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David A. Sullivan - One of the best experts on this subject based on the ideXlab platform.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
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impact of Androgen Deficiency on the lipid profiles in human meibomian gland secretions
Advances in Experimental Medicine and Biology, 2002Co-Authors: Benjamin D Sullivan, James E. Evans, M R Dana, David A. SullivanAbstract:Our previous research has indicated that Androgen Deficiency may be a critical etiologic factor in the pathogenesis of meibomian gland dysfunction, tear film instability and evaporative dry eye.1–3 We hypothesize that this may be due, at least in part, to significant alterations in the lipid profile of meibomian gland secretions.3 To test this hypothesis, we examined whether Androgen Deficiency, such as that occurring during aging in both sexes, complete Androgen insensitivity syndrome (CAIS), the use of anti-Androgen therapy and Sjogren’s syndrome (SS),4–7 is associated with significant changes in the fatty acid (FA) patterns of neutral and polar lipids in meibomian gland secretions. In addition, we determined whether lipid profiles could be used to separate individuals into clinically identifiable groups.
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effect of Androgen Deficiency on the human meibomian gland and ocular surface
The Journal of Clinical Endocrinology and Metabolism, 2000Co-Authors: Kathleen L Krenzer, James E. Evans, David M Ullman, Jennifer M Cermak, Dorothy Bazzinotti Tolls, Reza Dana, David A. SullivanAbstract:The purpose of this study was to determine whether the chronic use of antiAndrogen medications leads to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, decreased tear film stability, and evaporative dry eye. Subjects taking antiAndrogen therapy for prostatic indications, as well as age-related controls, were asked to complete a questionnaire that assessed dry eye symptoms and then were given a complete anterior segment examination. Moreover, meibomian gland secretions were obtained from each eye and analyzed by high-performance liquid chromatography/mass spectrometry for the relative content of cholesterol, cholesterol esters, wax esters, diglycerides, triglycerides, and specific molecular species in the diglyceride fraction. Our results demonstrate that patients taking antiAndrogen treatment, compared with age-related controls, had a: 1) significant increase in the frequency of appearance of tear film debris, an abnormal tear film meniscus, irregular posterior lid margins, conjunctival tarsal injection, and orifice metaplasia of the meibomian glands; 2) significant increase in the degree of ocular surface vital dye staining; 3) significant decrease in the tear film breakup time and quality of meibomian gland secretions; and 4) significant increase in the frequency of light sensitivity, painful eyes, and blurred vision. In addition, the use of antiAndrogen pharmaceuticals was associated with significant changes in the relative amounts of lipids in meibomian gland secretions. Our findings indicate that chronic Androgen Deficiency is associated with meibomian gland dysfunction and dry eye.
David J. Handelsman - One of the best experts on this subject based on the ideXlab platform.
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blood testosterone threshold for Androgen Deficiency symptoms
The Journal of Clinical Endocrinology and Metabolism, 2004Co-Authors: S Kelleher, Ann J. Conway, David J. HandelsmanAbstract:There are few systematic studies of the relationship between blood testosterone concentrations and the symptoms of overt Androgen Deficiency. Because most testosterone preparations are relatively short-term, the rapid changes in blood testosterone concentrations they cause make it difficult to define any testosterone threshold. By contrast, subdermal testosterone implants provide stable blood testosterone concentrations over days to weeks, while gradually declining to baseline over 5–7 months. Hence, this provides an opportunity to define a blood testosterone threshold for Androgen Deficiency symptoms by observing Androgen-deficient men as their familiar Androgen Deficiency symptoms return as testosterone pellets slowly dissolve. Among 52 Androgen-deficient men who underwent 260 implantations over 5 yr, at the time of return of Androgen Deficiency symptoms the blood total and free testosterone concentrations were highly reproducible within individuals (F 0.8, P 0.49 and F 1.4, 0.24, respectively) but varied markedly between men (F 167 and F 138, both P < 0.001), indicating that each person had a consistent testosterone threshold for Androgen Deficiency symptoms that differed markedly between individuals. The most reported symptoms of Androgen Deficiency were lack of energy, lack of motivation, and reduced libido. The symptomatic threshold was significantly lower in men with secondary hypogonadism compared with men with primary or mixed hypogonadism (total, 9.7 0.5 nmol/liter vs. 11.7 0.4 nmol/liter and 10.2 0.3 nmol/liter, P 0.006; free, 146 10 pmol/liter vs. 165 6 pmol/ liter and 211 18 pmol/liter, P 0.002) but was not affected by the underlying cause of hypogonadism or by specific symptoms of any severity. Despite a wide range in individual thresholds for Androgen Deficiency symptoms, the mean blood testosterone threshold corresponded to the lower end of the eugonadal reference range for young men. The implications of these observations for the development of more specific quality-of-life measures, as well as for other potential Androgen Deficiency states such as chronic diseases and aging, remain to be determined. (J Clin Endocrinol Metab 89: 3813–3817, 2004)
