Otro comentario sobre el mismo articulo del seguimiento de nevus displásicos.

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Observation May Be Acceptable for Moderately Dysplastic Nevi With Positive Margins

By Marilynn Larkin

October 22, 2018

 
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NEW YORK (Reuters Health) - Routine skin surveillance is a "reasonable" approach to managing moderately dysplastic nevi with positive histologic margins, although patients with two or more such nevi are at increased risk of developing cutaneous melanoma at a different site, researchers say.

"Dysplastic nevi/clinically atypical nevi (moles) have been identified as risk factors for melanoma; however, the majority of melanomas arise as new lesions on the skin," Dr. Caroline Lee of Beth Israel Deaconess Medical Center in Boston told Reuters Health by email.

"Unlike other models of dysplasia having a clear trajectory towards cancer, as seen in cervical dysplasia," she said, "dysplastic nevi are not proven to be obligate precursors for melanoma."

"There is little evidence to guide the management of biopsied dysplastic nevi with positive margins," she noted, "with much clinical variation in the care of moderately dysplastic nevi in particular."

To investigate, Dr. Lee and colleagues studied 438 patients (mean age 46.7; 55.9% men) with 467 moderately dysplastic lesions at nine U.S. academic dermatology sites. Patients were followed for a mean of 6.9 years.

As reported online October 10 in JAMA Dermatology, no patient developed cutaneous melanoma at a biopsy site, but 100 (22.8%) developed a cutaneous melanoma at a different site.

The risk of developing a cutaneous melanoma at a separate site was significantly associated with a history of cutaneous melanoma (odds ratio, 11.74) and with previously biopsied dysplastic nevi (OR, 2.55).

A central dermatopathologic review of 40 random representative case slides showed agreement in 35 of the cases (87.5%).

Of the remaining cases, two (5%) were interpreted as mildly dysplastic nevi and two as moderately to severely dysplastic nevi.

One case was interpreted as melanoma in situ. A review of the case with the host site revealed that the patient had not had a clinical recurrence at the biopsy site after five years of follow-up

Dr. Lee affirmed, "Our findings underscore that dysplastic nevi are not obligate precursors for melanoma, but rather, are phenotypic markers for patients at risk for melanoma."

Dr. Kelly Nelson of The University of Texas MD Anderson Cancer Center in Houston, coauthor of a related editorial, told Reuters Health the study "represents a significant multi-institutional collaborative effort to add to the paucity of dysplastic nevi management literature."

"In caring for my patients, I make every attempt to remove lesions concerning for melanoma in their clinical entirety with a small margin of normal skin," she said by email. "When the scenario arises of a dysplastic nevus with moderate atypia and microscopically positive margins on histopathologic review, and the interpretation by our . . . dermatopathologists aligns with my clinical impression, I am very comfortable monitoring the site for longitudinal clinical recurrence."

"In the setting of high patient anxiety, or when my clinical concern for the lesion is discordant from the dermatopathology interpretation, we proceed with a conservative therapeutic excision," Dr. Nelson concluded.

SOURCE: http://bit.ly/2CtgSdf and http://bit.ly/2Cs0jP8

JAMA Dermatol 2018.

Reuters Health Information © 2018 

Cite this article: Observation May Be Acceptable for Moderately Dysplastic Nevi With Positive Margins - Medscape - Oct 19, 2018.

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Nevus displasticos y su seguimiento...

COMMENTARY

Dysplastic Nevi: Monitoring and Management

Graeme M. Lipper, MD

DISCLOSURES 

October 25, 2018

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Dysplastic Nevi 

Since their original characterization by Clark and colleagues in 1978,^[1] dysplastic nevi have posed a management dilemma, given their position in the gray area between benign melanocytic nevi and malignant melanoma. Even their histologic typing is the subject of debate, with some pathologists preferring to avoid the common grading system of mild, moderate, or severe atypia.^[2]

Dysplastic nevi are benign melanocytic tumors containing clonal populations of hyperproliferative melanocytes. Strictly speaking, dysplastic nevus is a histologic diagnosis, characterized by architectural disorder and cytologic atypia. "Atypical nevus" is the clinical correlate, typified by the classic ABCD criteria of asymmetry, border irregularity, color variegation, and size > 6 mm.

