The Question of Adolescent and Postadolescent Acne: The Nigerian Experience.

Introduction: Differences between adolescent and postadolescent acne are increasingly being recognized. This study aimed to document the clinical profile of facial acne vulgaris and, additionally, to compare adolescent to postadolescent acne and any gender-based differences. Methods: Cross-sectional descriptive study of 261 facial acne vulgaris patients was conducted from February 2021 to March 2022 at three dermatology clinics. Patients had their anthropometric measurements, type of acne lesions, and severity and scarring assessed. Results: A total of 261 patients (75.5% females) with a mean age of 24.5 (±7.4) years were diagnosed to have facial acne vulgaris. The severity of acne was mild in 44.8%, moderate in 48.3%, and severe in 6.9%. Acne was noninflammatory in 69.7%, inflammatory in 13.0%, and mixed in 17.2%. Adolescent and postadolescent acne significantly differed in the type of acne, BMI, type of acne lesions, and acne scarring. Gender-based differences included BMI, lesions of acne, and severity. Conclusion: There is an increasing prevalence of postadolescent acne with persistent being the most common category. There are significant differences between adolescent and postadolescent acne: type of acne, BMI, type of acne lesions, and acne scarring. Gender-based differences exist in both adolescent and postadolescent acne.

Epigenetic modifications associated with genes implicated in cytokine storm: The potential biotherapeutic effects of vitamins and minerals in COVID-19.

Cytokine storm is a phrase used to refer to an abrupt upsurge in the circulating levels of various pro-inflammatory cytokines, causing increased stimulation and activity of immune cells during disease conditions. The binding of pattern recognition receptors to pathogen-associated molecular patterns during COVID-19 infection recruits response machinery involving the activation of transcription factors and proteins required for a robust immune response by host cells. These immune responses could be influenced by epigenetic modifications as evidenced by significant variations in COVID-19 pathophysiology and response to therapy observed among patients across the globe. Considering that circulating levels of interleukin 1, tumor necrosis factor-α, and interleukin 6 are significantly elevated during cytokine storm in COVID-19 patients, genetic and epigenetic variations in the expression and function of these proteins could enhance our understanding of the disease pathogenesis. Treatment options that repress the transcription of specific cytokine genes during COVID-19 infection could serve as possible targets to counteract cytokine storm in COVID-19. Therefore, the present article reviews the roles of cytokines and associated genes in the COVID-19 cytokine storm, identifies epigenetic modifications associated with the disease progression, and possible ameliorative effects of some vitamins and minerals obtained as epigenetic modifiers for the control of cytokine storm and disease severity in COVID-19 patients. PRACTICAL APPLICATIONS: COVID-19 causes mortality and morbidity that adversely affect global economies. Despite a global vaccination campaign, side effects associated with vaccination, misconceptions, and a number of other factors have affected the expected successes. Cytokine storm in COVID-19 patients contributes to the disease pathogenesis and response to therapy. Epigenetic variations in the expression of various cytokines could be implicated in the different outcomes observed in COVID-19 patients. Certain vitamins and minerals have been shown to interfere with the expression and activity of cytokines implicated in cytokine storm, thereby counteracting observed pathologies. This review examines cytokines implicated in cytokine storm in COVID-19, epigenetic modifications that contribute to increased expression of identified cytokines, specific foods rich in the identified vitamins and minerals, and suggests their possible ameliorative benefits. The article will be beneficial to both scientists and the general public who are interested in the role of vitamins and minerals in ameliorating COVID-19.

Eruptive neurofibromas in pregnancy.

Neurofibromatosis type 1 is the most common inherited nervous system disorder affecting 1 in 3500 live births. Cutaneous neurofibromas, the most characteristic feature of the disease, begin to appear in adolescence and continue throughout adulthood. Although neurofibromas have been noted to increase in size or number during pregnancy, there have been very few reports of eruption of a large number of lesions during this period. We report a case of a 24-year-old Nigerian woman of 32-week gestation who presented with a history of sudden eruption of neurofibromas during the current pregnancy and the previous one 3 years earlier. We discuss how hormones and growth factors contribute to the increase in numbers of neurofibromas during pregnancy, which is occasionally severe, as in our case, and the complications which may arise in the mother and fetus.

