Mesothelioma Diagnosis
By KhmengWat.com
Diagnosing mesothelioma is often difficult, because the symptoms are similar to those of a number of other conditions. Diagnosis begins with a review of the patient's medical history, including any Read more...
|
|
Inhaled corticosteroids and adrenal insufficiency: prevalence and clinical presentation.
Page: 769Authors: Molimard, Mathieu 1 2 3; Girodet, Pierre-Olivier 1 3; Pollet, Clothilde 1; Fourrier-Reglat, Annie 1 2 3; Daveluy, Amelie 1 3; Haramburu, Francoise 2 3; Fayon, Michael 1 3 4; Tabarin, Antoine 1 3 (Source: Drug Safety) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Inhaled corticosteroids and adrenal insufficiency: prevalence and clinical presentation
(Source: Drug Safety)
Correspondence: lack of evidence for adrenal insufficiency after single-dose etomidate
(Source: Archives of Surgery)
Correspondence: lack of evidence for adrenal insufficiency after single-dose etomidate--reply
(Source: Archives of Surgery)
Generalized pigmentation due to addison disease.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18700116">Related Articles</a></td></tr></table>
<p><b>Generalized pigmentation due to Addison disease.</b></p>
<p>Dermatol Online J. 2008;14(2):13</p>
<p>Authors: Kumar R, Kumari S, Ranabijuli PK</p>
<p>A 10-year-old boy presented with generalized hyperpigmentation, abdominal pain, change in behavior and, no weight gain for 2 years. On examination, he had hypotension and generalized hyperpigmentation that was more marked on gingival mucosa and frictional sites. Serum cortisol was markedly decreased and his CT scan abdomen showed adrenal atrophy. On the basis of clinical and laboratory findings, a diagnosis of Addison disease was made.</p>
<p>PMID: 18700116 [PubMed - in process]</p> (Source: Dermatol Online J)
The tryptophan 620 allele of the lymphoid tyrosine phosphatase (ptpn22 gene) predisposes to autoimmune addison's disease.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18710467">Related Articles</a></td></tr></table>
<p><b>The tryptophan 620 allele of the lymphoid tyrosine phosphatase (PTPN22 gene) predisposes to autoimmune Addison's disease.</b></p>
<p>Clin Endocrinol (Oxf). 2008 Aug 15;</p>
<p>Authors: Roycroft M, Fichna M, McDonald D, Owen K, Zurawek M, Gryczyńska M, Januszkiewicz-Lewandowska D, Fichna P, Cordell H, Donaldson P, Nowak J, Pearce S</p>
<p>Objective: Previous studies of the association between autoimmune Addison's disease (AAD) and a non-synonymous single nucleotide polymorphism in the PTPN22 gene (C1858T, pR620W; SNP ID# rs2476601) have shown conflicting results. We aimed to examine this association using additional cohorts of AAD subjects from the UK and Poland. Design: DNA samples were obtained from UK and Polish AAD subjects (n=251 and 87, respectively) and ethnically matched healthy controls subjects (n=429 and 236, respectively). Genotyping for the C1858T PTPN22 marker was performed by PCR-RFLP assay. Meta-analysis of the results, together with those from 3 other populations was performed using RevMan v5.0 software. Results: In 251 UK AAD subjects the frequency of the PTPN22 1858T allele was 12.2% compared to 7.8% in healthy UK controls; p=0.008. Similarly, in 87 Polish AAD subjects the PTPN22 1858T allele was found in 19.5% of alleles compared to 11.7% in healthy Polish subjects; p=0.010. A meta-analysis, combining these result with published data for 3 other populations, involving 797 AAD subjects and 2032 controls in total, showed that the 1858T allele was associated with AAD susceptibility with a pooled odds ratio of 1.44 (95% CI: 1.21-1.72) (P=5.6x10(-5)), under a fixed effects model. Conclusion: This study confirms the association between the PTPN22 1858T-allele and AAD in an expanded UK cohort and in the previously unstudied Polish population. This meta-analysis allows for the first time a reliable estimate of the strength of effect of this autoimmune disease susceptibility allele across different European Caucasian populations.</p>
<p>PMID: 18710467 [PubMed - as supplied by publisher]</p> (Source: Clinical Endocrinology) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Adrenal insufficiency in sepsis.
