Abnormal Hormone Profiles Research Articles

A differential expression of an identical mutation in CYP17A1 gene in two infertility patients: a case report

Background17-Hydroxylase deficiency is the rarest form of congenital adrenal hyperplasia, a disorder that affects steroidogenesis, causing abnormal hormone levels. Studies have shown a clear association between 17-hydroxylase deficiency and primary infertility, but a definite protocol to treat the disorder has not been determined yet.Case presentationCase I presents a 24-year-old Caucasian Israeli-Arab female who experienced 6 years of infertility. Before her initial visit to our clinic, she underwent three laparoscopic ovarian cystectomies, had an unsuccessful in vitro fertilization cycle, and was treated with combined oral contraceptives. Her hormonal profile was tested, and the results led to genetic counseling and the diagnosis of non-classical congenital adrenal hyperplasia. She was treated with estradiol, glucocorticoids, and transdermal testosterone. After hormonal levels were lowered, in vitro fertilization cycles were initiated, and the patient had a spontaneous ovulation. In case II, a 20-year-old Caucasian Israeli-Arab female presented for infertility evaluation owing to her oligomenorrhea. Her vitals and physical examination had normal results. The investigation of her abnormal hormonal profile led her to be referred to genetic testing, where the results showed the same genetic mutation as seen in case I.ConclusionBoth cases highlight the distinctiveness of the condition, where an identical mutation in the gene responsible for the same enzyme can bring about diverse phenotypes. Case I offers a potential treatment protocol for this rare disorder.

10-Day-Old Male Infant With Electrolyte Derangement and Abnormal Calciotropic Hormone Profile.

10-Day-Old Male Infant With Electrolyte Derangement and Abnormal Calciotropic Hormone Profile.

Melatonin in Endometriosis: Mechanistic Understanding and Clinical Insight.

Endometriosis is defined as the development of endometrial glands and stroma outside the uterine cavity. Pathophysiology of this disease includes abnormal hormone profiles, cell survival, migration, invasion, angiogenesis, oxidative stress, immunology, and inflammation. Melatonin is a neuroendocrine hormone that is synthesized and released primarily at night from the mammalian pineal gland. Increasing evidence has revealed that melatonin can be synthesized and secreted from multiple extra-pineal tissues where it regulates immune response, inflammation, and angiogenesis locally. Melatonin receptors are expressed in the uterus, and the therapeutic effects of melatonin on endometriosis and other reproductive disorders have been reported. In this review, key information related to the metabolism of melatonin and its biological effects is summarized. Furthermore, the latest in vitro and in vivo findings are highlighted to evaluate the pleiotropic functions of melatonin, as well as to summarize its physiological and pathological effects and treatment potential in endometriosis. Moreover, the pharmacological and therapeutic benefits derived from the administration of exogenous melatonin on reproductive system-related disease are discussed to support the potential of melatonin supplements toward the development of endometriosis. More clinical trials are needed to confirm its therapeutic effects and safety.

Tartary Buckwheat (Fagopyrum tataricum) Ameliorates Lipid Metabolism Disorders and Gut Microbiota Dysbiosis in High-Fat Diet-Fed Mice.

Jinqiao II, a newly cultivated variety of tartary buckwheat (Fagopyrum tataricum), has been reported to exhibit a higher yield and elevated levels of functional compounds compared to traditional native breeds. We aimed to investigate the potential of Jinqiao II tartary buckwheat to alleviate lipid metabolism disorders by detecting serum biochemistry, pathological symptoms, gene expression profiling, and gut microbial diversity. C57BL/6J mice were provided with either a normal diet; a high-fat diet (HFD); or HFD containing 5%, 10%, and 20% buckwheat for 8 weeks. Our results indicate that Jinqiao II tartary buckwheat attenuated HFD-induced hyperlipidemia, fat accumulation, hepatic damage, endotoxemia, inflammation, abnormal hormonal profiles, and differential lipid-metabolism-related gene expression at mRNA and protein levels in response to the dosages, and high-dose tartary buckwheat exerted optimal outcomes. Gut microbiota sequencing also revealed that the Jinqiao II tartary buckwheat elevated the level of microbial diversity and the abundance of advantageous microbes (Alistipes and Alloprevotella), lowered the abundance of opportunistic pathogens (Ruminococcaceae, Blautia, Ruminiclostridium, Bilophila, and Oscillibacter), and altered the intestinal microbiota structure in mice fed with HFD. These findings suggest that Jinqiao II tartary buckwheat might serve as a competitive candidate in the development of functional food to prevent lipid metabolic abnormalities.

