The first step is to decide if the hair loss is accompanied by inflammation and scarring of the scalp. The signs of inflammation are redness and scaling and the tell tale sign of scarring is destruction . . . → Read More: My hair is falling out. Why am I loosing my hair?]]> I am going to describe how a dermatologist will approach a patient with the problem of hair loss.

The first step is to decide if the hair loss is accompanied by inflammation and scarring of the scalp. The signs of inflammation are redness and scaling and the tell tale sign of scarring is destruction of the hair follicle itself.

Most hair loss problems can therefore be divided into scarring hair loss (alopecia) and non scarring alopecia.

In the case of scarring alopecia a scalp biopsy will most likely be required to diagnose the cause of the scarring alopecia. A biopsy is a small surgical procedure where a 3-5mm piece of skin is removed from the scalp and 1 or 2 sutures are inserted to close the little wound.

In the case of non-scarring alopecia further subdivision of the non-scarring alopecia is based on the distribution of the hair loss on the scalp.

If the hair loss occurs in round isolated patches, Alopecia Areata is the most likely diagnosis.

If the hair loss occurs diffusely over the whole scalp, Telogen Effluvium is the most likely diagnosis.

If the hair loss occurs in the classic male pattern baldness or equivalent female pattern baldness distribution, Androgenetic Alopecia is the most likely diagnosis.

Although there are other, less common patterns, the vast majority of hair loss cases will follow one of the above patterns.

I will post articles about the specific hair loss patterns in future.

The word Scabies is derived from the Latin word Scabere, which means "to scratch".

Scabies is caused by infection of the skin with a small (0.5mm) insect called Sarcoptes Scabiei. The infection is most often spread by direct skin contact with an infected person or less often by sitting or sleeping in a . . . → Read More: Scabies infection]]>

The word Scabies is derived from the Latin word Scabere, which means "to scratch".

Scabies is caused by infection of the skin with a small (0.5mm) insect called Sarcoptes Scabiei. The infection is most often spread by direct skin contact with an infected person or less often by sitting or sleeping in a space where an infected person has been. Once the female mite is on the skin it burrows into the top layer of the skin where she will lay her eggs.

The symptoms of Scabies starts a few weeks after exposure in people that have never had Scabies before. If someone had Scabies previously, reinfection can cause symptoms to appear in a few days. The rash can appear anywhere on the skin, but is more common in the skin folds areas, genital area, around the wrists, elbows, side of the hands and between the fingers. In young children the side of the feet is commonly affected. The initial sign of infection is a small, red, scaly or pearly-looking bump. Itching can be severe, especially at night. As the condition persists signs of scratching will start to dominate and eventually the affected areas start looking eczema-like.

The diagnosis of Scabies is made by scraping a red bump, mounting the scraping sample on a glass slide and then seeing the insect under the microscope. Sometimes the mite cannot be found in this way in which case the diagnosis is based on the patients symptoms and the clinical signs found on examination of the skin.

Scabies can be treated easily in most cases. Ascabiol lotion (Benzyl benzoate) is an often used treatment option. Tetmosol soap (Sulfiram 5%) is often prescribed by some practitioners, but does not work very well if used in isolation. Ascabiol lotion is applied from the neck downwards and left overnight. In the morning it is washed off. The procedure is repeated after one week.

The symptoms of Scabies might take weeks to resolve, even after the Scabies mites have been killed by treatment. This is because parts of the dead mite will remain in the skin and need to be shed off over time.

Overzealous use of Ascabiol lotion can lead to skin irritation, which is often the presenting complaint when patients come to our clinic.

Keratosis Pilaris is a hair follicle condition. It can be thought of as hair follicle eczema. It most commonly affects the hair follicles of the upper arms, but can also affect hair follicles on the upper legs and occasionally on the face and other areas.

Keratosis Pilaris affects the hair follicle in . . . → Read More: What is Keratosis Pilaris?]]>

Keratosis Pilaris is a hair follicle condition. It can be thought of as hair follicle eczema. It most commonly affects the hair follicles of the upper arms, but can also affect hair follicles on the upper legs and occasionally on the face and other areas.