<table border="0" width="100%"><tr><td align="left"/></tr></table>
<p><b>Adrenal insufficiency in sepsis.</b></p>
<p>Curr Pharm Des. 2008;14(19):1882-6</p>
<p>Authors: Annane D</p>
<p>The role of the hypothalamic-pituitary adrenal axis in the host response to infection is crucial. The initial inflammatory response to sepsis activates the endogenous release of cortisol, which in turn modulates the synthesis and release of both pro- and anti-inflammatory mediators to restrict inflammation in infected tissues. However, a number of factors, including vascular or ischemic damage, inflammation and apoptosis within the hypothalamic-pituitary adrenal axis, as well as use of drugs that alter cortisol metabolism, may cause adrenal insufficiency. One major problem ICU physicians are faced with is the diagnosis of sepsis-induced adrenal insufficiency at the bedside. A multidisciplinary international task force has recently recommended that sepsis induced adrenal insufficiency is best recognized by basal cortisol of less than 10 microg/dl or change in cortisol of less than 9 microg/dl after administration of corticotrophin. The diagnostic value of measuring salivary free cortisol in this setting remains to be investigated. While sepsis adrenal insufficiency is undoubtedly associated with a poor prognosis, the indication and practical modalities of corticosteroids therapy remained controversial. Based on the two largest randomised, placebo-controlled trials, many investigators, myself included, contend that septic shock patients with hypotension poorly responsive to fluid replacement and vasopressors should receive a seven day treatment with the combination of hydrocortisone at a dose of 200 mg per day and fludrocortisone at the dose of 50 microg per day.</p>
<p>PMID: 18691099 [PubMed - in process]</p> (Source: Current Pharmaceutical Design)
The altered adrenal axis and treatment with glucocorticoids during critical illness.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18695699">Related Articles</a></td></tr></table>
<p><b>The altered adrenal axis and treatment with glucocorticoids during critical illness.</b></p>
<p>Nat Clin Pract Endocrinol Metab. 2008 Aug 12;</p>
<p>Authors: Mesotten D, Vanhorebeek I, Van den Berghe G, </p>
<p>Critical illness is generally hallmarked by activation of the hypothalamic-pituitary-adrenal axis. The development of very high levels of cortisol has been associated with severe illness and a raised risk of death. Likewise, a response that is inadequate relative to the degree of stress, termed relative adrenal insufficiency (also known as critical-illness-related corticosteroid insufficiency) has been associated with increased mortality. Much controversy exists with regard to the definition and biochemical testing of an adequate adrenal response to critical illness, which hampers diagnosis. High doses of glucocorticoids have been shown to have no effect in this setting and might be harmful. Moderate doses have been advocated, however, for critically ill patients with inflammatory conditions, such as acute respiratory distress syndrome and septic shock syndrome. Initial results from proof-of-concept studies were promising but thus far have not been reproduced in large, multicenter trials, although the latter were underpowered to yield definite conclusions. The role of glucocorticoid therapy in intensive care, therefore, remains uncertain. Until the debate has been settled, we recommend that use of glucocorticoid therapy in critically ill patients should continue to be based on the clinician's judgment and that routine adjuvant use should be avoided.</p>
<p>PMID: 18695699 [PubMed - as supplied by publisher]</p> (Source: Nature Clinical Practice Endocrinology and Metabolism)
Corticotropin tests for hypothalamic-pituitary adrenal insufficiency: a meta-analysis.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18697868">Related Articles</a></td></tr></table>
<p><b>Corticotropin Tests for Hypothalamic-Pituitary Adrenal Insufficiency: A Meta-Analysis.</b></p>
<p>J Clin Endocrinol Metab. 2008 Aug 12;</p>
<p>Authors: Kazlauskaite R, Evans AT, Villabona CV, Abdu TA, Ambrosi B, Atkinson AB, Choi CH, Clayton RN, Courtney CH, Gonc EN, Maghnie M, Rose SR, Soule SG, Tordjman K, </p>
<p>Context: Diagnostic value of tests for detecting hypothalamic-pituitary adrenal insufficiency (HPAI) is controversial. Objective: To compare standard-dose and low-dose corticotropin tests for diagnosing HPAI. Data Sources: PubMed database from 1966 to 2006 for studies reporting diagnostic value of standard-dose or low-dose corticotropin tests, with patient-level data obtained from original investigators. Study Selection: Eligible studies had more than 10 patients; all subjects were evaluated because of suspicion for chronic HPAI; and patient-level data was available. We excluded studies with no accepted reference standard for HPAI (insulin hypoglycemia or metyrapone test), if test subjects were in the intensive care unit, or if only normal healthy subjects were used as controls. Data Extraction: We constructed receiver operator characteristic (ROC) curves using patient-level data from each study, and then merged results to create summary ROC curves, adjusting for study size and cortisol assay method. Diagnostic value of tests was measured by calculating area under the ROC curve (AUC) and likelihood ratios. Data Synthesis: Patient-level data from 13 of 23 (57%) studies (679 subjects) were included in the meta-analysis. The areas under the ROC curves were: low-dose corticotropin test 0.92 (95% CI: 0.89-0.94), and standard-dose corticotropin test 0.79 (95% CI: 0.74-0.84). Among patients with paired data (7 studies, 254 subjects), diagnostic value of low-dose corticotropin test was superior to standard-dose test, AUC 0.94 and 0.85, respectively (P<0.001). Conclusions: Low-dose corticotropin test was superior to standard-dose test for diagnosing chronic HPAI, however it has technical limitations.</p>
<p>PMID: 18697868 [PubMed - as supplied by publisher]</p> (Source: The Journal of Clinical Endocrinology and Metabolism)
Myosin-vb functions as a dynamic tether for peripheral endocytic compartments during transferrin trafficking
Background:
Myosin-Vb has been shown to be involved in the recycling of diverse proteins in multiple cell types. Studies on transferrin trafficking in HeLa cells using a dominant-negative myosin-Vb tail fragment suggested that myosin-Vb was required for recycling from perinuclear compartments to the plasma membrane. However, chemical-genetic, dominant-negative experiments, in which myosin-Vb was specifically induced to bind to actin, suggested that the initial hypothesis was incorrect both in its site and mode of myosin-Vb action. Instead, the chemical-genetic data suggested that myosin-Vb functions in the actin-rich periphery as a dynamic tether on peripheral endosomes, retarding transferrin transport to perinuclear compartments.
