Testosterone is an anabolic and androgenic steroid hormone therapeutically used to produce male sex characteristics. It has also been shown to have a modulating effect on proinflammatory biomarkers. Critical illness is characterised by a proinflammatory and catabolic state and is accompanied by altered testosterone production, which may persist into the recovery phase. Testosterone may, therefore be a potential therapeutic option in critical illness. This paper reviews normal testosterone physiology, and the changes seen during critical illness and systematically reviews testosterone therapy during both the acute and chronic phases of critical illness.

The misuse of anabolic androgenic steroid associated or not with physical workouts disrupts gastrointestinal (GI) function homeostasis. Our goal was to investigate the effects of nandrolone decanoate (ND) and moderate swimming on the GI transit of solid meals, GI motor contractility, and intestinal histology in rats. Male Wistar rats were allocated to four groups that received intramuscular injections of ND (5.0 mg/kg) or vehicle (60.0 µL) and were submitted or not to swimming sessions (60 min, 5% body weight overload) for 4 weeks. Gastric emptying, intestinal transit, in vitro GI contractility, intestinal morphometry, and duodenal mucosal mast cells were evaluated in all experimental groups. ND treatment accelerated gastric emptying, slowed small intestine transit time, enhanced gastric carbachol-mediated reactivity, decreased crypt depth and villus height, reduced mucosal thickness, and increased the circular and longitudinal muscle layer thickness of the duodenum in sedentary rats. Moderate exercise accelerated intestinal transit time and reduced submucosa thickness. In vehicle-treated animals, a strong negative correlation was found between intestinal transit and mucosal mast cells, which was reversed by ND treatment. Combining ND treatment and swimming accelerated gastric emptying, increased duodenal cholinergic reactivity, inhibited the sodium nitroprusside relaxing response, increased the number of duodenal mast cells, decreased villus height, and increased the thickness of all muscle layers. ND changed the morphological and functional properties of the GI tract over time, with intense dysmotility, especially in sedentary animals, but moderate exercise seemed to have played a compensatory role in these harmful effects in the gut. (GI homeostasis (ND meals contractility 5.0 50 5 0 (5. mg/kg mgkg mg kg 60.0 600 60 (60. µL (6 min overload weeks emptying morphometry carbacholmediated carbachol mediated reactivity height vehicletreated treated animals response layers dysmotility gut 5. (5 60. 6 (

The overexpression of the prostate cancer antigen 3 (PCA3) gene is well-defined as a marker for prostate cancer (PCa) diagnosis. Although widely used in clinical research, PCA3 molecular mechanisms remain unknown. Herein we used phage display technology to identify putative molecules that bind to the promoter region of PCA3 gene and regulate its expression. The most frequent peptide PCA3p1 (80%) was similar to the Rho GTPase activating protein 21 (ARHGAP21) and its binding affinity was confirmed using Phage Bead ELISA. We showed that ARHGAP21 silencing in LNCaP prostate cancer cells decreased PCA3 and androgen receptor (AR) transcriptional levels and increased prune homolog 2 (PRUNE2) coding gene expression, indicating effective involvement of ARHGAP21 in androgen-dependent tumor pathway. Chromatin immunoprecipitation assay confirmed the interaction between PCA3 promoter region and ARHGAP21. This is the first study that described the role of ARHGAP21 in regulating the PCA3 gene under the androgenic pathway, standing out as a new mechanism of gene regulatory control during prostatic oncogenesis. PCA (PCA3 welldefined well defined PCa (PCa diagnosis research unknown expression PCAp p PCA3p 80% 80 (80% ARHGAP (ARHGAP21 ELISA ARHGAP2 AR (AR PRUNE2 PRUNE (PRUNE2 androgendependent dependent pathway oncogenesis (PCA 8 (80 (ARHGAP2 (PRUNE (8 (ARHGAP (

Abstract Objective This study aimed to translate and validate the Estro-Androgenic-Symptom Questionnaire in Women (EASQ-W) into Brazilian Portuguese language, as we hypothesized that this tool would be consistent for addressing the specific context of hormonal symptoms in menopause. Methods In a cross-sectional study, a total of 119 women with Genitourinary Syndrome of Menopause (GSM) and 119 climacteric women without GSM were included. The EASQ-W was translated, and its psychometric properties were rigorously examined. Participants completed questionnaires covering sociodemographic details, the EASQ-W, and the Menopause Rating Scale (MRS). A subgroup of 173 women was re-invited after 4 weeks for test-retest analysis of the EASQ-W. Additionally, the responsiveness of the questionnaire was evaluated in 30 women who underwent oral hormonal treatment. Results The internal consistency of the EASQ-W was found to be satisfactory in both GSM and control groups (Cronbach’s alpha ≥ 0.70). Notably, a floor effect was observed in both groups; however, a ceiling effect was only evident in the sexual domain of the GSM group. Construct validity was established by comparing the EASQ-W with the MRS, yielding statistically significant correlations (0.33831-0.64580, p < 0.001). The test-retest reliability over a 4-week period was demonstrated to be satisfactory in both the GSM and control groups (ICC 0.787-0.977). Furthermore, the EASQ-W exhibited appropriate responsiveness to oral hormonal treatment (p < 0.001). Conclusion This study successfully translated and validated the Estro-Androgenic-Symptom Questionnaire in Women (EASQ-W) into Brazilian Portuguese, with satisfactory internal consistency, test-retest reliability, and construct validity. EstroAndrogenicSymptom Estro Androgenic Symptom EASQW EASQ W (EASQ-W language menopause crosssectional cross sectional 11 (GSM included examined details EASQW, W, MRS. MRS . (MRS) 17 reinvited re invited testretest test retest EASQW. W. Additionally 3 Cronbachs Cronbach s 0.70. 070 0.70 0 70 0.70) Notably however group 0.338310.64580, 033831064580 0.33831 0.64580, 33831 64580 (0.33831-0.64580 0.001. 0001 0.001 001 0.001) 4week week ICC 0.7870.977. 07870977 0.787 0.977 787 977 0.787-0.977) Furthermore 1 (MRS 07 0.7 7 338310 0.338310.64580 03383106458 033831 0.3383 064580 0.64580 3383 6458 (0.33831-0.6458 000 0.00 00 7870 0.7870.977 0787097 0787 0.78 0977 0.97 78 97 0.787-0.977 0. 0.338310.6458 0338310645 03383 0.338 06458 0.6458 338 645 (0.33831-0.645 0.0 0.7870.97 078709 078 097 0.9 9 0.787-0.97 0.338310.645 033831064 0338 0.33 0645 0.645 33 64 (0.33831-0.64 0.7870.9 07870 09 0.787-0.9 0.338310.64 03383106 033 0.3 064 0.64 6 (0.33831-0.6 0.7870. 0.787-0. 0.338310.6 0338310 03 06 0.6 (0.33831-0. 0.7870 0.787-0 0.338310. (0.33831-0 0.787- 0.338310 (0.33831- (0.33831 (0.3383 (0.338 (0.33 (0.3 (0. (0 (