In Silico Analysis of PORD Mutations on the 3D Structure of P450 Oxidoreductase.

Cytochrome P450 oxidoreductase (POR) is a membrane-bound flavoprotein that helps in transferring electrons from its NADPH domain to all cytochrome P450 (CYP450) enzymes. Mutations in the POR gene could severely affect the metabolism of steroid hormones and the development of skeletal muscles, a condition known as Cytochrome P450 oxidoreductase deficiency (PORD). PORD is associated with clinical presentations of disorders of sex development, Antley and Bixler’s syndrome (ABS), as well as an abnormal steroid hormone profile. We have performed an in silico analysis of POR 3D X-ray protein crystal structure to study the effects of reported mutations on the POR enzyme structure. A total of 32 missense mutations were identified, from 170 PORD patients, and mapped on the 3D crystal structure of the POR enzyme. In addition, five of the missense mutations (R457H, A287P, D210G, Y181D and Y607C) were further selected for an in-depth in silico analysis to correlate the observed changes in POR protein structure with the clinical phenotypes observed in PORD patients. Overall, missense mutations found in the binding sites of POR cofactors could lead to a severe form of PORD, emphasizing the importance of POR cofactor binding domains in transferring electrons to the CYP450 enzyme family.

Hyper-androgenemia and obesity in early-pubertal girls

PurposeThe aim of this study was to examine the hormonal profile in early-pubertal girls with obesity. We hypothesized that these patients might already present hormonal alterations with POCS-like features.MethodsCross-sectional study in a sample of 283 peri-pubertal girls (prepubertal and early-puberty subgroups), aged 6.1–12.0 years, diagnosed with obesity (BMI-SDS > 2.0, 97th percentile), so-called obesity group. They all underwent clinical examination and blood testing for hormonal measurements (leptin, TSH, FT4, IGF-1, IGFBP3, prolactin, insulin, FSH, LH, estradiol, ACTH, cortisol, 17-OH-P, DHE-S, androstenedione, testosterone and free testosterone). A control group was recruited: 243 healthy girls, aged 6.3–12.1 years, with normal BMI status.ResultsPrepubertal girls with obesity had significantly higher values (p < 0.05) for BMI-SDS, leptin, insulin and HOMA-IR levels than control group. Early-pubertal girls with obesity also had significantly higher values (p < 0.05) for BMI-SDS, leptin, IGF-1, IGFBP3, insulin and HOMA-IR, LH, ratio LH/FSH, ACTH, DHE-S, androstenedione, testosterone and free testosterone levels than control group. In early-pubertal girls with obesity (not prepubertal girls), there was a positive correlation (p < 0.01) between leptin levels with LH, androstenedione and testosterone, and HOMA-IR with LH and testosterone levels. There was also a positive correlation (p < 0.01) between IGF-1 levels with LH, androstenedione, DHE-S and testosterone; and LH levels with testosterone.ConclusionThe results obtained support our hypothesis that an abnormal hormonal profile with POCS-like features can already be detected (insulin resistance and hyperinsulinemia, increased secretion of LH and ACTH, and overproduction of ovarian and adrenal androgens) in early-pubertal girls with obesity.