Dysplastic nevi are common in people of Northern European descent, with prevalence estimates ranging from 7% to 24%.^[3] Although dysplastic nevi may progress to cutaneous melanoma, most lack the genetic mutations characteristic of cutaneous melanoma, such as CDKN2A, TP53, NF1, RAC1, and PTEN.^[4]

Malignant transformation of dysplastic nevus to cutaneous melanoma is rare, with one study estimating a dysplastic nevus-to-melanoma transformation rate of 1 in 30,089 nevi in males and 1 in 39,809 nevi in females.^[5] Nevertheless, patients with multiple dysplastic nevi and/or a family history of dysplastic nevus syndrome have a greater risk of developing cutaneous melanoma, with relative risk estimates ranging from 1.6 for individuals with one dysplastic nevus to 10.5 for those with five or more.^[6]

Given the high prevalence of dysplastic and atypical nevi, most dermatologists opt to monitor patients with multiple atypical nevi, only biopsying those lesions with clinical and dermatoscopic signs of severe atypia. Regardless of the technique (shave, saucerization, punch, excisional), many of dysplastic nevi show positive histologic margins, even in cases with no residual clinical pigmentation. Should all such lesions be re-excised to ensure no chance of recurrence? And what is the risk of opting to follow for any repigmentation instead?

Development of Cutaneous Melanoma From Excised Dysplastic Nevi

To address this practical concern, Kim and colleagues^[7] conducted a retrospective multicenter cohort study of 467 moderately dysplastic nevi with positive histologic margins, gathered from 438 patients (193 women and 245 men; mean age, 46.7 years; 96.7% white). Patients were followed for a mean of 6.9 years (range, 3.0-21.3 years) for development of cutaneous melanoma at a biopsy site or elsewhere on the body. This study did not assess severely dysplastic nevi or nevi that were only partially biopsied.

Among the study cohort, 33.2% had a personal history of melanoma, 50.4% had at least one previously biopsied dysplastic nevus, and 23.8% had a family history of melanoma. The primary methods of biopsy were saucerizations or shave excision (46.4%), punch excision (45.3%), or elliptical excision (7.7%). Key study results included:

• 52.7% of dysplastic nevi were interpreted as mild to moderate, and 47.3% were interpreted as moderate

• Histology was positive at the peripheral (89.9%), deep (3.6%), and both (6.5%) margins

• After a mean follow-up of 6 years, no melanomas developed at prior biopsy sites

• 100 patients (22.8%) developed a subsequent primary melanoma at a distant cutaneous site, and three of these patients developed metastatic melanoma

• Melanoma risk factors included a history of melanoma (odds ratio [OR], 11.74) and two or more biopsy-confirmed dysplastic nevi (OR, 2.55)

  
  

  Viewpoint

  This study of moderately dysplastic nevi with positive histologic margins is consistent with previous smaller studies^[8,9] and supports the practice of monitoring such biopsy sites without re-excision. During an average follow-up of 6 years, no cutaneous melanomas were observed. They also confirmed dysplastic nevi as an independent risk factor for cutaneous melanoma, which has been well documented elsewhere. These observations were specific to an almost exclusively white study population.

  One clinical consideration that was not addressed is what to do when repigmentation does occur within or near the scar of a previously biopsied dysplastic nevus. Should the recurrent pigmentation be re-excised? Does it make any difference whether the repigmentation occurs within the biopsy scar or extends beyond its clinical borders? What percentage of these recurrent pigmented lesions are dysplastic nevi with the same or higher grade dysplasia?

  Finally, most biopsied dysplastic nevi (69.5%) in this retrospective cohort were truncal, raising the remote possibility that dysplatic nevi removed from other cutaneous sites (eg, acral, face, genital) with positive margins may pose a greater future malignant melanoma risk.

  1. Clark WH Jr, Reimer RR, Greene M, Ainsworth AM, Mastrangelo MJ. Origin of familial malignant melanomas from heritable melanocytic lesions 'The B-K mole syndrome'. Arch Dermatol. 1978;114:732-738. Abstract

  2. Farber MJ, Heilman ER, Friedman RJ. Dysplastic nevi. Dermatol Clin. 2012;30:389-404. Abstract

  3. Tucker MA. Melanoma epidemiology. Hematol Oncol Clin North Am. 2009;23:383-395. Abstract

  4. Melamed RD, Aydin IT, Rajan GS, et al. Genomic characterization of dysplastic nevi unveils implications for diagnosis of melanoma. J Invest Dermatol. 2017;137:905-909. Abstract