Results:
In this study, we employed both approaches, with the addition of overexpression of full-length wild-type myosin-Vb and switching the order of myosin-Vb inhibition and transferrin loading, to distinguish between these hypotheses. Overexpression of full-length myosin-Vb produced large peripheral endosomes. Chemical-genetic inhibition of myosin-Vb after loading with transferrin did not prevent movement of transferrin from perinuclear compartments; however, virtually all myosin-Vb-decorated particles, including those moving on microtubules, were halted by the inhibition. Overexpression of the myosin-Vb tail caused a less-peripheral distribution of early endosome antigen-1 (EEA1).
Conclusions:
All results favored the peripheral dynamic tethering hypothesis. (Source: BioMed Central)
Despite additive ban, some parents voice worry
Samantha Rosenberg eyed the toy plastic cellphone that her 9-month-old daughter has chewed so much, the color is fading. She wondered if the shiny plaything, and others that fill her home, are endangering Addison's health. (Source: washingtonpost.com - Health) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Despite additive ban, some parents voice worry
Samantha Rosenberg eyed the toy plastic cellphone that her 9-month-old daughter has chewed so much, the color is fading. She wondered if the shiny plaything, and others that fill her home, are endangering Addison's health. (Source: washingtonpost.com - Health)
Underlying medical conditions.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18675594">Related Articles</a></td></tr></table>
<p><b>Underlying medical conditions.</b></p>
<p>Best Pract Res Clin Obstet Gynaecol. 2008 Jul 31;</p>
<p>Authors: Lombaard H, Pattinson RC</p>
<p>More than half of maternal deaths in the UK are due to pre-existing medical conditions, and medical emergencies often mimic acute obstetric conditions. An acute flare of systemic lupus erythaematosus, a thyroid storm or a phaeochromocytoma have many of the signs and symptoms of imminent eclampsia. Similarly, severe postpartum haemorrhage can result in diagnostic difficulties of medical conditions such as Addison's syndrome or acute renal failure. An acute collapse can be due to a pulmonary embolus, myocardial infarction, tachyarrhythmia or myasthenia gravis. These conditions are rare; however, unless they are considered in a differential diagnosis, they will not be diagnosed, to the detriment of the woman and her infant. This chapter deals with acute medical conditions occurring uncommonly in pregnant women. An obstetrician should know the initial steps to take in the emergency management of these cases.</p>
<p>PMID: 18675594 [PubMed - as supplied by publisher]</p> (Source: Best Practice & Research. Clinical Obstetrics & Gynaecology)
The tumour suppressor cyld is a negative regulator of rig-i-mediated antiviral response
Constantin S Friedman, Marie Anne O'Donnell, Diana Legarda-Addison, Aylwin Ng, Washington B Cardenas, Jacob S Yount, Thomas M Moran, Christopher F Basler, Akihiko Komuro, Curt M Horvath, Ramnik Xavier & Adrian T Ting (Source: EMBO Reports AOP)
A single-tube screen for salmonella and shigella.
<table border="0" width="100%"><tr><td align="left"/></tr></table>
<p><b>A single-tube screen for salmonella and Shigella.</b></p>
<p>Am J Clin Pathol. 2008 Aug;130(2):284-9</p>
<p>Authors: Procop GW, Wallace JD, Tuohy MJ, Lasalvia MM, Addison RM, Reller LB</p>
<p>Salmonella and Shigella species are routinely sought in stool specimens submitted for culture. It is a common practice to screen lactose-negative colonies by using triple sugar iron agar, lysine iron agar, and Christensen urea agar to determine if further identification is necessary. We designed and evaluated a novel combination of media, which are layered in a single tube, for screening isolates suspected to possibly represent Salmonella or Shigella. We tested this media combination with 106 Salmonella, 56 Shigella, and 56 other gram-negative bacilli.All Salmonella and Shigella isolates tested were appropriately characterized as possible Salmonella or Shigella by using an algorithm developed for use with this media combination. Similarly, 53 (95%) of 56 other gram-negative bacilli were appropriately screened as non -Salmonella and non -Shigella isolates. This unique media combination provides the most important biochemical reactions needed to screen for Salmonella and Shigella in a single-tube format, which decreases labor by two thirds (ie, 1 tube is inoculated vs 3).</p>
<p>PMID: 18628099 [PubMed - in process]</p> (Source: American Journal of Clinical Pathology)
You can be a country doctor
Are you looking for a practice opportunity in rural Texas? The Texas Organization of Rural and Community Hospitals and the Office of Rural and Community Affairs will conduct HealthFind on Aug. 23 at the Hotel-Intercontinental in Addison. (Source: Blogged_Arteries) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Enoxaparin sodium/nadroparin calcium: adrenal haematoma leading to adrenal insufficiency, and thrombocytopenia in an elderly patient: case report
(Source: Reactions)
Fluticasone propionate overdose: hypercorticism and adrenal insufficiency in a child following inhalation: case report
(Source: Reactions)
Enoxaparin sodium/nadroparin calcium: adrenal haematoma leading to adrenal insufficiency, and thrombocytopenia in an elderly patient: case report.
Page: 14 (Source: Reactions Weekly)
Fluticasone propionate overdose: hypercorticism and adrenal insufficiency in a child following inhalation: case report.
Page: 17 (Source: Reactions Weekly)
Insulin gene polymorphisms in type 1 diabetes, addison's
disease and the polyglandular autoimmune syndrome type ii
Background:
Polymorphisms within the insulin gene can influence insulin expression in the pancreas and especially in the thymus, where self-antigens are processed, shaping the T cell repertoire into selftolerance, a process that protects from beta-cell autoimmunity.