Keratosis Pilaris affects the hair follicle in 2 ways. It causes the mouth of the hair follicle to become slightly elevated due to overproduction (hyperkeratosis) of skin in the area. That is why the condition feels rough to the touch. Secondly, it causes inflammation of the hair follicle, which results in the spotty reddish appearance of the affected area.

The roughness combined with the redness can be unsightly and a source of embarrassment to patients.

Like asthma and hay fever, the condition can not be cured, but it can be improved.

The roughness can be treated with a moisturiser that contains Urea or Salicylic acid. It takes a few weeks to see good results. Sometimes retinoid containing creams, like Differin cream, needs to be used in addition to the moisturiser. An achievable goal is to improve the roughness by 80%.

The redness is more difficult to treat. It improves slightly when the roughness improves, but in most cases additional anti-inflammatory preparations like mild topical corticosteroids, Protopic or Elidel must be used for short periods. An achievable goal is to improve the redness by 50%.

The keep the Keratosis Pilaris under control daily use of moisturisers, with or without a retinoid cream and intermittent use of anti-inflammatory preparations are required.

Remember, the goal of treatment is improvement and not cure.

“Red bumps with or without a superimposed pussy . . . → Read More: What are pimples?]]> From a dermatologist’s point of view the term pimple is meaningless. Some people use the term “pimples” as a synonym for Acne. Other people use the term to refer to any red bump with a superimposed pussy area (pustule) or without a superimposed pussy area (papule).

“Red bumps with or without a superimposed pussy area” can be found in a long list of skin conditions, only one of which is Acne. To confirm the diagnosis of Acne in someone presenting with “pimples” one or more of the following additional findings are required:

• Black heads (open comedomes)
• White heads (closed comedomes)
• Scarring
• Distribution of the pimples on the face, chest and back

So, if you have pimples, but none of the above findings, you probably do not have Acne!

Some dermatologists believe that Perioral dermatitis does really exist and that patients that fit the clinical picture of Perioral dermatitis has Rosacea. . . . → Read More: What is Perioral dermatitis?]]> Perioral dermatitis is a type of dermatitis that occurs only around the mouth, nose and eyes. It does not have to be present in all of the areas at the same time.

Some dermatologists believe that Perioral dermatitis does really exist and that patients that fit the clinical picture of Perioral dermatitis has Rosacea. Rosacea and Perioral dermatitis can sometimes be present in the same patient. Because it is always more likely that a patient has 1 condition rather than two, the finding of both Rosacea and Perioral dermatitis in the same patient support to the thesis that the 2 conditions are in fact the same. Furthermore, when looking at a sample of skin under the microscope, both Rosacea and Perioral dermatitis displays the same type of inflammation, knows as a granulomatous peri-folliculitis. The word granulomatous refers to a collection of macrophages (a type of white blood cell). Peri-folliculitis means that the “collection of macrophages” is lying in close proximity to a hair follicle.

Whether or not Rosacea and Perioral dermatitis are the same disease or two separate diseases is an academic question and not very important from a treatment perspective. The fact is that the clinical picture known as Perioral dermatitis is quite classic and most often easily recognizable and treatable.

Classically young female patients are affected. The rash consists of small red bumps (knows as papules) and occasionally small pimples (knows a pustules) occurring around the mouth, nose and eyes. Interestingly, a small margin of skin around the edge of the lips are always unaffected. As mentioned before not all 3 of these areas has to be affected at the same time.

More than 80% of patients with Perioral dermatitis have been applying corticosteroid-containing creams to the face, before the rash started to appear. In the remaining cases the cause is unclear, but the excessive use of facial products seem to be another common factor.

The treatment of this condition involves the elimination of all (if possible) facial products. If topical corticosteroid-containing creams have been used they should be tapered off slowly and not stopped suddenly, because this will lead to a flare-up of the condition.

