Background: Use of sodium-glucose cotransporter-2 (SGLT2) inhibitors has been associated with Fournier gangrene (FG), a rare urologic emergency characterized by necrotizing infection of the external genitalia, perineum, and perianal region.
Objective: To describe and compare reported cases of FG in diabetic adults receiving treatment with SGLT2 inhibitors or other antiglycemic agents.
Design: Descriptive case series.
Setting: U.S. Food and Drug Administration (FDA) Adverse Event Reporting System and published case reports.
Patients: Adults receiving SGLT2 inhibitors or other antiglycemic agents.
Measurements: Clinical and laboratory data.
Results: The FDA identified 55 unique cases of FG in patients receiving SGLT2 inhibitors between 1 March 2013 and 31 January 2019. The patients ranged in age from 33 to 87 years; 39 were men, and 16 were women. Time to onset after initiation of SGLT2-inhibitor therapy ranged from 5 days to 49 months. All patients had surgical debridement and were severely ill. Reported complications included diabetic ketoacidosis (n = 8), sepsis or septic shock (n = 9), and acute kidney injury (n = 4). Eight patients had fecal diversion surgery, 2 patients developed necrotizing fasciitis of a lower extremity that required amputation, and 1 patient required a lower-extremity bypass procedure because of gangrenous toes. Three patients died. For comparison, the FDA identified 19 FG cases associated with other antiglycemic agents between 1984 and 31 January 2019: metformin (n = 8), insulin glargine (n = 6), short-acting insulin (n = 2), sitagliptin plus metformin (n = 2), and dulaglutide (n = 1). These patients ranged in age from 42 to 79 years; 12 were men, and 7 were women. Two patients died.
Limitation: Inability to establish causality or incidence, variable quality of reports, possible underreporting, and confounding by indication.
Conclusion: FG is a newly identified safety concern in patients receiving SGLT2 inhibitors. Physicians prescribing these agents should be aware of this possible complication and have a high index of suspicion to recognize it in its early stages.
Primary Funding Source: None.
PMID
31060053 [ - as supplied by publisher]
Sent from my iPhone
Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica
Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574
Please excuse the shortness of this message, as it has been sent from a mobile device.
Treatment Outcomes of Topical Calcineurin Inhibitor Therapy for Patients With Vitiligo: A Systematic Review and Meta-analysis | Dermatology | JAMA Dermatology | JAMA Network
Treatment Outcomes of Topical Calcineurin Inhibitor Therapy for Patients With Vitiligo: A Systematic Review and Meta-analysis | Dermatology | JAMA Dermatology | JAMA Network
Treatment Outcomes of Topical Calcineurin Inhibitor Therapy for Patients With Vitiligo A Systematic Review and Meta-analysis
Key Points
QuestionWhat outcomes are associated with topical calcineurin inhibitor (tacrolimus and pimecrolimus) therapy in patients with vitiligo?
FindingsIn this meta-analysis of 46 studies including 1499 patients, topical calcineurin inhibitor monotherapy produced an at least mild response in 55.0% of the patients, at least moderate response in 38.5%, and a marked response in 18.1% after a median treatment duration of 3 months. At least moderate responses were achieved in 47.3% of children, 57.5% of lesions on the face and neck, and in 72.9% of participants when topical calcineurin inhibitors were used in combination with phototherapy.
MeaningTopical calcineurin inhibitors appear to have significant therapeutic effects on vitiligo and it seems that their use should be encouraged in patients with vitiligo.
Abstract
ImportanceTopical calcineurin inhibitors (TCIs), including tacrolimus and pimecrolimus, have been widely used for the treatment of vitiligo; however, the efficacy of TCI monotherapy is often underestimated.
ObjectivesTo estimate the treatment responses to both TCI monotherapy and TCI accompanied by phototherapy for vitiligo, based on relevant prospective studies, and to systematically review the mechanism of action of TCIs for vitiligo treatment.
Data SourcesA comprehensive search of the MEDLINE, Embase, Web of Science and Cochrane Library databases from the date of database inception to August 6, 2018, was conducted. The main key words used were vitiligo, topical calcineurin inhibitor, tacrolimus, pimecrolimus, and FK506.
Study SelectionOf 250 studies initially identified, the full texts of 102 articles were assessed for eligibility. A total of 56 studies were identified: 11 studies on the TCI mechanism, 36 studies on TCI monotherapy, 12 studies on TCI plus phototherapy, and 1 study on TCI maintenance therapy.