OBESITY-RELATED ALTERATIONS IN PROTEIN EXPRESSION IN HUMAN FOLLICULAR FLUID

Obesity has a complex and significant impact on female reproduction. Prior research demonstrates that obesity is associated with decreased chances of conception, longer time-to-pregnancy, decreased response to medications in patients undergoing in vitro fertilization (IVF), and poorer IVF outcomes. In addition, obesity has been shown to directly alter the follicular microenvironment resulting in abnormal hormonal and metabolomic profiles. While proteomics has previously been employed to investigate follicular fluid in women with PCOS, there is a paucity of data investigating the impact of obesity in normo-ovulatory women. This study aimed to compare the proteomic composition of follicular fluid from normal vs. obese women without a history of PCOS or other ovulatory dysfunction undergoing IVF. Follicular fluid from 8 normal weight women (NW) and 8 women with obesity (OW) undergoing IVF was analyzed for proteomic content. Women undergoing IVF and without a history of PCOS, ovulatory dysfunction, endometriosis and diminished ovarian reserve were eligible for study inclusion. At the time of oocyte retrieval, follicular fluid from the 2nd and/or 3rd follicle from each ovary was collected and cryopreserved. Follicular fluid was subsequently thawed, and the most abundant proteins depleted using the ProteoMinerTM depletion kit (Biorad). Individual samples were then proteoylsed with Trypsin and labeled with a TMT 10-plex kit (ThermoFisher). Liquid chromatography mass-spectrometry (LC-MS) analysis was then performed through the University of Michigan proteomics core. Proteome Discoverer (v2.4) was used for data analysis. The ratio of protein abundance from obese/normal weight samples was calculated and the error rate corrected by utilization of the Benjamini-Hochberg method. Statistical significance was determined by a p<0.05. Western blotting was performed for validation of a subset of proteins. The mean age of NW vs OW was similar (32.88 vs 32.63 yrs). The mean BMI of NW was 21.1 kg/m2 compared with a BMI of 37.05kg/m2 in OW. A total of 1174 proteins were identified with >= 2 peptides present. 25 proteins were found to be significantly altered in the follicular fluid from women with obesity. 19 of these proteins were upregulated while 6 were downregulated. Notably, C-reactive protein was 11-fold higher in the follicular fluid from OW compared with NW (p<0.0001). Confirmatory western blots were consistent with the LC-MS findings. In this study we utilized high-resolution LC-MS to identify 1174 proteins in human follicular fluid. Further we found significant alterations in the proteomic composition of follicular fluid from women with obesity vs normal weight women without a history of ovulatory dysfunction. Future studies are needed to validate these findings in larger populations of patients and to further explore the mechanisms of these altered proteins in the pathophysiology of obesity.

Prevalence of Subclinical Hypothyrodism in Patients with Acute Myocardial Infarction

The present study shows an association of Prevalence of Subclinical Hypothyrodism (SCH) with Myocardial Infarction (MI). 200 patients with Acute MI of Adult (age > 18 years) males and females were selected. We observed that female Patients belonging to Age group of 51-60(15.5%) were more prone to MI. Study depicts SCH were observed in 16% of MI patients and Euthyroid was observed in 84% Patients. No gender difference was noted in abnormal thyroid hormone profile in male and female group. A higher prevalence of MI was seen in age group 51-60 years in both male and female accounting for 26% and 15.5%respectively. A statistically higher prevalence of STEMI was seen in SCH and Euthyroid Patients (77.5%) as compared to NSTEMI in SCH and Euthyroid Patients (22.5%). Physicians should be encouraged to educate the people about the risks of diabetes, hypertension and smoking. Furthermore, abnormal thyroid status increases risk of coronary artery disease and cardiovascular mortality affecting ventricular function, serum cholesterol levels, and heart rate and rhythm.

