Iatrogenic Cushing's Syndrome Due to Topical Ocular Glucocorticoid Treatment Daisuke Fukuhara, Toshihiko Takiura, Hiroshi Keino, Annabelle A

Total Page:16

File Type:pdf, Size:1020Kb

Iatrogenic Cushing's Syndrome Due to Topical Ocular Glucocorticoid Treatment Daisuke Fukuhara, Toshihiko Takiura, Hiroshi Keino, Annabelle A Iatrogenic Cushing’s Syndrome Due to Topical Ocular Glucocorticoid Treatment Daisuke Fukuhara, MD, PhD, a Toshihiko Takiura, MD, a Hiroshi Keino, MD, PhD, b Annabelle A. Okada, MD, PhD,b Kunimasa Yan, MD, PhDa Iatrogenic Cushing’s syndrome (CS) is a severe adverse effect of systemic abstract glucocorticoid (GC) therapy in children, but is extremely rare in the setting of topical ocular GC therapy. In this article, we report the case of a 9-year- old girl suffering from idiopathic uveitis who developed CS due to topical ocular GC treatment. She was referred to the ophthalmology department with a complaint of painful eyes, at which time she was diagnosed with bilateral iridocyclitis and started on a treatment of betamethasone sodium phosphate eye drops. Six months after the initiation of topical ocular GC treatment, she was referred to our pediatric department with stunted growth, truncal obesity, purple skin striate, buffalo hump, and moon face. Because her serum cortisol and plasma adrenocorticotropic hormone levels were undetectable, she was diagnosed with iatrogenic CS. After the Departments of aPediatrics, and bOphthalmology, Kyorin doses of topical ocular GC were reduced, the clinical symptoms of CS were University School of Medicine, Mitaka, Tokyo, Japan improved. The fact that the amount of topical ocular GC with our patient was Dr Fukuhara conceptualized and designed the apparently less than that of similar previous cases tempted us to perform study and drafted the initial manuscript; genetic analysis of her NR3C1 gene. We found that our patient had a single Dr Takiura carried out the initial analyses and heterozygous nucleotide substitution in the 3′ untranslated region of the reviewed and revised the manuscript; Drs Keino and Okada reviewed and revised the manuscript; NR3C1 gene, which may explain why she developed CS. However, additional Dr Yan oversaw the data and critically reviewed investigations are required to determine if our findings can be extrapolated the manuscript; and all authors approved the to other patients. In conclusion, clinicians should be aware that even fi nal manuscript as submitted and agree to be accountable for all aspects of the work. extremely low doses of topical ocular steroid therapy can cause DOI: 10.1542/peds.2016-1233 iatrogenic CS. Accepted for publication Oct 10, 2016 Address correspondence to Kunimasa Yan, MD, PhD, Department of Pediatrics, Kyorin University School Iatrogenic Cushing’s syndrome different and depends on genetic of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181- (CS) is a severe adverse effect of and acquired factors. 3 The actions 8611, Japan. E-mail: [email protected] glucocorticoid (GC) therapy in both of GCs are mediated by the GC PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, children and adults, and is mostly receptor (GR), which acts as a 1098-4275). caused by long-term and abundant ligand-activated transcription Copyright © 2017 by the American Academy of systemic GC administration. Topical factor regulating the transcription Pediatrics GC treatment with nasal drops or of thousands of GC-responsive FINANCIAL DISCLOSURE: The authors have ointment rarely induces iatrogenic genes in a positive or negative indicated they have no fi nancial relationships CS. 1, 2 GC treatment via eye drops fashion. 4 It is currently known that relevant to this article to disclose. is commonly used to treat ocular 4 functionally characterized single- FUNDING: No external funding. inflammatory diseases, including nucleotide polymorphisms (SNPs) POTENTIAL CONFLICT OF INTEREST: The authors juvenile idiopathic uveitis. This of GR (9β, ER22/23EK, BclI and have indicated they have no potential confl icts of interest to disclose. treatment causes local adverse N363S) modulate GC sensitivity. 