Data Extraction and SynthesisTwo reviewers independently extracted data on study design, patients, intervention characteristics, and outcomes. Random-effects meta-analyses using the generic inverse variance weighting were performed for the TCI monotherapy and TCI plus phototherapy groups.
Main Outcomes and MeasuresThe primary outcomes were the rates of at least mild (≥25%), at least moderate (≥50%), and marked (≥75%) repigmentation responses to treatment. These rates were calculated by dividing the number of participants in an individual study who showed the corresponding repigmentation by the total number of participants who completed that study.
ResultsIn the 56 studies included in the analysis, 46 (1499 patients) were selected to evaluate treatment response. For TCI monotherapy, an at least mild response was achieved in 55.0% (95% CI, 42.2%-67.8%) of 560 patients in 21 studies, an at least moderate response in 38.5% (95% CI, 28.2%-48.8%) of 619 patients in 23 studies, and a marked response in 18.1% (95% CI, 13.2%-23.1%) of 520 patients in 19 studies after median treatment duration of 3 months (range, 2-7 months). In the subgroup analyses, face and neck lesions showed an at least mild response in 73.1% (95% CI, 32.6-83.5%) of patients, and a marked response in 35.4% (95% CI, 24.9-46.0%) of patients. For TCI plus phototherapy, an at least mild response to TCI plus phototherapy was achieved in 89.5% (95% CI, 81.1-97.9%) of patients, and a marked response was achieved in 47.5% (95% CI, 30.6-64.4%) of patients.
Conclusions and RelevanceThe use of TCIs, both as a monotherapy and in combination with phototherapy, should be encouraged in patients with vitiligo.
Sent from my iPhone
Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica
Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574
Please excuse the shortness of this message, as it has been sent from a mobile device.
FDA Approves First Treatment for Paediatric Patients With Lupus
The US Food and Drug Administration (FDA) has approved belimumab (Benlysta) intravenous (IV) infusion for treatment of children with systemic lupus erythematosus (SLE).
This is the first time that the FDA has approved a treatment for paediatric patients with SLE.
Belimumab has been approved for use in adult patients since 2011.
"The agency expedited the review and approval of this application because belimumab IV fulfils an unmet need for therapies, specifically in paediatric patients with SLE," said Janet Woodcock, MD, FDA Center for Drug Evaluation and Research, Rockville, Maryland. "While there is no cure for lupus, treatment can help our youngest patients control their disease with the hope of improving their quality of life and lowering their risk of long-term organ damage and disability."
While childhood-onset SLE is rare, when diagnosed, it is generally more active in children and adolescents than in adult patients, particularly in how it impacts organs such as the kidneys and central nervous system. As a result of the disease starting early in life, paediatric patients with SLE are at a higher risk for developing increased organ damage and complications from the disease as well as adverse events from the lifelong treatments usually required.
The efficacy of belimumab IV for the treatment of SLE in paediatric patients was studied over 52 weeks in 93 children with SLE. The proportion of paediatric patients achieving the composite primary endpoint, the SLE response index (SRI-4), was higher in children receiving belimumab IV plus standard therapy compared with placebo plus standard therapy.
Pediatric patients who received belimumab IV plus standard therapy also had a lower risk of experiencing a severe flare, as well as longer duration of time until a severe flare occurred (160 days vs 82 days).
The drug's safety and pharmacokinetic profiles in paediatric patients were consistent with those in adults with SLE.
The doctor and patient information for belimumab includes a warning for mortality, serious infections, hypersensitivity, and depression, based on data from clinical studies in adults with SLE.
The drug should not be administered with live vaccines.
The manufacturer is required to provide a Medication Guide to inform patients of the risks associated with belimumab.
The most common side effects of belimumab include nausea, diarrhoea, and fever. Patients also commonly experienced infusion reactions, so healthcare professionals are advised to pre-treat patients with an antihistamine.
SOURCE: US Food and Drug Administration
Sent from my iPhone
Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica
Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574
Please excuse the shortness of this message, as it has been sent from a mobile device.
A diet high in ultra-processed foods is associated with elevated risk for cardiovascular disease (CVD) and mortality, suggest a pair of studies in The BMJ.
In the first study, over 100,000 adults in France who were free of CVD at baseline provided roughly six 24-hour dietary records over 2 years. During a median 5 years' follow-up, CVD event rates were higher among people in the top quarter of ultra-processed food consumption, compared with the bottom quarter (277 vs. 242 per 100,000 person-years). Each absolute increase of 10 in the percentage of ultra-processed food consumed was associated with 11%–13% increased risk for cardiovascular, coronary heart, and cerebrovascular diseases.