Invited Lecture 2: Endocrine disrupting chemicals in ocean ecosystem and human health risks

Brief Biosketch He is the author of 5 books and edited 7 books (chapters). He has published peer-reviewed articles in several reputed journals. He is serving as a Course Coordinator for Undergraduate (MD) teaching: Environmental health. There are 2 notified research grants in his credit: CIHR Project Grant (Spring 2019) and NSERC along with 3 ongoing projects. He was awarded Faculty of Medicine, Memorial University Outstanding Research Excellence Award (2015) and SSHRC Travel Grants Competition, Annual conference of International Society of Environmental Epidemiology, Basel, Switzerland (2013). His area of research interest is Environmental contamination and ecosystem health, Climate change and health, Indigenous health, Global Health and Social epidemiology. Endocrine disrupting chemicals (EDCs) are the exogenous substances that can cause adverse health effects through disruption to the body's endocrine systems. This can result in changes to circulating hormone concentrations, which act as signals to regulate growth, metabolism and reproduction. Hormones are maintained at very low concentrations in the bloodstream; therefore, even low levels of EDC exposure can have large consequences on endocrine homeostasis. The potential adverse health effects resulting from exposure to EDCs, including developmental abnormalities, abnormal hormonal profiles, disorders of the reproductive systems, increased incidence of cancer, and alterations to both the immune and nervous systems. There are numerous chemicals used in our day to day basis have endocrine disruption property, such as pesticides, flame retardants, and various other industrial chemicals. Humans are exposed to those chemicals from direct exposures while using them, and also from the diet. EDCs reach environment from deposition via industrial effluents or direct application and also through wastewater and landfills. Eventually, these chemicals destine to aquatic ecosystems, such as rivers, ponds, lakes, seas and oceans. Humans further get exposed to EDCs by eating marine products. The bio-accumulative and bio-magnification nature of EDCs result in their very high levels in large predatory fish and marine mammals. Studies show the people who regularly eat marine products contaminated with EDCs encounter various forms of adverse health outcomes such as thyroid hormone disruptions, infertility, and other endocrine diseases. Despite extensive literature available in industrialized countries, studies conducted in resource constraint countries are very few. Therefore, more research needed to generate further evidence.

PO-01-080 Intracytoplasmic Sperm Injection (ICSI) Outcome Using Cryopreserved Testicular Sperm from Non-Obstructive Azoospermic Infertile Men with Varicocele

To study the outcome of ICSI using cryopreserved testicular sperm from infertile men with varicocele-associated non-obstructive azoospermia (NOA). The study included 40 infertile men with NOA who underwent ICSI with cryopreserved testicular sperm. Twenty two patients had clinically palpable varicocele (group 1) and 18 had no detectable abnormality in their genital examination (group2). Diagnosis of varicocele was confirmed by scrotal color Doppler ultrasound. Diagnosis of azoospermia was confirmed by repeated absence of sperms in centrifuged semen pellets. Men with abnormal hormonal profiles, genetic abnormalities or genitourinary anomalies suggestive of obstructive pathology were excluded. Couples with known female factor infertility were excluded. ICSI was done using mature MII oocytes with good morphology. The pronuclear formation was assessed at 17 ± 1 hours following injection. Embryo quality was assessed on day 3 (67 ± 2 hours) and day 5. Positive clinical pregnancy was considered upon finding of gestational sac(s) and fetal pulsation by trans-vaginal US, 15 days after BHCG assessment. Results were presented as mean ± standard deviation (SD) for continuous variables and frequency and percentage (%) for categorical variables. P-value <0.05 was significant.

