To the Editor: As many as 42% of Americans report utilizing social media to access health information.1 Despite this trend, a minority of dermatology-related social media posts are produced by board-certified dermatologists.2 During clinical encounters, dermatologists regularly rely on verbal instruction or educational text to convey complex information to patients.3 However, through the production of high-quality, publicly available online learning tools, dermatologists have the opportunity to improve continued access to and retention of health information.

*City Facial Plastics, New York, New York; †Pilaris Dermatology, New York, New York The authors have indicated no significant interest with commercial supporters. G. Linkov: Conception and Design, Manuscript drafting, Review. K. Sukhdeo and E. Grand: Analysis and Interpretation, Manuscript drafting, Review. The JetPeel machine and PRP handpieces were kindly loaned for the study by NYLO Aesthetics (New York, NY).

The precise and reliable diagnosis of hair loss disorders is essential for developing a successful management plan. It is, thus, the responsibility of the dermatologist to select the appropriate diagnostic tools to effectively evaluate patients presenting with hair loss concerns. Fortunately, there is a growing body of noninvasive and invasive diagnostic resources, each with advantages and disadvantages. For the practicing dermatologist, tactile assessments and direct visualization are enhanced with scoring instruments, questionnaires, handheld trichoscopy, and scalp biopsy. For research and clinical study purposes, the more precise, high-resolution tools such as videodermoscopy, optical coherence tomography, and phototrichograms, may be useful.

To the Editor: We read with great interest the letter by Sharun and Pawde1 in response to our article "Evaluation of Platelet-Rich Plasma as a Treatment for Androgenetic Alopecia: A Randomized Controlled Trial."2 We thank Sharun and Pawde for their thoughtful comments and agree that interindividual variability in platelet-rich plasma (PRP) concentrations of platelets and growth factors exists.3,4 PRP preparation systems differ in methodology, which contributes to PRP variability. Although different preparation methods yield disparate PRP components, including platelet concentrations,5 Shaik et al4 recently reported no significant differences in growth factor secretion per platelet when comparing PRP prepared by using 2 different preparation systems.

Introduction: We present 2 cases in which typically irreversible lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) showed signs of reversal. Case Presentation: A 27-year-old Caucasian man presented with hair loss and intense pruritus on the vertex scalp for 4 years with biopsy-proven LPP and having failed multiple pharmacologic modalities. Six months after adding oral tofacitinib and later dapsone, he demonstrated reduced scalp visibility, evidence of crown and vertex hair regrowth, and elimination of itch. A 45-year-old premenopausal Hispanic woman presented with eyebrow loss for 3.75 years and hair loss for 9 months with biopsy-proven FFA. After beginning oral finasteride and hydroxychloroquine, triamcinolone injections, and topical minoxidil, she initially worsened over 11 months but subsequently improved over 6 months, demonstrating hair and eyebrow regrowth, reduction in glabella-hairline distance, and new absence of frontal hair line hyperkeratosis and inflammation. Discussion/Conclusion: Cicatricial alopecia involves inflammation with JAK-STAT upregulation. We report a positive clinical response in LPP to tofacitinib, a JAK1/3 inhibitor, and dapsone, an anti-neutrophilic agent. FFA is believed to involve autoimmune and/or hormonal processes. Here we report a positive clinical response to androgenic and immune modulators.