In the second study, Spanish researchers assessed food-frequency questionnaires from 20,000 adults. During a median follow-up of 10 years, 2% of participants died. People who were in the top quarter of ultra-processed food consumption (five or more servings daily) had a 62% higher mortality risk than participants in the bottom quarter (less than two servings daily).
Editorialists write: "The dietary advice is relatively straightforward: eat less ultra-processed food and more unprocessed or minimally processed food."
Walking at least 4400 steps daily might help improve survival in older women, a JAMA Internal Medicine study suggests — welcome news for people who don't hit the much-promoted goal of 10,000 steps daily.
Nearly 17,000 older women wore a hip accelerometer for 7 days to collect step counts. Participants were then divided into quartiles based on the median number of daily steps: 2700, 4400, 5900, and 8400.
During roughly 4 years' follow-up, 3% of the women died. After adjustment for confounders like age, smoking, and comorbid conditions, women in the three higher quartiles of daily steps had significantly lower mortality risks — reductions of 46%, 53%, and 66%, respectively — than those in the lowest quartile. Mortality declined with increasing steps until roughly 7500 steps per day, at which point the benefit leveled off.
The researchers conclude, "These findings may serve as encouragement to the many sedentary individuals for whom 10,000 steps/d pose an unattainable goal."
The Food and Drug Administration (FDA) has granted Breakthrough Therapy designation to pomalidomide (Pomalyst®), a thalidomide analogue, for the treatment of patients with Kaposi sarcoma. Breakthrough Therapy is a process designed to expedite the development and review of drugs that are intended to treat a serious condition and preliminary clinical evidence indicates that the drug may demonstrate substantial improvement over available therapy.
Pomalidomide is being investigated as a potential treatment for patients with HIV-positive Kaposi sarcoma who have previously received systemic chemotherapy as well as in patients with HIV-negative Kaposi sarcoma. There are currently no FDA-approved treatments for HIV-positive patients who are refractory or intolerant of systemic chemotherapy.
Read Dr. Heymann's analysis of new pitfalls in the diagnosis of Kaposi sarcoma in DW Insights and Inquiries.
Sent from my iPhone
Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica
Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574
Please excuse the shortness of this message, as it has been sent from a mobile device.
Life is just a bowl of cherry angiomas | American Academy of Dermatology
Life is just a bowl of cherry angiomas
By Warren R. Heymann, MD May 29, 2019 Vol. 1, No. 13
"Dr. Heymann, I've noticed a number of these spots appearing lately."
"They're called cherry angiomas — totally benign."
"Why I am getting them?"
"Maturity."
"You mean I'm getting old!"
"I did not say that — you did!"
"I don't like them. Can you take them off?"
"Easily, especially with the laser. It would be considered a cosmetic procedure."
"You mean Medicare won't pay for it?"
"Correct."
"Forget it — I'll live with them."
I imagine this conversation occurs daily in every dermatologist's office. Of all the cutaneous entities I have never thought much about, cherry angiomas (CAs, aka senile angioma, Campbell de Morgan spot) top the list. It is high time to take a fresh look at these common lesions and ask pertinent questions – notably what are they and why do they appear?
The following is the entry on CAs from the Andrews textbook (1):
These round, slightly elevated, ruby-red papules 0.5–6 mm in diameter are the most common vascular anomalies. It is a rare 30-year-old person who does not have a few, and the number increases with age. Probably every 70-year-old person has some senile angiomas. Most are on the trunk; they are rarely seen on the hands, feet, or face. Early lesions may mimic petechiae. When lesions are surrounded by a purpuric halo, amyloidosis should be suspected. Eruptive lesions have been described after nitrogen mustard therapy. Light electrodesiccation or laser ablation with intense pulsed light (IPL) and long-pulse Nd : YAG laser systems can be effective. Shave excision can also be performed, but most patients accept reassurance and do not request removal.
In a meticulous study of 488 patients who were at least 40 years old, having at least one truncal CA, Fettahlioglu Karaman observed a pale halo around CAs in 5.1% of the patients or in 2.0% of the lesions. It was more prevalent in patients aged 60 years or older with more than 4 lesions, being more frequent around lesions larger than 3 mm. (2) I am not sure if I have ever noticed these haloes, or, if so, just ignored them. It remains to be determined if haloes are associated with the evolution of CAs.