3, 5 effects, such as glaucoma or cataracts. On the other hand, 1 patient However, iatrogenic CS is extremely exhibiting manifestations of GC To cite: Fukuhara D, Takiura T, Keino H, et al. rare. hypersensitivity caused by a novel Iatrogenic Cushing’s Syndrome Due to Topical The sensitivity to endogenous NR3C1 gene mutation has been Ocular Glucocorticoid Treatment. Pediatrics. 2017; 139(2):e20161233 and synthetic GCs is individually described previously.6 In this article, Downloaded from www.aappublications.org/news by guest on September 30, 2021 PEDIATRICS Volume 139 , number 2 , February 2017 :e 20161233 CASE REPORT we report the case of a 9-year-old girl on her physical findings and low NR3C1 gene, rs13306585, which is suffering from idiopathic uveitis who endogenous cortisol and ACTH levels, located in the 3′ untranslated region developed CS due to topical ocular we diagnosed her with CS, which was (3′-UTR). No other mutations or GC treatment but had only a single most likely due to excess absorption polymorphisms were identified. nucleotide variation rather than such of ocular GC. Therefore, we started SNPs or mutation. oral methotrexate treatment to reduce the amount of eye drops of DISCUSSION betamethasone sodium phosphate. In this article, we report an extremely CASE REPORT Consequently, her weight gain rare case of iatrogenic CS due to A 9-year-old girl was referred to the decreased while her height increased topical ocular GC treatment. Synthetic ophthalmology department with to a typical SD ( Fig 1D). Six months GCs are one of the most important a complaint of painful eyes. Her after the initiation of methotrexate and widely used drugs in both adults medical history was unremarkable, treatment, she exhibited morning and children. They are used to treat a without any ocular injury or serum cortisol and plasma ACTH variety of disorders, such as allergies surgery. In addition, she did not levels of 10.1 μg/dL and 42.6 pg/mL, and dermatological, inflammatory, complain of any joint pain or bowel respectively, as well as no clinical and autoimmune diseases, because symptoms. She was diagnosed with symptoms of CS ( Fig 1C). they have a striking antiinflammatory bilateral iridocyclitis and started and immunosuppressive effect. All Amplifi cation and Sequencing of the on a treatment of betamethasone clinicians are aware that prolonged NR3C1 Gene sodium phosphate eye drops (0.1% use of systemic GCs at high doses solution). The frequency of eye drops Written informed consent was results in severe adverse effects. was increased to up to 6 times per obtained from the parents of the However, topical GC therapy day due to uncontrollable ocular patient. We performed genotyping uncommonly results in those adverse inflammation. She was referred to of the coding sequence, which effects, and ocular GC therapy is an our pediatric department after 6 comprised exons 2 through 9, extremely rare cause compared with months of treatment, at which time and the intron–exon junctions of nasal and dermatological therapies. 1, 2 she presented with purple skin the NR3C1 gene, including the 4 β There are 2 major potential routes striae. She was not taking any oral or functional GR SNPs (9 , rs6198; to absorb topical ocular GCs into parenteral GCs, nor was she taking ER22/23EK, rs6189, and rs6190; circulation. One is the conjunctiva, any other medication. BclI, rs41423247; and N363S, rs6195) using Sanger sequencing as which is thin and vascular, and Physical examination at our described below. Genomic DNA was facilitates rapid diffusion, and outpatient clinic revealed that she isolated from peripheral blood by the other is the nasal mucosa via was afebrile with a heart rate of 