Résumé La neurofibromatose de type 1 est le trouble du système nerveux héréditaire le plus répandu, touchant 1 naissance sur 3 500 naissances vivantes. Les neurofibromes cutanés, la caractéristique la plus caractéristique de la maladie, commencent à apparaître à l'adolescence et se poursuivent à l'âge adulte. Bien que l'on ait noté une augmentation de la taille ou du nombre des neurofibromes au cours de la grossesse, très peu de cas d'éruption d'un grand nombre de lésions ont été rapportés au cours de cette période. Nous rapportons le cas d'une femme nigérienne de 24 semaines de gestation nigérienne présentant des antécédents d'éruption soudaine de neurofibromes au cours de la grossesse en cours et la précédente trois ans plus tôt. Nous discutons de la manière dont les hormones et les facteurs de croissance contribuent à l'augmentation du nombre de neurofibromes pendant la grossesse, parfois sévère, comme dans notre cas, ainsi que des complications pouvant survenir chez la mère et le fœtus.

Modulatory role of rutin on 2,5-hexanedione-induced chromosomal and DNA damage in rats: validation of computational predictions.

The aim of this study was to evaluate the potentials of rutin on 2,5-hexanedione-induced toxicities. Two successive phases were involved using in silico and in vivo approaches. The in silico was adopted for potential oral toxicity and docking. The in vivo was carried-out in two stages for two weeks; the ameliorative (stage 1, first week), preventive, and curative studies (stage 2, extended to second week). In stage 1, rats were divided into four groups of seven each (distilled water, 3% (v/v) 2,5-hexanedione, 10 mg/kg rutin, and co-administration). In stage 2, the experimental groups were given either rutin or 2,5-hexanedione and treated in reverse order. Lipid peroxidation, protein carbonyl, and DNA fragmentation in tissues and bone marrow cells micronucleus were determined. The predicted Median lethal dose (LD50) of >5000 mg/kg and toxicity class of five (5) indicates the safety of rutin when orally administered. 2,5-Hexanedione comfortably docked in to the active sites of SOD (-22.857Kcal/mol; KI = 0.9621 µM), GPx (-11.2032Kcal/mol; KI = 0.9813 µM), and CAT (-16.446Kcal/mol; KI = 0.9726 µM) with strong hydrogen bond and hydrophobic interactions. However, only strong hydrophobic interaction was observed in the case of DNA (-3.3296Kcal/mol; KI = 0.9944). In vivo findings revealed deleterious effects of 2,5-hexanedione through induction of oxidative and chromosomal/DNA damage characterized by higher level of malondialdehyde, micronuclei formations, and DNA fragmentation. These have invariably, validates the findings from in silico experiments. Furthermore, rutin was able to ameliorate, protect, and reverse these effects, and was relatively non-toxic corroborating toxicity predictions. Rutin exhibited counteractive effects on 2,5-hexanedione-induced oxidative, chromosomal, and DNA damage.

Sickling-preventive effects of rutin is associated with modulation of deoxygenated haemoglobin, 2,3-bisphosphoglycerate mutase, redox status and alteration of functional chemistry in sickle erythrocytes.

Sickle cell anaemia is a hereditary disease branded by an upsurge in generation of ROS, irregular iron release and little or no antioxidant activity which can lead to cellular injuries due to oxidative stress resulting in severe symptoms including anaemia and pain. The disease is caused by a mutated version of the gene that helps make haemoglobin, the protein that carries oxygen in red blood cells. We used in silico and in vitro experiments to examine the antisickling effects of rutin for the first time by means of before and after induction approaches in sickle erythrocytes. Rutin was docked against deoxy-haemoglobin and 2,3-bisphosphoglycerate mutase, revealing binding energies (-27.329 and -25.614 kcal/mol) and Ki of 0.989µM and 0.990 µM at their catalytic sites through strong hydrophobic and hydrogen bond interactions. Sickling was thereafter, induced at 3 h with 2% metabisulphite. Rutin prevented sickling maximally at 12.3µM and reversed same at 16.4µM, by 78.5% and 69.9%, one-to-one. Treatment with rutin significantly (P < 0.05) reinvented the integrity of erythrocytes membrane as evident from the practical % haemolysis compared to induced erythrocytes. Rutin also significantly (P < 0.05) prevented and reversed lipid peroxidation relative to untreated. Likewise, GSH, CAT levels were observed to significantly (P < 0.05) increase with concomitant significant (P < 0.05) decrease in SOD activity based on administration of rutin after sickling induction approach. Furthermore, FTIR results showed that treatment with rutin favourably altered the functional chemistry, umpiring from shifts and functional groups observed. It can thus be deduced that, antisickling effects of rutin may be associated with modulation of deoxy-haemoglobin, 2,3-bisphosphoglycerate mutase, alteration of redox homeostasis and functional chemistry of sickle erythrocytes.

