Archive for September, 2008

Acne: Uncommon Association

They are miscellaneous groups of diseases which coexist with acne . (1) Acne excoriee: This usually occurs in females. Two types are there, first without any inflammatory lesion and the other with mild primary inflammatory acne lesions. This is usually seen in a female who ‘fiddle’ with the skin and exacerbate the small lesion. Contact dermatitis should be excluded. Patient commonly suffer from personality or psychological problem.

Read more...

Check Your BMI & Health Status

Here is a ready for checking (BMI) list. In the first left column your height in centimeters and to the right of that column your body weight. The nos. 17,18.5, 20, 22, 25, 30, 35 and 40 denotes BMI. The BMI of 18.5 to 30 is the normal range. BMI above 30 is obesity and not good for health. BMI below 18.5 is underweight, it is also not good for health.

If your weight and height do not match in the list you can calculate your own BMI by the following formula:

Body Mass Index or BMI (Quetelet’s index)

Weight (in kg)

=————————-

Height ²(in meters)

Acne: Severe Forms (The Other Four)

Here remaining four severe forms of acne are discussed:

(3) Gram-Negetive Folliculitis: This is a complication of long term antibiotic therapy for treatment of acne. Usually oral antibiotic are responsible and less commonly topical antibiotics. Common presentation is sudden eruption of multiple, follicular pustules (with pus ) or nodules. Examination of samplings reveals gram-negative organisms like klebsiella, proteas, Escherchia coli (e.coli) or pseudomonas. Treatment is stopping of antibiotics and replace them with ampicillin (250mg four times/day) or trimethoprime (600mg/day). But relapses are common and response is slow. So nowadays isotretinoin is the treatment of choice, with this relapses are less common.

(4) Pyoderma Faciale: Also known as rosacea fulminans. Though it is a variant of acne it is more related to rosasea. This is severe form of facial dermatosis. It is uncommon and occurs by suddenly producing eruptions of pustules and nodules, mainly in face. Common age group is 20-40 years of females, usually followed by stress; comedones are rare and there is no systemic involvement. Pyoderma faciale is reported to be associated with daily high dose of vitamin B complex and with Chron’s disease, but the cause of association is not known.

Treatment is with minocycline (100-200mg/day) and intra-lesional steroids. But the treatment of choice is oral isotretinoin 0.5mg/kg/day for 4-6 months. To reduce exacerbation oral prednisolone (0.5 to 1mg/kg/day) is used and tapered to zero over 4 weeks should be given. The prednisolone should be started 2-3 weeks before starting isotretinoin. Other alternative is metronidazole and dapsone.

(5) SAPHO syndrome: SAPHO is sinuvitis, acne, pustulosis, hyperostosis and osteitis. It is associated with recurrent chronic multifocal osteomyelitis which have skin disorders. Severe acne is one of the less frequently associated disorder. This may due to immunological reaction to a particular bacterial antigen.

(6) Vasculitis/pyoderma Gangresisum acne: This occurs in otherwise mild acne patients. There is sudden onset of severe vasculitic and pyoderma gangrenosum like lesions. There is severe scarring as a consequence. The cause of this devastating acne may be due to immunological reaction to P.acnes. These patients do not respond to isotretinoin but can be controlled to some extent by oral steroids and azathioprine (200mg/day) it given for 2-3 moths.

Acne: Severe Forms

There are mainly six severe forms of acne. They are (1) acne conglobata, (2) acne fulminans, (3) gram-negative folliculitis, (4) pyoderma faciale (also known rosasea fulminans), (5) SAPHA syndrome and (6) pyoderma gangrenosum acne.

The first two are discussed here:

(1) Acne conglobata: This is very uncommon but very severe form of acne. This is particularly seen in males and usually occurs in the trunk and upper limbs. Unlike common acne, facial lesions are less common in acne conglobata. This type of acne starts in early teens and increases in severity in second and third decade. This is characterized by multiple inflammatory papules and tender (painful) nodules. They frequently fuse together to form draining sinuses (sinus is a channel with opening outside). Large scaring and multiple blackheads are also seen. There may be malignant (cancerous) change in the scar. Rarely it is seen with folliculitis decalvans which is very rare and chronic progressive hair disease that produce scaring alopecia (baldness of head). There is extensive scaring. Familial cases of acne conglobata has been reported. It may persist up to the age of 40-50 years.