80 using the DNeasy Blood & Tissue Kit the lacrimal drainage system. In beats per minute and blood pressure (Qiagen, Hilden, Germany, catalog addition, the topically applied GC, of 104/60 mm Hg. Her body weight number 69504). These sequences which penetrates the eye via the and height were 49.6 kg (+1.7 SD) were validated via polymerase cornea, can also be absorbed into and 140.8 cm (–0.3 SD), respectively. chain reaction amplification by circulation. In this process, the lipid- Her physical signs included truncal using TaKaRa Ex Taq (TaKaRa rich corneal epithelium works as a obesity, buffalo hump, moon face, Bio, Inc, Otsu, Shiga, Japan, catalog barrier to intraocular penetration and femoral skin striae, which are number RR001A) according to the for hydrophilic derivatives, such as representative clinical findings of manufacturer’s protocol. Primers betamethasone sodium phosphate. CS ( Fig 1B). These findings were were designed to amplify each locus However, the presence of intraocular not observed the previous year ( Fig ( Table 1). The PCR products were inflammation is suggested to 7 1A). She was at a prepubertal stage, analyzed via Sanger sequencing by accelerate the penetration of GCs. defined to be grade 1 on the Tanner using the 3500 Dx Genetic Analyzer Therefore, there is a possibility scale. At this time, she was diagnosed (Applied Biosystems, Foster City, that the concentrations of GCs were with stunted growth ( Fig 1D). CA) according to the manufacturer’s relatively high in the blood in our patient. Laboratory findings revealed no protocol. abnormal data with the peripheral Although the potential systemic blood, biochemistry, or urinalysis. effects of topical GCs are less Her serum cortisol and plasma RESULTS clearly defined, a 50% decrease in adrenocorticotropic hormone (ACTH) We identified a single heterozygous endogenous GC production was levels at 8.00 AM were <1.0 μg/dL A to G nucleotide substitution at observed in male volunteers given and <2 pg/mL, respectively. Based position 3584 in exon 9 of the 0.1% dexamethasone
Recommended publications
  • Hypertensive Encephalopathy As the Initial Manifestation of Cushing's
    The Journal of Medical Research 2016; 2(6): 144-145 Case Report Hypertensive encephalopathy as the initial manifestation JMR 2016; 2(6): 144-145 November- December of Cushing’s syndrome ISSN: 2395-7565 © 2016, All rights reserved Alagoma Iyagba*1, Arthur Onwuchekwa1 www.medicinearticle.com 1 Department of Internal Medicine, University of Port Harcourt Teaching Hospital, Port Harcourt, Rivers State, Nigeria Abstract A 65-year old lady was rushed into the accident and emergency department with a two-day history sudden onset severe generalized throbbing headache associated with restlessness, irritability, irrational talk, projectile vomiting and loss of consciousness of three hours duration. On examination, she had moon face, buffalo hump, and truncal obesity with body mass index was 45.84kg/m2. Her blood pressure was 190/120 mmHg. Serum cortisol done at 0800 hrs the next day was elevated with a value of 511 ng/ml. 1 mg overnight dexamethasone was 148 ng/ml. The diagnosis of hypertension secondary to Cushing’s syndrome should be strongly considered in any hypertensive obese patients regardless of age with typical ‘cushingoid facies’. An assessment of serum cortisol in such patients would be beneficial in diagnosing this condition and optimizing treatment outcomes. Keywords: Cushing’s, Hypertension, Encephalopathy. INTRODUCTION Cushing’s syndrome is the constellation of a large group of signs and symptoms resulting from prolonged pathologic hypercortisolism caused by excessive adrenocorticotropic hormone (ACTH) secretion by tumors in the pituitary gland or elsewhere, or by ACTH-independent cortisol secretion from adrenal tumors[1]. It is one of the endocrine causes of hypertension with profound cardiovascular and neurological effects.