Methods:
We investigated the role of the -2221Msp(C/T) and -23HphI(A/T) polymorphisms within the insulin gene in patients with a monoglandular autoimmune endocrine disease [patients with isolated type 1 diabetes (T1D, n= 317), Addison's disease (AD, n=107) or Hashimoto's thyroiditis (HT, n=61)], those with a polyglandular autoimmune syndrome type II (combination of T1D and/or AD with HT or GD, n=62) as well as in healthy controls (HC, n=275).
Results:
T1D patients carried significantly more often the homozygous genotype "CC" -2221Msp(C/T) and "AA" -23HphI(A/T) polymorphisms than the HC (78.5% vs. 66.2%, p=0.0027 and 75.4% vs. 52.4%, p=3.7X10-8, respectively).
The distribution of insulin gene polymorphisms did not show significant differences between patients with AD, HT, or APS-II and HC.
Conclusions:
We demonstrate that the allele "C" of the -2221Msp(C/T) and "A" -23HphI(A/T) insulin gene polymorphisms confer susceptibility to T1D but not to isolated AD, HT or as a part of the APS-II. (Source: BioMed Central) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Insulin gene polymorphisms in type 1 diabetes, addison's disease and the polyglandular autoimmune syndrome type ii
Background:
Polymorphisms within the insulin gene can influence insulin expression in the pancreas and especially in the thymus, where self-antigens are processed, shaping the T cell repertoire into selftolerance, a process that protects from ?-cell autoimmunity.
Methods:
We investigated the role of the -2221Msp(C/T) and -23HphI(A/T) polymorphisms within the insulin gene in patients with a monoglandular autoimmune endocrine disease [patients with isolated type 1 diabetes (T1D, n = 317), Addison's disease (AD, n = 107) or Hashimoto's thyroiditis (HT, n = 61)], those with a polyglandular autoimmune syndrome type II (combination of T1D and/or AD with HT or GD, n = 62) as well as in healthy controls (HC, n = 275).
Results:
T1D patients carried significantly more often the homozygous genotype "CC" -2221Msp(C/T) and "AA" -23HphI(A/T) polymorphisms than the HC (78.5% vs. 66.2%, p = 0.0027 and 75.4% vs. 52.4%, p = 3.7 × 10-8, respectively).The distribution of insulin gene polymorphisms did not show significant differences between patients with AD, HT, or APS-II and HC.
Conclusion:
We demonstrate that the allele "C" of the -2221Msp(C/T) and "A" -23HphI(A/T) insulin gene polymorphisms confer susceptibility to T1D but not to isolated AD, HT or as a part of the APS-II. (Source: BMC Medical Genetics - Latest articles)
Replacement therapy of oral hydrocortisone in adrenal insufficiency: the influence of gastrointestinal factors
Expert Opinion on Drug Metabolism & Toxicology , June 2008, Vol. 4, No. 6, Pages 749-758.
Background: Replacing glucocorticoids in primary adrenal insufficiency (AI) or Addison's disease (AD) is today based on oral replacement therapy with hydrocortisone in a conventional immediate-release tablet. It is recognised that physiological ... (Source: Expert Opinion: Expert Opinion on Drug Metabolism & Toxicology: Table of Contents)
Late-onset adrenal hypoplasia congenita caused by a novel mutation of the
dax-1
gene
Abstract Mutation in the orphan nuclear receptor DAX-1 gene causes X-linked adrenal hypoplasia congenita (AHC). Affected male children
classically suffer a salt-losing crisis and adrenal insufficiency in their early infancy or, in some rare exceptions, with
late-onset subtype. We report here a patient manifesting late-onset adrenal hypoplasia congenita caused by the premature truncation
of the C-terminus of the DAX-1 molecule, which is essential for its function as a transcriptional repressor. A 12-year-old
boy was referred to us after being afflicted with generalized skin pigmentation for about 3 years, fatigue and headache. Primary
adrenal insufficiency was determined on the basis of a low plasma cortisol level (3.9 ?g/dl) despite an extremely high ACTH
level (1200 pg/ml). Replacement therapy with hydrocortisone and fludorocortisone acetate was initiated soon thereafter. Hypogonadotropic
hypogonadism was confirmed at the age of 18 years, at which time sexual infantilism had become apparent. Direct sequencing
of the peripheral lymphocyte-derived DNA revealed a novel 1033del13 mutation on the ligand-binding domain of the NR0B1 (DAX-1) gene, which generated a premature stop codon truncating the C-terminus. This mutation was considered de novo since
we could not find it in his mother. This case demonstrates that even a truncated protein lacking the major functional domain
of DAX-1 can present late-onset and latent adrenal failure.
Content Type Journal ArticleCategory Original PeperDOI 10.1007/s00431-008-0779-xAuthors
Fan Yang, Tottori University Division of Pediatrics and Perinatology, Faculty of Medicine Yonago 683?8504 JapanKeiichi Hanaki, Tottori University School of Health Sciences, Faculty of Medicine Nishi-cho 86 Yonago 683?8503 JapanTomoe Kinoshita, Tottori University Division of Pediatrics and Perinatology, Faculty of Medicine Yonago 683?8504 JapanYuki Kawashima, Tottori University Division of Pediatrics and Perinatology, Faculty of Medicine Yonago 683?8504 JapanJun-ichi Nagaishi, Tottori University Division of Pediatrics and Perinatology, Faculty of Medicine Yonago 683?8504 JapanSusumu Kanzaki, Tottori University Division of Pediatrics and Perinatology, Faculty of Medicine Yonago 683?8504 Japan
Journal European Journal of PediatricsOnline ISSN 1432-1076Print ISSN 0340-6199 (Source: European Journal of Pediatrics)
Electric pool bikes
I am investigating the possibility of providing electric pool bikes for use by community staff for short journeys.