The treatment of Perioral dermatitis involves the use of oral tetracycline antibiotics for a few months. Sometimes this is combined with antibiotic creams, but in general it is better to avoid as many creams as possible. Most often this approach results in complete clearance of the skin condition in a few weeks.

Perioral dermatitis is associated with the use of facial products. Most patients with Perioral dermatitis are using multiple different types of facial products. The use of corticosteroid containing creams over extended . . . → Read More: Perioral dermatitis treatment]]> Perioral dermatitis is sometimes also called Perioral-nasal-ocular dermatitis (PONOD) or periorificial dermatitis, because the rash can also appear around the nose and eyes.

Perioral dermatitis is associated with the use of facial products. Most patients with Perioral dermatitis are using multiple different types of facial products. The use of corticosteroid containing creams over extended periods are strongly linked to the development of Perioral dermatitis. One of the most important aspects of the treatment of Perioral dermatitis is therefore the gradual elimination of all non-essential facial products.

Depending on the severity of the Perioral dermatitis the above process is started while taking an oral Tetracycline antibiotic, like Minocycline, Doxycycline or Lymecycline. Normally this antibiotic must be continued for at least 3 months (or until the rash has disappeared) and is then tapered off over a 2 month period.

Paradoxically, the early phases of the treatment of Perioral dermatitis might involve using a mild topical corticosteroid cream on the face to calm down the active redness and inflammation. The most commonly used corticosteroid cream contains Mometasone furoate. This is initially applied daily until the redness subsides and then tapered off as soon as possible.

The tapering off process of the corticosteroid cream normally occurs over a few weeks. The average patient will use the corticosteroid cream daily for about 5 days, on alternate days for about 4 days, twice a week for about 2 weeks and after that maybe once or twice a month. There is however considerable variation.

While the corticosteroid cream is tapered off the oral antibiotic is continued until the rash has been absent for at least a month. Only then is the oral antibiotic also tapered off. It is extremely important that during this treatment period all non essential facial products (yes all!) must be gradually eliminated. If this is not entirely possible then try to eliminate as many facial products as you can. Only after all facial products have been stopped and the Perioral dermatitis has been clear for at least one month, can facial products be gradually reintroduced one by one.

Perioral dermatitis is normally quite responsive to the above treatment regime and most patients will experience a marked improvement in only a few days to weeks.

There are a few causes of Cradle cap, including Seborrheic dermatitis, Atopic Dermatitis and Plaque Psoriasis. Seborrheic dermatitis is . . . → Read More: What is Cradle Cap?]]> Cradle cap is a term used to refer to any red scaly rash on the scalp of babies. Cradle cap is not a medical diagnosis, but simply a descriptive term, like the term diaper dermatitis.

There are a few causes of Cradle cap, including Seborrheic dermatitis, Atopic Dermatitis and Plaque Psoriasis. Seborrheic dermatitis is the most common cause of cradle cap. Before Cradle Cap can be treated, the specific cause of the Cradle cap must first be diagnosed. To diagnose the cause of the Cradle cap your doctor will have to examine the baby from head to toe.

A concomitant rash in the skin-folds and the nappy area might indicate Seborrheic dermatitis, whereas a generally dry skin might indicate Atopic Dermatitis as the cause of the Cradle cap. Nobody knows exactly why babies develop Seborrheic dermatitis or Atopic Dermatitis. The theory is that Seborrheic dermatitis is related to the overgrowth of the yeast Pityrosporum ovale which was recently renamed Malassezia furfur. The yeast overgrows because of overactive oil glands on the scalp. The oil glands become overactive because of genetic influences or perhaps because of hormones passed to the baby from the mother.  Seborrheic dermatitis is not due to bad hygiene or a bad diet! Perhaps as many as 50% of babies born in the developed world have some degree of cradle cap.

Once the diagnosis is made, treatment can be started. The following treatment options will apply especially to Cradle cap caused by Seborrheic dermatitis.

The are really 2 aspects of Cradle cap to treat; scaling and redness. The scaling develops from the areas of redness. Once the redness is resolved the scaling will cease. Initially however, treatment is targeted at both scaling and redness.