Functional analysis of monocarboxylate transporter 8 mutations in Japanese Allan-Herndon-Dudley syndrome patients

Monocarboxylate transporter 8 (MCT8) facilitates T3 uptake into cells. Mutations in MCT8 lead to Allan-Herndon-Dudley syndrome (AHDS), which is characterized by severe psychomotor retardation and abnormal thyroid hormone profile. Nine uncharacterized MCT8 mutations in Japanese patients with severe neurocognitive impairment and elevated serum T3 levels were studied regarding the transport of T3. Human MCT8 (hMCT8) function was studied in wild-type (WT) or mutant hMCT8-transfected human placental choriocarcinoma cells (JEG3) by visualizing the locations of the proteins in the cells, detecting specific proteins, and measuring T3 uptake. We identified 6 missense (p.Arg445Ser, p.Asp498Asn, p.Gly276Arg, p.Gly196Glu, p.Gly401Arg, and p.Gly312Arg), 2 frameshift (p.Arg355Profs*64 and p.Tyr550Serfs*17), and 1 deletion (p.Pro561del) mutation(s) in the hMCT8 gene. All patients exhibited clinical characteristics of AHDS with high free T3, low-normal free T4, and normal-elevated TSH levels. All tested mutants were expressed at the protein level, except p.Arg355Profs*64 and p.Tyr550Serfs*17, which were truncated, and were inactive in T3 uptake, excluding p.Arg445Ser and p.Pro561del mutants, compared with WT-hMCT8. Immunocytochemistry revealed plasma membrane localization of p.Arg445Ser and p.Pro561del mutants similar with WT-hMCT8. The other mutants failed to localize in significant amount(s) in the plasma membrane and instead localized in the cytoplasm. These data indicate that p.Arg445Ser and p.Pro561del mutants preserve residual function, whereas p.Asp498Asn, p.Gly276Arg, p.Gly196Glu, p.Gly401Arg, p.Gly312Arg, p.Arg355Profs*64, and p.Tyr550Serfs*17 mutants lack function. These findings suggest that the mutations in MCT8 cause loss of function by reducing protein expression, impairing trafficking of protein to plasma membrane, and disrupting substrate channel.

Changes in the thyroid hormone profiles in children with nephrotic syndrome.

PurposeWe compared thyroid hormone profiles in children with nephrotic syndrome (NS) during the nephrotic phase and after remission.MethodsThis study included 31 pediatric NS patients. The thyroid hormone profiles included serum levels of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), and free T4.ResultsOf the 31 patients, 16 (51.6%) showed abnormal thyroid hormone profiles: 6 had overt hypothyroidism, 8 had subclinical hypothyroidism, and 2 had low T3 syndrome. The mean serum T3, T4, and free T4 levels in the nephrotic phase and after remission were 82.37±23.64 and 117.88±29.49 ng/dL, 5.47±1.14 and 7.91±1.56 µg/dL, and 1.02±0.26 and 1.38±0.23 ng/dL, respectively; the levels were significantly lower in the NS nephrotic phase (P=0.0007, P<0.0001, and P=0.0002). The mean serum TSH levels during the nephrotic phase and after remission were 8.05±3.53 and 4.08±2.05 µIU/ mL, respectively; they were significantly higher in the nephrotic phase (P=0.0005). The urinary protein/ creatinine ratio during the nephrotic phase was significantly correlated with serum T3, T4, and free T4 levels (r=-0.5995, P=0.0032; r=-0.5797, P=0.0047; r=-0.5513, P=0.0078) as well as with TSH levels (r=0.5022, P=0.0172). A significant correlation was found between serum albumin and serum T3 levels during the nephrotic phase (r=0.5385, P=0.0018) but not between serum albumin and T4, TSH, or free T4 levels. These significant correlations all disappeared after remission.ConclusionAbnormal thyroid hormone profile findings were observed in 51.6% of pediatric patients with NS. Thyroid hormone levels normalized after remission, regardless of levothyroxine therapy.