  5. Tsao H, Bevona C, Goggins W, Quinn T. The transformation rate of moles (melanocytic nevi) into cutaneous melanoma: a population-based estimate. Arch Dermatol. 2003;139:282-288. Abstract

  6. Goldstein AM, Tucker MA. Dysplastic nevi and melanoma. Cancer Epidemiol Biomarkers Prev. 2013;22:528-532. Abstract

  7. Kim CC, Berry EG, Marchetti MA, et al; Pigmented Lesion Subcommittee, Melanoma Prevention Working Group. Risk of subsequent cutaneous melanoma in moderately dysplastic nevi excisionally biopsied but with positive histologic margins. JAMA Dermatol. 2018 Oct 10 [Epub ahead of print] Abstract

  8. Goodson AG, Florell SR, Boucher KM, Grossman D. Low rates of clinical recurrence after biopsy of benign to moderately dysplastic melanocytic nevi. J Am Acad Dermatol. 2010;62:591-596. Abstract

  9. Hocker TL, Alikhan A, Comfere NI, Peters MS. Favorable long-term outcomes in patients with histologically dysplastic nevi that approach a specimen border. J Am Acad Dermatol. 2013;68:545-551. Abstract

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Antifúngicos y sol...

Voriconazole Use Tied To Higher Risk Of Cutaneous Squamous Cell Carcinoma In Patients With Lung Transplant Or Hematopoietic Cell Transplant, Review Indicates.

Dermatology Advisor (10/26) reported researchers found in a "systematic literature review and meta-analysis" that "use of voriconazole is associated with an increased risk for cutaneous squamous cell carcinoma (SCC) in patients with lung transplant (LT) or hematopoietic cell transplant (HCT)." The findings were published in the Journal of the American Academy of Dermatology

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Cierre inmediato no siempre es lo mejor

Some Patients Undergoing Mohs Procedures For Skin Tumors May Benefit From Delayed Reconstruction, Study Indicates.

MedPage Today (10/26, Lyles) reported researchers found in a retrospective study that "for select patients undergoing Mohs procedures for skin tumors, delaying reconstruction enhanced viability of full-thickness skin grafts and composite grafts and decreased postoperative complication rates." The findings were published in JAMA Facial Plastic Surgery. In an accompanying editorial, Jeffrey Moyer, MD, and Shi Yang, MD, both of the University of Michigan Medical School, wrote that the study's results "would seem to be counterintuitive because the prevailing belief is that an increased interval between [Mohs micrographic surgery] and repair has little meaningful effect on the ultimate reconstructive outcome or might actually be detrimental rather than beneficial."

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Tincion para Histoplasma

   Diagnostic tip: CD42b IHC stain for Histoplasma          

 

There are currently no antibodies specific for Histoplasma, which makes diagnosis challenging. While performing immunohistopathology on a biopsy of bone marrow infected with histoplasmosis, Ku and colleagues noticed that H. capsulatumexpresses a cell surface marker called CD42b (glycoprotein Ib), which is normally used to identify megakaryocytes and the platelets they produce. Further characterisation is needed to show whether this antibody is suitable for development into new diagnostics.

 

►  Find out more: Ku et al (2018) Use of CD42b immunohistochemical stain for the detection of Histoplasma

 

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Shingrix mas efectiva que Zostavax

Recombinant Zoster Vaccine More Efficacious Than Live Vaccine

By Amy Orciari Herman

Edited by André Sofair, MD, MPH, and William E. Chavey, MD, MS

The adjuvant recombinant subunit herpes zoster vaccine (Shingrix) seems to prevent more zoster cases than the live attenuated vaccine (Zostavax) — but may also cause more injection site reactions — according to a network meta-analysis in The BMJ.

Researchers examined data from 22 trials examining the efficacy of the vaccines in adults aged 50 and older. Among the findings:

• For preventing confirmed zoster infection, the recombinant vaccine was more efficacious than the live vaccine or placebo, whereas there was no difference between the live vaccine and placebo. 
• For suspected zoster, the recombinant vaccine was again more efficacious than the live vaccine or placebo, and the live vaccine was superior to placebo.
• Both vaccines were superior to placebo for preventing postherpetic neuralgia.
• Injection site reactions were more common with the recombinant vaccine than with the live vaccine.
• Serious adverse events did not differ across the groups.

