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Sunday, June 19, 2011

TÌM Y VĂN QUA PUBMED

http://www.statistics.vn/KyNangNghienCuu/TimTaiLieu/68-pubmedsearch

Papa (lyric)- Paul Anka

Wednesday, June 08, 2011

A Shorter, Simpler Treatment Option for Latent Tuberculosis?

In a large, CDC-sponsored trial, combination therapy weekly for 3 months was as effective as single-drug therapy daily for 9 months.

On May 16, the results of one of the largest U.S. government clinical trials on tuberculosis (TB) preventive therapy were reported in an oral presentation at the 2011 meeting of the American Thoracic Society. In this randomized study, 3 months of directly observed combination therapy (rifapentine 900 mg plus isoniazid 900 mg once weekly) was compared with the current standard regimen — 9 months of nonobserved monotherapy (isoniazid 300 mg daily) — in 8053 individuals with latent TB infection, predominantly in the U.S. and Canada. Participants were evaluated 33 months after enrollment. Because of concern about drug interactions, HIV-infected individuals taking antiretrovirals were excluded.

TB disease developed in 7 participants in the 3-month combination-treatment group, compared with 15 in the 9-month isoniazid-monotherapy group. The proportion of participants who completed the regimen was substantially higher in the 3-month treatment group (82% vs. 69%). The new regimen was found to be safe.

Comment: These findings suggest that weekly combination therapy for 3 months is as effective as the current standard therapy in areas with low to medium TB incidence. Revised guidelines for treatment of latent TB in the U.S. will likely feature this new regimen. However, additional research is needed before the regimen can be recommended in countries with a high TB incidence — especially those with high rates of HIV infection.

Neil M. Ampel, MD

Published in Journal Watch Infectious Diseases May 25, 2011

Thursday, June 02, 2011

Griseofulvin vs. Terbinafine for Tinea Capitis: Which Is Ahead?

Each agent has its uses in this common fungal infection in children.

Since the late 1950s, griseofulvin has been the treatment of choice for tinea capitis; it is very safe and inexpensive and is available in tablet or liquid forms. The main disadvantages are long treatment duration (6–8 weeks) and erratic absorption. Shorter treatment and longer tissue retention of drug have increased use of newer antifungal agents (terbinafine, itraconazole, and fluconazole) for adult fungal skin infections. These agents, however, are much more expensive, dosage forms are limited, and data regarding pediatric use are few.

Investigators performed a meta-analysis of randomized, controlled trials to compare griseofulvin with terbinafine for tinea capitis treatment in children and adults. Seven studies involving 2163 subjects were included, and clinical and mycological cure rates and adverse effects were compared. No significant differences in efficacy were found between griseofulvin (mean duration, 8 weeks; range, 6–12 weeks) and terbinafine (mean duration, 4 weeks; range, 2–6 weeks). Terbinafine was more efficacious for Trichophyton species and griseofulvin forMicrosporum species. Both agents had good safety profiles. The authors recommend that pretreatment and intermittent laboratory investigations are unnecessary in terbinafine treatment of healthy children because adverse side effects are rare, and the tests do not effectively predict these rare reactions.

Comment: Head-to-head studies of tinea capitis treatment in the U.S. are limited by FDA-required dosing of griseofulvin at 10 mg/kg/day, an outdated and inadequate dosage for Trichophyton tonsurans. Current U.S. practice for the microsize griseofulvin suspension is to use 20–25 mg/kg/day (the dose would need to be converted if ultramicrosize tablets are prescribed). In this meta-analysis of studies from around the world, griseofulvin dosing ranged from 6 to 20 mg/kg/day. Despite suboptimal dosing in many, griseofulvin beat terbinafine for Microsporum canis infections. Ideally, pretreatment fungal cultures can guide our choice of agent. Terbinafine works well against T. tonsuranswhen treatment duration is adequate, but terbinafine oral granules are prohibitively expensive; therefore, I prescribe tablets for children (cut in half, if needed). Itraconazole is another alternative to griseofulvin for M. canis infection in children. For T. tonsurans, I still prescribe a lot of griseofulvin: It's safe, it's cheap, and it works well when given correctly.

