• Acne is almost always seen in the teenage years,
• severity of disease differs per individuals
• Peak severity is in the late teenage years But acne may persist into the third decade and beyond, particularly in females.

Main Problem- issues relate to under-treatment and lack of clinical interest or insight into the patient’s condition.

Aetiology or Causes-
There are three pathogenetic factors :

1. Increased sebum excretion. There is a clear relation between severity of acne and sebum excretion rate. In the complete absence of sebum, acne does not occur, however, acne may improve in the third and fourth decades despite high sebum excretion. Sebum excretion is therefore necessary for the development of acne but is not sufficient to cause acne on its own.
2. Infection with Propionibacterium acnes. This bacterium colonises the pilosebaceous ducts and acts on lipids to produce a number of pro-inflammatory factors.
3. Occlusion or blockage of the pilosebaceous unit.

Clinical features
Lesions are usually limited to

• face,
• shoulders,
• upper chest and back.
• upper arms

Seborrhoea (greasy skin) is often clinically obvious.

• Open comedones (blackheads) due to plugging by keratin and sebum of the pilosebaceous orifice, or closed comedones (whiteheads) due to accretions of sebum and keratin deeper in the pilosebaceous ducts, are usually evident.
• Inflammatory papules, nodules and cysts occur , with one or two types of lesion predominating.
• Scarring may follow.

Scars ( Source Wikipedia)
Physical acne scars - “Icepick” scars. This is because the scars tend to cause an indentation in the skin’s surface. There are a range of treatments available. Although quite rare, the medical condition Atrophia Maculosa Varioliformis Cutis also results in “acne-like” depressed scars on the face.
Ice pick scars: Deep pits, that are the most common and a classic sign of acne scarring.
Box car scars: Angular scars that usually occur on the temple and cheeks, and can be either superficial or deep, these are similar to chickenpox scars.
Rolling scars: Scars that give the skin a wave-like appearance.
Hypertrophic scars: Thickened, or keloid scars.

Before treatment.

Clinical variants of acne.

Conglobate acne refers to severe acne with many abscesses and cysts, marked scarring and sinus formation.
Acne fulminans refers to the presence of severe acne accompanied by fever, joint pains and markers of systemic inflammation such as a raised ESR.
Acne excoriée refers to the effects of scratching or picking, principally on the face of teenage girls with acne.
Infantile acne is rare and is thought to be due to the sebotrophic effects of maternal hormones on the infant.

• A mild form of acne dominated by the presence of comedones may be due to exogenous substances such as tars, chlorinated hydrocarbons or oily cosmetics.
• A primarily pustular rash may also be seen in those being treated with corticosteroids, lithium, oral contraceptives and anticonvulsants. These forms of acne are usually clinically distinct from the usual variety developing in adolescence.
• Individuals with moderate or even severe acne very rarely have any other systemic disorder. However, individuals with polycystic ovary syndrome are more likely to have severe acne, and clinical hints-for instance, menstrual irregularities-require investigation. If there is associated cutaneous virilism or other features of an androgen-secreting tumour, further investigations and expert endocrinological assessment are warranted.

Investigations
- rarely required.

Management

• Tretinoin cream.
• Benzoyl peroxide.
• Local antibiotics (clindamycin or erythromycin) are used more widely than previously
• The principal oral antibiotic is oxytetracycline, taken on an empty stomach not with food, in a dose of up to 1.5 g a day if tolerated. In general, oxytetracycline has a good safety profile even with long-term use.
• Minocycline may be used if the response to oxytetracycline is inadequate or because of the ease of dosing. It is, however, associated with autoimmune hepatitis and remains a second- rather than first-choice drug.
• Before an antibiotic is deemed not to have worked, the individual must be treated continuously for up to 3 months. If after 3 months there is little response to oxytetracycline the patient should be changed to erythromycin up to 1 g per day in divided doses. Patients need to remain under review.
• In women, oestrogen-containing oral contraceptives can be a useful adjunct in therapy. There is a small reduction in sebum secretion with oral oestrogens. An oral anti-oestrogen, cyproterone acetate, is occasionally added in doses of 50-100 mg daily on days 5-14 of the cycle to enhance the effects of sebum reduction. If these topical and systemic agents fail to produce an adequate clinical response within 3-6 months the patient should be referred for specialist opinion and consideration for treatment with isotretinoin (13 cis-retinoic acid).
• Isotretinoin has revolutionised the treatment of severe or moderate acne in patients unresponsive to other therapy.