Redness can be treated with mild topical corticosteroids. Corticosteroids is not dangerous if used correctly and sparingly. Do not let anybody tell you different, because mild topical corticosteroids can rapidly improve the condition and make your baby feel better. Mild topical corticosteroids should be applied once of twice per day while there is redness. If there is no redness do not apply any corticosteroids.

Ketoconazole containing shampoos can also help. Ketoconazole is an anti-fungal that will help to eradicate yeasts. It is a good idea to dilute the Ketoconazole shampoo perhaps 50:50 or greater initially, to make sure the shampoo does not irritate the babies skin. Use the shampoo every second day initially. Ketoconazole creams can also be applied once or twice per day to the red areas.

Scaling is treated by moisturising the skin. Many different oil and creams can be used for this. Examples include Vaseline, over-the-counter moisturizers, olive oil, borage oil, tea-tree oil, aloe gel etc.

Cradle cap due to Seborrheic dermatitis will resolve spontaneously within a few months in the vast majority of babies.

Topical Pimecrolimus (Elidel) become available for prescription around 2001. Pimecrolimus (Elidel) cream comes in one strength (1%) and is available in 30g, 60g and 100g tubes.

The most important use for Pimecrolimus (Elidel) cream is to treat Atopic . . . → Read More: What is Pimecrolimus (Elidel)?]]> Pimecrolimus (Elidel) is an immunosuppressant derived from Ascomycin. Ascomycin is produced by the fungus Streptomyces hygroscopicus.

Topical Pimecrolimus (Elidel) become available for prescription around 2001. Pimecrolimus (Elidel) cream comes in one strength (1%) and is available in 30g, 60g and 100g tubes.

The most important use for Pimecrolimus (Elidel) cream is to treat Atopic Dermatitis. The manufacturer recommends that Pimecrolimus (Elidel) should only be used for age 2yr and older, but is has been used successfully in younger children. Pimecrolimus (Elidel) works by inhibiting the molecule Calcineurin that is essential for activating T-lymphocytes. T-lymphocytes, which are white blood cells, play an active role in Atopic Dermatitis. When T-lymphocytes become activated they help to induce a flare-up of Atopic Eczema.

Pimecrolimus (Elidel) is most often used as a third line treatment for Atopic Dermatitis. First line treatment is emollients and second line treatment is topical corticosteroids. Pimecrolimus (Elidel) is often prescribed when it is difficult or impossible for eczema-sufferers to wean themselves of topical corticosteroids. The extra immunosuppressive effect of the Pimecrolimus (Elidel) should allow most patients to reduce the topical corticosteroids needed to control the dermatitis.

A comparison of Pimecrolimus (Elidel) with Tacrolimus 0.03% showed no significant differences in efficacy at 6 weeks after treatment started. Tacrolimus 0.1% is more potent that Pimecrolimus (Elidel) and 0.03% Tacrolimus.

Side effects from using Pimecrolimus (Elidel) cream are mild. About 4% of people using Pimecrolimus (Elidel) will experience a burning or stinging sensation where they apply the Pimecrolimus (Elidel). The burning sensation disappears in about 15 minutes. It only occurs in the first week or two and in active patches of dermatitis.

The long-term risks (years) of using Pimecrolimus (Elidel) is unclear. The biggest concern about Pimecrolimus (Elidel) cream is that it might raise the risk of developing skin cancers. People using Pimecrolimus (Elidel) cream should limit their exposure to sunlight. In animal studies Pimecrolimus (Elidel) speeded up the cancer-forming effects of sunlight. There have been a few people that have developed a skin cancer while using Pimecrolimus (Elidel). Four of these were skin lymphomas.

The skin cancers occurred on average 90 days after the start of therapy. It is unclear if Pimecrolimus (Elidel) caused the skin cancers or whether the skin cancers would have developed anyway. Until long-term data becomes available Pimecrolimus (Elidel) will probably remain an important third line treatment for eczema-sufferers finding it difficult or impossible to wean themselves of topical corticosteroids.