Treatment is very difficult. Treatment can be of long term high dose antibiotics, dapsone (an anti-leprosy drug) and topical therapy (local therapy). Oral isotretinoin is the treatment of choice, which is given for 4-6 month at the dose of 1mg/kg/day. It is combine with antibiotics like erythromycin or trimethoprim. Short and intermittent courses of oral steroids can be used. Some time surgery may be required.

(2) Acne Fulminans: This was previously described as ulcerative form of acne conglobata. This is also very uncommon. This is immunologically induced systemic disease, antigen of which is P. acnes. The patients are usually young males and they suddenly develop extensive inflammatory lesions, mainly on trunk. The patients also suffer from fever, joint pain, lack of appetite, weight loss and lethargy. Bone involvement is common. There is enlargement of spleen. Bone involvement is usually in the form of osteolysis (bone erosion) which can be seen in x-ray. The prognosis of bone lesion are very good.

Testosterone treatment and oral isotretinoin can induce acne fulminans. Acne fulminans like lesion is seen in Epstein-Barr virus infection, so patients with sudden exacerbation of acne should be checked for infectious mononucleosis (caused by Epstein-Barr virus)

Treatment is oral prednisolone (steroid) 0.5 to1mg/kg/day and gradually tapered to zero in six weeks. Bone pain, fever and lethargy are treated symptomatically with salicylates (aspirin) and physiotherapy. For underlying skin lesion oral antibiotics are required. Crusts have to be removed with emollient oil which is followed by use of a steroid and antiseptic cream for 2-3 weeks.

Treatment of acne & Acne Scar

Acne can be a major problem in adolescence. Cause of acne is mainly due to four reasons namely excess sebum production (seborrhea), formation of comedones (comedogenesis), inflammation and presence of bacteria propinibacterium acnes.

Acne cream treatment is one of the best forms of treatment. It is used for treatment of acne. Acne creams can be of antibiotic to kill the causative bacteria of acne i.e. propinibacterium acnes or it may be of keratolytic property (peeling effect) like benzoyl peroxide. Benzoyl peroxide is mainly keratolytic, but it has some antibacterial property as well.

Read more...

Physiological & Environmental Factors That Influence Acne

The following are the physiological and environmental factors that may help or aggravate acne: (1) Diet: A large number of foods are blamed for acne, like pork fat and chocolate, but there is no scientific proof. Chocolate have no influence on acne whatsoever, severe diet restriction reduces seborrhea, but this is not a routine treatment. Several studies have been done about diet and acne. A study was done in Papua New Guinea and Ache­­­ hunters in Paraguay and in the study not a single male or female was found with acne, and it was proposed that diet was responsible for that. But since the above populations live in close communities so genetic factors also must be important. The authors of the study suggested that western diet has a high glycemic index (diet rich in food which trigger insulin and insulin-like growth factor secretion). This induces seborrhea and comedones and acne. Acne also occurs less frequently in Japan, Zambia and Nigeria, where diets are different from that of western countries. But lower incidence of acne may be due to genetic and other environmental factors.

Read more...

4th Cause of Acne (out of 4 main causes)

The exact mechanism of inflammation in acne is not clear. A comedone is present in about 88% of inflamed papules and duct rupture is seen in one third of papular in 36 hours after the onset of inflammation. But two third of ducts are ruptured by 72 hours. Inflammatory mediators (interleukins, tumor necrosis factor TNF & prostaglandins) move through the duct into the dermis. The inflammation in dermis is not produced by bacteria but it is most likely due to inflammatory mediators that diffuse from follicles which are produced by the microorganism P. acnes.

Read more...

3rd Cause of Acne (out of 4 main causes)

Acne is not infectious. But three major organisms have been identified and isolated from the surface of skin and from pilocebaceous duct of patients with acne. They are propionibacterium acnes (P.acne), staphylococcus epidermidis and malasazzia furfur (causative agent for acne rosasae ). Propionibacterium has three subgroups and they are P. acnes, P. granulosum and P. avidum. P. acnes is most important in pathogenesis & to lesser extent P. granulosurm are also involved.

