Posted by admin on Feb 13, 2010 in
medical Demodicosis is a infestation caused by mite from Demodex species, belongs to class arachnida called Demodex folliculorum or Demodicid, It is a tiny mite that lives in the pores of hair follicle. Demodex folliculorum is commonly found on the nose, forehead, scalp, cheek, chin, and eyelashes of adult and it’s number continue to increase with the increasing age of an individual and is often associated with blackheads, acne , rosacea, and skin irritations.
Adult Demodex folliculorum has an appearance of worm with four pair of short legs. It’s size ranges from 0.1mm to 0.4 mm; has a needle like mouth. The body is covered with layer of scales which helps the mite to anchor itself in to the hair follicle. The mite doesn’t have the excretory system. The mite copulates outside the hair follicle then female mite moves to a new hair follicle and lays up to 25 eggs in the hair follicle. The larva grows in to a adult mite in the hair follicle. During the day the mite stays in the hair follicle and feed on sebaceous secretion, and at night, it come out of the hair follicle onto the surface to the skin to mate and female mite moves to a new follicle and lays eggs over there. The whole cycle takes about14 to 18 days.
The mite stay in the hair follicle with head-down. When too many mites get buried into the same follicle, it may cause the hair fall and induce inflammation around the hair follicle.
The infection by demodex mite depends on the ability of individuals gene to induce immune response against the mite. The body reacts to the existence mites and induces an inflammatory response as it tries to rebuff the mites.
It has been observed that eighty-eight percent of individuals with thin hair have Demodex Folliculorum in their body, in contrast to 9% in individuals with normal hair density. The incidence of demodex in the hair follicle of a individual varies with age , it has been reported that about 25% of demodex is seen in about 20 years of age, 30% in 50 years , and up 50% in 80 years age.
Demodicids are mostly present in adults and they are usually harmless; they do not transmit diseases to others by close contact but infection occurs when large number of these mites congregate in a single follicle. It produces itching and inflammatory lesion at the site of hair follicle, as it is commonly found on the face, it’s often regarded as the ‘face mite’.Infection is commonly noticed in adults with oily skin; persons using heavy cosmetics, and those who don’t wash off cosmetics thoroughly.
The demodex infection is characterized by itchy erythematous edematous papules, pustules on the face and scalp. The infestation may be frequently free of symptoms. However, Demodicidosis is characterized by the presence of an erythematous papulo- pustular rash on the face. The inflammation is either acute and chronic in nature. Our observation was also similar but our patients had extensive areas of involvement face, scalp, back, ‘V’ area of the chest, axilla and forearm.
Treatment with topical Permethrine5% for 5-7 consecutive days, and the other drugs which have been used effectively are Gamma benzinehexachliride, Oral Ivermectin, Metronidazole 2% cream and oral. In our personal cases we had used Permethrine 5% topical cream effectively with rapid clearance of symptoms and lesions.
For Scientific english editing and Medical Writing Services visitwww.manuscriptedit.com
Tags: "Editing, academic, English, manuscript, medical, proofreading, research paper, scientific, service", writing
Posted by admin on Feb 13, 2010 in
medical Sweet’s syndrome is eponym for acute febrile neutrophilic dermatosis coined by Dr Sweet from Plymouth, England, who first described this condition in 1964. It is characterized by acute fever, leukocytosis; with sudden appearance of tender erythematous papules, nodules, and plaques. The edema is so intense that the papules and nodules often resemble vesicles so often the description used for the papule is pseudovesicle. The plaques are formed by coalition of papules that gives an arcuate appearance. Sweet’s syndrome is common in middle-aged women, but men, children are also be affected. Hematological investigation shows neutrophilia with diffuse infiltrate of neutrophils in the middle and upper dermis of skin biopsy.