ABSTRACT Hair is not only a matter of personal image, below is a clinical case of a patient with long-standing androgenic alopecia and lupus with suboptimal results after some previous treatments, the management of alopecia is a medical challenge because it is not only an aesthetic condition but also possible risk factors for psychiatric pathologies, timely diagnosis and treatment is important. There are numerous treatments for androgenic alopecia from topical treatments, oral route and mesotherapy among others. In this particular case, a satisfactory response is presented after starting oral and topical minoxidil.

RESUMEN El cabello no solo es una cuestión de imagen personal, a continuación, se expone un caso clínico de una paciente con alopecia androgénica y lupus eritematoso sistémico (LES) de larga data con resultados subóptimos luego de algunos tratamientos realizados con anterioridad, el manejo de la alopecia es un desafío médico pues no solo se trata de un padecimiento estético si no de posibles factores de riesgo para patologías psiquiátricas, por lo que es importante el diagnóstico y tratamiento oportunos. Existen numerosos tratamientos para la alopecia androgénica desde tratamientos tópicos, vía oral, mesoterapia, entre otros. En este caso en particular se presenta la respuesta satisfactoria tras el inicio de minoxidil vía oral y tópica.

SUMMARY Hypercalcemia is a frequent condition in clinical practice and when the most frequent causes are excluded, etiological diagnosis can be challenging. A rare cause of PTH-independent hypercalcemia is described in the present case report. A male adult with a history of androgenic-anabolic steroids abuse, and injection of mineral oil and oily veterinary compound containing vitamins A, D and E into muscles for local hypertrophy presented with hypercalcemia, nephrocalcinosis, and end-stage renal disease. On physical examination, the presence of calcified subcutaneous nodules and calcification of musculature previously infused with oily substances drew attention. Laboratory tests confirmed hypercalcemia of 12.62 mg/L, low levels of PTH (10 pg/mL), hyperphosphatemia (6.0 mg/dL), 25(OH)D of 23.3 ng/mL, and elevated 1,25(OH)2D (138 pg/mL). Imaging exams showed diffuse calcification of muscle tissue, subcutaneous tissue, and organs such as the heart, lung, and kidneys. The patient was diagnosed with PTH-independent hypercalcemia secondary to foreign body reaction in areas of oil injection. The patient underwent treatment with hydrocortisone for 10 days, single dose zoledronic acid and hemodialysis. He evolved with serum calcium levels of 10.4 mg/dL and phosphorus of 7.1 mg/dL. In addition, sertraline and quetiapine were prescribed to control body dysmorphic disorder. The medical community should become aware of new causes of hypercalcemia as secondary to oil injection since this should become increasingly frequent due to the regularity with which such procedures have been performed. excluded challenging PTHindependent independent report androgenicanabolic androgenic anabolic abuse nephrocalcinosis endstage end stage disease examination attention 1262 12 62 12.6 mgL mg L mg/L (1 pg/mL, pgmL pg/mL , pg mL pg/mL) 6.0 60 6 0 (6. mg/dL, mgdL dL mg/dL) 25OHD OHD 25 OH 233 23 3 23. ngmL ng ng/mL 1,25OH2D 125OH2D 1,25 2D 1 138 (13 pg/mL. . tissue heart lung kidneys days hemodialysis 104 4 10. 71 7 7. addition disorder performed 126 12. ( 6. (6 2 25OH2D 125 1,2 13 1,

Resumen Los métodos tradicionales para obtener líneas puras u homocigotas involucran varias generaciones de autofecundación con un requerimiento importante de tiempo. La obtención de plantas haploides y doble haploides, representa una alternativa que reduce a una generación, la producción de líneas con alelos idénticos en todos sus cromosomas. El objetivo de este trabajo fue implementar el protocolo de obtención de embriones androgénicos en poblaciones de chile mulato y ancho del programa de mejoramiento de chile en el Campo Experimental Bajío del Instituto Nacional de Investigaciones Forestales, Agrícolas y Pecuarias durante 2019 y 2020. Treinta genotipos de chile comprendidos en dos poblaciones. a) población criolla heterogénea de chiles mulato y ancho con característica de esterilidad masculina citoplasmática; y b) población de cruzas interespecíficas de chile ancho con chile habanero (C. annuum x C. chinense) resistentes a geminivirus (PepGMV) y Phytophthora sp., fueron sometidas a tratamiento de inducción androgénica. El tratamiento consistió en N 6 -furfuriladenina (cinetina) (0.01 mg L-1) y ácido 2,4-diclorofenoxiacético (2,4-D) (0.01 mg L-1) para la inducción de embriogénesis somática y posteriormente de cinetina (0.1 mg L-1) para la inducción de germinación de embriones. La duplicación cromosómica se realizó por medio de colchicina (0.5%) previo a su adaptación in vivo. La población conformada por genotipos derivados de cruzas interespecíficas obtuvo mayor eficiencia de plantas regeneradas doble haploides entre 4.29% y 14.67%, mientras que la población criolla generó embriones en menor proporción entre 1.02% y 5.26%. Estos resultados son los primeros reportados para obtención de plantas doble haploides de chiles mulato y ancho.

Abstract Traditional methods to obtain pure or homozygous lines involve several generations of self-fertilization with a significant time requirement. The obtaining of haploid and double haploid plants represents an alternative that reduces the production of lines with identical alleles in all their chromosomes to one generation. The objective of this work was to implement the protocol for obtaining androgenic embryos in populations of mulato and ancho chili of the chili improvement program in the Bajío Experimental Field of the National Institute of Forestry, Agricultural and Livestock Research during 2019 and 2020. Thirty chili genotypes included in the two populations mentioned below were subjected to androgen induction treatment. a) heterogeneous landrace population of mulato and ancho chilies with characteristic of cytoplasmic male sterility; and b) population of interspecific crosses of ancho chili with habanero chili (C. annuum x C. chinense) resistant to geminiviruses (PepGMV) and Phytophthora sp. The treatment consisted of N 6-furfuryladenine (kinetin) (0.01 mg L-1) and 2,4-dichlorophenoxyacetic acid (2,4-D) (0.01 mg L-1) for the induction of somatic embryogenesis and subsequently of kinetin (0.1 mg L-1) for induction of embryo germination. Chromosomal duplication was performed by colchicine (0.5%) prior to adaptation in vivo. The population made up of genotypes derived from interspecific crosses obtained greater efficiency of double haploid regenerated plants, between 4.29% and 14.67%, while the landrace population generated embryos in a smaller proportion, between 1.02% and 5.26%. These results are the first reported to obtain double haploid plants of mulato and ancho chilies.