Read more...

2nd Cause of Acne (out of 4 main causes)

An important cause of acne is ductal hyper cornification that can be seen as microcomedones histologically. Clinically they can be seen as blackheads, whiteheads and macrocomedones. There is strong correlation between acne and number & size of microcomedones. Comedones are due to abnormal proliferation and differentiation of ductal keratinocytes . They are due to retention of hyper proliferating ductal keratinocytes . The hyper proliferation has been confirmed by an increase in H-thymidine labeling of comedones.

Read more...

Causes of Acne

There are four major causative factors involved in development of acne:

1. Seborrhea (excess production of sebum)
2. Comedogenesis (comedo formation due to hyper-cornification of pilosebaseous glands).
3. Colonization of pilosebaceous duct with P. acnes (Propionibacterium acnes).
4. The production of inflammation.

At first we will discus the first cause i.e. Seborrhea.

(1) Seborrhea:

Patients with excess sebum production complain of greasy skin (seborrhea). For development of acne active functional sebaceous glands are required. Acne patients male or female on an average secrete more sebum than normal person and there is strong correlation between acne severity and sebum secretion. Normal person secrete about 0.7µg of sebum per square centimeter per minute. Patient with mild acne secrete about 1.2µg, moderate patients secrete about 1.5µg and severe acne patient secrete more than 1.8µg/cm2/minute. Sebaceous activity is dependent on androgenic sex hormone of gonadal or adrenal origin. So, high levels of sebum may be due to high androgen production, increase availability of free androgen due to less sex hormone binding globulin (SHBG) and increased capacity of the intracellular receptor to bind androgen.

Plasma testosterone (male sex hormone) levels are not high in males with acne. But in females there may be high or low testosterone level. But most studies have shown that SHBG are below normal, consequently free testosterone level is above normal. In many studies it is found that patients with acne some have high testosterone level. Some of them have low SHBG, some of the patients have high free testosterone level. Androgenic hormonal balance is disturbed to some degree in 50% to 75% of the patients with acne. But at least a quarter of the cases there is no hormonal imbalance. If acne is only related to systemic hormone levels, than acne should be present in back, face and chest. But it is seen only on face.

Sebum secretion varies from follicle to follicle. In acne patients the sebum is heterogeneous but in normal persons sebum is homogenous. From the above fact it is clear that some of the follicles are prone to acne. There is increased 5-alpha-reduction of testosterone to its active metabolite 5-alpha-DTH, & this is supported by high 5?-reductase activity in acne prone regions and abnormally high amount of 5-alpha-androstenidiols in the urine of female acne patients.

Androgen action on sebaceous gland may be independent of serum hormone levels. There are two forms of 5-alpha-reductase, type I and type II. 5-alpha-reduetase Type I is responsible for acne for two reasons. Firstly fenesteride which is an inhibitor of 5-alpha-reductase Type II, do not reduce sebum production. Secondly, patients with deficiency of 5-alpha-reductase II have normal sebum production. The above points prove that 5-alpha-reduetase Type I is responsible for acne.

In clinical practice it not required to check for endocrinopathy (pathology of hormone producing glands) except for females with sudden severe acne which is not responding to conventional treatment.

Finally acne may be due to change in skin lipid composition irrespective of sebum secretion . Sebum consists of mixture of wax, cholesterol, squalene, sterol esters, triglycerides and polar lipids. As the sebum passes through pilosebaseous duct, bacteria mainly P. acne hydrolyze (break) triglycerides into Free Fatty Acids (FFA). The lipids may be responsible for ductal hyper-cornification or may be used by bacteria for growth. Samplings from acne patients have shown that they have higher levels of squalene and wax, lower levels of fatty acids and more common occurrence of particular free fatty acids. In acne patients linoleic acid (a free fatty acid) is reduced significantly in comedonal lipids and this may be related to hyper cornification of pilosebaseous duct.