Histologically, CAs are circumscribed vascular proliferations of venule-like blood vessels in a thickened papillary dermis. In a study of 23 lesions, Fernandez-Flores and Colmenero demonstrated that all cases showed intense expression of Wilms tumor protein 1 (WT1) in 80-100% of endothelial cells. WT1 is expressed by "actively growing" endothelia, either tumoral or reactive. Additionally, Ki67 staining displayed proliferation by the endothelia in all lesions. These findings support the theory that CAs are either vascular tumors, or reactive vascular proliferations, but not vascular malformations. (3)
Other findings challenge that conclusion. Klebanov et al sequenced 323 cancer-relevant genes in 10 CAs from 6 women and 4 men, with a median age of 54 years. Five samples (50%) revealed somatic missense mutations in GNAQ and GNA11. Individually, these mutational hot spots are known to be involved in entities that include congenital and anastomosing hemangiomas, hepatic small-vessel neoplasms (Q209), port-wine stains, and Sturge-Weber syndrome (R183). Both hot spots are associated with blue nevi, melanoma associated with blue nevus, and uveal melanoma. The authors suggest that these mutations may lead to aberrations in vessel formation rather than endothelial proliferation. Additionally, these findings could help explain the panoply of features observed in phakomatosis pigmentovascularis. (4) In an accompanying editorial, Siegel notes that the GNAQ and GNA11 mutations in CAs demonstrate how we continually acquire somatic mutations throughout life, confirming that humans are mosaics. (5)
Perhaps both mosaic mutations and a proliferative component are involved. Could angiogenic factors be at play? In a captivating article, Darjani et al performed a case-control study of 122 cases with CAs and 122 control subjects without CAs. Demographic characteristics, number of CAs, and serum lipid profile were collected for all subjects. Mean levels of the total cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein were higher in patients with CAs compared to control subjects in which differences were significant for total cholesterol, low-density lipoprotein, and triglyceride (P < 0.05) but not for high-density lipoprotein level. The authors hypothesized that CAs may form in response to angiogenic agents that were elaborated to compensate for the occlusive effects of atherogenic agents. (6) Although I do not plan on checking a lipoprotein profile in every patient with CAs, this is an intriguing study that warrants further exploration.
The lyrics "Life is just a bowl of cherries. Don't take it serious; it's too mysterious" could easily be applied to CAs. Clinically, they are not serious, but understanding their pathophysiology remains a mystery. As we learn more about the genetics and molecular pathway(s) to their appearance, novel topical therapies, akin to rapamycin for angiofibromas, could be in the offing.
Point to remember: Although cherry angiomas appear when we get older and wiser, our knowledge about their pathogenesis is in its infancy.
Our expert's commentary
Jason B. Lee, MD Clinical Vice Chair Director, Jefferson Dermatopathology Center Director, Residency and Dermatopathology Fellowship Director, Jefferson Pigmented Lesion Clinic Jefferson University Hospitals
In his current commentary, Dr. Heymann reflects on how little we know about a commonly encountered vascular lesion, namely cherry angioma. The same can be said of seborrheic keratosis, another frequently confronted lesion that we know very little about its underlying pathogenesis. Dr. Heymann, in his usual incisive and playful way, highlights 4 small studies on cherry angiomas and their relevance to our clinical practice. The study by Karaman will now make me look for a subtle halo around each cherry angioma. In the rare instances in which I observed a halo, I just assumed the phenomenon was because of a compensatory vasoconstrictive effect, nothing more. Fernandez-Flores and Colmenero affirm my view that a cherry angioma is a benign vascular neoplasm, never thought otherwise. I do not believe they are a marker of hyperlipidemic state as Durjani et al. suggest.
In my clinical practice, I have only observed an association with pregnancy on rare occasions. Though I am not as optimistic as Dr. Heymann that someday we might come up with a topical therapy for cherry angiomas by understanding the genetic basis of the proliferative process, I welcome the genetic studies on such a common banal entity. I have always asked why basic scientists often gravitate toward studying rare conditions. I understand that the idea is to apply the knowledge learned from studying the rare conditions to more common ones. Why not study the common conditions and attempt to apply the knowledge to the rare ones? By understanding the underpinning genetic basis of the proliferative process in cherry angiomas, additional insight may be gained in other rarer proliferative vascular processes, both benign and malignant such as glomeruloid hemangioma, hemangioendotheliomas, and angiosarcomas. Contrary to the suggestion by Klebanov et al. that cherry angiomas are rarely sampled, they are not infrequently removed for diagnostic and therapeutic reasons, being mistaken for pyogenic granuloma when traumatized. There are plenty of paraffin-embedded blocks of cherry angiomas in our dermatopathology laboratory for the next generation of studies.