Rational and design of an overfeeding protocol in constitutional thinness: Understanding the physiology, metabolism and genetic background of resistance to weight gain

BackgroundConstitutional thinness (CT) is a natural state of underweight (13–17.5kg/m2) without the presence of any eating disorders and abnormal hormonal profile, and with preserved menses in women. We previously conducted a four-week fat overfeeding study showing weight gain resistance in CT women and one of our main results was the identification of an energy gap: a positive energy balance (higher energy intake than energy expenditure). ObjectiveThis new overfeeding study is designed to confirm the energy gap and propose mechanistic hypothesis. DesignA 2-week overfeeding (daily consumption of one bottle of Renutryl® Booster (600kcal, 30g protein, 72g carbohydrate, 21g fat) on top of the dietary intake) is performed to compare 15 women and men in each CT group (Body Mass Index [BMI]<18.5kg/m2) to their controls (BMI 20–25kg/m2). Bodyweight, food intake, energy expenditure (canopy, calorimetric chamber and Actiheart), body composition (DXA), appetite regulatory hormone profiles after a test meal, proteomics, metabolomics, urinary metabolic profiles, stool microbiome and lipids, fat and muscle transcriptomics are monitored before and after overfeeding. Results and conclusionsData inter-linking will be able to be established with results of this study. The findings could possibly open to therapeutic approaches to help CT patients to gain weight as well as provide a better understanding of energy regulation with regard to treat obesity (resistance to weight loss), a mirror image of CT (resistance to weight gain).

MENSTRUAL CHANGES AND PREGNANCY OUTCOMES AMONG PHYSIOTHERAPISTS EXPOSED TO NON-IONIZING RADIATIONS

Introduction: Excessive exposure to radiofrequency (RF), electromagnetic fields (EMFs) from the diathermy devices could result in adverse pregnancy / reproductive outcomes. Aim of Work: to assess the menstrual changes, hormonal profile and pregnancy outcomes among female physiotherapists exposed to non-ionizing radiations. Materials and Methods: a prospective study, included 120 female workers at the physiotherapy departments with 160 healthy controls (non-exposed), who were allocated into two groups: pregnant (50 physiotherapists and 75 controls) and non-pregnant (70 physiotherapists and 85 controls). Outcome measures in the pregnant group included pregnancy outcome while in non-pregnant group were menstrual irregularities, abnormal uterine bleeding and abnormal hormonal profile. Results: There was a highly significant difference between the exposed pregnant and controls regarding low birth weight (p 0.05). Conclusion: female physiotherapists have no increased risks for menstrual irregularities, abnormal hormonal profile or adverse pregnancy outcome except for low birth weight which needs future research.

Abnormal Sex Hormone Profile in Women with End Stage Kidney Disease

Abnormal Sex Hormone Profile in Women with End Stage Kidney Disease

The effect of hormone therapy on all-cause and cardiovascular mortality in women with chronic kidney disease: protocol for a systematic review and meta-analysis.

BackgroundChronic kidney disease affects approximately one in ten North Americans and is associated with a high risk of cardiovascular disease. Chronic kidney disease in women is characterized by an abnormal sex hormone profile and low estradiol levels. Since low estradiol levels are associated with an increased cardiovascular risk in healthy women, our objective is to determine the effect of hormone therapy on all-cause mortality, cardiovascular mortality, and cardiovascular morbidity in women with chronic kidney disease.Methods/designStudies examining hormone therapy for adult women with chronic kidney disease will be included. The primary outcome is all-cause or cardiovascular mortality and morbidity. We will search electronic bibliographic databases (MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials (CENTRAL)) along with relevant conference proceedings, table of contents of journals, and review articles. Two investigators will independently screen identified abstracts and select observational cohort studies, case–control studies, and randomized controlled trials examining hormone therapy in women with chronic kidney disease. These investigators will also independently abstract data from relevant full-text journal articles and assess risk of bias. Where possible, these data will be summarized using pooled or combined estimates for the risk ratio or hazard ratio of all-cause mortality, cardiovascular mortality, and cardiovascular morbidity in women with chronic kidney disease with and without hormone therapy. A random effects model will be used, and meta-regression and subgroup analyses will be used to explore potential source of heterogeneity.DiscussionGiven the high burden of cardiovascular disease in women with chronic kidney disease, this study will help guide clinical practice by summarizing current evidence on the use of hormone therapy for prevention of all-cause mortality, cardiovascular mortality, and cardiovascular morbidity in this population.Systematic review registrationThe final protocol was registered with PROSPERO (CRD42014014566).