The CDC currently recommends the recombinant vaccine over the live vaccine for healthy adults aged 50 and older.

The BMJ article (Free)

Background: NEJM Journal Watch General Medicine coverage of CDC's 2018 adult immunization schedule (featuring zoster recommendations)(Free)

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Etanercept en PsoAR

24-10-2018 | Rheumatology | News | Article

ACR/ARHP 2018

Etanercept outperforms methotrexate for PsA

medwireNews: Etanercept has greater efficacy than methotrexate for the treatment of psoriatic arthritis (PsA), suggest phase III trial results presented at the 2018 ACR/ARHP Annual Meeting in Chicago, Illinois, USA.

"This is a trial that was necessary but never done," lead author Philip Mease (Swedish Medical Center and University of Washington, Seattle, USA) told medwireNews.

He explained that etanercept and methotrexate "are used a lot, and we just didn't have this data before to be able to support our use of these drugs."

As outlined in a late-breaking poster presentation, Mease and colleagues randomly assigned 851 methotrexate- and biologic-naïve patients with active PsA to receive once weekly treatment with etanercept 50 mg, methotrexate 20 mg, or a combination of both agents for a total of 48 weeks.

At the 24-week follow-up, ACR20 response rates were significantly higher among patients receiving etanercept alone or alongside methotrexate than with methotrexate alone, at 60.9% and 65.0% versus 50.7%, respectively. The corresponding rates at week 48 were 83.1% and 80.4% versus 70.7%.

Etanercept use was also associated with a significantly higher likelihood of achieving minimal disease activity (MDA; defined as tender and swollen joint counts ≤1; Psoriasis Area and Severity Index score ≤1 or psoriasis-affected body surface area ≤3%; visual analog scale [VAS] pain score ≤15; patient global disease activity VAS ≤20, HAQ-DI ≤0.5; and tender entheseal points ≤1). Specifically, the MDA rates at week 24 were 35.9% and 35.7% versus 22.9% for patients taking etanercept monotherapy and combination therapy versus methotrexate monotherapy, respectively.

Mease said that all three treatment arms experienced improvements in enthesitis and dactylitis scores over the study period, with numerically greater improvements for patients given etanercept or combination therapy versus methotrexate.

"So etanercept does better but not hugely better," and these results show that "methotrexate works" in terms of ACR and MDA responses, as well as enthesitis, dactylitis, and skin responses, said Mease.

However, "the one area where there was a question mark was in its ability to inhibit radiographic progression," he remarked. Mean changes in modified total Sharp Score from baseline to week 48 were –0.04 points for patients receiving etanercept monotherapy, –0.01 points for those given the combination of both drugs, and 0.08 points for patients given methotrexate alone.

Mease concluded that monotherapy with etanercept did as well as the combination of etanercept and methotrexate, which "tells me I'm doing fine if I drop methotrexate" from the combination.

By Claire Barnard

medwireNews is an independent medical news service provided by Springer Healthcare. © 2018 Springer Healthcare part of the Springer Nature group

This information is brought to you by medwireNews and is not sponsored by, nor a part of, the American College of Rheumatology

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Edulcorantes afectan glicemia...

Sweeteners Disrupt Blood Glucose Via Effects on Gut Bacteria

Liam Davenport

October 09, 2018

BERLIN — Low-calorie sweeteners appear to impair glucose uptake and control by disrupting the gut microbiome, Australian researchers have shown for the first time in findings that suggest artificial sweeteners could potentially play havoc with glucose-lowering medications in patients with diabetes.

In a study of healthy individuals presented here at the European Association for the Study of Diabetes (EASD) 2018 Annual Meeting, Richard L. Young, PhD, head of the Intestinal Nutrient Sensing Group, University of Adelaide, South Australia, and colleagues showed that a low-calorie sweetener capsule altered the gut ecosystem in favor of pathogenic bacteria compared with placebo.

Young told a press conference that "2 weeks' supplementation with sweeteners in capsules increases glucose absorption and glycemic responses to glucose, and decreases glucose-evoked increases in the incretin glucagon-like peptide 1 (GLP-1)."

He added, "I hope I've convinced you that [sweeteners] trigger changes in the gut microbiome, including its functional properties."

Asked by Medscape Medical News whether, based on their impact on GLP-1 levels, low-calorie sweeteners could affect the efficacy of diabetes medications, he said, "There's definitely the possibility that they could interact."

