieved independent of lamivudine once Liv. 52 HB was initiated.
4.)    Safe to use during pregnancy by initial observations as no adverse events were reported except for occassional bloating sensations of the stomach.
Further continuing evaluations –
1.)    The status of the baby at birth with respect to HbsAg.
2.)    Since AST and ALT values have been attained at a normal value and are sustained; a long term use may have a potential impact on HCV status as well.
3.)    The patient shall remain under observation for 2 years with observations made 6 monthly since studies show reversal of Hepatitis B status as positive.
4.)    Since patients with a dual status of Hepatits B and Hepatitis C positive are at a long term risk of developing Liver Cancer, the extended evaluations may lend a scope into evaluating a possible role in Liver Cancer.




Saturday, March 10, 2012

ONYCHOMYCOSIS - NAIL FUNGAL INFECTION

ONYCHOMYCOSIS - NAIL FUNGAL INFECTION


The nail infections of the fungal type are the thickening and discoloration of the toe nails. There are certain types of fungi that feed on the toe nails, that is, keratin. Fungi grow in dark and moist environments and some footwear are ideal for the growth of the fungi. When your nail catches a fungal infection, it gets chalky, brown and yellow.

The nail would become brittle. The nail will become loose and thicken and it is likely that the infection would spread to the other nails too. You must see the skin expert for advice if you tend to have thickened nails. Nail infection can happen at any age although it happens with increasing age. Attention must be paid to the changes in nails and this may lead to local infections too.

There are quite a variety of treatments available for fungal infections of nails and these treatments are general as well as surgical. A thickened nail has to undergo a diagnosis.

Lacquers, ointments and creams are to be applied topically and these can be bought from the pharmacist while other medicines would need a prescription. Many nails are not resolved even with the application of drugs. The nails have to be cut short for the drug to get penetrated. This is generally done with the help of a file.  A small nail drill can also be used. There are tablets available for the infection and these can be taken orally. However, only taking tablets would not help in the cure as ointments have to be applied. Surgery is often used for removing a fungus affected nail. The nail is sometimes fully removed and then the new nail can be treated with drugs.

A nail infection is not much harmful but it should be stopped from getting enhanced and if regular and proper care is taken, it would be easier to come out of this nail problem.

Friday, March 09, 2012

URTICARIA - SHEETAPITTA


Urticaria

This is a vascular reaction of the skin characterized by the transient appearance of elevated patches which are redder of paler than the surrounding skin and often attended by itching. In Ayurveda this is called Shita pitta.
Allergens, taking cold bath immediately after exercise, when the body is hot , and mental excitement are the most important factors for the causation of this disease .Intestinal worms and exposure to the cold wind often cause Urticaria .these patches appear all over the body suddenly or gradually. There may be severe itching .The patient is usually constipated He may get attacks of cold, cough, bronchitis and stomach disorder.

Monday, March 05, 2012

ALOPECIA

ALOPECIA

Hair loss… 
 
Hair loss is a problem of many people and most of them get frustrated because they spent a lot for things promoted widely via television and media channels. Commercial products of 100% efficacy cannot be a cure for each and every type of alopecia because there are so many triggerring factors causing alopecia or hair loss. [hereditary, stress, hormones, medicines, irregular food habits, environment etc]. As per Ayurveda the answer is Prakriti [basic nature]. Just like human fingerprints each individual has unique basic nature so the treatment and its result may vary from person to person. (PRAKRUTI ASSESSMENT). Ayurveda is India's traditional, natural system of medicine that has been practiced for more than 5,000 years. Ayurveda means the "science of life".

World Health Organization [WHO] has recognized Ayurveda as prime alternative therapy. Ayurveda is the ancient Indian medical science, the origin of which can be traced back from Vedas which are the ancient books of knowledge, or science, from India.

Ayurveda believes in three doshas which are vata, pitta, and kapha.
Each person has a unique blend of the three doshas, known as the person's prakriti [basic nature].
Due to this Ayurvedic treatment is always individualized. In Ayurveda, a disease is viewed as a state of imbalance in one or more of a person's doshas.

'Alopecia' is a medical terminology which is used for various types of hair loss. There are different types of alopecia like androgenetic alopecia, diffuse alopecia, traction alopecia, cicatricial alopecia etc. But among all, alopecia areata is a highly unpredictable, autoimmune skin disease resulting in the loss of hair on the scalp and elsewhere on the body.