Abstract Background Anabolic androgenic steroid (AAS) abuse has been associated with coronary artery disease (CAD). Pericoronary fat attenuation (pFA) is a marker of coronary inflammation, which is key in the atherosclerotic process. Objective To evaluate pFA and inflammatory profile in AAS users. Methods Twenty strength-trained AAS users (AASU), 20 AAS nonusers (AASNU), and 10 sedentary controls (SC) were evaluated. Coronary inflammation was evaluated by mean pericoronary fat attenuation (mPFA) in the right coronary artery (RCA), left anterior descending coronary artery (LAD), and left circumflex (LCx). Interleukin (IL)-1 (IL-1), IL-6, IL-10, and TNF-alpha were evaluated by optical density (OD) in a spectrophotometer with a 450 nm filter. P<0.05 indicated statistical significance. Results AASU had higher mPFA in the RCA (-65.87 [70.51-60.70] vs. -78.07 [83.66-72.87] vs.-78.46 [85.41-71.99] Hounsfield Units (HU), respectively, p<0.001) and mPFA in the LAD (-71.47 [76.40-66.61] vs. -79.32 [84.37-74.59] vs. -82.52 [88.44-75.81] HU, respectively, p=0.006) compared with AASNU and SC. mPFA in the LCx was not different between AASU, AASNU, and SC (-72.41 [77.17-70.37] vs. -80.13 [86.22-72.23] vs. -78.29 [80.63-72.29] HU, respectively, p=0.163). AASU compared with AASNU and SC, had higher IL-1, (0.975 [0.847-1.250] vs. 0.437 [0.311-0.565] vs. 0.530 [0.402-0.780] OD, respectively, p=0.002), IL-6 (1.195 [0.947-1.405] vs. 0.427 [0.377-0.577] vs. 0.605 [0.332-0.950] OD, p=0.005) and IL-10 (1.145 [0.920-1.292] vs. 0.477 [0.382-0.591] vs. 0.340 [0.316-0.560] OD, p<0.001). TNF-α was not different between the AASU, AASNU, and SC groups (0.520 [0.250-0.610] vs. 0.377 [0.261-0.548] vs. 0.350 [0.182-430]), respectively. Conclusion Compared with ASSNU and controls, AASU have higher mPFA and higher systemic inflammatory cytokines profile suggesting that AAS may induce coronary atherosclerosis through coronary and systemic inflammation. (AAS CAD. CAD . (CAD) (pFA process strengthtrained strength trained , (AASU) 2 (AASNU) 1 (SC (mPFA RCA, (RCA) LAD, (LAD) LCx. (LCx) IL1 IL (IL)- IL1, (IL-1) IL6, IL6 6, 6 IL10, IL10 10, TNFalpha TNF alpha OD (OD 45 filter P005 P 0 05 P<0.0 significance 65.87 6587 65 87 (-65.8 70.5160.70 70516070 70.51 60.70 70 51 60 [70.51-60.70 vs 78.07 7807 78 07 -78.0 83.6672.87 83667287 83.66 72.87 83 66 72 [83.66-72.87 vs.78.46 vs7846 78.46 46 vs.-78.4 85.4171.99 85417199 85.41 71.99 85 41 71 99 [85.41-71.99 HU (HU) respectively p<0.001 p0001 p 001 71.47 7147 47 (-71.4 76.4066.61 76406661 76.40 66.61 76 40 61 [76.40-66.61 79.32 7932 79 32 -79.3 84.3774.59 84377459 84.37 74.59 84 37 74 59 [84.37-74.59 82.52 8252 82 52 -82.5 88.4475.81 88447581 88.44 75.81 88 44 75 81 [88.44-75.81 p=0.006 p0006 006 72.41 7241 (-72.4 77.1770.37 77177037 77.17 70.37 77 17 [77.17-70.37 80.13 8013 80 13 -80.1 86.2272.23 86227223 86.22 72.23 86 22 23 [86.22-72.23 78.29 7829 29 -78.2 80.6372.29 80637229 80.63 72.29 63 [80.63-72.29 p=0.163. p0163 p=0.163 163 p=0.163) 1, IL-1 0.975 0975 975 (0.97 0.8471.250 08471250 0.847 1.250 847 250 [0.847-1.250 0437 437 0.43 0.3110.565 03110565 0.311 0.565 311 565 [0.311-0.565 0530 530 0.53 0.4020.780 04020780 0.402 0.780 402 780 [0.402-0.780 p=0.002, p0002 p=0.002 002 p=0.002) IL- 1.195 1195 195 (1.19 0.9471.405 09471405 0.947 1.405 947 405 [0.947-1.405 0427 427 0.42 0.3770.577 03770577 0.577 377 577 [0.377-0.577 0605 605 0.60 0.3320.950 03320950 0.332 0.950 332 950 [0.332-0.950 p=0.005 p0005 005 1.145 1145 145 (1.14 0.9201.292 09201292 0.920 1.292 920 292 [0.920-1.292 0477 477 0.47 0.3820.591 03820591 0.382 0.591 382 591 [0.382-0.591 0340 340 0.34 0.3160.560 03160560 0.316 0.560 316 560 [0.316-0.560 p<0.001. TNFα α 0.520 0520 520 (0.52 0.2500.610 02500610 0.250 0.610 610 [0.250-0.610 0377 0.37 0.2610.548 02610548 0.261 0.548 261 548 [0.261-0.548 0350 350 0.35 0.182430, 0182430 0.182 430 182 [0.182-430]) (CAD (AASU (AASNU (RCA (LAD (LCx (IL) (IL-1 4 P00 P<0. 65.8 658 8 (-65. 5160 70.5160.7 7051607 7051 70.5 6070 60.7 7 5 [70.51-60.7 78.0 -78. 6672 83.6672.8 8366728 8366 83.6 7287 72.8 [83.66-72.8 vs.78.4 vs784 7846 78.4 vs.-78. 4171 85.4171.9 8541719 8541 85.4 7199 71.9 9 [85.41-71.9 (HU p<0.00 p000 00 71.4 714 (-71. 4066 76.4066.6 7640666 7640 76.4 6661 66.6 [76.40-66.6 79.3 793 3 -79. 3774 84.3774.5 8437745 8437 84.3 7459 74.5 [84.37-74.5 82.5 825 -82. 4475 88.4475.8 8844758 8844 88.4 7581 75.8 [88.44-75.8 p=0.00 72.4 724 (-72. 1770 77.1770.3 7717703 7717 77.1 7037 70.3 [77.17-70.3 80.1 801 -80. 2272 86.2272.2 8622722 8622 86.2 7223 72.2 [86.22-72.2 78.2 782 6372 80.6372.2 8063722 8063 80.6 7229 [80.63-72.2 p016 p=0.16 16 0.97 097 97 (0.9 8471 0.8471.25 0847125 0847 0.84 1250 1.25 25 [0.847-1.25 043 43 0.4 3110 0.3110.56 0311056 0311 0.31 0565 0.56 31 56 [0.311-0.56 053 53 0.5 4020 0.4020.78 0402078 0402 0.40 0780 0.78 [0.402-0.78 1.19 119 19 (1.1 9471 0.9471.40 0947140 0947 0.94 1405 1.40 94 [0.947-1.40 042 42 3770 0.3770.57 0377057 0577 0.57 57 [0.377-0.57 060 0.6 3320 0.3320.95 0332095 0332 0.33 0950 0.95 33 95 [0.332-0.95 1.14 114 14 9201 0.9201.29 0920129 0920 0.92 1292 1.29 92 [0.920-1.29 047 3820 0.3820.59 0382059 0382 0.38 0591 0.59 38 [0.382-0.59 034 34 0.3 3160 0.3160.56 0316056 0316 0560 [0.316-0.56 0.52 052 (0.5 2500 0.2500.61 0250061 0250 0.25 0610 0.61 [0.250-0.61 037 2610 0.2610.54 0261054 0261 0.26 0548 0.54 26 54 [0.261-0.54 035 35 182430 0.182430 018243 0182 0.18 18 [0.182-430] (IL (IL- P0 P<0 65. (-65 516 70.5160. 705160 705 70. 607 60. [70.51-60. 78. -78 667 83.6672. 836672 836 83. 728 72. [83.66-72. vs.78. vs78 784 vs.-78 417 85.4171. 854171 854 85. 719 71. [85.41-71. p<0.0 p00 (-71 406 76.4066. 764066 764 76. 666 66. [76.40-66. 79. -79 84.3774. 843774 843 84. 745 74. [84.37-74. 82. -82 447 88.4475. 884475 884 88. 758 75. [88.44-75. p=0.0 (-72 177 77.1770. 771770 771 77. 703 [77.17-70. 80. -80 227 86.2272. 862272 862 86. 722 [86.22-72. 637 80.6372. 806372 806 [80.63-72. p01 p=0.1 0.9 09 (0. 0.8471.2 084712 084 0.8 125 1.2 [0.847-1.2 04 0. 0.3110.5 031105 031 056 [0.311-0.5 0.4020.7 040207 040 078 0.7 [0.402-0.7 1.1 11 (1. 0.9471.4 094714 094 140 1.4 [0.947-1.4 0.3770.5 037705 057 [0.377-0.5 06 0.3320.9 033209 033 095 [0.332-0.9 0.9201.2 092012 092 129 [0.920-1.2 0.3820.5 038205 038 059 [0.382-0.5 03 0.3160.5 031605 [0.316-0.5 0.2500.6 025006 025 0.2 061 [0.250-0.6 0.2610.5 026105 026 054 [0.261-0.5 18243 0.18243 01824 018 0.1 [0.182-430 P< (-6 70.5160 70516 [70.51-60 -7 83.6672 83667 [83.66-72 vs.78 vs7 vs.-7 85.4171 85417 [85.41-71 p<0. p0 (-7 76.4066 76406 [76.40-66 84.3774 84377 [84.37-74 -8 88.4475 88447 [88.44-75 p=0. 77.1770 77177 [77.17-70 86.2272 86227 [86.22-72 80.6372 80637 [80.63-72 (0 0.8471. 08471 08 12 1. [0.847-1. 0.3110. 03110 [0.311-0. 0.4020. 04020 [0.402-0. (1 0.9471. 09471 [0.947-1. 0.3770. 03770 [0.377-0. 0.3320. 03320 [0.332-0. 0.9201. 09201 [0.920-1. 0.3820. 03820 [0.382-0. 0.3160. 03160 [0.316-0. 0.2500. 02500 02 [0.250-0. 0.2610. 02610 [0.261-0. 1824 0.1824 01 [0.182-43 (- 70.516 [70.51-6 - 83.667 [83.66-7 vs.7 vs.- 85.417 [85.41-7 p<0 76.406 [76.40-6 84.377 [84.37-7 88.447 [88.44-7 p=0 77.177 [77.17-7 86.227 [86.22-7 80.637 [80.63-7 ( 0.8471 [0.847-1 0.3110 [0.311-0 0.4020 [0.402-0 0.9471 [0.947-1 0.3770 [0.377-0 0.3320 [0.332-0 0.9201 [0.920-1 0.3820 [0.382-0 0.3160 [0.316-0 0.2500 [0.250-0 0.2610 [0.261-0 [0.182-4 [70.51- [83.66- [85.41- p< [76.40- [84.37- [88.44- p= [77.17- [86.22- [80.63- [0.847- [0.311- [0.402- [0.947- [0.377- [0.332- [0.920- [0.382- [0.316- [0.250- [0.261- [0.182- [70.51 [83.66 [85.41 [76.40 [84.37 [88.44 [77.17 [86.22 [80.63 [0.847 [0.311 [0.402 [0.947 [0.377 [0.332 [0.920 [0.382 [0.316 [0.250 [0.261 [0.182 [70.5 [83.6 [85.4 [76.4 [84.3 [88.4 [77.1 [86.2 [80.6 [0.84 [0.31 [0.40 [0.94 [0.37 [0.33 [0.92 [0.38 [0.25 [0.26 [0.18 [70. [83. [85. [76. [84. [88. [77. [86. [80. [0.8 [0.3 [0.4 [0.9 [0.2 [0.1 [70 [83 [85 [76 [84 [88 [77 [86 [80 [0. [7 [8 [0 [