1.James WD, et al (eds). Andrews' Diseases of the Skin, 12th edition. Elsevier, 2015, pp 590. 2.Fettahlioglu Karaman B. Halo formation around cherry angiomas: A rare but substantial finding. Med Sci Monit 2018 Jul 20; 24: 5050-5053. 3.Fernandez-Flores A, Colmenero I. Campbell de Morgan spots (cherry angiomas) show endothelial proliferation. Am J Dermatopathol 2018; 40: 894-898). 4.Klebanov N, Lin WM, Artomov M, Shaughnessy M, et al. Use of targeted next-generation sequencing to identify activating hot spot mutations in cherry angiomas. JAMA Dermatol 2019; Jan 2 [Epub ahead of print]. 5.Siegel DH. Cherry angiomas- further expanding the phenotype with somatic GNAQ and GNA11 mutations. JAMA Dermatol 2019; Jan 2 [Epub ahead of print]. 6.Durjani A, Rafiei R, Shafaei S, Rafiei E, et al. Evaluation of lipid profile in patients with cherry angioma. Dermatol Res Pract 2018; May 13;2018:4639248.
All content found on Dermatology World Insights and Inquiries, including: text, images, video, audio, or other formats, were created for informational purposes only. The content represents the opinions of the authors and should not be interpreted as the official AAD position on any topic addressed. It is not intended to be a substitute for professional medical advice, diagnosis, or treatment.
A new analysis, published in JAMA Internal Medicine, adds to the evidence that nonfasting lipid measurements are as clinically useful as fasting measurements.
Nearly 8300 adults at increased cardiovascular (CV) risk had fasting and nonfasting lipid levels measured 4 weeks apart. Participants' total, LDL, and HDL cholesterol levels showed "negligible" differences between their fasting and nonfasting samples, while triglycerides were "modestly higher" in nonfasting samples.
During a median 3 years' follow-up, some 210 major coronary events occurred. Nonfasting and fasting lipid levels were similarly associated with incident coronary events — a finding that persisted in a subanalysis of patients without prior vascular disease. Additionally, nonfasting and fasting levels showed high agreement in terms of classifying patients into CV risk categories.
The researchers say their findings "provide robust evidence and more impetus for physicians to more broadly adopt nonfasting measurement of lipid levels for routine practice, in a manner consistent with ... recent guideline recommendations."
OBJECTIVE: Topical corticosteroids (CSs) are commonly used to treat inflammatory skin conditions including eczema and psoriasis. Although topical CS package inserts describe hyperglycemia and glycosuria as adverse drug reactions, it is unclear whether topical CS use in real life is also associated with an increased risk of type 2 diabetes (T2D).
RESEARCH DESIGN AND METHODS: Two matched case-control studies and one cohort study were conducted using routinely collected health care data from Denmark and the U.K. A total of 115,218 and 54,944 adults were identified as case subjects with new-onset T2D in the Danish and U.K. case-control study, respectively. For the Danish cohort study, 2,689,473 adults were included. The main exposure was topical CSs, and the outcome was incident T2D.
RESULTS: Topical CS was significantly associated with T2D in the Danish (adjusted odds ratio [OR] 1.25 [95% CI 1.23-1.28]) and U.K. (adjusted OR 1.27 [95% CI 1.23-1.31]) case-control studies. Individuals who were exposed to topical CSs had significantly increased risk of incident T2D (adjusted hazard ratio 1.27 [95% CI 1.26-1.29]). We observed significant dose-response relationships between T2D and increasing potency of topical CSs in the two Danish studies. The results were consistent across all sensitivity analyses.
CONCLUSIONS: We found a positive association between topical CS prescribing and incident T2D in Danish and U.K. adult populations. Clinicians should be cognizant of possible diabetogenic effects of potent topical CSs.
1.Limpie pilas, canoas, estañones, baldes, bebederos de animales u otros recipientes útiles que puedan acumular agua.
2.Tape todos los recipientes donde almacene agua.
3.Vuelque botes, pangas u otro tipo de embarcaciones.
4.Rellene huecos de árboles, floreros de cementerios, blocks, tapias, entre otros.
5.Recicle todos los materiales de plástico, aluminio o vidrio que puedan acumular agua.