    [Show full text]
  • Chapter 13. Secondary Hypertension
    Hypertension Research (2014) 37, 349–361 & 2014 The Japanese Society of Hypertension All rights reserved 0916-9636/14 www.nature.com/hr GUIDELINES (JSH 2014) Chapter 13. Secondary hypertension Hypertension Research (2014) 37, 349–361; doi:10.1038/hr.2014.16 OVERVIEW AND SCREENING approximately 5–10% of hypertensive patients,984,985 and it is the most Hypertension related to a specific etiology is termed secondary frequent in endocrine hypertension. In addition, frequent etiological hypertension, markedly differing from essential hypertension, of factors for secondary hypertension include renal parenchymal hyper- which the etiology cannot be identified, in the condition and tension and renovascular hypertension. A study reported that sleep therapeutic strategies. Secondary hypertension is often resistant hyper- apnea syndrome was the most frequent factor for secondary hyper- tension, for which a target blood pressure is difficult to achieve by tension.517 The number of patients with secondary hypertension standard treatment. However, blood pressure can be effectively may further increase with the widespread diagnosis of sleep apnea reduced by identifying its etiology and treating the condition. There- syndrome. fore, it is important to suspect secondary hypertension and reach an Generally, the presence of severe or resistant hypertension, juvenile appropriate diagnosis. hypertension and the rapid onset of hypertension suggest the possi- Frequent etiological factors for secondary hypertension include bility of secondary hypertension. In such hypertensive patients, a close renal parenchymal hypertension, primary aldosteronism (PA), reno- inquiry on medical history, medical examination and adequate vascular hypertension and sleep apnea syndrome. Renal parenchymal examinations must be performed, considering the possibility of hypertension is caused by glomerular diseases, such as chronic secondary hypertension.
    [Show full text]
  • HEMADY (Dexamethasone Tablets), for Oral Use Chronic Use
    HIGHLIGHTS OF PRESCRIBING INFORMATION These highlights do not include all the information needed to use • Gastrointestinal Perforation: Avoid use in active or latent peptic ulcers, HEMADYTM safely and effectively. See full prescribing information for diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative HEMADY. colitis, since they may increase the risk of a perforation. (5.7) • Osteoporosis: Increased risk; monitor for changes in bone density with HEMADY (dexamethasone tablets), for oral use chronic use. (5.8) Initial U.S. Approval: 1958 • Behavioral and Mood Disturbances: May include euphoria, insomnia, mood swings, personality changes, severe depression, and psychosis. --------------------------- INDICATIONS AND USAGE -------------------------­ Monitor for signs and symptoms and manage promptly. (5.10) HEMADY is a corticosteroid indicated in combination with other anti­ • Kaposi’s Sarcoma: Kaposi’s sarcoma has been reported to occur in patients myeloma products for the treatment of adults with multiple myeloma. (1) receiving corticosteroid therapy, most often for chronic conditions. (5.11) • Embryo-Fetal Toxicity: Can cause fetal harm. Advise females of ----------------------- DOSAGE AND ADMINISTRATION ---------------------­ reproductive potential of the potential risk to a fetus. (5.13, 8.1) Recommended Dosage: 20 mg or 40 mg orally once daily, on specific days depending on the protocol regimen. (2) ------------------------------ ADVERSE REACTIONS ----------------------------­ The most common adverse reactions are