Resumo Fundamento O uso abusivo de esteroides anabólicos androgênicos (EAA) tem sido associado à doença arterial coronariana (DAC). A atenuação de gordura pericoronária (AGp) é um marcador de inflamação coronária, a qual exerce um papel chave no processo aterosclerótico. Objetivo Avaliar AGp e perfil inflamatório em usuários de EAA. Método Vinte indivíduos que realizavam treinamento de força, usuários de EAA (UEAA), 20 não usuários de EAA (NUEAA), e 10 indivíduos sedentários controle (SC) foram avaliados. Inflamação coronária foi avaliada por atenuação de gordura pericoronária média (AGPm) artéria coronária direita (ACD), artéria descendente anterior esquerda (ADA) e artéria circunflexa (ACX). Interleucina (IL)-1 (IL-1), IL-6, IL-10, e TNF-alfa foram avaliados por densidade ótica (DO) em um espectrofotômetro com um filtro de 450 nm. Um p<0,05 indicou significância estatística. Resultados Os UEAA apresentaram maior AGPm na ACD [-65,87 (70,51-60,70) vs. -78,07 (83,66-72,87) vs.-78,46 (85,41-71,99] unidades Hounsfield (HU), respectivamente, p<0,001) e AGPm na ADA [-71,47 (76,40-66,610 vs. -79,32 (84,37-74,59) vs. -82,52 (88,44-75,81) HU, respectivamente, p=0,006) em comparação aos NUEAA e CS. A AGPm na ACX não foi diferente entre os grupos UEAA, NUEAA e CS [-72,41 (77,17-70,37) vs. -80,13 (86,22-72,23) vs. -78,29 (80,63-72,29) HU, respectivamente, p=0,163). Em comparação aos NUEAA e aos CS, o grupo UEAA apresentaram maiores níveis de IL-1 [0,975 (0,847-1,250) vs. 0,437 (0,311-0,565) vs. 0,530 (0,402-0,780) DO, respectivamente, p=0,002), IL-6 [1,195 (0,947-1,405) vs. 0,427 (0,377-0,577) vs. 0,605 (0,332-0,950) DO, p=0,005) e IL-10 [1,145 (0,920-1,292) vs. 0,477 (0,382-0,591) vs. 0,340 (0,316-0,560) DO, p<0,001]. TNF-α não foi diferente entre os grupos UEAA, NUEAA e CS [0,520 (0,250-0,610) vs. 0,377 (0.261-0,548) vs. 0,350 (0,182-430)]. Conclusão Em comparação aos NUEAA e controles, os UEAA apresentam maior AGPm e maior perfil de citocinas inflamatórias sistêmicas, sugerindo que os EAA podem induzir aterosclerose por inflamação coronária e sistêmica. (EAA DAC. DAC . (DAC) (AGp aterosclerótico força , (UEAA) 2 NUEAA, (NUEAA) 1 SC (SC (AGPm ACD, (ACD) (ADA ACX. (ACX) IL1 IL (IL)- IL1, (IL-1) IL6, IL6 6, 6 IL10, IL10 10, TNFalfa TNF alfa DO (DO 45 nm p005 p 0 05 p<0,0 estatística 65,87 6587 65 87 [-65,8 70,5160,70 70516070 70,51 60,70 70 51 60 (70,51-60,70 vs 78,07 7807 78 07 -78,0 83,6672,87 83667287 83,66 72,87 83 66 72 (83,66-72,87 vs.78,46 vs7846 78,46 46 vs.-78,4 85,4171,99 85417199 85,41 71,99 85 41 71 99 (85,41-71,99 HU (HU) respectivamente p<0,001 p0001 001 71,47 7147 47 [-71,4 76,4066,610 764066610 76,40 66,610 76 40 610 (76,40-66,61 79,32 7932 79 32 -79,3 84,3774,59 84377459 84,37 74,59 84 37 74 59 (84,37-74,59 82,52 8252 82 52 -82,5 88,4475,81 88447581 88,44 75,81 88 44 75 81 (88,44-75,81 p=0,006 p0006 006 72,41 7241 [-72,4 77,1770,37 77177037 77,17 70,37 77 17 (77,17-70,37 80,13 8013 80 13 -80,1 86,2272,23 86227223 86,22 72,23 86 22 23 (86,22-72,23 78,29 7829 29 -78,2 80,6372,29 80637229 80,63 72,29 63 (80,63-72,29 p=0,163. p0163 p=0,163 163 p=0,163) IL- 0,975 0975 975 [0,97 0,8471,250 08471250 0,847 1,250 847 250 (0,847-1,250 0437 437 0,43 0,3110,565 03110565 0,311 0,565 311 565 (0,311-0,565 0530 530 0,53 0,4020,780 04020780 0,402 0,780 402 780 (0,402-0,780 p=0,002, p0002 p=0,002 002 p=0,002) 1,195 1195 195 [1,19 0,9471,405 09471405 0,947 1,405 947 405 (0,947-1,405 0427 427 0,42 0,3770,577 03770577 0,577 377 577 (0,377-0,577 0605 605 0,60 0,3320,950 03320950 0,332 0,950 332 950 (0,332-0,950 p=0,005 p0005 005 1,145 1145 145 [1,14 0,9201,292 09201292 0,920 1,292 920 292 (0,920-1,292 0477 477 0,47 0,3820,591 03820591 0,382 0,591 382 591 (0,382-0,591 0340 340 0,34 0,3160,560 03160560 0,316 0,560 316 560 (0,316-0,560 p<0,001. p<0,001] TNFα α 0,520 0520 520 [0,52 0,2500,610 02500610 0,250 0,610 (0,250-0,610 0377 0,37 0.2610,548 02610548 0.261 0,548 261 548 (0.261-0,548 0350 350 0,35 0,182430. 