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recombinant human chorionic gonadotropin but not dihydrotestosterone alone stimulates osteoblastic collagen synthesis in older men with partial age related Androgen Deficiency
The Journal of Clinical Endocrinology and Metabolism, 2004Co-Authors: Christian Meier, David J. Handelsman, Peter Liu, Mark Jimenez, James De Wintermodzelewski, Markus J SeibelAbstract:Several randomized trials of Androgen supplementation in older men have been undertaken. However, the relative contributions of testosterone (T) and estrogens on bone metabolism in aging men are controversial. Within the setting of two double-blind, placebo-controlled studies, we evaluated the effect of dihydrotestosterone (DHT) and recombinant human chorionic gonadotropin (rhCG) on bone turnover in healthy, community-dwelling older men with partial Androgen Deficiency (total T < or = 15 nmol/liter). In the first study, 35 men (age 68.3 +/- 6.8 yr; baseline T, 13.9 +/- 3.3 nmol/liter) were randomized to receive either daily transdermal DHT (n = 17) or placebo for 3 months. In the second study, 40 men (age 67.4 +/- 5.4 yr; baseline T, 11.4 +/- 2.2 nmol/liter) were randomized to receive either rhCG s.c. (n = 20), two injections weekly, or placebo for 3 months. The following parameters were measured before, monthly during, and 1 month after treatment: serum T, estradiol (E2), and LH; markers of bone formation, serum amino-terminal propeptide of type I procollagen (S-PINP) and osteocalcin; markers of bone resorption, serum carboxyterminal cross-linked telopeptide of type I collagen and urinary deoxypyridinoline. Compared with placebo, treatment with DHT significantly increased serum DHT and suppressed LH and T levels, whereas E2 concentrations and markers of bone turnover did not change. In contrast, rhCG therapy significantly increased both T and E2, with the increases in E2 being supraphysiological. At the same time, rhCG significantly increased S-PINP concentrations with peak levels after 1 month (Delta40%; P = 0.02 compared with placebo). In contrast, serum osteocalcin and carboxyterminal cross-linked telopeptide of type I collagen and urinary deoxypyridinoline levels did not change. The change in S-PINP levels correlated with the change in E2 levels (r = 0.59; P = 0.02) but not with a change in T. We conclude that in older men with partial age-related Androgen Deficiency, rhCG treatment stimulates osteoblastic collagen formation proportionally to increased E2 concentrations but does not alter markers of mature osteoblastic function or bone resorption. In contrast, treatment with a pure, nonaromatizable Androgen (DHT) has no effect on bone turnover despite a 20-fold increase in serum levels. Bone resorption was not accelerated during unchanged (DHT) or increased (rhCG) E2 levels, suggesting that minimal E2 levels are needed to maintain stable resorption, although direct Androgen receptor-mediated effects cannot be excluded. If Androgen supplementation is required for aging men, aromatizable Androgens with sufficient endogenous estrogenic activity may have the most beneficial effects on bone.
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11 Androgen Deficiency and replacement therapy in men
The Medical Journal of Australia, 2004Co-Authors: David J. Handelsman, Jeffrey D ZajacAbstract:Androgen Deficiency is a clinical diagnosis confirmed by hormone assays. Among younger men, Androgen Deficiency is usually due to underlying hypothalamopituitary or testicular disorders. Androgen replacement therapy should be started after proof of Androgen Deficiency and should continue lifelong with monitoring. Men presenting with erectile dysfunction should be evaluated for Androgen Deficiency, but it is an uncommon cause; if overt Androgen Deficiency is confirmed, an underlying disorder needs further specialist investigation. In the absence of characteristic underlying testicular or pituitary disorders, new diagnosis of Androgen Deficiency in older men is difficult because of the non-specific symptoms and the decline in blood testosterone levels seen in healthy ageing and chronic medical disorders. There remains no convincing evidence that Androgen therapy is either effective treatment or safe for older men unless they have frank Androgen Deficiency.