    [Show full text]
  • Cholesterol (Precursor of Steroid Hormones)
    Unit IV – Problem 5 – Biochemistry: Biosynthesis of Steroid Hormones & Steroid Hormone Receptor - Cholesterol (precursor of steroid hormones): It is composed of 27 carbons with four rings and a hydroxyl group (-OH) attached at carbon 3 and is found in cell membrane (why?) → to regulate membrane fluidity and permeability. Cholesterol from diet will be packaged in chylomicrons (in the gut) to be transported into lymph and then into plasma. Cholesterol is synthesized de novo (from scratch) in the cytosol of the liver. - Steroid Hormones: The rate-limiting irreversible step in steroid hormone synthesis is represented by the conversion of cholesterol into pregnenolone (which contains 21 carbons) via the enzyme desmolase. How to name steroids? 21 carbons: pregnanes (pregnenolone). 19 carbons: androstanes (testosterone). 18 carbons: estranges (estrogen). - Classes of steroid hormones: Mineralocorticoids: from zona glomerulosa of adrenal cortex. Glucocorticoids: from zona fasciculate of adrenal cortex. Androgens: from testes and zona reticularis of adrenal cortex. Estrogens and progestogens: from ovaries and placenta. - Synthesis of steroid hormones: Enzyme Sex Mineralocorticoids Cortisol Labs Presentation deficiency hormones XY: Hypertension, 17α- pseudohermaphroditism ↑ ↓ ↓ hypokalemia and hydroxylase XX: lack secondary ↓DHT sexual development Hypotension, Infancy: salt wasting; hyperkalemia, ↑ 21- childhood precocious ↓ ↓ ↑ renin activity and ↑ hydroxylase puberty; XX: 17- virilization hydroxyprogesterone ↓ aldosterone, ↑ 11- 11β- Hypertension (low deoxycorticosterone ↓ ↑ XX: virilization hydroxylase renin) (results in ↑ BP) - Glucocorticoids (natural): Synthesized in zona fasciculate of adrenal cortex. Regulated by: Corticotrophin-releasing hormone (CRH) which is secreted from the hypothalamus and then stimulating the anterior pituitary gland to produce adrenocorticotropic hormone (ACTH) which in turn will enhance the synthesis of cortisol from zona fasciculata. Functions of cortisol (BIG FIB): ↑ Blood pressure.
    [Show full text]
  • Cushings Disease
    put together by Alex Yartsev: Sorry if i used your images or data and forgot to reference you. Tell me who you are. [email protected] Cushings Disease History of Presenting Illness - weight gain, BUFFALO HUMP with supraclav fat pads, moon face, central obesity - purple stretch marks , HEADACHE, POLYURIA, NOCTURIA, GALACTORHHOEA? - easy bruising , Changes in pigmentation?? DARKER? Acanthisis Nigricans? - skin thinning . It can only be ACTH SECRETING ADENOMA!! - irregular menses hirsutism . - difficulty climbing stairs, getting out of a low chair, and raising their arms. - Depression CUSHINGOID FEATURES WITH HIRSUITISM AND - cognitive dysfunction VIRILISATION? BUT NO PIGMENT CHANGES?? - emotional lability Think about an ADRENAL CARCINOMA!! - bone disease (fractures) - STOMACH ULCERS from corticosteroid excess - Appetite Gain! ACUTELY cortisol excess causes EUPHORIA - Exacerbation of diabetes CHRONICALLY cortisol excess causes DEPRESSION - Hypokalemia (weakness ) - hypernatremia ELECTROLYTES ALL WRONG? MUCH ACNE, FLORID HYPERTENSION, OEDEMA, HIGH GLUCOSE, …BUT : NO FAT REDISTRIBUTION? ACUTE ONSET? Sounds like an ECTOPIC NEOPLASTIC SOURCE Differential Diagnoses - Hypothalamic disease (too much CRH) - Primary Cushing Disease (ACTH-secreting pituitary adenoma) - Adrenal cortisol-secreting adenoma - Ectopic Neoplastic Source of cortisol eg. lung cancer ( disease of decrepit old men) - Use + Abuse of corticosteroid medication - Hypercortisolism secondary to alcoholism - Depression - Hypothyroidism ~ADRENAL CRISIS~ - Hypoadrenalism