Perfect etiology of alopecia areata is not known but medical science believes that the affected hair follicles are mistakenly attacked by a person's own immune system (white blood cells), resulting in the arrest of the hair growth stage.

Alopecia areata -

1.) usually starts as one or more small, round, smooth bald patches on the scalp.
2.) It can progress to total scalp hair loss (alopecia totalis)
3.) complete body hair loss (alopecia universalis).

(LIFE TIME SKIN CLINIC REGISTRATION)

Saturday, March 03, 2012

FREE ONLINE SKIN CLINIC



FREE AYURVEDIC SKIN CLINIC

This is an online Ayurvedic skin clinic where you can consult for free and buy your prescriptions online by paying through your email. This will also feature articles on skin issues from time to time.

LEUCODERMA

Vitiligo is a widespread disorder now a days. Generally it happens due to autoimmunity which is the most known reason. Depigmentation of skin happens first which acquires skin area in shape of a spot or patch forming vitiligo spots. No one can predict its spreading without medicines. This all depends on how far a person’s immunity is affected as per our studies.

Facial vitiligo is a very bad situation in the life of a vitiligo patient. As the face gets a white spot it almost disturbs the psychosomatic state of the person’s mind. One can feel embarrassed and get into deep depression after onset of facial vitiligo.

Signs and symptoms

The most notable symptom of vitiligo is depigmentation of patches of skin that occurs on the extremities. Although patches are initially small, they often enlarge and change shape. When skin lesions occur, they are most prominent on the face, hands and wrists. Depigmentation is particularly noticeable around body orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Some lesions have hyperpigmentation around the edges. Patients who are stigmatised for their condition may experience depression and similar mood disorders.

Treatment

There are a number of treatments that treat vitiligo. Treatment options generally fall into four groups.

UVB phototherapy

Exposing the skin to UVB light from UVB lamps is the most common treatment for vitiligo. The treatments can be done at home with a domestic UVB lamp or in a clinic. Normally a small lamp is needed if the spot is small. Treatment can take a few weeks if the spots are on the neck and face and if they existed not more than 3 years. If the spots are on the hands and legs and have been there more than 3 years, it can take a few months. In a clinic the treatments are done 2-3 times a week, and at home every day, which makes the home treatments more effective. If the spots are on a large area of the body, full body treatment in a clinic or hospital will be needed. Both UVB broadband and UVB narrowband lamps can be used.[8][9] However these treatments are unreliable at best.[citation needed] There is no treatment that totally repigments the skin. Adding a psoralen, a photosensitizer that increases the effect of the UV light, can aid in partial repigmentation.
Studies have shown that immunomodulator creams such as Protopic and Elidel also cause repigmentation in some cases, when used with UVB narrowband treatments. A 1997 report suggests that combining vitamin B12 and folic acid supplements with sun exposure caused repigmentation in 52% of cases.

PUVA phototherapy

Ultraviolet light (UVA) treatments are normally carried out in a hospital clinic. Psoralen and ultraviolet A light (PUVA) treatment involves taking a drug which increases the skin's sensitivity to ultraviolet light. The skin is then exposed to high doses of ultraviolet A light. Treatment is required twice a week for 6–12 months or longer. Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn-type reactions or skin freckling.
Narrowband ultraviolet B (UVB) phototherapy is now used more commonly than PUVA as it is less damaging to the skin. 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.
A few preliminary trials have been carried out using the herb ginkgo biloba. A small-scale open-label pilot clinical trial found the progression of vitiligo stopped in all participants and indicated an average repigmentation of vitiligo lesions of 15%. The authors concluded that "larger, randomized double-blind clinical studies are warranted and appear feasible".

Transplanting melanocytes

In October 1992, a scientific report was published of successfully transplanting melanocytes to vitiligo affected areas, effectively repigmenting the region. The procedure involved taking a thin layer of pigmented skin from the patient's gluteal region. Melanocytes were then separated out to a cellular suspension that was expanded in culture. The area to be treated was then denuded with a dermabrader and the melanocytes graft applied. Between 70 and 85 percent of patients experienced nearly complete repigmentation of their skin. The longevity of the repigmentation differed from person to person.

Skin camouflage

In mild cases, vitiligo patches can be hidden with makeup or other cosmetic camouflage solutions. If the affected person is pale-skinned, the patches can be made less visible by avoiding sunlight and sun tanning of unaffected skin.

Reversal

The traditional treatment is the application of corticosteroid cream.