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a double blind placebo controlled randomized clinical trial of recombinant human chorionic gonadotropin on muscle strength and physical function and activity in older men with partial age related Androgen Deficiency
The Journal of Clinical Endocrinology and Metabolism, 2002Co-Authors: Peter Liu, Susan M Wishart, David J. HandelsmanAbstract:Despite partial Androgen Deficiency, the safety and efficacy of Androgen therapy in older men remains controversial because controlled studies of testosterone have given equivocal results. Human chorionic gonadotropin (hCG) can be conveniently and infrequently self-administered, and it increases not only circulating testosterone but also estradiol and other testicular steroids. We evaluated the efficacy and safety of 3 months of treatment with sc recombinant hCG (r-hCG, Ovidrel) on muscle mass, strength, mobility, and physical activity in ambulant, community-dwelling men more than 60 yr old having partial Androgen Deficiency (testosterone ≤ 15 nmol/liter, twice). Forty eligible men (mean age, 67 yr; range, 60–85 yr) were randomized to receive r-hCG (5000 IU, 250 μg) or placebo by twice weekly sc self-injection and were studied before treatment, monthly during treatment, and 1 month after treatment. All completed the study, and treatment groups were well matched. r-hCG significantly increased body weight (...
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a double blind placebo controlled randomized clinical trial of recombinant human chorionic gonadotropin on muscle strength and physical function and activity in older men with partial age related Androgen Deficiency
The Journal of Clinical Endocrinology and Metabolism, 2002Co-Authors: Peter Liu, Susan M Wishart, David J. HandelsmanAbstract:Despite partial Androgen Deficiency, the safety and efficacy of Androgen therapy in older men remains controversial because controlled studies of testosterone have given equivocal results. Human chorionic gonadotropin (hCG) can be conveniently and infrequently self-administered, and it increases not only circulating testosterone but also estradiol and other testicular steroids. We evaluated the efficacy and safety of 3 months of treatment with sc recombinant hCG (r-hCG, Ovidrel) on muscle mass, strength, mobility, and physical activity in ambulant, community-dwelling men more than 60 yr old having partial Androgen Deficiency (testosterone < or = 15 nmol/liter, twice). Forty eligible men (mean age, 67 yr; range, 60-85 yr) were randomized to receive r-hCG (5000 IU, 250 microg) or placebo by twice weekly sc self-injection and were studied before treatment, monthly during treatment, and 1 month after treatment. All completed the study, and treatment groups were well matched. r-hCG significantly increased body weight (approximately 1 kg; P < 0.05) and lean body mass ( approximately 2 kg; P < 0.001) and reduced fat mass (approximately 1 kg, P < 0.05). However, anthropometric measures of skinfold thickness (biceps, triceps, subscapular, suprailiac) and circumferences (midarm, waist, hip, and midthigh), including the waist-hip ratio, did not change significantly. Shoulder and knee strength (peak torque), as measured by isokinetic and isometric dynamometry, was not significantly increased, nor was physical activity (accelerometry and Physical Activity Scale for Elderly self-report) or gait and balance (modified Guralnik and Frailty and Injuries: Cooperative Studies of Intervention Techniques performance batteries) altered. Total and free testosterone and estradiol were markedly (150%; P < 0.001) and stably increased, whereas LH, FSH, and urea were significantly decreased. Testis volume was significantly decreased (approximately 5 ml; P < 0.05). There were no significant changes in hemoglobin, osteocalcin, or prostate-specific antigen, and the International Prostate Symptom Score did not change. Three men developed nipple tenderness that did not progress to gynecomastia. We conclude that 3 months of treatment with twice weekly r-hCG demonstrates sustained Androgenic effects on hormones and muscle mass but has no effect on muscle strength or physical functioning.
Thomas G Travison - One of the best experts on this subject based on the ideXlab platform.