He pointed out that posters presented during the meeting also suggest that some of the effects of "some of the GLP-1 receptor agonists are certainly mediated through changes in the microbiome, which is an emerging phenomenology." He added: "I think that the microbiome is not often considered by clinicians as a first-pass way of understanding of mechanisms."

Approached for comment, session cochair Ellen E. Blaak, PhD, professor of physiology of fat metabolism, NUTRIM School of Nutrition and Translational Research, Maastricht University, the Netherlands, said that the results are "interesting."

She said she would like to see more long-term data; however, she added that the issue of what is used as placebo in such studies is important. "Do you take sugar sweetened beverages as the placebo?" she asked. "Then the results will be different."

Blaak also pointed out that there needs to be a balance between the beneficial effects of artificial sweeteners in moderate amounts, "which may help you to comply with lifestyle interventions," as they can help with weight control, and the potential adverse events when taken to excess, "so I think there are two sides to it."

Research in Mice Shows Sweeteners Disrupt Gut Microbiome

Young began his presentation by noting that "the vast majority [of sweeteners] are fairly recent entrants to the food chain, and the number of products that are available for low-calorie sweeteners is expanding exponentially."

He added, "Of course, they're increasingly marketed towards the health conscious sector of the market."

Previous studies have indicated, however, that a high intake of low-calorie sweeteners is associated with poorer glycemic control and that HbA_1c levels increase with increasing consumption of beverages that contain them.

At last year's meeting, as reported by Medscape Medical News, Young and his team showed that sweeteners were, compared with placebo, associated with a 20% increase in 3-O-methyl-glucose absorption and a 24% increase in plasma glucose levels (P < .05 for both), again in healthy volunteers. The low-calorie sweeteners were also associated with a significant 34% reduction in GLP-1 levels versus placebo (P < .05).

And research in mice has shown that low-calorie sweetener supplementation can cause changes in the gut microbiome, as well as alter microbial carbohydrate-related metabolic pathways, increasing fecal short-chain fatty acid production, Young said.

Noting that the majority of studies in humans have been of limited duration and none have assessed glucose absorption, for the current analysis, Young said his team randomized 40 nondiabetic individuals to a low-calorie sweetener tablet containing sucralose 92 mg and acesulfame potassium 52 mg, which is equivalent to approximately 1.2 L of sweetened beverage per day, or placebo.

Participants took the tablets three times daily for 2 weeks with a standardized evening meal. Complete data were available for 16 patients assigned to placebo and 17 patients assigned to the low-calorie sweetener arm. The two groups had similar baseline patient and clinical characteristics.

Sweeteners Decrease "Good" Bacteria, Increase "Bad" Ones

Participants' gut microbiomes were assessed using stool samples collected before and after the 2-week treatment period. The team wanted to determine whether low-calorie sweetener supplementation altered the human gut microbiome in a way that predicts host glycemic changes.

Young explained, "We were able to see a number of different species emerging...In essence, we saw a loss of health-associated bacterium."

There were decreases in levels of Eubacterium cylindroides, as well as in levels of the beneficial and fermentative Bifidobacterium, Lactobacillus, and Bacteroides populations, which are correlated with augmented glucose absorption (P ≤ .001 for all). There were also reductions in levels of Butyrivibrio populations, which have been shown to be correlated with attenuated GLP-1 release (P ≤ .001).

"In contrast, we saw increases in a number of gut pathogens that are normally low or absent in health," Young said. Specifically, there was an increase in 11 opportunistic gut pathogens, including Klebsiella, Porphyromonas, and Finegoldia (P ≤ .001 for all).

"In healthy nondiabetic subjects, 2 weeks of low-calorie sweetener supplementation was sufficient to disrupt gut bacteria and increase the abundance of those which are normally absent in healthy individuals," the team summarizes.

The observed decrease in fermentative bacteria populations and changes in the pathways used by bacteria to harvest energy "predicted a deterioration in the body's ability to regulate glucose," they add.

"Our findings support the concept that such sweeteners worsen blood sugar control in healthy subjects by disrupting the regulation of glucose uptake and disposal, as well as from changes in the balance of gut bacteria. This highlights the clinical relevance of dietary low-calorie sweetener patterns to overall blood sugar control."