To the Editor: Medical therapy for androgenetic alopecia (AGA) is limited to 2 FDA-approved therapies, topical minoxidil and oral finasteride.1Shapiro J. Otberg N. Hair Loss and Restoration.2nd ed. CRC Press, Taylor & Francis Group, Boca Raton2015: 220Google Scholar Platelet-rich plasma (PRP), a concentrated suspension of platelets in plasma harvested from venous blood, is an emerging treatment for AGA.2Alves R. Grimalt R. Randomized placebo-controlled, double-blind, half-head study to assess the efficacy of platelet-rich plasma on the treatment of androgenetic alopecia.Dermatol Surg. 2016; 42: 491-497Crossref PubMed Scopus (112) Google Scholar, 3Alves R. Grimalt R. Platelet-rich plasma in combination with 5% minoxidil topical solution and 1 mg oral finasteride for the treatment of androgenetic alopecia: a randomized placebo-controlled, double-blind, half-head study.Dermatol Surg. 2017; Google Scholar, 4Gentile P. Cole J.P. Cole M.A. et al.Evaluation of not-activated and activated PRP in hair loss treatment: role of growth factor and cytokine concentrations obtained by different collection systems.Int J Mol Sci. 2017; : 18Google Scholar The mechanism of hair growth from PRP remains undefined but presumably involves the release of several growth factors from platelets.5Li Z.J. Choi H.I. Choi D.K. et al.Autologous platelet-rich plasma: a potential therapeutic tool for promoting hair growth.Dermatol Surg. 2012; 38: 1040-1046Crossref PubMed Scopus (222) Google Scholar Investigations of PRP for hair loss show augmentation of hair growth but mostly test PRP as monotherapy.2Alves R. Grimalt R. Randomized placebo-controlled, double-blind, half-head study to assess the efficacy of platelet-rich plasma on the treatment of androgenetic alopecia.Dermatol Surg. 2016; 42: 491-497Crossref PubMed Scopus (112) Google Scholar, 3Alves R. Grimalt R. Platelet-rich plasma in combination with 5% minoxidil topical solution and 1 mg oral finasteride for the treatment of androgenetic alopecia: a randomized placebo-controlled, double-blind, half-head study.Dermatol Surg. 2017; Google Scholar, 4Gentile P. Cole J.P. Cole M.A. et al.Evaluation of not-activated and activated PRP in hair loss treatment: role of growth factor and cytokine concentrations obtained by different collection systems.Int J Mol Sci. 2017; : 18Google Scholar, 5Li Z.J. Choi H.I. Choi D.K. et al.Autologous platelet-rich plasma: a potential therapeutic tool for promoting hair growth.Dermatol Surg. 2012; 38: 1040-1046Crossref PubMed Scopus (222) Google Scholar However, most of the AGA patients in dermatologic clinics considering PRP are on ≥1 other therapeutic agent. Therefore, to better counsel patients, we assessed whether the benefit of PRP is maintained while employed in combination with other hair restorative modalities. With institutional review board approval, we assembled the records of 24 AGA patients who received PRP while using concomitant hair restoration therapy. PRP was prepared by venipuncture of 8 mL of blood then centrifuged for 5 minutes at 1500 g (RegenKit-BCT-1, New York, NY). The supernatant harvested contained 1.6 times the normal blood concentration of platelets (total 5 mL). Baseline trichologic assessments of hair density and diameter (Folliscope, Seoul, South Korea) at the anterior crown (midline part 12 cm from glabella) were taken before an initial scalp treatment consisting of PRP on 2 consecutive months. Scalp injections, directed to areas of alopecia, deposited 0.1 mL PRP ∼1 cm deep and spaced 1 cm apart. Patients were then reassessed; if hair density increased >10 hairs/cm2 over baseline, monthly treatments were continued for 4 additional months followed by maintenance injections every 3-6 months. Mean trichoscopic measurements throughout the treatment course (average 6 months; range 2-24 months) were compared with baseline by using unequal t tests. All PRP patients used topical 5% minoxidil and 83.3% (20/24) used oral antiandrogen medications (Table I). Positive response to PRP was seen in 70.8% (17/24) of patients 2 months after initial injections. Overall, mean hair density after PRP showed a statistically significant increase from baseline on the anterior crown (+24.5 hairs/cm2, P = .022; Table II). Hair density with PRP increased >10% over baseline in 62.5% (15/24) of patients and >20% over baseline in 33.3% (8/24) of patients. One patient had an increase in hair density of >50%. Changes in hair shaft diameter did not reach statistical significance.Table IDemographics and baseline characteristics of androgenetic alopecia patients treated with PRP while on concomitant hair restoration therapyCharacteristicAll patients, % (N)Patients with positive response, % (N)Patients with no response, % (N)Total no. PRP patients24177Sex Female79.2 (19/24)76.5 (13/17)85.7 (6/7) Male20.8 (5)23.5 (4/17)14.3 (1/7)Age of AGA onset, y, average (range)29.9 (13-57)35 (13-57)18.6 (15-22)Age of treatment, y, average (range)41.9 (23-73)43.9 (23-73)36.9 (23-73)Race White70.8 (17/24)76.5 (13/17)57.1 (4/7) Asian16.7 (4/24)11.8 (2/17)28.6 (2/7) Hispanic12.5 (3/24)11.8 (2/17)14.3 (1/7)Family history of alopecia75 (18/24)82.4 (14/17)57.1 (4/7)Physical examination Frontotemporal thinning33.3 (9/24)47.1 (8/17)14.3 (1/7) Centroparietal thinning29.2 (8/24)35.3 (6/17)28.6 (2/7) Vertex thinning12.5 (3/24)17.6 (3/17) Diffuse thinning20.8 (5/24)17.6 (3/17)28.6 (2/7)Hair loss treatment Topical 5% minoxidil100 (24/24)100 (17/17)100 (7/7) Finasteride∗Men received 1 mg and women 5 mg.70.8 (17/24)70.6 (12/17)71.4 (5/7) Spironolactone25 (6/24)29.4 (5/17)14.3 (1/7) Dutasteride4.2 (1/24)0 (0/17)14.3 (1/7) Flutamide4.2 (1/24)0 (0/17)14.3 (1/7) Hair transplant4.2 (1/24)0 (0/17)14.3 (1/7) Laser therapy4.2 (1/24)0 (0/17)14.3 (1/7)Length of hair loss treatment before initiating PRP 0-4 months41.7 (10/24)47.1 (8/17)28.6 (2/7) 4+ months58.3 (14/24)52.9 (9/17)71.4 (5/7)Two-month treatment evaluation Positive response (Δ >10 hairs/cm2)70.8 (17/24) No response (Δ <10 hairs/cm2)29.2 (7/24)AGA, Androgenetic alopecia; PRP, platelet-rich plasma.∗ Men received 1 mg and women 5 mg. Open table in a new tab Table IIBaseline trichoschopic measurements versus mean follow-up trichoscopic measurements from 24 patients after initial PRP injectionsCharacteristicPatients, NBaseline (range)SDFollow-up mean (range)SDP valueAll patients, hairs/cm224154.8 (85-202)31.3179.3 (86-232)39.8.022Positive response, hairs/cm217163.1 (106-202)28.7198.1 (143.8-232)26.48.23E-04No response, hairs/cm27134.7 (85-172)29.9133.9 (86-174.5)28.5.957Hair shaft diameter, microns2346.1 (34-72)10.250.6 (35.5-65)8.7.115PRP, Platelet-rich plasma; SD, standard deviation. Open table in a new tab AGA, Androgenetic alopecia; PRP, platelet-rich plasma. PRP, Platelet-rich plasma; SD, standard deviation. Limitations of this study include the retrospective design, no blinding, and no control population. Prior reports and our own experience show PRP can be used as a standalone therapy to achieve enhanced hair growth in most but not all patients. However, as shown here, AGA patients opting for PRP are typically on multiple modalities and any newly developed therapy will likely be incorporated as an additional treatment. PRP may also serve to benefit patients' unresponsive to medical therapy. Our results of PRP as combination therapy demonstrated a significant increase in density of hairs but not caliber. These findings represent real-world outcomes that can be used to inform patients' decision-making, as PRP represents a substantially time-consuming financial and emotional investment.