0182430 0,182 430 182 (0,182-430)] controles sistêmicas sistêmica (DAC (UEAA (NUEAA (ACD (ACX (IL) (IL-1 4 p00 p<0, 65,8 658 8 [-65, 5160 70,5160,7 7051607 7051 70,5 6070 60,7 7 5 (70,51-60,7 78,0 -78, 6672 83,6672,8 8366728 8366 83,6 7287 72,8 (83,66-72,8 vs.78,4 vs784 7846 78,4 vs.-78, 4171 85,4171,9 8541719 8541 85,4 7199 71,9 9 (85,41-71,9 (HU p<0,00 p000 00 71,4 714 [-71, 4066 76,4066,61 76406661 7640 76,4 66610 66,61 61 (76,40-66,6 79,3 793 3 -79, 3774 84,3774,5 8437745 8437 84,3 7459 74,5 (84,37-74,5 82,5 825 -82, 4475 88,4475,8 8844758 8844 88,4 7581 75,8 (88,44-75,8 p=0,00 72,4 724 [-72, 1770 77,1770,3 7717703 7717 77,1 7037 70,3 (77,17-70,3 80,1 801 -80, 2272 86,2272,2 8622722 8622 86,2 7223 72,2 (86,22-72,2 78,2 782 6372 80,6372,2 8063722 8063 80,6 7229 (80,63-72,2 p016 p=0,16 16 0,97 097 97 [0,9 8471 0,8471,25 0847125 0847 0,84 1250 1,25 25 (0,847-1,25 043 43 0,4 3110 0,3110,56 0311056 0311 0,31 0565 0,56 31 56 (0,311-0,56 053 53 0,5 4020 0,4020,78 0402078 0402 0,40 0780 0,78 (0,402-0,78 1,19 119 19 [1,1 9471 0,9471,40 0947140 0947 0,94 1405 1,40 94 (0,947-1,40 042 42 3770 0,3770,57 0377057 0577 0,57 57 (0,377-0,57 060 0,6 3320 0,3320,95 0332095 0332 0,33 0950 0,95 33 95 (0,332-0,95 1,14 114 14 9201 0,9201,29 0920129 0920 0,92 1292 1,29 92 (0,920-1,29 047 3820 0,3820,59 0382059 0382 0,38 0591 0,59 38 (0,382-0,59 034 34 0,3 3160 0,3160,56 0316056 0316 0560 (0,316-0,56 0,52 052 [0,5 2500 0,2500,61 0250061 0250 0,25 0610 0,61 (0,250-0,61 037 2610 0.2610,54 0261054 0261 0.26 0548 0,54 26 54 (0.261-0,54 035 35 182430 0,182430 018243 0182 0,18 18 (0,182-430) (IL (IL- p0 p<0 65, [-65 516 70,5160, 705160 705 70, 607 60, (70,51-60, 78, -78 667 83,6672, 836672 836 83, 728 72, (83,66-72, vs.78, vs78 784 vs.-78 417 85,4171, 854171 854 85, 719 71, (85,41-71, [-71 406 76,4066,6 7640666 764 76, 6661 66,6 (76,40-66, 79, -79 84,3774, 843774 843 84, 745 74, (84,37-74, 82, -82 447 88,4475, 884475 884 88, 758 75, (88,44-75, p=0,0 [-72 177 77,1770, 771770 771 77, 703 (77,17-70, 80, -80 227 86,2272, 862272 862 86, 722 (86,22-72, 637 80,6372, 806372 806 (80,63-72, p01 p=0,1 0,9 09 [0, 0,8471,2 084712 084 0,8 125 1,2 (0,847-1,2 04 0, 0,3110,5 031105 031 056 (0,311-0,5 0,4020,7 040207 040 078 0,7 (0,402-0,7 1,1 11 [1, 0,9471,4 094714 094 140 1,4 (0,947-1,4 0,3770,5 037705 057 (0,377-0,5 06 0,3320,9 033209 033 095 (0,332-0,9 0,9201,2 092012 092 129 (0,920-1,2 0,3820,5 038205 038 059 (0,382-0,5 03 0,3160,5 031605 (0,316-0,5 0,2500,6 025006 025 0,2 061 (0,250-0,6 0.2610,5 026105 026 0.2 054 (0.261-0,5 18243 0,18243 01824 018 0,1 (0,182-430 p< [-6 70,5160 70516 (70,51-60 -7 83,6672 83667 (83,66-72 vs.78 vs7 vs.-7 85,4171 85417 (85,41-71 [-7 76,4066, 764066 666 66, (76,40-66 84,3774 84377 (84,37-74 -8 88,4475 88447 (88,44-75 p=0, 77,1770 77177 (77,17-70 86,2272 86227 (86,22-72 80,6372 80637 (80,63-72 [0 0,8471, 08471 08 12 1, (0,847-1, 0,3110, 03110 (0,311-0, 0,4020, 04020 (0,402-0, [1 0,9471, 09471 (0,947-1, 0,3770, 03770 (0,377-0, 0,3320, 03320 (0,332-0, 0,9201, 09201 (0,920-1, 0,3820, 03820 (0,382-0, 0,3160, 03160 (0,316-0, 0,2500, 02500 02 (0,250-0, 0.2610, 02610 0. (0.261-0, 1824 0,1824 01 (0,182-43 [- 70,516 (70,51-6 - 83,667 (83,66-7 vs.7 vs.- 85,417 (85,41-7 76,4066 76406 (76,40-6 84,377 (84,37-7 88,447 (88,44-7 p=0 77,177 (77,17-7 86,227 (86,22-7 80,637 (80,63-7 [ 0,8471 (0,847-1 0,3110 (0,311-0 0,4020 (0,402-0 0,9471 (0,947-1 0,3770 (0,377-0 0,3320 (0,332-0 0,9201 (0,920-1 0,3820 (0,382-0 0,3160 (0,316-0 0,2500 (0,250-0 0.2610 (0.261-0 (0,182-4 (70,51- (83,66- (85,41- 76,406 (76,40- (84,37- (88,44- p= (77,17- (86,22- (80,63- (0,847- (0,311- (0,402- (0,947- (0,377- (0,332- (0,920- (0,382- (0,316- (0,250- (0.261- (0,182- (70,51 (83,66 (85,41 (76,40 (84,37 (88,44 (77,17 (86,22 (80,63 (0,847 (0,311 (0,402 (0,947 (0,377 (0,332 (0,920 (0,382 (0,316 (0,250 (0.261 (0,182 (70,5 (83,6 (85,4 (76,4 (84,3 (88,4 (77,1 (86,2 (80,6 (0,84 (0,31 (0,40 (0,94 (0,37 (0,33 (0,92 (0,38 (0,25 (0.26 (0,18 (70, (83, (85, (76, (84, (88, (77, (86, (80, (0,8 (0,3 (0,4 (0,9 (0,2 (0.2 (0,1 (70 (83 (85 (76 (84 (88 (77 (86 (80 (0, (0. (7 (8 (0 (