Defective CFTR-regulated granulosa cell proliferation in polycystic ovarian syndrome

Polycystic ovarian syndrome (PCOS) is one of the most frequent causes of female infertility, featured by abnormal hormone profile, chronic oligo/anovulation, and presence of multiple cystic follicles in the ovary. However, the mechanism underlying the abnormal folliculogenesis remains obscure. We have previously demonstrated that CFTR, a cAMP-dependent Cl(-) and HCO3 (-) conducting anion channel, is expressed in the granulosa cells and its expression is downregulated in PCOS rat models and human patients. In this study, we aimed to investigate the possible involvement of downregulation of CFTR in the impaired follicle development in PCOS using two rat PCOS models and primary culture of granulosa cells. Our results indicated that the downregulation of CFTR in the cystic follicles was accompanied by reduced expression of proliferating cell nuclear antigen (PCNA), in rat PCOS models. In addition, knockdown or inhibition of CFTR in granulosa cell culture resulted in reduced cell viability and downregulation of PCNA. We further demonstrated that CFTR regulated both basal and FSH-stimulated granulosa cell proliferation through the HCO3 (-)/sAC/PKA pathway leading to ERK phosphorylation and its downstream target cyclin D2 (Ccnd2) upregulation. Reduced ERK phosphorylation and CCND2 were found in ovaries of rat PCOS model compared with the control. This study suggests that CFTR is required for normal follicle development and that its downregulation in PCOS may inhibit granulosa cell proliferation, resulting in abnormal follicle development in PCOS.

The Prevalence and Patterns of Endocrinopathies Amongs Azoospermic Male Partners at a Fertility Clinic in Benin City

Aim and Objective: We undertook this study to evaluate the prevalence, trend and patterns of endocrine abnormalities among azoospermic male partners of infertile couples investigated for male infertility in our fertility centre. Setting: A private IVF hospital treating infertility with assisted reproduction technology in Benin City, Nigeria. Methodology: A prospective, observational and a descriptive study of the analysis of the hormonal profile of azoospermic male partners of the infertile couples, who presented at St Augustine Medical center, Benin City, Nigeria over a five-year period from May 2007 through December 2012 was undertaken. Results: A total of 686 men were investigated for infertility within this period, fifty-eight (8.45%) of them with a mean age of 43.72±1.5years were found to be azoospermic. Of the 58 azoospermic men, fourty-eight (82.76%) had one or more abnormal hormonal profile parameter, while ten (17.24%) had a normal hormone profile pattern. Of the forty-eight Azoospermic men with abnormal hormone profile pattern, twenty-two (37.93%) had increased serum FSH and LH, mildly increased prolactin and low testosterone, 15 (25.86%) had increased serum FSH, normal LH and prolactin with reduced testosterone, 4 (6.9%) had increased serum LH, normal FSH and prolactin with reduced testosterone, 2 (3.45%) had low LH, FSH and testosterone with high prolactin while 5 (10.42%) had elevated prolactin levels, normal gonadotrophins (LH & FSH) and low testosterone. Ejaculate volume was normal in 48(82.76%) of the azoospermic men when the mean semen volume was 3.30±0.19mls; and mean serum hormone levels were LH; 9.54 ± 0.89, FSH; 22.77± 2.70, Prolactin; 18.54± 2.50, Testosterone; 3.01 ± 0.22. The ejaculate volume was low in 10 (17.24%) men with a mean semen volume of 0.89±0.07 and mean serum hormone levels; LH; 13.75±3.12, FSH; 23.48±4.45, Prolactin; 15.87±2.46, Testosterone; 3.08±0.46. Conclusion: Endocrinopathies are common among azoospermic male partners of infertile couples in Benin City. The most prevalent pattern of endocrinopathy suggests testicular failure. Majority of men don't show-up early enough for infertility screening. Azoospermia was most prevalent among business men followed by civil servants. The main reason for the endocrinopathies is not clear, but exposures to certain environmental/occupational factors which can disrupt endocrine function are likely to be contributory.