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effects of testosterone replacement on pain catastrophizing and sleep quality in men with opioid induced Androgen Deficiency
Pain Medicine, 2016Co-Authors: Grace Huang, Thomas G Travison, Robert R Edwards, Shehzad BasariaAbstract:Objective. The objective of this investigation was to determine the effects of testosterone administration on pain catastrophizing and sleep quality in adult men with opioid-induced Androgen Deficiency. Design. Sixty-two men aged 18–64 years using opioid analgesics for chronic non-cancer pain with total testosterone levels < 350 ng/dl were randomized to 14 weeks of transdermal testosterone gel or placebo gel daily. Total testosterone levels were measured by liquid chromatography mass spectrometry and free testosterone was calculated using the law of mass action equation. Outcomes were assessed by administering validated instruments such as Pain Catastrophizing Scale (PCS) and Insomnia Severity Index (ISI) at baseline and 14 weeks. Results. Baseline characteristics were similar between the two groups. Mean (SD) total testosterone concentrations increased from 223 ± 86 to 775 ± 555 ng/dl in the testosterone group, but did not meaningfully change in placebo group. Mean changes in PCS and ISI scores during intervention did not differ significantly between groups and were not related to changes in on-treatment serum testosterone concentrations. Conclusion. In this 14-week trial, testosterone administration in men with opioid-induced Androgen Deficiency was not associated with improvements in pain catastrophizing or sleep quality.
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effects of testosterone replacement on metabolic and inflammatory markers in men with opioid induced Androgen Deficiency
Clinical Endocrinology, 2016Co-Authors: Grace Huang, Thomas G Travison, Marcello Maggio, Robert R Edwards, Shehzad BasariaAbstract:SummaryObjective Symptomatic Androgen Deficiency is common in patients taking opioid analgesics, and testosterone replacement in these men improves libido, quality of life and body composition. However, the effects of testosterone replacement on metabolic and inflammatory markers in this setting have not been evaluated. This is important as opiate use itself has been associated with metabolic abnormalities. The objective of this investigation was to determine the effects of testosterone administration on metabolic and inflammatory markers in adult men with opioid-induced Androgen Deficiency. Methods Sixty-four nondiabetic men aged 18 to 64 years using opioid analgesics for chronic noncancer pain with total testosterone levels <12 nmol/l were randomized to 14 weeks of transdermal testosterone gel or placebo gel daily. Total testosterone levels were measured by liquid chromatography mass spectrometry, and free testosterone was calculated using the law-of-mass-action equation. Metabolic parameters, inflammatory markers and oral glucose tolerance test (OGTT) were evaluated at baseline and 14 weeks. Results Baseline characteristics were similar between the two groups. Testosterone concentrations increased from 7·7 ± 3·0 to 27 ± 19 nmol/l in the testosterone group, but did not meaningfully change in placebo group. Mean changes in metabolic and inflammatory markers during intervention did not differ significantly between groups and were not related to changes in on-treatment serum testosterone concentrations. Glucose and insulin response to the 75 g OGTT also did not differ between groups. Conclusion In this 14-week trial, testosterone administration in men with opioid-induced Androgen Deficiency was not associated with worsening of metabolic and inflammatory markers.
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effects of testosterone replacement in men with opioid induced Androgen Deficiency a randomized controlled trial
Pain, 2015Co-Authors: Shehzad Basaria, Thomas G Travison, Daniel P Alford, Philip E Knapp, Kjersten Teeter, Christine Cahalan, Richard Eder, Kishore M Lakshman, Eric BachmanAbstract:Symptomatic Androgen Deficiency is common in patients taking opioid analgesics, as these drugs potently suppress the hypothalamic-pituitary-gonadal axis. However, the efficacy of testosterone replacement in this setting remains unclear. The objective of this trial was to evaluate the efficacy of testosterone replacement on pain perception and other Androgen-dependent outcomes in men with opioid-induced Androgen Deficiency. We conducted a randomized, double-blind, parallel placebo-controlled trial at an outpatient academic research center. Participants were men aged 18 to 64 years on opioid analgesics for chronic noncancer pain, and total testosterone levels were <350 ng/dL. Participants were randomly assigned to 14 weeks of daily transdermal gel that contained 5 g of testosterone or placebo. Primary outcomes were changes in self-reported clinical pain and objectively assessed pain sensitivity. Sexual function, quality of life, and body composition were also assessed. The mean age was 49 years. The median total and free testosterone levels at baseline were 243 ng/dL and 47 pg/mL and 251 ng/dL and 43 pg/mL in the testosterone and placebo arm, respectively. Of the 84 randomized participants, 65 had follow-up data on efficacy outcomes. Compared with men assigned to the placebo arm, those assigned to testosterone replacement experienced greater improvements in pressure and mechanical hyperalgesia, sexual desire, and role limitation due to emotional problems. Testosterone administration was also associated with an improvement in body composition. There were no between-group differences in changes in self-reported pain. In conclusion, in men with opioid-induced Androgen Deficiency, testosterone administration improved pain sensitivity, sexual desire, body composition, and aspects of quality of life.