Abstract The androgenic hormone testosterone protects against pharmacological-induced damage to pancreatic islets in rodent models of diabetes. The increased production of reactive oxygen species damage the pancreatic islets through oxidative stress and apoptosis. The precise protective mechanism of testosterone has yet to be determined. The aim of this study was to evaluate the effect of post-gonadectomy testosterone substitution on the expression of two key antioxidant enzymes, Mn-dependent superoxide dismutase and catalase. The protein expression of the enzymes was examined by immunohistochemistry in male rats: intact, gonadectomized, and gonadectomized followed by testosterone substitution. mRNA expression was analyzed by reverse transcription-quantitative polymerase chain reaction on pancreatic islets cultured with testosterone, dihydrotestosterone (DHT) or the vehicle. Testosterone increased the protein level of MnSOD in pancreatic tissue and its mRNA expression in cultured pancreatic islets. DHT (a non-aromatizing androgen) had similar effects. For catalase, only the mRNA expression increased by testosterone treatment. Testosterone induced overexpression of MnSOD protein and mRNA in pancreatic islets through a mechanism unrelated to androgen aromatization, most likely involving androgen receptors, demonstrating the implications of testosterone in preventing damage to insulin-producing cells by oxidative stress.

Resumen El aumento de la producción de especies reactivas de oxígeno daña a los islotes pancreáticos por estrés oxidativo y apoptosis en algunos modelos de diabetes en roedores. Se ha observado que la testosterona los protege contra este daño, sin embargo, no se conoce el mecanismo por el cual esta hormona ejerce su protección. El objetivo de este estudio fue evaluar el efecto de la administración de testosterona a ratas macho gonadectomizadas sobre la expresión de las enzimas antioxidantes, superóxido dismutasa dependiente de Mn (MnSOD) y catalasa. La expresión de las enzimas a nivel de la proteína, se estudió por inmunohistoquímica en ratas macho intactas, gonadectomizadas y gonadectomizadas tratadas con testosterona. La expresión del ARNm se analizó por retrotranscripción y reacción en cadena de la polimerasa en tiempo real, en islotes pancreáticos cultivados con testosterona, dihidrotestosterona (DHT) o vehículo. En el caso de la catalasa, el tratamiento con testosterona solamente aumentó la expresión del ARNm. La testosterona indujo la sobreexpresión de la proteína de MnSOD y del ARNm en los islotes pancreáticos a través de un mecanismo no relacionado con la aromatización androgénica, en el que muy probablemente intervienen los receptores de andrógenos, lo que demuestra la participación de la testosterona en la prevención de los daños causados por el estrés oxidativo en las células productoras de insulina.

