BACKGROUNDCosmetic procedures for antiaging carry inherent risks of adverse events. One that has not yet been well characterized is transitory or permanent alopecia. This is attributable to numerous mechanisms including pressure, ischemia, inflammation, and necrosis. Cases of postcosmetic procedure alopecia have been reported after mesotherapy as well as hyaluronic acid filler, deoxycholic acid, and botulinum toxin injections.OBJECTIVEThis review serves to describe the currently known causes of postcosmetic procedure alopecia and the mechanisms by which alopecia is attained. Furthermore, this review highlights the risk of unregulated mesotherapy injections for cosmetic enhancement and to bring attention to the increasing number reports of alopecia after these procedures.METHODSA systematic review of the literature from 2000 to 2022 was conducted looking for keywords such as “alopecia,” “cosmetic procedures,” “mesotherapy,” and “hyaluronic acid” in Google Scholar and PubMed.RESULTSTen articles met the criteria set forth in the authors' literature review. Many of the procedures resulted in partial or complete resolution of alopecia.CONCLUSIONAlopecia after cosmetic injection procedures is an underreported adverse effect. More research is needed to further characterize the risk of alopecia after mesotherapy and other injection procedures.

4646 Background: Hepatocellular carcinoma (HCC) represents >90% of primary liver neoplasms and develops mainly in patients with liver cirrhosis. Risk factor identification for development of HCC in patients with cirrhosis is of great relevance due to its high incidence and poor prognosis when detected at advanced stages. The aim of our study was to identify HCC development-associated risk factors in a cohort of patients with hepatitis virus-related chronic liver disease and cirrhosis. Materials and Methods: Patients with diagnosis of hepatitis virus-related cirrhosis from January 1980 to January 2000 were included. Patients were followed with abdominal US and determination of AFP levels, physical examination, and biochemical tests every 3–6 months. The endpoint in this study was defined as development of HCC. Liver histology was evaluated according to the METAVIR. Results: 282 patients met the inclusion criteria; most (86%) had a serologic diagnosis of hepatitis C virus, and only 14% had hepatitis B virus at the time of diagnosis of cirrhosis, while 56 and 37% were classified as Child A and B, respectively; only 7% as Child C. Histological activity was mild in 59% of patients; moderate and severe in 41%. Mean annual incidence was 1.87%; 22 and 35% of patients developed HCC at 10 and 15 years of follow-up, respectively. Diagnosis of HCC was made by histopathology in 37% and by tumoral lesion-associated AFP elevation confirmed by imaging studies in 63%. In multivariate analysis, 3 variables were associated with HCC: moderate to severe histological activity; platelet count <105 103/mm3, and alpha- fetoprotein >5 ng/mL. We divided patients into two groups according to regression coefficient: low and high-risk; patients assigned to the low-risk group showed 5, 10, and 15-year HCC incidences of 3.4, 6.4, and 6.4%, respectively, in contrast to patients from the high-risk group, who showed incidences of 17.8, 33.5, and 56.8%, respectively. Conclusions: We found three HCC-associated variables: histological activity; platelet count and alpha-fetoprotein levels. Patients considered as high-risk for developing hepatocellular carcinoma must be considered candidates for closer follow-up. No significant financial relationships to disclose.

Methods: Blood, plasma and serum samples were spiked with known quantities of human DNA. To optimize the yield of DNA, we investigated the effects of changes in the blood collection and processing, storage and DNA extraction protocols. We compared two DNA purification methods, the QIAamp blood DNA kit (QIAGEN) (with and without proteinase K pre-digestion) and phenol/chloroform DNA extraction after heat denaturation (5 minutes at 95˚C). Extracted DNA was quantified using the PicoGreen assay and its quality was checked by conventional PCR analysis for the p53 gene. Results: Using the standard QIAamp protocol, the efficiency of DNA extraction from serum was 13.8 ± 5.9% (Mean ± SD). Pre-incubation with proteinase K (0.4 mg/ml, QIAGEN) at 37˚C for 2 hours significantly increased the DNA recovery (p<0.0001, unpaired t-test), but longer incubation time and incubation at 50˚C did not improve the DNA yield further. Further improvements in the efficiency of the QIAamp protocol were obtained by increasing the volume of elution buffer, but reloading the columns and using different buffers did not improve the yield. Using the phenol/chloroform extraction method after heat denaturation, the efficiency of DNA extraction was 52.7 ± 4.6% (Mean ± SD), which is significantly better than the QIAamp protocol (p<0.0001, unpaired t-test). Delays in processing blood samples reduced the DNA yield. Importantly, all the recovered DNA was of quality suitable for PCR analysis. Conclusions: We recommend that blood samples are held on ice for no more than 1 hour before plasma/serum separation by double spin. Because of its higher efficiency, low-cost and good quality products for PCR analysis, we prefer the phenol/chloroform circulating DNA isolation method with heat denaturation.