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correlates of low testosterone and symptomatic Androgen Deficiency in a population based sample
The Journal of Clinical Endocrinology and Metabolism, 2008Co-Authors: Susan A Hall, Andre B Araujo, Gretchen R Esche, Thomas G Travison, Rachel E Williams, Richard V Clark, John B MckinlayAbstract:Context: Risk factors for low testosterone and symptomatic Androgen Deficiency (AD) may be modifiable. Objective: Our objective was to examine demographic, anthropometric, and medical correlates of low testosterone and symptomatic AD. Design: Data were used from the Boston Area Community Health Survey, an epidemiological study conducted from 2002–2005. Setting: Data were obtained from a community-based random sample of racially and ethnically diverse men. Patients or other Participants: Data were available for 1822 men. Main Outcome Measures: Multivariate logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for associations of covariates with 1) low testosterone and 2) symptomatic AD. The operational definition of low testosterone was serum total testosterone less than 300 ng/dl and free testosterone less than 5 ng/dl; symptomatic AD was defined as the additional presence of symptoms: any of low libido, erectile dysfunction, or osteoporosis or two or more of sleep disturbance, depressed mood, lethargy, or diminished physical performance. Results: Factors associated with low testosterone included age (OR = 1.36; 95% CI= 1.11–1.66, per decade), low per-capita income ($6000 or less per household member vs. more than $30,000; OR = 2.86; 95% CI = 1.39–5.87), and waist circumference (per 10-cm increase; OR = 1.75; 95% CI = 1.45–2.12). Only age (OR = 1.36; 95% CI = 1.04–1.77), waist circumference (OR = 1.88; 95% CI = 1.44–2.47), and health status (OR = 0.21; 95% CI = 0.05–0.92, excellent vs. fair/poor) were associated with our construct of symptomatic AD. Of all variables, waist circumference was the most important contributor in both models. Conclusions: Waist circumference is a potentially modifiable risk factor for low testosterone and symptomatic AD. Manifestation of symptoms may be a consequence of generally poor health status.
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treatment of symptomatic Androgen Deficiency results from the boston area community health survey
JAMA Internal Medicine, 2008Co-Authors: Susan A Hall, Andre B Araujo, Gretchen R Esche, Thomas G Travison, Rachel E Williams, Richard V Clark, John B MckinlayAbstract:Background: Despite the aging of the US population and increasing sales of prescription testosterone, treatment patterns for Androgen Deficiency (AD) are poorly understood. We describe patterns and correlates of testosterone treatment in community-dwelling men. Methods: The Boston Area Community Health Survey is an observational study of a population-based random sample of racially and ethnically diverse men representative of Boston, Massachusetts. Data collected by inperson interview from April 2002 to June 2005 included health status, socioeconomic status, access to medical care, and use of prescription medications. A venous blood sample was collected. The operational definition of untreated AD was serum total testosterone level less than 300 ng/dL (to convert to nanomoles per liter, multiply by 0.0347) and free testosterone level less than 5 ng/dL, and the presence of at least 1 specific symptom (low libido, erectile dysfunction, or osteoporosis) or 2 or more less-specific symptoms (sleep disturbance, depressed mood, lethargy, or diminished physical performance) and not using prescription testosterone. Any man who was using testosterone was considered to have treated AD. Results: Data were available for 1486 Boston Area Community Health Survey participants (mean age, 46.4 years; age range, 30-79 years). A total of 5.5% (95% confidence interval, 3.5-8.5) men met the criteria for having untreated, symptomatic AD, and 0.8% (95% confidence interval, 0.4-1.4) met the criteria for having treated AD. Considering all cases, the proportion treated was 12.2%. Men with untreated AD seemed to have adequate access to care. Conclusions: Under our assumptions, a large majority (87.8%) of 97 men in our groups with AD were not receiving treatment despite adequate access to care. The reasons for this are unknown but could be due to unrecognized AD or unwillingness to prescribe testosterone therapy.