Resumen: La hiperplasia de glándulas sebáceas es un hallazgo benigno y transitorio, común en el período neonatal. Secundariamente al estímulo hormonal androgénico se produce un hipercrecimiento de las glándulas, con mayor frecuencia en nariz y mejillas, donde existen en mayor densidad. La hiperplasia de glándulas en una localización ectópica, llamada gránulos de Fordyce (GF), es excepcional en el período neonatal. Se han reportado en aproximadamente 1% de los recién nacidos, y con frecuencia se localizan en la mucosa oral. Los GF se describen como lesiones papulares de aspecto vesiculoso blanco amarillentas de 1-3 mm2, que podrían confundir al neonatólogo o al pediatra con entidades infecciosas, dando lugar a pruebas invasivas y tratamientos innecesarios. Se describen tres casos clínicos de neonatos con diagnóstico de hiperplasia sebácea ectópica localizada en mucosa oral, con el objetivo de revisar la etiología, las características clínicas, los diagnósticos diferenciales y la evolución de esta entidad benigna. Conclusiones: la hiperplasia sebácea ectópica en mucosa oral de neonatos es un hallazgo benigno autolimitado que se presenta con baja frecuencia. El reconocimiento clínico de esta entidad es importante para evitar diagnósticos incorrectos y tratamientos innecesarios.

Summary: Sebaceous gland hyperplasia is a common transient and benign finding in neonates. After androgenic hormonal stimulation, there is a gland overgrowth mainly in the nose and cheeks where there is a greater density of glands. Ectopic sebaceous gland hyperplasia, called Fordyce’s Granules (FG), is exceptional in neonates and it is reported in approximately 1% of newborns and frequently located in the oral mucosa. FGs are described as 1-3mm2 yellowish-white papular and vesicular lesions. Neonatologists or pediatricians may confuse these clinical features with infectious diseases, leading to invasive tests and unnecessary treatment. We describe three clinical cases of neonates with diagnosis of ectopic sebaceous gland hyperplasia located in the oral mucosa, with the aim of reviewing the etiology, clinical characteristics, differential diagnoses and evolution of this benign entity. Conclusions: ectopic sebaceous gland hyperplasia of the lips is a self-limited benign finding occurring infrequently in newborns. The clinical recognition of this entity is important to avoid inaccurate diagnoses or unnecessary treatment.

Resumo: A hiperplasia das glândulas sebáceas é um achado benigno e transitório comum nos neonatos. Secundário ao estímulo hormonal androgênico, há um hipercrescimento das glândulas com mais frequência no nariz e nas bochechas onde há uma maior densidade das glândulas. A hiperplasia das glândulas num local ectópico, chamado Fordyce Granules (FG), é excepcional no período neonatal, e ela é relatada em aproximadamente 1% dos recém-nascidos e muitas vezes está localizada na mucosa oral. Os FGs são descritos como lesões vesiculares brancas amareladas de 1-3mm2, o que poderia confundir o neonatologista ou pediatra com entidades infecciosas, levando a testes invasivos e tratamentos desnecessários. Descrevemos três relatos clínicos de recém-nascidos com diagnóstico de hiperplasia sebácea ectópica localizada na mucosa oral, com o objetivo de rever a etiologia, características clínicas, diagnósticos diferenciais e evolução desta entidade benigna. Conclusões: hiperplasia sebácea ectópica na mucosa oral de recém-nascidos é um achado benigno autolimitante que ocorre com baixa frequência. O reconhecimento clínico desta entidade é importante para evitar diagnósticos incorretos e tratamentos desnecessários.

Abstract One research line in criminal behavior studies 2D:4D ratio as predictor of aggression and violent behavior has been established, given that there are sexually dimorphic behaviors associated with the influence of testosterone on brain organization. However, results have been mixed. The aim of this study was to explore the differences in the 2D:4D ratio among offending and non-offending Colombian men in four groups (N = 139). A comparative study was conducted with three groups of offenders sentenced in a Colombian penitentiary: (1) sexual offenders against children (n = 34), (2) sexual offenders against adult women (n = 31), and (3) non-sexual violent offenders (n = 26); as well as one group (4) men with no criminal record (n = 48). The 2D:4D ratio was measured using the hand scanning technique and three digital measurements were analyzed with the Autometric software: right hand ratio, left hand ratio, and difference between the right and left hand ratios (Dr - Iz). Although, in all groups, right-digit ratio was lower that left-digit ratio (negative Dr–l ratio) and, in non-offending men this difference was not significant, no strong significant differences were found between groups in any measure of 2D:4D ratio used (right hand, left hand or Dr−l). The results support the idea that these associations are too weak to consider them predictors of sexual or non-sexual criminal behavior. The risk factors determining sexual or non-sexual criminal behavior, seems to go beyond intra-uterine effects and involve complex interactions between heritability, epigenetics, and pre-natal and post-natal life events.