BACKGROUND:Platelet-rich plasma (PRP) shows promise as an androgenetic alopecia (AGA) treatment. OBJECTIVE:To conduct a randomized placebo-controlled split-scalp study to investigate the effects of PRP on hair regrowth and thickness. METHODS:Two 7.6-cm × 7.6-cm squares were tattooed on the scalps of 35 study participants with AGA. Areas were randomly assigned to intradermal injection with PRP or saline. Participants received 3 monthly treatment sessions with evaluation 3 months after the final treatment. RESULTS:Hair density in the PRP-treated area was significantly increased compared with baseline at all visits. At the final assessment, hair density in PRP-treated areas increased from 151 ± 39.82 hairs/cm2 at baseline to 170.96 ± 37.14 hairs/cm2, a mean increase of approximately 20 hairs/cm2 (P < .05). However, hair density in placebo-treated areas also increased from 151.04 ± 41.99 hairs/cm2 to 166.72 ± 37.13 hairs/cm2 (P < .05). There was no significant difference in hair density change between the 2 groups (P > .05). No serious adverse events were reported. LIMITATIONS:Possible PRP diffusion due to split-scalp study design as well as microinjections causing microinjury to both sides. CONCLUSION:PRP may have benefit in increasing hair density.

Drug-induced hyperpigmentation (DIH) is a common side effect of several medication classes, including atypical psychoactive agents.1 Mirtazapine is an antidepressant with antiadrenergic and antiserotonergic activity. Indications for mirtazapine use include major depressive disorder and other mood disorders, anxiety, and insomnia. Typical potential adverse effects of mirtazapine include drowsiness, weight gain, xerostomia, and increased appetite.2 However, reports of hyperpigmentation are extraordinarily rare.

Tracking trichologic responses of hair restoration therapy requires sequential quantitative assessments. Visualization of the same scalp location(s) facilitates direct comparison of change. Current localization methods rely on either triangulated measurement from anatomic landmarks or skin tattooing. The former process lacks precision, whereas the latter leaves a visible mark that is undesirable to patients.