R M Sullivan - One of the best experts on this subject based on the ideXlab platform.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
James E. Evans - One of the best experts on this subject based on the ideXlab platform.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
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Androgen Deficiency meibomian gland dysfunction and evaporative dry eye
Annals of the New York Academy of Sciences, 2002Co-Authors: David A. Sullivan, James E. Evans, Benjamin D Sullivan, F Schirra, Hideki Yamagami, Stephen M Richards, Debra A Schaumberg, Tomo Suzuki, R M SullivanAbstract:Abstract: Objective. We have recently discovered that women with primary and secondary Sjogren's syndrome are Androgen-deficient. We hypothesize that this hormone insufficiency contributes to the meibomian gland dysfunction, tear film instability, and evaporative dry eye that are characteristic of this autoimmune disorder. If our hypothesis is correct, we predict: (1) that Androgens regulate meibomian gland function, control the quality and/or quantity of lipids produced by this tissue, and promote the formation of the tear film's lipid layer; and (2) that Androgen Deficiency, due to an attenuation in Androgen synthesis (e.g., during Sjogren's syndrome, menopause, aging, complete Androgen-insensitivity syndrome [CAIS] and anti-Androgen use), will lead to meibomian gland dysfunction and evaporative dry eye. The following studies were designed to test these predictions. Methods. Experimental procedures included clinical studies, animal models, and histological, biochemical, molecular biological, and biomedical engineering techniques. Results. Our results demonstrate that: (1) Androgens regulate the meibomian gland. This tissue contains Androgen receptor mRNA, Androgen receptor protein within acinar epithelial cell nuclei, and Types 1 and 2 5α-reductase mRNAs. Moreover, Androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) Androgen Deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye. Thus, we have found that anti-Androgen therapy in men is associated with meibomian gland disease, a decreased tear film breakup time, and functional dry eye. Furthermore, we have discovered that Androgen receptor dysfunction in women with CAIS is associated with meibomian gland changes and a significant increase in the signs and symptoms of dry eye. Of interest, we have also found that Androgen Deficiency is associated with significant and striking alterations in the neutral and polar lipid patterns of human meibomian gland secretions. Conclusions. Our findings show that the meibomian gland is an Androgen target organ and that Androgen Deficiency may promote meibomian gland dysfunction and evaporative dry eye. Overall, these results support our hypothesis that Androgen Deficiency may be an important etiologic factor in the pathogenesis of evaporative dry eye in women with Sjogren's syndrome.
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impact of Androgen Deficiency on the lipid profiles in human meibomian gland secretions
Advances in Experimental Medicine and Biology, 2002Co-Authors: Benjamin D Sullivan, James E. Evans, M R Dana, David A. SullivanAbstract:Our previous research has indicated that Androgen Deficiency may be a critical etiologic factor in the pathogenesis of meibomian gland dysfunction, tear film instability and evaporative dry eye.1–3 We hypothesize that this may be due, at least in part, to significant alterations in the lipid profile of meibomian gland secretions.3 To test this hypothesis, we examined whether Androgen Deficiency, such as that occurring during aging in both sexes, complete Androgen insensitivity syndrome (CAIS), the use of anti-Androgen therapy and Sjogren’s syndrome (SS),4–7 is associated with significant changes in the fatty acid (FA) patterns of neutral and polar lipids in meibomian gland secretions. In addition, we determined whether lipid profiles could be used to separate individuals into clinically identifiable groups.
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effect of Androgen Deficiency on the human meibomian gland and ocular surface
The Journal of Clinical Endocrinology and Metabolism, 2000Co-Authors: Kathleen L Krenzer, James E. Evans, David M Ullman, Jennifer M Cermak, Dorothy Bazzinotti Tolls, Reza Dana, David A. SullivanAbstract:The purpose of this study was to determine whether the chronic use of antiAndrogen medications leads to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, decreased tear film stability, and evaporative dry eye. Subjects taking antiAndrogen therapy for prostatic indications, as well as age-related controls, were asked to complete a questionnaire that assessed dry eye symptoms and then were given a complete anterior segment examination. Moreover, meibomian gland secretions were obtained from each eye and analyzed by high-performance liquid chromatography/mass spectrometry for the relative content of cholesterol, cholesterol esters, wax esters, diglycerides, triglycerides, and specific molecular species in the diglyceride fraction. Our results demonstrate that patients taking antiAndrogen treatment, compared with age-related controls, had a: 1) significant increase in the frequency of appearance of tear film debris, an abnormal tear film meniscus, irregular posterior lid margins, conjunctival tarsal injection, and orifice metaplasia of the meibomian glands; 2) significant increase in the degree of ocular surface vital dye staining; 3) significant decrease in the tear film breakup time and quality of meibomian gland secretions; and 4) significant increase in the frequency of light sensitivity, painful eyes, and blurred vision. In addition, the use of antiAndrogen pharmaceuticals was associated with significant changes in the relative amounts of lipids in meibomian gland secretions. Our findings indicate that chronic Androgen Deficiency is associated with meibomian gland dysfunction and dry eye.