Sweet’s syndrome is characterized by four features: tender erythematous plaques with arcuate border and the plaque studded with pseudovesicles. The other associated features are: fever; conjunctivitis, leukocytosis, and papillary dermal infiltration of neutrophils in the skin biopsy. Fever and neutrophilia is not a consistent feature. The diagnosis is mostly based on the typical skin eruption and characteristic histological finding in skin biopsy.
Based on the clinical setting the SS is classified into classical or idiopathic sweet’s syndrome, malignancy-associated SS and Drug-induced Sweet’s syndrome. Classical Sweet’s syndrome (CSS) usually presents in women between the ages of 30 to 50 years, it is often preceded by an upper respiratory tract infection and may be associated with inflammatory bowel disease and pregnancy. The malignancy-associated Sweet’s syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals, whose Sweet’s syndrome is related hematologic dyscrasia in malignant associated SS. The dermatosis in MASS may precede, follow, or appear concurrently with the diagnosis of malignancy. The most commonly associated malignancy is acute myelogenous leukemia and approximately 20% of cases are associated with hematogenous malignancy. Drug-induced Sweet’s syndrome (DISS) most commonly occurs in patients who are receiving granulocyte-colony stimulating factor, hematopoietic growth factor and the lesions typically occur when the patient has leukocytosis and neutrophilia. SS may precede 3 months to 6 years before the manifestation of any associated disease or malignancy, so these patients needs to kept under prolonged follow up and regular clinical and hematological evaluation to know the early development of these condition. Because of this, it is believed to be reactive phenomenon or cutaneous marker of systemic diseases. At the same time, it is also suggested to be having genetic association but no genetic link has been identified till today.
The skin lesions predominantly occurs on the head, neck, legs, and arms, and particularly on the fore arm and cheeks. Development of fever (50%); arthralgia or arthritis (62%); eye involvement in the form of conjunctivitis or iridocyclitis (38%); and oral aphthus (13%) has been noted. Other organs affected are: bones, nervous system, kidneys, intestines, liver, heart, lungs, muscles and spleen. Rarely sweet’s syndrome lesions may turn bluish or grey and form abscess-like nodule and ulcerates known as ‘pustular vasculitis.
Hematological investigations of these patients frequently shows neutrophilia (in less than 50%), elevated ESR (greater than 30 mm/hr) (in 90%), and a slight increase in alkaline phosphatase (in 83%) cases, C-reactive protein (CRP); and p-ANCA (antineutrophil cytoplasmic antibody) is some. Skin biopsy shows mixed infiltrate of polymorphonuclear cells with nuclear fragmentation and histiocytes in the mid and papillary dermis of skin biopsy. The infiltrate is predominantly perivascular with swollen endothelial cell, and vessels, however, changes like: thrombosis; fibrin deposits, complement, or immunoglobulins are seen within the vessel walls; red blood cell extravasation ; inflammatory infiltration of vessel walls are absent in early lesions, unlike vasculitis. But, the features of vasculitis do not exclude the diagnosis of SS.
Sweets syndrome responds to systemic corticosteroids given at the dose of 0.5 to 1.5 mg/kg of body weight per day. It cases rapid improvement of the symptoms and skin lesions, so it’s regarded as the “gold standard” in the treatment for SS. The skin eruption, increase nerutrophil count and fever improve within 72 hours of treatment with corticosteroid. The complete clearance of skin lesions takes about 3 to 9 days, however, frequent recurrences is seen in one-third cases. Corticosteroids are tapered over 2 to 6 weeks. The disease may clear spontaneously in some patients. Other drug effective is oral potassium iodide, colchicines. dapsone, doycycline, clofazimineand and cyclosporine. These drugs are indicated, when the use of steroid is contraindicated. Our cases were given corticosteroid with complete clearance of their lesions with no relapse after discontinuation of corticosteroid.
For Scientific english editing and Medical Writing Services visitwww.manuscriptedit.com
Tags: "Editing, academic, English, manuscript, medical, proofreading, research paper, scientific, service", writing