Postmenopausal osteoporosis and breast cancer: The biochemical links and beneficial effects of functional foods.

Breast cancer as a multifactorial disease has been classified among the major causes of morbidity and mortality in women across the world, with a higher prevalence among post-menopausal women. Osteoporosis, a condition characterized by altered bone mineralization is also commonly found among post-menopausal women. Consequently, post-menopausal women are at risk of morbidity and mortality associated with breast cancer and postmenopausal osteoporosis. This may not be unconnected to the fact that, there may be existent biochemical links between the two mayhems, which might rally round between the cellular and molecular connectivity based on the actions and inactions of RANKL, estrogen, free radicals-induced oxidative stress and metabolic implications of age related obesity among others. Cells and tissues including breast and bone are more prone to oxidative stress with age, and oxidative stress could alter the activity of key proteins and pathways required for protection against breast cancer and osteoporosis. As a result, the potentials of antioxidant rich functional foods in preventing, managing and possibly treating breast cancer and postmenopausal osteoporosis cannot be overemphasised. This review mainly uses ISI, SCOPUS and PubMed indexed journals and books containing various experimental reports vacillating from humans, animals and in vitro studies in relation to breast cancer and postmenopausal osteoporosis, biochemical links and possible beneficial effects of functional foods. One distinct feature of the review is that it categorically intends to provide a critical appraisal on the said available experimental data within the variables of breast cancer and osteoporosis among females vis-à-vis the potentials of functional foods.

Metabolism and toxicological implications of commonly used chemopreventive drugs against breast cancer/carcinogenesis.

BACKGROUND: Breast cancer has been reported to be among the frequently diagnosed cancer in women worldwide despite advances in early detection and treatment. Several drugs are currently used for chemoprevention as a result of a number of drawbacks associated with breast cancer therapy. AIM: This review focuses on the metabolism and toxicological implications of these drugs against breast cancer/carcinogenesis. METHODOLOGY: Relevant articles on the commonly used anti-breast cancer drugs (raloxifene, tamoxifen, anastrozole, letrozole and exemestane) used in chemoprevention were searched using the major scientific databases including Scopus, Embase, PubMed/ Medline, Sciencedirect and Google Scholar. RESULTS: The mechanism of action of estrogen receptor modulators are basically mediated via binding to estrogen receptors leading agonistic and antagonistic effects, whereas that of aromatase inhibitors involved the suppression of estrogen concentration in plasma via inhibition or inactivation of aromatase. Both estrogen receptor and aromatase modulators are good candidates for breast cancer chemoprevention, with latter being the most appropriate. However, it has been observed that pharmacodynamics nature of these xenobiotics, often yields some undesirable outcomes after administration which may be linked to resistance and other biological side effects, following phase I/II reactions, bioactivation within and around breast tissue microenvironment vis-à-vis distant tissues. Various findings indicated the manifestation of genotoxicity, organ toxicity and oxidative/nitrosative stress at low, moderate and high doses, thereby complicating the already existing precarious condition. Moreover, interindividual variations were also observed amongst patients, suggesting a critical role of genetic polymorphism. Also, variable side effects including osteoporosis, musculoskeletal events, such as arthralgia and myalgia were found to be predominant. CONCLUSION: The aromatase inhibitors seem to be most appropriate when it comes to application by virtue of their metabolic functions and fates. The reason is that raloxifene and tamoxifen are not the ideal drugs to reduce the incidence of primary invasive breast cancer because their safety and efficacy don't reach the desired optimal agent level. However, adequate care should be taken while prescribing, as well as during and after treatment with constant close monitoring of patients for any possible biochemical and clinical manifestations vis-à-vis the issue of pharmacogenetics.