International Journal of DermatologyVolume 57, Issue 8 p. 913-914 Clinicopathologic Challenge Concentric targetoid scaly plaques in a patient with severe rheumatoid arthritis Mary E. Laird BA, Mary E. Laird BA The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorKumar Sukhdeo MD, PhD, Kumar Sukhdeo MD, PhD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorAnthony Ho BA, Anthony Ho BA The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorRachel K. Hoffmann MD, Rachel K. Hoffmann MD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorShane A. Meehan MD, Shane A. Meehan MD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorRandie H. Kim MD, PhD, Corresponding Author Randie H. Kim MD, PhD Randie.Kim@nyumc.org The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USA Correspondence Randie H. Kim, md, phd The Ronald O. Perelman Department of Dermatology 240 E 38th Street, 11th floor New York, NY, 10016 USA E-mail: Randie.Kim@nyumc.orgSearch for more papers by this author Mary E. Laird BA, Mary E. Laird BA The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorKumar Sukhdeo MD, PhD, Kumar Sukhdeo MD, PhD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorAnthony Ho BA, Anthony Ho BA The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorRachel K. Hoffmann MD, Rachel K. Hoffmann MD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorShane A. Meehan MD, Shane A. Meehan MD The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USASearch for more papers by this authorRandie H. Kim MD, PhD, Corresponding Author Randie H. Kim MD, PhD Randie.Kim@nyumc.org The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, NY, USA Correspondence Randie H. Kim, md, phd The Ronald O. Perelman Department of Dermatology 240 E 38th Street, 11th floor New York, NY, 10016 USA E-mail: Randie.Kim@nyumc.orgSearch for more papers by this author First published: 11 April 2018 https://doi.org/10.1111/ijd.13991 Funding: None. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume57, Issue8August 2018Pages 913-914 RelatedInformation

Lichen myxedematosus is condition characterized by localized areas of dermal deposition of mucin, presenting with firm papules localized to few areas of the body. The condition needs to be excluded from scleromyxedema, which, in addition to the firm papular eruption, has areas of induration and is usually associated with a monoclonal gammopathyand systemic symptoms. We present a 62-year-old woman with a several-year history of asymptomatic, firm papules over the face and arms with no evidence of thyroid disease or a monoclonal gammopathy,which is consistent with a diagnosis of localized lichen myxedematosus, the discrete papular variant. The patient is being treated with a topical calcineurininhibitor.

Despite recent advances in treatment, precursor-B-cell acute lymphoblastic leukemia (B-ALL) remains a challenging clinical entity. Recent genome-wide studies have uncovered frequent genetic alterations involving activating RAS pathway mutations and loss of the INK4A/ARF locus suggesting their important role in the pathogenesis, relapse, and chemoresistance of B-ALL. Therefore, to better understand the oncogenic mechanisms by which these alterations might promote B-ALL and to develop an in vivo preclinical model of relapsed B-ALL, we engineered mouse strains with induced somatic KrasG12D pathway activation and/or loss of Ink4a/Arf during early stages of B-cell development.

Despite recent advances in treatment, human precursor B-cell acute lymphoblastic leukemia (B-ALL) remains a challenging clinical entity. Recent genome-wide studies have uncovered frequent genetic alterations involving RAS pathway mutations and loss of the INK4A/ARF locus, suggesting their important role in the pathogenesis, relapse, and chemotherapy resistance of B-ALL. To better understand the oncogenic mechanisms by which these alterations might promote B-ALL and to develop an in vivo preclinical model of relapsed B-ALL, we engineered mouse strains with induced somatic KrasG12D pathway activation and/or loss of Ink4a/Arf during early stages of B-cell development. Although constitutive activation of KrasG12D in B cells induced prominent transcriptional changes that resulted in enhanced proliferation, it was not sufficient by itself to induce development of a high-grade leukemia/lymphoma. Instead, in 40% of mice, these engineered mutations promoted development of a clonal low-grade lymphoproliferative disorder resembling human extranodal marginal-zone lymphoma of mucosa-associated lymphoid tissue or lymphoplasmacytic lymphoma. Interestingly, loss of the Ink4a/Arf locus, apart from reducing the number of apoptotic B cells broadly attenuated KrasG12D-induced transcriptional signatures. However, combined Kras activation and Ink4a/Arf inactivation cooperated functionally to induce a fully penetrant, highly aggressive B-ALL phenotype resembling high-risk subtypes of human B-ALL such as BCR-ABL and CRFL2-rearranged. Ninety percent of examined murine B-ALL tumors showed loss of the wild-type Ink4a/Arf locus without acquisition of highly recurrent cooperating events, underscoring the role of Ink4a/Arf in restraining Kras-driven oncogenesis in the lymphoid compartment. These data highlight the importance of functional cooperation between mutated Kras and Ink4a/Arf loss on B-ALL.