Mary Wu Chang, MD

Published in Journal Watch Dermatology May 20, 2011

Wednesday, March 09, 2011

Access Dermatology March Update

  1. Topical heparin and levomenol combination reduces pruritus in atopic dermatitis
  2. Differences in FCER1A N222K mutation between Japanese and Polish patients with atopic dermatitis
  3. A novel biomarker identifies Bak as a candidate serum biomarker in melanoma
  4. Comparison of drug survival rates for adalimumab, etanercept and infliximab in psoriasis patients
  5. Benefit-risk analysis favors adalimumab over methotrexate in psoriasis study
  6. Serum prolactin levels may be a proxy measure of psoriasis disease activity
  7. HLA-DR alleles are associated with skin warts induced by human papillomavirus
  8. Genital psoriasis: A literature review of its epidemiology, presentation, diagnosis and treatment
  9. Social and environmental factors may influence pediatric eczema expression: U.S. national data survey
  10. Serum neopterin levels in spontaneous urticaria and atopic dermatitis
  11. Study suggests link between psoriasis, atherosclerosis and erectile dysfunction
  12. Full spectrum light phototherapy shows efficacy and safety in atopic dermatitis
  13. Facial melanoma management outcomes and the role of sentinel lymph node biopsy
  14. Study shows no significant association between vitiligo and thyroid dysfunction
  15. AAD News: Sun avoidance to slow down aging may predispose women to vitamin D deficiency
  16. AAD News: Study identifies predictors of response to treatments for Sezary syndrome
  17. AAD News: Atopic dermatitis increases risk for infective endocarditis in children with cardiac anomalies
  18. AAD News: History of nevus-associated melanoma predisposes patients to second malignancy of the same origin
  19. AAD News: TNF inhibitors do not reduce MI risk or increase malignancy risk in patients with psoriasis
To be able to read these news and more, please visit www.accessdermatology.com

Wednesday, February 16, 2011

Amyloidosis Cutis Dyschromica in Two female siblings: cases report

Yang WenLin email, Lin YangYang email, Yang Jian email and Lin WenSheng email

BMC Dermatology 2011, 11:4doi:10.1186/1471-5945-11-4




Abstract (provisional)

Background

Cutaneous amyloidosis has been classified into primary cutaneous amyloidosis (PCA, OMIM #105250), secondary cutaneous amyloidosis and systemic cutaneous amyloidosis. PCA is the deposition of amyloid in previously apparent normal skin without systemic involvement. Amyloidosis cutis dyschromica (ACD) is a rare distinct type of PCA. Here, the unique clinical and histological findings of two Chinese female siblings with ACD were described. Cases presentations: Patient 1 was a 34-year-old female, presented with mildly pruritic, diffuse mottled hyperpigmentation and hypopigmentation. The lesions involved all over the body since she was 10 years old. There were a few itchy blisters appearing on her arms, lower legs and truck, especially on the sun-exposed areas in summer. Some hypopigmented macules presented with slight atrophy. Patient 2 was 39-year-old, the elder sister of patient 1. She had similar skin lesions since the same age as the former. The atrophy and blisters on the skin of the patient with amyloidosis cutis dyschromica have not been described in previous literature. Histological examinations of the skin biopsies taken from both patients revealed amyloid deposits in the whole papillary dermis. Depending on the histological assessment, the two cases were diagnosed as amyloidosis cutis dyschromica.

Conclusion

The two cases suggest that the atrophy and blisters may be the uncommon manifestations of amyloidosis cutis dyschromica. It alerts clinicians to consider the possibility of ACD when meeting patients with cutaneous dyschromia. Skin biopsy is essential and family consultation of genetic investigation is very important in such cases.







Tuesday, February 15, 2011

Severe refractory erythema nodosum leprosum successfully treated with the tumor necrosis factor inhibitor etanercept; Ramien ML, Wong A, Keystone JS;

Erythema nodosum leprosum (ENL), or type II reaction, is a common complication of lepromatous leprosy that can cause significant patient debility. First-line therapy includes prednisone and thalidomide, with clofazimine reserved for patients who do not respond to first-line treatment. We present the case of a 33-year-old woman with ENL that failed to respond adequately to conventional therapy over a 6-year period. Because of the severe nature of her disease and the adverse effects of therapy that she experienced, a trial of etanercept was undertaken, which led to full resolution of her ENL. The rationale behind our choice of therapy and its future implications are discussed.

Dermatitis May Be More Cause Than Effect of Food Allergies

THURSDAY, Feb. 10 (HealthDay News) -- One of the most common forms of eczema, the chronic inflammatory skin disease, may actually precede the onset of food allergies, rather than be the product of existing allergies, new research suggests.

This means that parents of children with the specific skin condition, known as atopic dermatitis, should be on the lookout for signs of food allergies in their children.

"Considering that 6 to 10% of children have atopic dermatitis and that up to one-third of those individuals may have documented food allergy, the number of these children affected by food allergies may be significant," Dr. Jon M. Hanifin, a dermatologist and professor at Oregon Health & Science University, said in a news release from the American Academy of Dermatology.

Hanifin presented his team's findings Feb. 4 in New Orleans at the annual meeting of the American Academy of Dermatology.

Their conclusions stem from a five-year study that focused on children aged 3 months to 18 months old who had atopic dermatitis, which is characterized by red, cracked and itchy skin.

The researchers found that about 15% of the children had food allergies, including those with the mildest form of the disease. Children with more severe disease had a greater risk for developing allergies, they said.

Experts note that research presented at meetings has not been subjected to the same type of rigorous scrutiny given to research published in peer-reviewed medical journals.

Hanifin added that people with atopic dermatitis produce relatively large amounts of an antibody known as IgE, which normally is generated when foreign proteins enter the bloodstream, which is key to the onset of an allergic reaction.