Young said that he and his colleagues will test the causal nature of the association between low-calorie sweetener-related changes in the microbiome and glycemic changes through "experiments in both healthy individuals and individuals with type 2 diabetes, who are particularly high consumers of this type of product."

The study was funded by the Australian National Health and Medical Research Council. The authors have reported no relevant financial relationships.

European Association for the Study of Diabetes (EASD) 2018 Annual Meeting; October 5, 2018; Berlin, Germany. Abstract 241.

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Cite this article: Sweeteners Disrupt Blood Glucose Via Effects on Gut Bacteria - Medscape - Oct 09, 2018.

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La ingesta de Cafe reduce la rosacea...

Coffee May Reduce Rosacea Risk

Diana Swift

October 18, 2018

Far from promoting rosacea, a higher intake of caffeinated coffee is associated with a reduced risk of rosacea, researchers report in an article published online October 17 in JAMA Dermatology. 

Caffeine from other sources, such as caffeinated soda, tea, and chocolate appear to have no such protective impact, report Suyun Li, PhD, an epidemiologist at the School of Public Health, Qingdao University, Shandong, China, and colleagues.

The researchers analyzed data from the longitudinal Nurses' Health Study II cohort and found a dose–response association with increasing ingestion of both caffeine generally and coffee specifically, which counters the notion of limiting caffeine intake and coffee consumption to prevent rosacea flares.

The absolute risk of incident rosacea fell by 132 per 100,000 person-years for the highest versus the lowest quintile of caffeine intake and, similarly, by 131 per 100,000 person-years for caffeinated coffee consumption of at least four servings a day versus less than one serving per month. A benefit was not seen with decaffeinated coffee.

The effect translated to a 23% reduction in risk with at least four servings of coffee a day (hazard ratio (HR), 0.77; 95% CI, 0.69 - 0.87; P < .001 for trend). For decaffeinated coffee, the HR was 0.80 but the reduction was not significant (95% CI, 0.56 - 1.14; P = .39 for trend).

The authors note that higher caffeine intake was associated with being a current or past smoker and oral contraceptive user, as well as with somewhat older age and higher alcohol consumption.

"The finding that consuming caffeine from coffee protects from the risk of developing rosacea may have clinical and public health implications and may inform clinical practice to address patients' queries," senior author Wen-Qing Li, PhD, from the Department of Dermatology, Warren Alpert Medical School, Brown University in Providence, Rhode Island, told Medscape Medical News. "Public messages are warranted with regard to the potential protective effect of coffee and caffeine against rosacea development."

In a related editorial, Mackenzie R. Wehner, MD, MPhil, from the University of Pennsylvania in Philadelphia, and colleagues write, "This study provides evidence that patients with rosacea need not avoid coffee, and it offers all of us one more reason to continue drinking coffee regularly."

Li and colleagues analyzed data from 82,737 participants in the Nurses' Health Study II who responded in the 2005 survey to a question on rosacea. There were 4945 incident cases of clinically diagnosed rosacea during 1,120,051 years of follow-up. The mean age at entry of all cohort participants was 50.5 years, whereas the mean age of caffeine consumers across quintiles was about 36 years. Analyses were adjusted for potential confounders such as age, race, body mass index, and lifestyle factors.

According to the authors, caffeine may act through an effect on vascular contractility, with increased intake reducing symptoms by decreasing vasodilation. Caffeine also contains antioxidants and has immunosuppressant effects, which may mitigate inflammation. Caffeine can also modulate levels of hormones such as adrenaline, noradrenaline, and cortisol, which can impact rosacea.

The authors speculate that although other compounds in coffee could lower risk, the lack of effect from decaffeinated coffee undermines that explanation. They suggest that the heat in decaffeinated coffee, which lacks the compensatory protection of caffeine, might counteract the beneficial effect of drinking coffee.

Previous case-control studies and reviews have reported differing effects from caffeine or coffee consumption on rosacea risk. An Estonian case-control study and a literature review from France found no significant difference in risk between groups consuming different amounts of caffeine, while a case-control study from Poland reported an increased risk in coffee drinkers.

The lack of effect from noncoffee sources of caffeine is likely because of the low absolute caffeine content of these foods and beverages, the authors explain. "Further studies are required to explain the mechanisms of action of these associations, to replicate our findings in other populations, and to explore the relationship of caffeine with different rosacea subtypes," they write.

The editorialists point out that the perennial question remains whether it is caffeine, coffee, or a combination of both that is responsible for the protective effect.