1) I wondered whether anyone had any information on such vehicles which they would be able to let me have or could suggest alternative sources of such information.
2) I also needs to... (Source: Networks Talk)
A novel dax1 gene mutation in a turkish infant with x-linked adrenal hypoplasia congenita
Abstract Adrenal hypoplasia congenita (AHC) is a rare inherited disorder of the adrenal cortex commonly manifested as an early onset
adrenal insufficiency syndrome. A novel DAX1 (NR0B1) gene mutation was detected in a Turkish newborn boy presenting with primary adrenal insufficiency. He was from a family
with a history of unexplained death of three male siblings in the neonatal period. This report highlights the value of mutational
analysis of the DAX1 gene for definitive diagnosis of AHC as well as for genetic counselling because this disorder shows an
X-linked genetic pattern of transmission, providing the possibility of finding new cases even in presymptomatic individuals.
Content Type Journal ArticleCategory Short ReportDOI 10.1007/s00431-008-0778-yAuthors
Esra Arun Ozer, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir TurkeyAysun Kaya, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir TurkeyMunevver Yildirimer, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir TurkeyOzlem Guler, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir TurkeySule Can, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir TurkeyHalil Aydinlioglu, Izmir Tepecik Training and Research Hospital Department of Neonatology Izmir Turkey
Journal European Journal of PediatricsOnline ISSN 1432-1076Print ISSN 0340-6199 (Source: European Journal of Pediatrics) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
New therapies for sepsis.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18473886">Related Articles</a></td></tr></table>
<p><b>New therapies for sepsis.</b></p>
<p>Curr Top Med Chem. 2008;8(7):603-14</p>
<p>Authors: Cunnington A, Nadel S</p>
<p>Sepsis is a common clinical problem that is responsible for an increasing number of deaths. Many new therapies for severe sepsis have been developed but few have shown benefit in rigorous clinical trials. To date the most successful therapies are relatively simple clinical interventions: appropriate broad spectrum antibiotics; early goal directed therapies to restore tissue oxygen delivery; physiological dose hydrocortisone in patients with relative adrenal insufficiency; intensive insulin therapy to maintain normoglycemia; and lung-protective ventilation strategies. The only adjunctive therapy supported by strong evidence of benefit is Activated Protein C. Experimental therapies are being developed with improved in vitro and animal models and better understanding of the pathophysiology of sepsis in humans. Neutralization of the triggers of inflammation, such as endotoxin, and inhibition of the signal transduction mechanisms are promising new strategies. Statins may be beneficial in prevention of sepsis and as adjunctive treatments. Reconstitution of the immune response with interferon-gamma or granulocyte-macrophage colony stimulating factor may reverse immunoparesis in severe sepsis. Many other molecular targets have been identified for possible therapeutic intervention, but there are still fundamental difficulties to be overcome in demonstrating efficacy in clinical trials.</p>
<p>PMID: 18473886 [PubMed - indexed for MEDLINE]</p> (Source: Current Topics in Medicinal Chemistry)
Triamcinolone: adrenal insufficiency presenting as hypoglycaemia following epidural administration: case report.
Page: 29 (Source: Reactions Weekly)
Warfarin: adrenal haemorrhage leading to adrenal insufficiency in an elderly patient: case report.
Page: 30 (Source: Reactions Weekly)
The mary kay ash charitable foundation awards grant to fund innovative breast surgery training program
The American Society of Breast Disease announces the creation of the Mary Kay Ash Advanced Training Program in Oncoplastic Breast Surgery. The Addison-based Mary Kay Ash Charitable Foundation - a leading philanthropy in the field of cancers affecting women - has approved a two-year $225,000 grant to support this innovative program to train breast surgeons in the emerging field of oncoplastic surgery. (Source: Cancer / Oncology News From Medical News Today)
Polymorphisms in clec16a and ciita at 16p13 are associated with primary adrenal insufficiency.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18593762">Related Articles</a></td></tr></table>
<p><b>Polymorphisms in CLEC16A and CIITA at 16p13 are associated with primary adrenal insufficiency.</b></p>
<p>J Clin Endocrinol Metab. 2008 Jul 1;</p>
<p>Authors: Skinningsrud B, Husebye ES, Pearce SH, McDonald DO, Brandal K, Bøe Wolff A, Løvås K, Egeland T, Undlien DE</p>
<p>Context/objectives: It is known that different autoimmune diseases often share the same susceptibility genes. In this study we aimed to investigate if loci found associated with common autoimmune diseases in recent genome wide association studies, also could be susceptibility loci for autoimmune Addison's disease (primary adrenal insufficiency). Design/patients: A total of 139 tagging SNPs in eleven candidate genes (IL2, IL21, IL2RA, CLEC2D, CD69, ERBB3, PTPN11, SH2B3, CLEC16A, CIITA and PTPN2) were genotyped in a case/control study design consisting of Norwegian Addison's disease patients (n = 332) and Norwegian healthy control individuals (n = 1029). Five SNPs were subsequently selected for analysis in a United Kingdom sample set consisting of Addison's disease patients (n =210) and controls (n = 191). Results: Polymorphisms in CLEC16A and CIITA remained significantly associated with Addison's disease in the Norwegian sample set at the 0.05 level, even after correction for multiple testing. CLEC16A and CIITA are both located at 16p13, but linkage disequilibrium patterns and logistic regression analyses suggest that SNPs in these two genes are independently associated with Addison's disease. We were not able to confirm these associations in the UK material, however, this may well be due to limited sample size and lack of statistical power. Conclusion: Two alleles at 16p13 are independently associated with risk of Addison's disease in the Norwegian population, suggesting this chromosomal region to harbour common autoimmunity gene(s), CLEC16A and CIITA being possible independent candidates.</p>
<p>PMID: 18593762 [PubMed - as supplied by publisher]</p> (Source: The Journal of Clinical Endocrinology and Metabolism) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Triamcinolone: adrenal insufficiency presenting as hypoglycaemia following epidural administration: case report
(Source: Reactions)
Warfarin: adrenal haemorrhage leading to adrenal insufficiency in an elderly patient: case report
(Source: Reactions)
What causes idiopathic intracranial hypertension?