Low-dose Gamma Knife surgery for nonfunctioning pituitary adenomas

The primary concern when performing Gamma Knife surgery for pituitary adenoma is preservation of vision and pituitary function while achieving tumor growth control. Higher prescribed radiation doses are typically correlated with higher incidences of postradiosurgical hormone deficiencies. The goal of the present study was to retrospectively analyze the feasibility of using a lower prescribed radiation dose in the treatment of nonfunctioning pituitary adenomas and the effect of this dose on vision, pituitary function, and tumor growth control. The study was conducted in 38 patients with nonfunctioning pituitary adenomas, who were treated between January 2002 and July 2008. Twenty-one patients were available for follow-up (13 men and 8 women). The mean follow-up period was 44 months (range 24-90 months). Nineteen patients had previously undergone surgery. Pituitary dysfunction developed after surgery in 3 patients. One patient had an abnormal pituitary hormone profile before radiosurgery due to an attack of pituitary apoplexy. Visual field defects were present in 12 patients. The prescribed radiation dose was 12 Gy in all patients. The tumor volume ranged from 0.5 to 11.8 cm(3) (mean 4.8 cm(3)). The maximum dose to the visual pathway was kept below 10 Gy. The mean maximum dose delivered to the visual pathway was 7.9 Gy. The patients were followed up for a period of 24 to 90 months (mean 44 months). The size of the tumor decreased in 11 patients (52%) and remained stable in 9 patients (43%). In 1 patient there was tumor growth outside the previous radiation field (on the contralateral side). Among the 12 patients with visual field defects, 9 (75%) experienced an improvement and the remaining patients' vision remained stable. In only 4 patients was the visual improvement associated with tumor shrinkage. The hormone profile remained normal in all patients except for the 4 patients who had pituitary dysfunction before radiosurgery. The 12-Gy prescribed dose used in this study seems to be sufficient for producing tumor control while sparing the patient from radiation-induced pituitary dysfunction. In addition, visual improvement was reported in a number of cases. A larger series and longer follow-up are required to confirm these results.

Pharmacologic Interventions for Hidradenitis Suppurativa

Hidradenitis suppurativa is a chronic debilitating skin disease that is recalcitrant to treatment. The aim of this article was to conduct an evidence-based review of pharmacologic interventions for the treatment of hidradenitis suppurativa (HS). A systematic search of MEDLINE, EMBASE, and the Cochrane database was conducted to identify controlled trials (randomized controlled trials, cohorts, and case-control studies) published in English. The abstracts were examined using predetermined inclusion and exclusion criteria. The identified studies were used to develop the recommendations. Clinically relevant outcomes that were assessed were: clinical remission, patient global assessment, physician global assessment, number of skin lesions, and improvement in Hurley's stage, or Sartorius score. Overall there was sparse evidence to support the use of any treatment modality. There is fair evidence to support the use of antibacterials in HS and they should be used as first-line therapy (level II-1/grade B). There is fair evidence to support the use of intravenous infliximab in the treatment of advanced HS (Hurley's stage II and III). Given the high cost of anti-tumor necrosis factor therapy and its adverse-effect profile, intravenous infliximab should be offered to patients with severe disease affecting their daily activities who have failed antibacterial therapy (level I/grade B). There is insufficient evidence to support the use of antiandrogens in HS; consideration could be given to their use in women with mild to moderate disease (Hurley's stage I and II) who have failed antibacterial therapy and women with an abnormal hormone profile (level II-2/grade I). The existing evidence suggests that antibacterials and anti-tumor necrosis factor therapy are effective in the treatment of HS. Further research is required to confirm the efficacy of the different medications within these groups and to explore the efficacy of other treatment modalities.