The study was supported by a Research Career Development Award of Dermatology Foundation, Richard B. Salomon Faculty Research Award of Brown University, and National Institutes of Health grants for the Nurses' Health Study II. Two coauthors report a variety of ties with one or more of the following: Abbvie, Amgen, Sanofi, Regeneron, RTI Health Solutions, Astellas Canada, Prime Inc, Spire Learning, CME Outfitters, Janssen, Merck, Novartis, Pfizer, and the Eczema Society of Canada. The remaining authors and editorialists have reported no relevant financial relationships.

JAMA Dermatol. Published online October 17, 2018. Abstract, Editorial

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Treatments of Basal Cell Carcinoma | Annals of Internal Medicine | American College of Physicians

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Treatments of Primary Basal Cell Carcinoma of the Skin: A Systematic Review and Network Meta-analysisFREE

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Abstract

Background:

Most interventions for basal cell carcinoma (BCC) have not been compared in head-to-head randomized trials.

Purpose:

To evaluate the comparative effectiveness and safety of treatments of primary BCC in adults.

Data Sources:

English-language searches of MEDLINE, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Embase from inception to May 2018; reference lists of guidelines and systematic reviews; and a search of ClinicalTrials.gov in August 2016.

Study Selection:

Comparative studies of treatments currently used in adults with primary BCC.

Data Extraction:

One investigator extracted data on recurrence, histologic clearance, clinical clearance, cosmetic outcomes, quality of life, and mortality, and a second reviewer verified extractions. Several investigators evaluated risk of bias for each study.

Data Synthesis:

Forty randomized trials and 5 nonrandomized studies compared 18 interventions in 9 categories. Relative intervention effects and mean outcome frequencies were estimated using frequentist network meta-analyses. Estimated recurrence rates were similar for excision (3.8% [95% CI, 1.5% to 9.5%]), Mohs surgery (3.8% [CI, 0.7% to 18.2%]), curettage and diathermy (6.9% [CI, 0.9% to 36.6%]), and external-beam radiation (3.5% [CI, 0.7% to 16.8%]). Recurrence rates were higher for cryotherapy (22.3% [CI, 10.2% to 42.0%]), curettage and cryotherapy (19.9% [CI, 4.6% to 56.1%]), 5-fluorouracil (18.8% [CI, 10.1% to 32.5%]), imiquimod (14.1% [CI, 5.4% to 32.4%]), and photodynamic therapy using methyl-aminolevulinic acid (18.8% [CI, 10.1% to 32.5%]) or aminolevulinic acid (16.6% [CI, 7.5% to 32.8%]). The proportion of patients reporting good or better cosmetic outcomes was better for photodynamic therapy using methyl-aminolevulinic acid (93.8% [CI, 79.2% to 98.3%]) or aminolevulinic acid (95.8% [CI, 84.2% to 99.0%]) than for excision (77.8% [CI, 44.8% to 93.8%]) or cryotherapy (51.1% [CI, 15.8% to 85.4%]). Data on quality of life and mortality were too sparse for quantitative synthesis.

Limitation:

Data are sparse, and effect estimates are imprecise and informed by indirect comparisons.

Conclusion:

Surgical treatments and external-beam radiation have low recurrence rates for the treatment of low-risk BCC, but substantial uncertainty exists about their comparative effectiveness versus other treatments. Gaps remain regarding high-risk BCC subtypes and important outcomes, including costs.

Primary Funding Source:

Agency for Healthcare Research and Quality. (PROSPERO: CRD42016043353)

http://annals.org/aim/fullarticle/2702474/treatments-primary-basal-cell-carcinoma-skin-systematic-review-network-meta

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Skin Care Physicians of Costa Rica

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Dr. Warren Heymann: Laboratory Testing for Syphilitic Alopecia—Time to Renew Old Habits? | PracticeUpdate

Published in Dermatology

Expert Opinion / Commentary · October 16, 2018

Dr. Warren Heymann: Laboratory Testing for Syphilitic Alopecia—Time to Renew Old Habits?

Written by

 

 Warren R Heymann MD

I'm not sure how this happened. I used to check several laboratory studies in patients presenting with alopecia, including a rapid plasma reagin (RPR) for syphilis (in addition to a CBC, TSH, iron-binding studies, ANA, and vitamin D; testosterone and DHEAS would also be obtained if there was a hint of virilization). Now, it's usually just a CBC, ferritin, and TSH.