Physical measures

1. Cysts can be incised and drained under local anaesthetic.
2. Intralesional injections of triamcinolone acetonide (0.1-0.2 ml of a 10 mg/ml solution) hasten the resolution of stubborn cysts.
3. Scarring following acne is seen a lot less commonly if patients receive adequate care. Small, deep acne scars can be excised and other forms of more extensive but shallower scars can be treated by carbon dioxide laser.
4. Dermabrassion

Photo Therapy

1. Red and Blue light
2. Photodynamic therapy
3. Laser treatment.

SUBMITTED- DR. S. M. PALIKHE, MBBS .

Macule: A flat, colored lesion, <2 cm in diameter, not raised above the surface of the surrounding skin. A “freckle,” or ephelid, is a prototype pigmented macule. Patch: A large (>2 cm) flat lesion with a color different from the surrounding skin. This differs from a macule only in size.

Papule: A small, solid lesion, <0.5 cm in diameter, raised above the surface of the surrounding skin and hence palpable (e.g., a closed comedone, or whitehead, in acne). Nodule: A larger (0.5–5.0 cm), firm lesion raised above the surface of the surrounding skin. This differs from a papule only in size (e.g., a dermal nevomelanocytic nevus). Tumor: A solid, raised growth >5 cm in diameter.

Plaque: A large (>1 cm), flat-topped, raised lesion; edges may either be distinct (e.g., in psoriasis) or gradually blend with surrounding skin (e.g., in eczematous dermatitis).

Vesicle: A small, fluid-filled lesion, <0.5 cm in diameter, raised above the plane of surrounding skin. Fluid is often visible, and the lesions are translucent [e.g., vesicles in allergic contact dermatitis caused by Toxicodendron (poison ivy)].

Pustule: A vesicle filled with leukocytes. Note: The presence of pustules does not necessarily signify the existence of an infection. Bulla: A fluid-filled, raised, often translucent lesion >0.5 cm in diameter.

Wheal: A raised, erythematous, edematous papule or plaque, usually representing short-lived vasodilatation and vasopermeability.

Telangiectasia: A dilated, superficial blood vessel.

Description of Secondary Skin Lesions

Lichenification: A distinctive thickening of the skin that is characterized by accentuated skin-fold markings.

Scale: Excessive accumulation of stratum corneum.

Crust: Dried exudate of body fluids that may be either yellow (i.e., serous crust) or red (i.e., hemorrhagic crust).

Erosion: Loss of epidermis without an associated loss of dermis.

Ulcer: Loss of epidermis and at least a portion of the underlying dermis.

Excoriation: Linear, angular erosions that may be covered by crust and are caused by scratching.

Atrophy: An acquired loss of substance. In the skin, this may appear as a depression with intact epidermis (i.e., loss of dermal or subcutaneous tissue) or as sites of shiny, delicate, wrinkled lesions (i.e., epidermal atrophy).

Scar: A change in the skin secondary to trauma or inflammation. Sites may be erythematous, hypopigmented, or hyperpigmented depending on their age or character. Sites on hair-bearing areas may be characterized by destruction of hair follicles.

Nicotinamide and nicotinic acid are covered under genre Niacin of which Nicotinamide is essential part of NAD and NADP. NAD and NADP are required in essential biochemical reaction of the body where they act as hydrogen acceptors and donor for many enzymes. Tryptophan is the substrate for this vitamin and it can be synthesized by the body in limited amount.
• Absorption- stomach and small intestine.
• Sources- beans, milk, meat, and eggs lesser extent from cereal grains.
• The amino acid tryptophan can be converted to niacin with an efficiency of 60:1 by weight. Thus, the RDA for niacin is expressed in niacin equivalents.
• Conversion of tryptophan to niacin occurs with less efficacy in vitamin B6 and/or riboflavin deficiencies, or in the presence of isoniazid.
• The urinary excretion products of niacin include 2-pyridone and 2-methyl nicotinamide, can be measured for diagnois of Niacin deficiency.