Patient Presentation
A 14-year-old female came to the emergency room with a 3 week history of tinnitus that resolved 3 days prior to admission.
She had persistent blurred vision in her left eye and 2 days ago developed it in her right eye. She also complains of some neck pain and a headache that she was taking ibuprofen for. She denied any trauma.
The past medical history showed attention deficit disorder on methylphenidate and mild acne that was controlled with benzoyl peroxide.
The family history was negative for any hematological, neurological or ophthalmological disorders.
The review of systems showed no fever, nausea, vomiting, cough, diarrhea, difficulties walking, writing or speaking.
The pertinent physical exam showed vital signs of blood pressure = 145/105, pulse = 98, respiratory rate = 20, was afebrile, with a mini-mental status evaluation showing her to be alert and oriented x 3.
Her weight was > 95% for age with a body mass index of 35 kg/m2. Eye examination showed decreased light perception bilaterally, with papilledema and her venous pulsations could not be determined. Extraocular muscles were intact.
Neurologically cranial nerves III-XII were intact, deep tendon reflexes were normal, strength and tone were normal. She had normal sensation and was able to walk but had problems because of her vision.
She had no obvious ataxia.
The work-up included an emergency consultation with ophthalmology and neurology that confirmed decreased vision, papilledema and no venous pulsations.
She was taken to the pediatric intensive care unit, given intravenous Diamox®, Lasix® and Solumedrol®.
Magnetic resonance imaging revealed the diagnosis of a non-occulsive venous sinus thrombosis in the right transverse sinus, but it was questioned whether or it this alone could be the cause of her idiopathic intracranial hypertension.
A lumbar puncture was normal.
The patient's clinical course showed her to have a continued decrease in her vision over the next day and therefore a lumboperitoneal shunt was placed to decrease the intracranial pressure.
This stopped the visual decline but at discharge she had not regained her prior vision and had a discharge acuity of 20/150 in her right eye and 20/180 in her left eye.
The diuretics were stopped and she was to continue prednisone, tapering it over 1 month.
During her admission she was evaluated for her hypertension and her idiopathic hypertension was being controlled on propranolol at discharge.
She had a hematological evaluation for a hypercoagulable state that was negative, but would have repeated Protein C and Protein S levels drawn later as acute levels may not be accurate. She was placed on aspirin prophylaxis.
She was discharged to home with daily occupational therapy and physical therapy. She was to follow up with a local nutritionist for her obesity, with her local physician within the week and other specialists within the month.
http://www.pediatriceducation.org/pictures/viewer$282
Figure 63 - Axial (left) and sagittal (right) T1-weighted
magnetic resonance images of the brain demostrate a relatively small
bright (seen here as white) signal abnormality in the right
transverse sinus, concerning for venous sinus thrombosis.
Figure 64 - 06-30-08 - Magnetic resonance venogram obtained with
contrast demonstrates some irregularity in the contour of the right
transverse sinus, but it is still patent and there is flow within it,
demonstrating the thrombus is non-occlusive.
Discussion
Papilledema is described as congestion and elevation of the optic nerve head, blurring of the optic nerve disc margin, obliteration of the physiological optic cup, venous congestion with loss of spontaneous venous pulses, peripapillary splinter hemorrhages and edema of the peripapillary retina.
An image of papilledema from EyeRounds.org can be seen by clicking here.
Papilledema is a neurological emergency and needs prompt evaluation by specialists.
The causes of papilledema include:
Cataracts
Demyelinating diseases
Drugs
Glaucoma
Hypertension
Iridocyclitis
Meningo-encelphalitis
Optic atrophy
Tumor
Retinitis pigmenotosa
Idiopathic intracranial hypertension (IIH) is the proper term but many other terms are used such as benign intracranial hypertension or pseudotumor cerebri which is the term used by the National Library of Medicine.
IIH is defined as elevated intracranial pressure but no clinical laboratory or radiographic evidence of hydrocephalus, infection, tumor or vascular abnormality.
IIH has papilledema, normal or small cerebral ventricular system on radiographic imaging, no intracranial mass and normal cerebrospinal fluid.