    [Show full text]
  • High Blood Pressure: Secondary Hypertension
    High Blood Pressure: Secondary Hypertension What is secondary hypertension? Blood pressure is the force of the blood on the artery walls as the heart pumps blood through the body. High blood pressure caused by a disease or another known medical problem is called secondary hypertension. Most cases of secondary hypertension are caused by kidney or hormonal problems. Normal blood pressure ranges up to 120/80 ("120 over 80") but blood pressure can rise and fall with exercise, rest, or emotions. The pressures are measured in millimeters of mercury. The upper number (120) is the pressure when the heart pushes blood out to the rest of the body (systolic pressure). The bottom number (80) is the pressure when the heart rests between beats (diastolic pressure). • Healthy blood pressure is less than 120/80. • Pre-high blood pressure (prehypertension) is from 120/80 to 139/89. • Stage I high blood pressure ranges from 140/90 to 159/99. • Stage II high blood pressure is over 160/100. If repeated checks of your blood pressure show that it is higher than 140/90, you have hypertension. If you have prehypertension and other health problems, such as diabetes, you need treatment. How does it occur? Many medical conditions, diseases, and medicines can cause secondary hypertension, including: • narrowing of the arteries in the kidneys • narrowing of the aorta, a large blood vessel that supplies blood to the lower body • several types of kidney disease • excess secretion of a hormone called aldosterone from the adrenal gland • tumor of the adrenal gland • Cushing's syndrome, a disorder in which there is too much corticosteroid hormone in the blood • medicines such as estrogen and oral contraceptives • abuse of drugs such as amphetamines, alcohol, or diet pills • pregnancy.
    [Show full text]
  • Budesonide Prolongs Time to Relapse in Ilealand
    82 Gut 1996; 39: 82-86 Budesonide prolongs time to relapse in ileal and ileocaecal Crohn's disease. A placebo controlled one year study Gut: first published as 10.1136/gut.39.1.82 on 1 July 1996. Downloaded from R L6fberg, P Rutgeerts, H Malchow, C Lamers, A Danielsson, G Olaison, D Jewell, 0 0stergaard Thomsen, H Lorenz-Meyer, H Goebell, H Hodgson, T Persson, C Seidegard Abstract Corticosteroids are the most efficacious Background and Ains-To evaluate the medical treatment for active Crohn's disease efficacy and safety of the topical cortico- (CD)' with remission rates of 50 to 80 per cent steroid budesonide, given in an oral con- reported after short or intermediate courses of trolled release formulation for treatment.2A Well known adverse effects (for maintenance ofremission in patients with example, acne, moon face, hirsutism, buffalo ileal and ileocaecal Crohn's disease (CD). hump) and systemic side effects (that is, impact Patients and Methods-Out of 176 patients on adrenal gland function, hypertension, with active CD who had achieved remis- impaired glucose tolerance) make continued sion (CD activity index score s,S0) after 10 conventional corticosteroid treatment with high weeks' treatment with either budesonide or doses inadvisable. Some patients achieving prednisolone, 90 were randomised to remission with the use of corticosteroids, how- continue with once daily treatment of6 mg ever, may benefit from longterm treatment with budesonide, or 3 mg budesonide or placebo low doses (<7.5 mg/day) of prednisolone or for up to 12 months in a double blind, similar. In the European Cooperative CD multicentre trial.