6.Reutilice de una manera creativa y amigable con el ambiente, todos los recipientes de plástico, aluminio, vidrio y llantas.
7.Agujeree llantas que se encuentran en parques, y parqueos, para que no acumulen agua.
8.Entierre pipas, cocos, cáscaras o cualquier otro desecho orgánico.
9.Ponga bajo techo cualquier objeto que acumule agua y que no puede deshacerse de él.
10.Elimine solo en la basura: cualquier material de desecho capaz de acumular agua.
11.Fumigue aquellos sitios oscuros de su vivienda tales como: debajo de pilas, armarios, closet, etc.
12.Organícese con otros vecinos para que en su barrio no haya ninguna posibilidad de que el mosquito que transmite el dengue se reproduzca.
13.Protéjase si vive o visita un lugar donde haya transmisión activa de dengue, use repelente, especialmente, al amanecer y al atardecer y en las zonas más expuestas de su cuerpo.
Este correo es de interés único del destinatario. Si usted lo recibió por error, elimínelo, por favor. El mensaje está libre de virus. CCSS.
Bye-bye, bumps! How to get rid of razor bumps for good
Learn how to get rid of razor bumps fast and how to prevent them in the first place.
ByChrissy Callahan
It's an all-too-familiar scenario: You've just shaved and are ready to show off smooth legs in a flirty dress. But then you notice a raised, red bump that starts to feel tender to the touch — razor bumps strike again!
This beauty mishap always seems to wreak havoc at the most inopportune moments, but you don't have to accept razor bumps as inevitable. TODAY Styleconsulted dermatologists to unearth the secret behind avoiding and getting rid of razor bumps so you can feel ready for summer!
Anyone who's ever had a razor bump can tell you how aggravating these pesky raised bumps are. Typically found where a hair follicle emerges from the surface of the skin, razor bumps can sometimes be mistaken for acne.
"Depending on the color of your skin, razor bumps can look like red bumps in Caucasians, but in darker skin types the bumps are usually darker brown in color," said Dr. Noelani González, director of cosmetic dermatology at Mount Sinai West in New York City.
Much like acne, razor bumps can feel tender or painful when inflamed, but what you experience as a razor bump might be a bit different than what your friends see or feel.
"A razor bump is a colloquial term for redness and bumps after shaving, not something specific. But dermatologically, it can include any number of issues, most commonly folliculitis and pseudofolliculitis barbae," said Dr. Robert Anolik, a fellow of the American Academy of Dermatology.
When hair follicles become irritated, folliculitis can occur, causing redness and swelling (bumps). "It tends to appear dotted because the majority of the inflammation is at the hair root," Anolik said.
Pseudofolliculitis barbae, on the other hand, is a bit different. "It's an inflammatory reaction to the hair shaft reentering the skin — like with ingrown hairs," said Dr. Dendy Engelman, a dermatologist in New York City.
Shaving can be tedious, and it's sometimes tempting to rush through the process. But following these shaving best practices can help prevent pesky razor bumps down the line.
Shave in the right direction: "If you shave in many different directions, you increase the chances of razor bumps, irritation and even ingrown hairs," Engelman said. "It is best to shave in the direction your hair grows or against it."
Don't shave too close to the skin: "When you pull your skin taut to get that close shave, once you release it, your skin goes over that hair shaft that you just cut and the hair will start growing under your skin, causing the bumps. This is especially common if you have thick, coarse or curly hair," González said.
Use the best tools: "Prevent future razor bumps and ingrown hairs by making sure you are using a sharp razor," Engelman said. And don't forget to keep your razors clean, and swap them out often!
Exfoliate regularly: "Getting rid of dead skin cells on the surface before you shave can help you avoid hairs getting caught under your skin," González said.
Keep skin moisturized: "Use a moisturizing cream or shaving gel, and also moisturize right after you shave. Try using a moisturizer with salicylic acid or glycolic acid to gently exfoliate the skin," González said.
Try as you might, you can't always avoid a razor bump, and some people are just more naturally prone to them.
"Razor bumps are more common in darker skin types, and in people who have thick, coarse and curly hair. Same goes for those areas of the body that have thicker, coarse hairs like the pubic area and beard area in men," González said.
Razor bumps happen! And when they do, you typically want immediate relief. Although there's no instant cure-all for razor bumps, there are a few ways to help send them quickly on their way.
Douse your skin with cool water after shaving to help soothe it.