Gout is an inflammatory arthritis characterised by hyperuricemia, which, if poorly controlled, can lead to the development of tophi. We report the case of a 60-year-old Caucasian man with poorly controlled polyarticular tophaceous gout with multiple comorbidities (including renal failure) who presented with tophaceous ulcers of the upper extremity. These ulcers caused extreme pain, requiring chronic opiate medications, and were associated with decreased sensation and reduced ability to move the extremity. His hospital course was complicated by acute kidney injury, haemolytic anaemia and Clostridium difficile infection. He required 1 month of antibiotics and intensive wound care for his ulcers. This case highlights the diagnosis, natural history and management of an unusual complication of hyperuricemia.

The 'soak and smear' regimen is a highly effective method for localised topical therapy employed by dermatologists for widespread inflammatory skin conditions. The regimen involves application of topical medication under occlusion after soaking in water. Complications from this treatment method are rare. We present a case of multiple, generalised methicillin-resistant Staphylococcus aureus (MRSA)-positive furuncles arising in a patient as an unexpected consequence of therapy. The case highlights an unanticipated risk of a commonly employed treatment amid an epidemic of MRSA in the community.

Wnt signaling regulates self-renewal and fate commitment of stem and progenitor cells in development and homeostasis. Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) is a co-receptor for Wnt signaling that marks highly proliferative stem and progenitor cells in many epithelial tissue types. Wnt signaling instructs neural developmental and homeostatic processes; however, Lgr5 expression in the developing and adult brain has not been characterized. Here we report that Lgr5 is expressed in the postnatal cerebellum during the maturation and synaptogenesis of cerebellar granule neurons (CGNs), processes controlled by Wnt signaling. Using a transgenic reporter mouse for in vivo Lgr5 expression analysis and lineage tracing, we reveal that Lgr5 specifically identified CGNs and was restricted temporally to the CGN maturation phase within the internal granule layer, but absent in the adult brain. Cells marked by Lgr5 were lineage restricted, post-mitotic and long-lived. The ligand for Lgr5, R-spondin, was secreted in a paracrine fashion that evolved during the maturation of CGNs, which coincided with the Lgr5 expression pattern. Our findings provide potential new insight into the critical regulation of Wnt signaling in the developing cerebellum and support a novel role for Lgr5 in the regulation of post-mitotic cells.

Colon cancer is a deadly disease affecting millions of people worldwide. Current treatment challenges include management of disease burden as well as improvements in detection and targeting of tumor cells. To identify disease state-specific surface antigen signatures, we combined fluorescent cell barcoding with high-throughput flow cytometric profiling of primary and metastatic colon cancer lines (SW480, SW620, and HCT116). Our multiplexed technique offers improvements over conventional methods by permitting the simultaneous and rapid screening of cancer cells with reduced effort and cost. The method uses a protein-level analysis with commercially available antibodies on live cells with intact epitopes to detect potential tumor-specific targets that can be further investigated for their clinical utility. Multiplexed antibody arrays can easily be applied to other tumor types or pathologies for discovery-based approaches to target identification.

Glioblastoma (GBM) is the most common primary malignant brain tumor in adults with a median survival of 12-15 months with treatment consisting of surgical resection followed by ionizing radiation (IR) and chemotherapy. Even aggressive treatment is often palliative due to near universal recurrence. Therapeutic resistance has been linked to a subpopulation of GBM cells with stem cell-like properties termed GBM initiating cells (GICs). Recent efforts have focused on elucidating resistance mechanisms activated in GICs in response to IR. Among these, GICs preferentially activate the DNA damage response (DDR) to result in a faster rate of double-strand break (DSB) repair induced by IR as compared to the bulk tumor cells. IR also activates NOTCH and the hepatic growth factor (HGF) receptor, c-MET, signaling cascades that play critical roles in promoting proliferation, invasion, and resistance to apoptosis. These pathways are preferentially activated in GICs and represent targets for pharmacologic intervention. While IR provides the benefit of improved survival, it paradoxically promotes selection of more malignant cellular phenotypes of GBM. As reviewed here, finding effective combinations of radiation and molecular inhibitors to target GICs and non-GICs is essential for the development of more effective therapies.