Dermatologists know that there are three great mimickers that can be included in virtually every differential diagnosis—sarcoidosis, cutaneous T-cell lymphoma, and Osler's ultimate masquerader—syphilis.

Syphilis is on the rise in recent years, especially in men having sex with men.1

I applaud Costa et al for having diagnosed syphilis in the two cases they presented—I probably would have misdiagnosed diffuse alopecia areata.2 The first was a 14-year-old girl with a 4-month history of diffuse and poorly defined hair loss in the parieto‐occipital area and a loss of the distal third of the eyebrows (Fournier's sign). The second was a 23-year-old man with diffuse, unevenly distributed hair loss for the previous 3 months. Both patients had a positive VDRL (venereal disease research laboratory) and a positive FTA-Abs (fluorescent treponemal antibody absorption); both were treated with benzathine penicillin resulting in complete hair regrowth.

Admittedly, my point of reference is an image of "moth-eaten" syphilitic alopecia (SA) appearing in an ancient edition of Andrews. As Tognetti et al state3: "SA may clinically mimic a wide range of hair disorders, including alopecia areata (AA), trichotillomania, lichen planus pilaris, tinea capitis, telogen effluvium, and androgenetic alopecia. Thus, the diagnosis may be delayed, especially when SA is the unique manifestation of secondary syphilis and primary syphilis signs are absent or not reported (ie, essential SA)."

Here is something to chew on—would you have suspected lues in the following case?

Luo and Liu reported a 2‐year‐old boy with a 3‐month history of "moth‐eaten" scalp alopecia.4 Serological tests showed a positive RPR with a titer of 1:32, and Treponema pallidum particle agglutination (TPPA) positivity. His parents tested negative for syphilis, but his grandmother demonstrated a positive RPR (1:32) and TPPA positivity. Every day, the boy's grandmother chewed food before feeding it to him; apparently, this ritual occurs in the poorly educated of rural China. The boy was diagnosed with acquired syphilis via premasticated food; the only symptom was moth‐eaten alopecia.

The current hypothesis supporting the pathogenesis of SA is a vasculitis of peribulbar capillaries causing a perifollicular lymphocytic infiltration with scattered plasma cells that stops the hair cell cycle. The tropism of T. pallidum for the hair bulge epithelium and peribulbar capillaries has been demonstrated by scalp biopsies detecting spirochetes in the peribulbar region and penetrating into the follicle matrix.3

In conclusion, there are two types of SA: symptomatic SA, which is accompanied by other lesions of secondary syphilis, and essential SA, which is free from any other cutaneous manifestations.5 Although essential SA is considered extremely rare, I wonder how many cases I have missed. Perhaps it's time again to routinely check syphilis serologies in patients presenting with non-scarring alopecia.

Point to Remember: Consider checking for syphilis in patients presenting with alopecia without other features of lues. 

Disclaimer: First published on Dr. Warren Heymann's Dermatology Insights and Inquiries website on June 4, 2018. Republished with permission.

• References

1. Patton ME, Su JR, Nelson R, Weinstock H; Centers for Disease Control and Prevention (CDC). Primary and secondary syphilis – United States, 2005-2013. MMWR Morb Mortal Wkly Rep. 2014;63(18):402-406.
2. Costa MC, Peres AS, Queiróz AJR, et al. Nonspecific diffuse alopecia as a single manifestation of syphilis infection: clinical and trichoscopic features. Int J Dermatol. 2018;57(5):593-595.
3. Tognetti L, Cinotti E, Perrot JL, et al. Syphilitic alopecia: Uncommon trichoscopic findings. Dermatol Pract Concept. 2017;7(3):55-59.
4. Luo Y, Liu J. Image gallery: Moth-eaten alopecia as the only cutaneous symptom of acquired secondary syphilis in a 2-year-old boy. Br J Dermatol. 2017;177(5):e227.
5. Cao HL, Engle MY, Shen YF, Wang JY. Moth-eaten essential syphilitic alopecia. QJM. 2015;108(2):157-158.

http://www.practiceupdate.com/content/dr-warren-heymann-laboratory-testing-for-syphilitic-alopecia-time-to-renew-old-habits/72137

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Benjamin Hidalgo-Matlock

Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 2224-0654

Momentum Escazu: 2101-9574

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