Dealing with a tricky razor bump? Gonzálezsuggests combining a retinoid, topical steroid and/or an antibacterial product.
Consider using a toner with ingredients like aloe, witch hazel and willow bark to tackle inflammation and kill bacteria. But Anolikrecommends treading lightly, as toners can sometimes irritate raw skin.
If you notice regular razor bumps, González suggests visiting a board-certified dermatologist and trying laser hair removal to get to the root of the problem.
Board-certified dermatologist Mary Lupo recommends using a retinoid to prevent dead skin buildup that can keep hairs from clearing the surface of your skin. This one from Paula's Choice helps refresh skin with a blend of antioxidants.
Hate having to switch out razor blades? Opt for a rechargeable razor complete with a cleaning brush to keep your razor in the best shape possible and avoid razor bumps.
Cortisone and benzoyl peroxide go hand in hand as beauty cabinet must-haves, and this gel form of the multitasking ingredient can help soothe irritated skin.
4. CeraVe SA Lotion for Rough & Bumpy Skin, $13 (usually $16), Amazon
Moisturize and exfoliate the skin after shaving with this targeted lotion featuring salicylic acid.
Breaking the terbinafine laboratory habit for onychomycosis
By Warren R. Heymann, MD May 22, 2019 Vol. 1, No. 11
Are you a creature of habit when it comes checking laboratory tests for certain prescriptions? I am. I get nervous if the quantiferon TB test is not checked annually for patients on biologics. If my patient is on SSKI, I want to see a thyrotopin level (TSH) after two months. If I'm treating a patient for onychomycosis with terbinafine for a standard 12-week course, I routinely check a complete blood count (CBC) and liver function tests (LFTs) at baseline and at six weeks. Why? Because that is what I've been doing for years.
Fortunately, old paradigms are being challenged, leading to changes in management. I have become much less compulsive about checking serum potassium levels in young healthy women on spironolactone. I no longer worry about checking CBCs in patients on isotretinoin, while LFTs and lipids are obtained less frequently. Fewer laboratory studies finds favor with both patients and the health care economy. I'm delighted by any studies that assuage my obsessive tendencies.
Stolmeier et al. examined the rate of abnormal laboratory tests in 4985 healthy adults and children taking terbinfine orgriseofulvin for dermatophyte infections. The authors identified a low rate of laboratory test result abnormalities in patients taking terbinafine or griseofulvin. When laboratory test result abnormalities occurred, most were low grade and did not require subsequent laboratory test result evaluation nor discontinuation of the drugs in 99.9% of patients. Elevations in alanine aminotransferase (ALT) measurements were detected infrequently and were comparable to baseline detection rates for terbinafine, griseofulvin microsize, and griseofulvin ultramicrosize. Rates of elevated aspartate aminotransferase measurements (AST), anemia, lymphopenia, and neutropenia were also infrequent and comparable to baseline rates. The authors assert that routine interval laboratory test result monitoring appears to be unnecessary in adults and children without underlying hepatic or hematologic conditions taking terbinafine or griseofulvin for dermatophyte infections. They suggest that abandoning frequent laboratory monitoring can decrease unnecessary health care spending, decrease patient psychological angst associated with blood draws, and allow for expanded use of these effective oral medications. This study was designed to address interval laboratory testing, not baseline examinations. (1) This commentary will focus only on terbinafine for onychomycosis.
The package insert for terbinafine (oral granules) states that hepatotoxicity may occur in patients with and without pre¬existing liver disease. Pretreatment serum transaminase (ALT and AST) tests are advised for all patients before taking the drug. Any symptoms of persistent nausea, anorexia, fatigue, vomiting, right upper abdominal pain or jaundice, dark urine, or pale stools must be reported. Patients with these symptoms should discontinue taking the drug, and the patient's liver function should be immediately evaluated. (There is no comment about interval LFTs). Regarding hematologic effects, "cases of severe neutropenia have been reported; these were reversible upon discontinuation of terbinafine, with or without supportive therapy. If clinical signs and symptoms suggestive of secondary infection occur, a complete blood count with differential should be obtained." For patients with known or suspected immunodeficiency, physicians should consider monitoring complete blood counts if treatment continues for more than six weeks.