However, the researchers cautioned that the true determination of a food allergy requires careful testing with controlled exposures to particular foods followed by a rigorous analysis of ensuing reactions.

"In most cases," Hanifin said, "patients experience atopic dermatitis before food allergies, so it is important for parents of infants and small children affected by this skin condition to be aware of the risk of food allergies."

-- Alan Mozes

New Treatment for Celiac Disease?

Research Shows Blocking a Protein May Reverse Celiac Disease Symptoms

By Denise Mann
WebMD Health News

Reviewed by Laura J. Martin, MD

Feb. 9, 2011 -- Blocking an inflammatory protein called interleukin-15 (IL-15) may help treat the symptoms of celiac disease and prevent the development of celiac disease in certain at-risk people, according to new research in mice published in Nature.

Celiac disease is an autoimmune and inflammatory condition that is triggered by gluten, the protein found in wheat, barley, and rye. When people with celiac disease eat gluten, it triggers an inflammatory response that damages the lining of the small intestine. Symptoms include gas, bloating, cramping, and constipation. People with celiac disease are also at risk for nutritional shortfalls including vitamin B12, vitamin B1 (thiamine), vitamin K, vitamin D, calcium, iron, and folate. Risk factors for developing celiac disease include family history of celiac disease and/or a personal or family history of other autoimmune diseases, including rheumatoid arthritis (RA).

Gluten-free diets are the treatment of choice for celiac disease. Such foods are becoming increasingly available because of the dramatic uptick in rates of celiac disease and other conditions that may respond to gluten-free diets.

In the new study, researchers blocked IL-5 in mice genetically altered to have celiac disease and found that the disease symptoms were reversed, and the mice were once again able to eat gluten.

Is Blocking IL-15 the Key to Treating Celiac Disease?

"We have identified one mechanism by which people lose tolerance to gluten," says author Bana Jabri, MD, PhD, an associate professor of medicine and pathology and co-director of the Digestive Disease Research Core Center at the University of Chicago. "IL-15 may be a critical element that drives the loss of tolerance to gluten, and we can now think about pathways to block it and potentially develop therapies for celiac disease."

Medications that block IL-15 are being developed for other inflammatory diseases, including RA.

The new research also shows that retinoic acid, a vitamin-A derivative found in acne treatments such as Retin-A and Accutane, may be complicit in the onset of celiac disease.

"Vitamin A in these patients is a bad idea," she says. "Patients at risk should be careful about using retinoids." This may even include topical retinoids if they can enter the bloodstream, she says.

Those two molecules act together to promote inflammation, she says. "The vitamin A derivative seems to fuel the IL-15, but if you block IL-15, retinoids are OK," she says.

More Celiac Treatments Needed

"In the U.S., we need to increase awareness and diagnosis of celiac disease because less than 10% of patients are diagnosed," she says. "A gluten-free diet is currently the treatment of choice, but some patients only respond partially, and it is still socially a handicap."

The race is on to develop new therapies to treat or prevent celiac disease, she says.

"At this point, the new study holds theoretic promise," says Gerard Mullin, MD, an associate professor of medicine at Johns Hopkins School of Medicine and the director of Integrative Nutrition Services at the Johns Hopkins Hospital in Baltimore. "IL-15 may be a major player in driving the inflammatory response in celiac disease, and if we block it, you can tolerate gluten.

"A drug that blocks IL-15 may be most beneficial in people with really aggressive disease that doesn't respond to conventional dietary measures," Mullin says. For people with celiac disease, "today's day and age is better to live in than 10 years ago due to increased availability of gluten-free foods and gluten-free menu options."

Celiac disease is on the rise in the U.S., he says.

"The prevalence has jumped four to five times since the 1940s, but we are not clear why," Mullin says. "Many food experts have speculated that it is the way grains are processed here, but we do see it in Italy and other places."

Diagnosing celiac disease is not always straightforward, he says. Blood tests that look for the presence of certain antibodies are the first step. If the results are positive, many doctors will order a biopsy of the small intestine to confirm the diagnosis. This biopsy can also help assess the degree of damage, but "even the biopsy can miss it," he says.

Richard Desi, MD, a gastroenterologist at the Melissa L. Posner Institute for Digestive Health and Liver Disease at Mercy Medical Center in Baltimore, says that blocking IL-15 may well help some people with celiac disease.

"This may not be it for everybody, but maybe it can help some people," he says. "We are starting to understand celiac disease a lot more and diagnose it a lot more. The hope is that we will be able to come up with a treatment that doesn't just involve a gluten-free diet."

SOURCES: Richard Desi , MD, gastroenterologist, Melissa L. Posner Institute for Digestive Health and Liver Disease, Mercy Medical Center, Baltimore.Gerard Mullin, MD, associate professor of medicine, Johns Hopkins School of Medicine, Baltimore.Bana Jabri, MD, PhD, associate professor of medicine and pathology; co-director, Digestive Disease Research Core Center, University of Chicago.DePalo, R. Nature, 2011, manuscript received ahead of print.