The pathogenesis of IIH is not complete understood. Proposed mechanisms include increased cerebral blood volume, increased cerebrospinal fluid secretion, increased venous sinus pressure and decreased cerebrospinal fluid absorption. All or combinations of these problems can lead to intracranial hypertension.
IIH occurs from childhood (with an increasing incidence in adolescence) to adulthood. Infants and neonates usually do not have it.
In younger children there is an equal gender distribution of patients, but as age increases female predominate.
Patients often come to attention because of headache, nausea and/or vomiting, blurred vision or diplopia, dizziness, tinnitus and stiff neck.
Other presentations include anorexia, increasing head size, pain behind the orbit, photophobia, head tilt and preference for knee-chest position.
Patients can also be asymptomatic with papilledema noticed incidentally on physical examination.
The papilledema in IIH is usually bilateral but may be unilateral or asymmetric.
Treatment to decrease the intracranial pressure and to maintain vision include stopping possible causative drugs, diuretics (i.e. acetazolamide, furosemide), serial lumbar punctures, and operative procedures such as optic nerve sheath fenestration or placement of a lumboperitoneal shunt.
With prompt treatment, visual loss can be completely reversible, but some visual loss is reported in up to 17% of patients. Recurrence rate is between 6-12%
Learning Point
Causes and possible associations with IIH include:
Cardiovascular
Heart murmur
Mitral valve prolapse
Heart transplant*
Collagen Vascular
Behçet disease
Panuveitis
Polyangiitis overlap syndrome
Systemic lupus erythematosus
Drugs
Amiodarone
Antibiotics - minocycline and tetracycline
Chemotherapy - cytarabine
Contraceptives, oral and implantable
Danazol
Desmopressin
Human growth hormone
Steroids or steroid withdrawal
Lithium
Mesalamine
Nalidixic acid
Nitrofurantoin
Vitamin A, retinoic acid and similar drugs
Endocrine
Addison disease
Cushing disease
Hypocalcemia
Hypo or hyperthyroidism
Ovarian dysfunction
Vitamin D-dependent rickets
Vitamin A excess or deficiency
Gastrointestinal
Crohn's disease
Genetic
Guillain-Barré
Galactosemia
Miller-Fisher variant
Hematologic
Severe anemia
Hypercoagulable states*
Polycythemia vera
Wiskott-Aldrich syndrome
Infectious Disease
Illness with fever
Lyme disease*
Measles
Otitis media
Roseola
Sinusitis
Streptococcal B pharyngitis
Tonsillitis
Upper respiratory tract infection
Viral disease
Varicella
Pulmonary
Asthma
Chronic lung disease
Cystic fibrosis*
Renal
Renal failure*
Renal transplant*
Surgical/Trauma
Appendectomy
Head trauma*
Tonsillectomy and adenoidectomy
Miscellaneous
Malnutrition
Obesity
Postvaccination
Refeeding
Note: one paper (Rangwala and Liu, see To Learn More below) reviewed other reports which may not meet the standard criteria for IIH. This paper cites the following as possibly not meeting criteria for IIH: cystic fibrosis, head trauma, heart transplantation, hypercoagulable states, Lyme disease, renal failure and renal transplantation.
Questions for Further Discussion
1. What radiographic imaging tests should be performed to evaluate papilledema?
2. What disease processes are considered neurological emergencies?
3What disease processes are considered opthalmological emergencies?
Related Cases
Disease
Idiopathic Intracranial Hypertension
Pseudotumor cerebri
Benign Tumors
Blood and Blood Disorders
Eye Diseases
High Blood Pressure
Venous Sinus Thrombosis
Symptom/Presentation
Bleeding and Bruising
Blurred Vision
Hypertension
Neck Stiffness
Tinnitus
Visual Field Defects
Specialty
Ophthalmology
Neurology / Neurosurgery
Radiology / Nuclear Medicine / Radiation Oncology
Pharmacology / Toxicology
Age
Teenager
To Learn More
To view pediatric review articles on this topic from the past year check PubMed.
Information prescriptions for patients can be found at MedlinePlus for this topic: (Source: PediatricEducation.org)
The adrenal gland in aids
Abstract The adrenal gland has been known to be a common site of opportunistic infections and tumors that define the acquired immunodeficiency
syndrome (AIDS) ever since the first autopsy data were published. We have examined the adrenal glands of 66 AIDS patients
autopsied in New York City and tabulated and graded the findings in an attempt to estimate the likelihood of adrenal insufficiency
developing on the basis of these lesions. AIDSdefining conditions were found in the adrenal glands of 56% of patients, primarily
opportunistic infections (53%) and much less frequently neoplasms (3%). Cytomegaloviral (CMV) infection was by far the most
common type (42%), followed by mycobacterial (8%) and fungal infections (3%). There was one case eachof Kaposi?s sarcoma and lymphoma. Total necrosis of adrenal cortex was restricted to 2 cases of tuberculosis. CMV adrenalitis,
although the most common infection and often associated with necrosis, never resulted in more than 30% destruction of the
cortex. We conclude that although histopathological evidence of adrenal disease is common in AIDS, most such lesions are not
sufficiently extensive to result in adrenal insufficiency. In contrast to previous reports stressing the importance of CMV
adrenalitis as a possible cause of adrenocortical insufficiency, we now find tuberculosis the more likely cause of total cortical
destruction.