Despite the rarity of terbinafine-induced hepatoxicity, such reports exist. The hepatic injury is usually a mixed picture of cholestatic and hepatocellular disease, hypothetically due to a metabolic idiosyncratic reaction. Cases of hepatic failure attributed to terbinafine necessitating liver transplantation have been reported, an example being the case of a 50-year-old African-American man treated for onychomycosis. (2) The main treatment of drug-induced hepatic injury is drug withdrawal, with the presumption (not proven) that early withdrawal of the drug prevents progression of liver disease. For that reason, Kaushal et al. recommend "to monitor patients clinically and by measuring liver biochemistry through periodic blood tests after confirming normal liver function at the onset of therapy with terbinafine." (3)
Pillans and Boyd studied 12 cases of granulocytopenia associated with terbinafine use in Australia, one patient having agranulocytosis. The mean age of the participants was 64 years. Sex was reported in 11 patients and all but one was a woman. Time to onset of neutropenia/agranulocytosis was 4-5 weeks in most cases. Neutropenia was typically severe with neutrophil counts < or = 0.3 x 10(3)/mm3 in all but three of 11 patients where counts were given. Terbinafine was discontinued in all patients, five were hospitalized and one died of septic shock. Six patients received antibiotics and three were given granulocyte colony stimulating factor. The authors noted that it takes approximately 1 month or longer for the development of manifestations of neutropenia, which include fatigue, fever, sore throat and mouth ulceration. Withdrawal of terbinafine and appropriate management of febrile neutropenia will probably result in a favorable outcome, usually within a week. Patients should be warned about this potentially life-threatening adverse reaction and the warning symptoms. (4). Reversible agranulocytosis associated with oral terbinifine has also been reported in children. The authors, however, note that routine monitoring for hematologic side effects is not considered a requirement when treating immunocompetent adults. (5)
Will I change my terbinafine laboratory regimen when treating onychomycosis? I would be delighted to do so when the AAD creates guidelines clearly stating that laboratory studies (CBC, LFTs — baseline and/or interval) are no longer necessary. I applaud Stolmeier et al. for their efforts that give us a sense of perspective. Until those guidelines are available, however, I will likely keep my current routine, perhaps foregoing the CBC. I play a game with my residents — "which attorney would I rather be?" Imagine being the dermatologist who prescribed terbinafine for a patient who developed hepatic failure leading to a liver transplant. "Tell me doctor, why did you not check liver function studies?" Somehow, I think the jury would not be too impressed with hearing "the patient was afraid of needles, and I saved the health care system $100!" It would be much easier to justify not obtaining laboratory studies when that is the standard of care. I have the sense that we will be there soon, should the findings of Stolmeier et al. be confirmed.
Point to remember: Interval testing of hepatic function for patients on terbinafine is of little value.
Our expert's viewpoint
Joel M. Gelfand, MD, MSCE Professor of Dermatology and of Epidemiology Vice Chair of Clinical Research Medical Director, Dermatology Clinical Studies Unit Director, Psoriasis and Phototherapy Treatment Center University of Pennsylvania Perelman School of Medicine
How does a dermatologist who is also an epidemiologist handle the problem of low value safety lab testing? The study by Stolmeier and colleagues demonstrates that checking LFTs in patients on terbinifine is unlikely to change clinical management. Stated another way, there is no evidence that checking LFTs will prevent one of the most feared (but fortunately, extremely rare) side effects of terbinifine, fulminant hepatic necrosis. The data by Stolmeier can be used to counsel patients and allow them the choice of checking labs. An informed patient who opts out of lab monitoring will be a happy patient with an exceptionally low risk of experiencing a rare but serious liver complication that likely can't be mitigated by lab testing. An anxious patient who decides to pursue lab monitoring will appreciate being engaged in the decision-making process.
1.Stolmeier DA, Stratman HB, McIntee TJ, Stratman EJ. Utility of laboratory test result monitoring in patients taking oral terbinafine or griseofulvin for dermatophyte infections. JAMA Dermatol2018154: 1409-1416. 2.Perveze Z, Johnson MW, Rubin RA, Sellers M, et al. Terbinafine-induced hepatic failure requiring liver transplantation. Liver Trans 2007; 13: 162-164. 3.Kaushal M, Tolani P Kumar N, Sharma S. Terbinafine-induced liver injury. Natl Med J India 2017; 30: 321-323. 4.Pillans PI, Boyd IW. Toenails and agranulocytosis. Int Med J 2007; 37: 572-575. 5.Aguilar C, Mueller KK. Reversible agranulocytosis associated with oral terbinafine in a pediatric patient. J Am Acad Dermatol 2001; 45-632-634.
Sent from my iPhone
Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica
Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574
Please excuse the shortness of this message, as it has been sent from a mobile device.