    [Show full text]
  • View a Copy of This Licence, Visit
    Fushimi et al. BMC Endocrine Disorders (2021) 21:163 https://doi.org/10.1186/s12902-021-00818-2 CASE REPORT Open Access Concurrence of overt Cushing’s syndrome and primary aldosteronism accompanied by aldosterone-producing cell cluster in adjacent adrenal cortex: case report Yoshiro Fushimi, Fuminori Tatsumi, Junpei Sanada, Masashi Shimoda, Shinji Kamei, Shuhei Nakanishi, Kohei Kaku, Tomoatsu Mune and Hideaki Kaneto* Abstract Background: Various adrenal disorders including primary aldosteronism and Cushing’s syndrome lead to the cause of hypertension. Although primary aldosteronism is sometimes complicated with preclinical Cushing’s syndrome, concurrence of overt Cushing’s syndrome and primary aldosteronism is very rare. In addition, it has been drawing attention recently that primary aldosteronism is brought about by the presence of aldosterone-producing cell cluster in adjacent adrenal cortex rather than the presence of aldosterone-producing adenoma. Case presentation: A 67-year-old Japanese female was referred to our institution due to moon face and central obesity. Based on various clinical findings and data, we diagnosed this subject as overt Cushing’s syndrome and primary aldosteronism. Furthermore, in immunostaining for cytochrome P450 (CYP) 11B1, a cortisol-producing enzyme, diffuse staining was observed in tumorous lesion. Also, in immunostaining for CYP11B2, an aldosterone- producing enzyme, CYP11B2 expression was not observed in tumorous lesion, but strong CYP11B2 expression was observed in adjacent adrenal cortex, indicating
    [Show full text]
  • Patient Perceptions of Glucocorticoid Side Effects: a Cross-Sectional Survey of Users in an Online Health Community
    PEER REVIEW HISTORY BMJ Open: first published as 10.1136/bmjopen-2016-014603 on 3 April 2017. Downloaded from BMJ Open publishes all reviews undertaken for accepted manuscripts. Reviewers are asked to complete a checklist review form (http://bmjopen.bmj.com/site/about/resources/checklist.pdf) and are provided with free text boxes to elaborate on their assessment. These free text comments are reproduced below. ARTICLE DETAILS TITLE (PROVISIONAL) Patient perceptions of glucocorticoid side effects: a cross-sectional survey of users in an online health community. AUTHORS Costello, Ruth; Patel, Rikesh; Humphreys, Jennifer; McBeth, John; Dixon, Will VERSION 1 - REVIEW REVIEWER Russell, Anthony Univ Alberta,Canada REVIEW RETURNED 14-Oct-2016 GENERAL COMMENTS An interesting approach with unexpected answers. REVIEWER Michele Iudici Past address: Rheumatology Unit Second University of Naples, Italy REVIEW RETURNED 15-Nov-2016 http://bmjopen.bmj.com/ GENERAL COMMENTS The authors report an online cross-sectional survey aiming to identify the GC-related adverse events most important to patients. They analyzed data from 604 patients and reported the ranks for each side effect, without providing any additional analysis that can make the paper more interesting and appealing for the readers. For example they do have data on the number and time of pills intake on October 1, 2021 by guest. Protected copyright. per day. It would be interesting to investigate if patient's perception of some AEs could be related to these parameters (evening intake and sleep disturbances...intake during meals and digestive symptoms...). Moreover, authors could also in deepen analyze how the experience of an AEs impacts on patient's perception.
    [Show full text]
  • What Is Secondary Hypertension?
    Secondary Hypertension The Primary Care Perspective Stephen Koesters, MD Assistant Professor of Clinical Medicine Department of Pediatrics Division of General Medicine The Ohio State University’s Wexner Medical Center What Is Hypertension (JNC 7) 1 What is Hypertension • For Children/Adolescents: – Average SBP/DBP >/= 95th percentile for age, gender, and height. – “Prehypertension” is >/= 90th percentile – 3 separate readings on 3 separate viitisits. – Incidence appears to be increasing over time. What is Essential/Primary Hypertension • HTN with no identifiable cause • Often develops gradually over years • Much of HTN still falls in this category - up to 85% in many reports. • Likely a complex interaction between multiple risk factors/causes in many cases. 2 What is Secondary Hypertension? • Meets Criteria for HTN • Results from an identifiable, potentially correctable cause • Accounts for significant number of Resistant HTN cases • Estimated to account for 5-15% of cases of HTN • Prevalence of hypertension in adults between 20-30% (50-70 million people). Conservatively, probably 3-5 million people in U.S. affected. Associations with Hypertension • Family History – first degree relatives • Race – more common in African Americans • Physical Inactivity • Dyslipidemia • Obesity • Vitamin D deficiency 3 Unclear Association with HTN • Caffeine – May cause short spike in BP – No sustained effect noted – May be more significant in older/overweight • Stress/Anxiety/Type A – Clearly causes short-term increases – Unclear if sustained stress can truly cause HTN When to Suspect Secondary HTN • Early age of onset – Young adult without family history or risk factors – Onset prior to puberty • Severe or resistant HTN – Remember – fewer than 50% of patients well controlled on a single medication • Acute onset or change in control when previously stable • Malignant/End-organ changes • Abnormal exam findings (e.g.