De-pigmenting

In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol or hydroquinone may be considered to render the skin an even colour. The removal of all the skin pigment with monobenzone is permanent and vigorous sun-safety must be adhered to for life to avoid severe sun burn and melanomas. Depigmentation takes about a year to complete.

Non-segmental

In non-segmental vitiligo (NSV), there is usually some form of symmetry in the location of the patches of depigmentation. New patches also appear over time and can be generalized over large portions of the body or localized to a particular area. Vitiligo where little pigmented skin remains is referred to as vitiligo universalis. NSV can come about at any age, unlike segmental vitiligo, which is far more prevalent in teenage years.

Classes of non-segmental vitiligo include:

 Generalized Vitiligo - the most common pattern, wide and randomly distributed areas of depigmentation
Universal Vitiligo - depigmentation encompasses most of the body
Focal Vitiligo - one or a few scattered macules in one area, most common in children
Acrofacial Vitiligo - fingers and periorificial areas
Mucosal Vitiligo - depigmentation of only the mucous membranes

Segmental

Segmental vitiligo (SV) differs in appearance, etiology and prevalence from associated illnesses. Its treatment is different from that of NSV. It tends to affect areas of skin that are associated with dorsal roots from the spine and is most often unilateral. It spreads much more rapidly than NSV and, without treatment, it is much more stable/ static in course and it is associated with auto-immune diseases and a very treatable condition that responds to topical treatment.
Vitiligo is a disorder characterized by patchy loss of skin pigmentation due to immune attacks on melanocytes. While there is no significant proof or evidence for this, many doctors believe that it can be caused by defects in many genes. Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. The immune system genes are associated with other autoimmune disorders. In one case, the gene TYR, which makes the melanocyte more susceptible to the immune system in vitiligo, also makes the melanocyte more susceptible to the immune system in the skin cancer malignant melanoma. So people with vitiligo caused by the TYR gene are less likely to have malignant melanoma. A genomewide association study found 10 independent susceptibility loci for generalized vitiligo, responsible for 7.4% of the genetic risk. Some patients had vitiligo alone; others had generalized vitiligo with other autoimmune diseases. Most loci were associated with both forms. (The exception was PTPN22, which was only associated with generalized vitiligo.) In the MHC region, which controls the immune system, major association signals were identified in the class I gene region (between HLA-A and HLA-HGC9) and class II gene region (between HLA-DRB1 and HLA-DQA1). Outside the MHC region, association signals were identified near RERE, PTPN22, LPP, IL2RA, GZMB, UBASH3A and C1QTNF6 genes, which are associated with other autoimmune diseases. TYR encodes tyrosinase, which is not a component of the immune system, but is an enzyme of the melanocyte that catalyzes melanin biosynthesis, and a major autoantigen in generalized vitiligo. The major alleles of TYR are associated with vitiligo, and the minor alleles are associated with malignant melanoma. Vitiligo-associated 402R tyrosinase may be more efficiently presented to the immune system. Melanoma-associated 402Q may fail to be identified by the immune system. The transcriptional profile of melanocytes from vitiligo patients have been studied. Oligonucleotide microarrays containing approximately 16,000 unique genes were used to analyse mRNA expression in melanocytes from vitiligo patients and age-matched healthy controls. In total, 859 genes were identified as differentially expressed. Vitiligo is sometimes associated with autoimmune and inflammatory diseases,commonly thyroid overexpression and underexpression. A study comparing 656 people with and without vitiligo in 114 families found several mutations (single-nucleotide polymorphisms) in the NALP1 gene.The NALP1 gene, which is on chromosome 17 located at 17p13, is on a cascade that regulates inflammation and cell death, including myeloid and lymphoid cells, which are white cells that are part of the immune response. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity. Polymorphisms of CD4 were shown to be associated with the vitiligo and other autoimmune diseases like type I Diabetes Mellitus.
Among the inflammatory products of NALP1 are caspase 1 and caspase 5, which activate the inflammatory cytokine interleukin-1β. Interleukin-1β is expressed at high levels in patients with vitiligo. There are compounds which inhibit caspase and interleukin-1β, and so might be useful drugs for vitiligo and associated autoimmune diseases. In one of the mutations, the amino acid leucine in the NALP1 protein was replaced by histidine (Leu155->His). The original protein and sequence is highly conserved in evolution, and found in humans, chimpanzee, rhesus monkey, and bush baby, which means that it is an important protein and an alteration is likely to be harmful. Addison's disease (typically an autoimmune destruction of the adrenal glands) may cause vitiligo.