Resumen Una de las líneas de investigación de la conducta criminal estudia la relación 2D:4D como predictor de agresión y comportamiento violento, dada la conexión de este marcador biológico con la influencia de la testosterona en la organización del cerebro y los comportamientos sexualmente dimórficos más prevalentes en hombres. Los resultados han sido mixtos y, en general, se han encontrado tamaños de efecto débiles, aunque significativos, en la relación entre proporción 2D:4D y el comportamiento agresivo, con escasos estudios comparativos y con muestras forenses. El objetivo de este estudio fue explorar las diferencias en la relación 2D:4D entre hombres colombianos (N = 139) con y sin delitos en cuatro grupos. Para ello, .e realizó un estudio comparativo con tres grupos de delincuentes condenados en una cárcel de Colombia: (1) agresores sexuales de menores (n = 34); (2) agresores sexuales de mujeres adultas (n = 31); (3) delincuentes violentos no sexuales (n = 26), y uno de (4) hombres sin antecedentes delictivos (n = 48). Se midió la proporción 2D:4D usando la técnica de escaneo de las manos y se analizaron tres medidas digitales con el software Autometric: proporción de la mano derecha, mano izquierda y diferencia entre la proporción de las manos derecha e izquierda (Dr – Iz). Se encontraron diferencias significativas entre la diferencia de la proporción Dr-Iz en todos los grupos, en la que la 2D:4D de la mano derecha fue menor que la de la mano izquierda en todos los grupos. Sólo en los hombres sin antecedentes delictivos esta diferencia no fue significativa. Para evaluar las diferencias grupales en las relaciones 2D:4D, se ajustaron modelos tipo a ANOVA unidireccional con un solo grupo como predictor, seguidos de contrastes de Helmert para comparar las diferencias entre todos los grupos. El grupo predijo sólo la diferencia de las proporciones Dr – Iz, pero no las proporciones de la mano derecha o izquierda por separado. El grupo de hombres sin antecedentes delictivos, mostró una proporción 2D:4D de la mano izquierda significativamente menor (masculinizada) y una menor diferencia (más cercana a cero) entre las proporciones Dr-Iz comparado con los grupos de delincuentes. Sin embargo, los contrastes con cada grupo, mostraron que la diferencia sólo fue significativa con el grupo de delincuentes violentos no sexuales, pero no con los grupos de agresores sexuales. Se concluyó que no hubo diferencias significativas importantes y concluyentes entre los grupos en ninguna medida de la proporción 2D:4D utilizada (mano derecha, mano izquierda o Dr − Iz). Estos resultados respaldan la idea de que estas asociaciones son demasiado débiles para considerarlas predictores de conductas criminales sexuales o no sexuales. Los factores de riesgo que determinan el comportamiento delictivo sexual o no sexual parecen ir más allá de los efectos intrauterinos reflejados por el biomarcador 2D:4D y, posiblemente, involucrar interacciones complejas entre heredabilidad, epigenética y eventos de la vida prenatal y postnatal. Si la relación 2D:4D es un marcador indirecto válido y confiable de androgenización prenatal, no es algo que se pueda discutir con los datos aquí obtenidos. Sin embargo, si tiene más que un simple efecto detectado por casualidad en el comportamiento delictivo, esto también debería explorarse más a fondo no sólo en la mano derecha, como la mayoría de la investigación disponible lo ha hecho, sino en la mano izquierda y en la diferencia entre las proporciones 2D:4D Dr-Iz, para evaluar si su poder explicativo se mantiene bajo como hasta ahora o incluso inexistente.

Resumen En los últimos años han surgido informes de los novedosos estudios de imagen para aumentar la sensibilidad para detectar enfermedad metastásica temprana y por lo mismo, el reconocimiento de subgrupos biológicos de hombres en el escenario del cáncer de próstata avanzado recién diagnosticado en relación al manejo del tumor primario para mejorar la supervivencia general de estos pacientes considerados a tener enfermedad sistémica y con solo tratamiento de supresión androgénica, fatal a corto o mediano plazo.

Abstract In the last years, novel imaging studies have surged for increase the sensitivity in early metastatic disease detection. the recognition of biological subgroups of men with newly diagnosed advanced prostate cancer for the management of the primary tumor to improve the overall survival in this patients considered fatal in the short or medium term with systemic disease managed just with androgenic hormonal suppression.

Abstract Background Androgenetic alopecia in the pediatric population is rarely discussed in the literature. Although the prevalence of the metabolic syndrome is increased in patients with early-onset androgenetic alopecia, the presence of metabolic syndrome risk factors in pediatric androgenetic alopecia is unknown. Objective To evaluate the demographics, medical and family histories, clinical and trichoscopic features, androgenic hormones, and metabolic syndrome risk factors in pediatric androgenetic alopecia. Methods The medical reports of pediatric patients with androgenetic alopecia were reviewed. Results The study included 23 patients (12 females and 11 males) with a mean age of 15,3 ± 2,1 years. Sixteen patients had adolescent androgenetic alopecia and seven, had childhood alopecia. Nine patients reported a family history, all of whom had adolescent androgenetic alopecia. Hyperandrogenism was noted in three patients with adolescent androgenetic alopecia. The most common hair loss pattern was diffuse thinning at the crown with preservation of the frontal hairline which was noted in 10 patients (43.5%), six of whom were males. Fourteen patients (60.9%) had at least one metabolic syndrome risk factor. The most common risk factor was obesity or overweight (47.8%) followed by insulin resistance (21.7%), high fasting blood glucose (13%), high blood pressure (4.4%) and lipid abnormalities (4.4%). Study limitations Retrospective study; lack of a control group. Conclusion Pediatric androgenetic alopecia is often associated with metabolic syndrome risk factors. Therefore, androgenetic alopecia in the pediatric population may indicate a future metabolic syndrome which warrants an accurate and prompt diagnosis for early screening and treatment.