    [Show full text]
  • Corticosteroid Therapy in Inflammatory Bowel Diseases This Publication Is Sponsored by the Falk Foundation E.V
    The informed patient Corticosteroid therapy in inflammatory bowel diseases This publication is sponsored by the Falk Foundation e.V. The information herein represents the independent opinion of the author and does not necessarily reflect the opinion and recommendations of the Falk Foundation e.V. Not all products discussed may have a licence or indication in your country. Please consult your doctor regarding your country’s specific prescribing information. If you get any side effects, talk to your Doctor, pharmacist or nurse. This includes any possible side effects not listed in the package leaflet. You can also report side effects directly via the Yellow Card Scheme at www.mhra.gov.uk/yellowcard. By reporting side effects you can help provide more infor- mation on the safety of medicines. Publisher For further information please contact DR FALK PHARMA UK LTD Bourne End Business Park Cores End Road Bourne End Bucks SL8 5AS, UK © 2017 Falk Foundation e.V. 5th edition 2017 (UK) All rights reserved. (Bu80e 10-6/2010) U2 The informed patient Corticosteroid therapy in inflammatory bowel diseases Prof. Dr. Tilo Andus 1 Author: Prof. Dr. Tilo Andus Klinik für Allgemeine Innere Medizin, Gastroenterologie, Hepatologie und internistische Onkologie Krankenhaus Bad Cannstatt Klinikum Stuttgart Prießnitzweg 24 70374 Stuttgart Germany 2 The informed patient Contents Page Introduction 5 The natural role and regulation of corticosteroids in the body 7 • Anti-inflammatory properties of corticosteroids 12 • The effect of corticosteroids on metabolism 12
    [Show full text]
  • Secondary Causes of Obesity
    REVIEW Secondary causes of obesity Jocelyne G Karam & While the rising epidemic of obesity is primarily attributed to sedentary lifestyle, poor Samy I McFarlane† dietary habits and the aging of the population, secondary causes of obesity generally go †Author for correspondence undetected and untreated. These include endocrinological disorders, such as Cushing’s State University of New York, Division of Endocrinology, syndrome, polycystic ovary syndrome, hypogonadism and hypothyroidism, as well as Diabetes and Hypertension, genetic, syndromic and drug-related obesity. We present an overview of the major Department of Medicine, disorders associated with obesity, highlighting the pathophysiologic mechanisms and Box 50 Health Science Center at Brooklyn Kings County discussing diagnostic and treatment strategies that are most helpful to practicing Hospital Center, physicians in recognizing and treating these generally underdetected and 450 Clarkson Avenue, undertreated disorders. Brooklyn, NY 11203, USA Tel.: +1 718 270 3711; Fax: +1 718 270 6358; During the past few decades, prevalence of obes- recognized by physicians and specific therapeutic Email: smcfarlane@ downstate.edu ity has dramatically increased in the Western strategies should be planned in conjunction with world, including the USA where obesity has cur- diet and exercise. rently reached epidemic proportions. A compar- In this review, we provide the readers with a ison of data from two National Health and general overview of the secondary causes of obesity, Nutrition Examination Surveys (NHANES) has highlighting the pathophysiology, the clinical diag- shown that among US adults, the prevalence of nosis and the therapeutic options of each disorder. obesity increased from 15% (in the 1976–1980 Obesity is a state of excessive body weight asso- survey) to 32.9% (in the 2003–2004 survey) [1].
    [Show full text]