Fatty acid transporter expression and regulation is impaired in placental macrovascular endothelial cells in obese women.

OBJECTIVE: Fetal fatty acid (FA) delivery is ultimately controlled by placental transport. Focus has been the maternal-placental interface, but regulation at the feto-placental interface is unknown. METHODS: Placental macrovascular endothelial cells (EC) (n = 4/group) and trophoblasts (TB) (n = 5/group) were isolated from lean (pregravid BMI <25 kg/m2) and obese (body mass index (BMI) > 30) women. Fatty acid transporters FAT/CD36, FABPpm, FATP4, FABP 3, 4 and 5, PLIN2 and PPARα, δ, γ expression, was measured in EC and TB. Transporter response to 24 h palmitate (PA) was assessed. RESULTS: mRNA expression of FABP3, 4, 5 and PPARγ was 2- to 3-fold reduced in EC of obese versus lean women (p < .03), but not in TB. Protein level of FABPpm was 20% lower in obese (p < .05). Palmitate (PA) up-regulated CD36, FABP3, FABP4, and PLIN2 gene expression by 3- to 4-fold in lean but not obese EC (p < .05), while PA increased FABP4 and PLIN2 in lean and obese TB, and FABP5 in lean (p < .05) EC. PA exposure up-regulated peroxisome proliferator activated receptors (PPARs) 2-fold in lean and obese EC (p < .05), but not in TB. CONCLUSIONS: In obese women, FA transporter expression is lower in placental EC, but not TB, and less sensitive to saturated FA, compared to lean women. FA transport may be regulated at the feto-placental interface.

Eruptive Sebaceous Hyperplasia: A Rare Consequence of Systemic Corticosteroids.

BACKGROUND: Eruptive sebaceous hyperplasia is a rare and poorly understood consequence of immunosuppression, most commonly with cyclosporine, following organ transplantation. To date, there have been no reports documenting eruptive sebaceous hyperplasia associated with the utilization of immunosuppression outside of this clinical scenario. OBSERVATION: A 43-year-old Caucasian male with a significant history for Crohn's disease presented with the sudden appearance of multiple asymptomatic growths now present for several weeks. They were first noted two weeks following the initiation of a slow prednisone taper prescribed for a recent exacerbation of Crohn's disease. Skin examination revealed multiple 1-3mm, soft, skin colored to yellowish, dome-shaped, umbilicated papules on the forehead and the bilateral lateral/malar cheeks, clinically suggestive and confirmed histologically as sebaceous hyperplasia. CONCLUSION: To our knowledge, this is the first reported case of eruptive sebaceous hyperplasia secondary to the use of prednisone in a patient with Crohn's disease. This case brings awareness to the unique side effect of prednisone induced sebaceous hyperplasia, and demonstrates the importance of educating patients with Crohn's disease of this potential side effect when prescribing this medication.

J Drugs Dermatol. 2018;17(1):118-120.

Managing Seborrheic Keratoses: Evolving Strategies for Optimizing Patient Outcomes.

The seborrheic keratosis is the most common benign skin tumor of middle-aged and elderly adults, affecting nearly 83 million individuals in the US alone. Although these are benign lesions, many patients still undergo some form of treatment. Clinicians are frequently presented with a challenge when determining whether to remove a seborrheic keratosis, and which treatment modality to use when doing so. The most commonly used method of removal is cryotherapy, however there are numerous other options that can be employed with varying degrees of efficacy. In this article, we highlight the use of topical keratolytics, vitamin D analogues, and lasers, to name a few. We also address potential side effects associated with these treatment options, as well as discuss patients' preferences and concerns. We conclude with the most recent advances in topical treatments currently under clinical investigation, and offer treatment strategies aimed at maximizing patient satisfaction.

J Drugs Dermatol. 2017;16(11):1064-1068.

Effect of Maternal Obesity on Placental Lipid Metabolism.

Obese women, on average, give birth to babies with high fat mass. Placental lipid metabolism alters fetal lipid delivery, potentially moderating neonatal adiposity, yet how it is affected by maternal obesity is poorly understood. We hypothesized that fatty acid (FA) accumulation (esterification) is higher and FA ß-oxidation (FAO) is lower in placentas from obese, compared with lean women. We assessed acylcarnitine profiles (lipid oxidation intermediates) in mother-baby-placenta triads, in addition to lipid content, and messenger RNA (mRNA)/protein expression of key regulators of FA metabolism pathways in placentas of lean and obese women with normal glucose tolerance recruited at scheduled term Cesarean delivery. In isolated trophoblasts, we measured [3H]-palmitate metabolism. Placentas of obese women had 17.5% (95% confidence interval: 6.1, 28.7%) more lipid than placentas of lean women, and higher mRNA and protein expression of FA esterification regulators (e.g., peroxisome proliferator-activated receptor γ, acetyl-CoA carboxylase, steroyl-CoA desaturase 1, and diacylglycerol O-acyltransferase-1). [3H]-palmitate esterification rates were increased in trophoblasts from obese compared with lean women. Placentas of obese women had fewer mitochondria and a lower concentration of acylcarnitines, suggesting a decrease in mitochondrial FAO capacity. Conversely, peroxisomal FAO was greater in placentas of obese women. Altogether, these changes in placental lipid metabolism may serve to limit the amount of maternal lipid transferred to the fetus, restraining excess fetal adiposity in this population of glucose-tolerant women.

Prevalence of hormonal and endocrine dysfunction in patients with lichen planopilaris (LPP): A retrospective data analysis of 168 patients.

BACKGROUND: Studies on the pathophysiology and comorbidities associated with lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) are limited. OBJECTIVE: The purpose of this study was to determine the prevalence of androgen excess in the postmenopausal LPP population, in relation to demographics and comorbidities. METHODS: A retrospective data analysis of 413 patients with LPP, FFA, and LPP/FFA seen in the Department of Dermatology at the Cleveland Clinic Foundation in Ohio between 2005 and 2015 was conducted. Of this cohort, 168 patients met the inclusion criteria. RESULTS: Androgen excess was identified in 31.5% (n = 53) of the 168 patients with LPP and all subtypes (P < .001). Androgen deficiency was identified in 32.1% (n = 17) of the 53 patients with FFA (P < .001). The androgen excess group was significantly more likely to present with hirsutism, seborrheic dermatitis, polycystic ovary syndrome, ovarian cysts, or a combination of these (P < .001). LIMITATIONS: This study was limited by being retrospective. CONCLUSION: Our study demonstrated that LPP is associated with androgen excess, and FFA is associated with androgen deficiency.