Deficiency of Niacin:

Results in a condition called Pellagra which is a condition characterized by triad 3D- Dermatitis, Diarrhoea and Dementia.

Epidemiology and cause-

• In poor communities specially in Africa, where maize is used as staple diet. Maize chiefly contains unusable form of niacin called Niacytin. Pellagra can develop within 8 weeks if the regular diet is deficient in Niacin and Tryptophan.
• Hartnup’s Disease- a genetic disease in which there impaired absorption of AAs including tryptophan and results in Pellagra.
• Carcinoid Syndrome- Much of Tryptophan is utilized for formation of 5-HT resulting in Niacin deficiency.
• Contributing factors to Deficiency-Alcoholism, vitamin B6 deficiency, riboflavin deficiency, tryptophan deficiency

Clinical Features-

Dermatitis-

Casal Necklace

• Characterized by erythrema. Resembles sunburn over the part exposed to sunlight over the neck,limbs but sparing face giving a necklace appearance in neck called “ Casal’s Necklace” This rash is known as Casal’s necklace because it forms a ring around the neck; it is seen in advanced cases
• Vesicles, cracks, exudates and secondary infection can occur.

Diarrhoea-

• Non-infective inflammation of the GIT.
• Associated with loss of appetite, generalized weakness and irritability, abdominal pain, and vomiting. Bright red glossitis.

Dementia-

• Delerium in acute cases
• Dementia Apathy, disorientation in chronic cases

Vaginitis and esophagitis may also occur.

TREATMENT-

1. Nicotinamide or nicotinic acid 100-200mg PO Q8hrly or Parenteral route.

Side effects may be significant with higher doses.
Response is usually rapid.

more reading:http://dermatology.cdlib.org/1505/case_presentations/pellagra/nogueira.html

Reference- Davidson’s Principle and Practice of Medicine, Harrison’s Internal Medicine.

Why does penicillin anaphylaxis occur?

The core structure Beta lactams consists of a reactive bicyclic B lactam ring that acts as a hapten by covalently binding to tissue carrier proteins. 95% of tissue bound penicillin is found to be haptenated in the form of benzyl penicilloyl which is called the major determinant and 5% of tissue bound penicillin consist of 3 non-crossreactive metabolites called the minor determinants.

Most often immediate allergic reactions are caused by major determinants.

Sometimes modified penicillin such as ampicillin can produce allergic reaction in which the antigenic determinant is the side chain.

What are the manifestations of pencillin allergy?

1. Difficulty breathing or dyspnea
2. Wheezing due to bronchospasm
3. Drop in blood pressure (Hypotension)
4. Swelling of the throat or tongue (Angiodema)
5. Dizziness
6. Loss of consciousness
7. Rapid or weak pulse
8. Pruritis, Urticaria
9. Abdomen cramping, diarrhea

What precautions should be taken?

1. Skin testing by an allergist
2. Shared cross-reactivity can occur with cephalosporins, monobactams and carbapenams
3. Peolple who expereinced symptoms with penicllin previously like following should be more cautious:

• Rash, itching, urticaria, fever
• Wheezing, angioneuritic edema, serum sickness, exfoliative dermatitis

Treatment:

• Epinephrine or Adrenaline administration
  • 0.3-0.5 mL 1:1000 soln SC or IM q15min
  • 0.5-1 mL 1:10,000 soln IV; slow administration; repeat prn
  • 0.3-0.5 mL 1:1000 soln SL q15min
  • 1 mL 1:1000 soln ET in approximately 10 mL NS
  • IV infusion: 0.1-1 mcg/kg/min
• Airway management
• Inhaled beta-agonists
• Volume expansion by IV fluids
• Antihistaminics
• Corticosteroids
• Glucagon

Detail reading on treatment of anaphylaxis @ Medscape

Reference: Washington Manual of Medical Therapeutics 32nd edition