Content Type Journal ArticleCategory Special ArticleDOI 10.1007/BF02914483Authors
Heidrun Rotterdam, College of Physicians and Surgeons of Columbia University Department of Pathology New York New YorkFrancine Dembitzer, College of Physicians and Surgeons of Columbia University Department of Pathology New York New York
Journal Endocrine PathologyOnline ISSN 1559-0097Print ISSN 1046-3976
Journal Volume Volume 4
Journal Issue Volume 4, Number 1 / March, 1993 (Source: Endocrine Pathology)
Fluticasone propionate: adrenal insufficiency in a child followed by corticosteroid withdrawal symptoms: case report
(Source: Reactions) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Fluticasone propionate: adrenal insufficiency in a child followed by corticosteroid withdrawal symptoms: case report.
Page: 20 (Source: Reactions Weekly)
Addison's disease
Addison's disease ? Comprehensive overview covers symptoms, treatment of this disorder of the adrenal glands.Sponsored by:Chemotherapy.com - http://www.chemotherapy.com (Source: MayoClinic.com Full Feed)
P450 oxidoreductase deficiency - a new form of congenital adrenal hyperplasia.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18493134">Related Articles</a></td></tr></table>
<p><b>P450 oxidoreductase deficiency - a new form of congenital adrenal hyperplasia.</b></p>
<p>Endocr Dev. 2008;13:67-81</p>
<p>Authors: Flück CE, Pandey AV, Huang N, Agrawal V, Miller WL</p>
<p>Patients with adrenal insufficiency, genital anomalies and bony malformations resembling the Antley- Bixler syndrome (a craniosynostosis syndrome), are likely to have P450 oxidoreductase (POR) deficiency. Since our first report in 2004, about 26 recessive POR mutations have been identified in 50 patients. POR is the obligate electron donor to all microsomal (type II) P450 enzymes, including the steroidogenic enzymes CYP17A1, CYP21A2 and CYP19A1. POR deficiency may cause disordered sexual development manifested as genital undervirilization in 46,XY newborns as well as overvirilization in those who are 46,XX. This may be explained by impaired aromatization of fetal androgens which may also lead to maternal virilization and low urinary estriol levels during pregnancy. A role for the alternate 'backdoor' pathway of androgen biosynthesis, leading to dihydrotestosterone production bypassing androstenedione and testosterone, has been suggested in POR deficiency but remains unclear. POR variants may play an important role in drug metabolism, as most drugs are metabolized by hepatic microsomal P450 enzymes. However, functional assays studying the effects of specific POR mutations on steroidogenesis showed that several POR variants impaired CYP17A1, CYP21A2 and CYP19A1 activities to different degrees, indicating that each POR variant must be studied separately for each potential target P450 enzyme. Thus, the impact of POR mutations on drug metabolism by hepatic P450s requires further investigation.</p>
<p>PMID: 18493134 [PubMed - in process]</p> (Source: Endocrine Development)
Disorders of adrenal development.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18493131">Related Articles</a></td></tr></table>
<p><b>Disorders of adrenal development.</b></p>
<p>Endocr Dev. 2008;13:19-32</p>
<p>Authors: Ferraz-de-Souza B, Achermann JC</p>
<p>Human adrenal development is a complex and relatively poorly understood process. However, significant insight into some of the mechanisms regulating adrenal development and function is being obtained through the analysis of individuals and families with adrenal hypoplasia. Adrenal hypoplasia can occur: (1) secondary to defects in pituitary adrenocorticotropin (ACTH) synthesis, processing and release (secondary adrenal hypoplasia; e.g. HESX1, LHX4, SOX3, TPIT, pituitary POMC, PC1); (2) as part of several ACTH resistance syndromes (e.g. MC2R/ACTHR, MRAP, Alacrima, Achalasia, Addison disease), or as (3) a primary defect in the development of the adrenal gland itself (primary adrenal hypoplasia; e.g. DAX1/NR0B1 - dosage-sensitive sex reversal, adrenal hypoplasia congenita critical region on the X chromosome 1). Indeed, the X-linked form of primary adrenal hypoplasia due to deletions or mutations in the orphan nuclear receptor DAX1 occurs in around half of male infants presenting with a salt-losing adrenal crisis, where no obvious steroidogenic defect (e.g. 21-hydroxylase deficiency), metabolic abnormality (e.g. neonatal adrenoleukodystrophy) or physical cause (e.g. adrenal haemorrhage) is found. Establishing the underlying basis of adrenal failure can have important implications for investigating associated features, the likely long-term approach to treatment, and for counselling families about the risk of other children being affected.</p>
<p>PMID: 18493131 [PubMed - in process]</p> (Source: Endocrine Development)
Acute hypothalamic?pituitary?adrenal response in traumatic brain injury with and without extracerebral trauma
Abstract
Objective Endocrine disturbances are common after traumatic brain injury (TBI). Hypothalamic?pituitary?adrenal (HPA) axis response in
TBI patients may be related with hemodynamic status. However, its relationship with outcome is unclear. Our objective was
to evaluate HPA axis response in the acute phase after TBI in patients with or without extracerebral trauma (ECT), and to
investigate the impact of systemic injury and the mechanisms underlying HPA response.
Methods We prospectively studied 165 patients with moderate to severe TBI. Between 24 and 48 h after TBI, blood samples were taken
for plasma adrenocorticotrophin hormone (ACTH) and baseline cortisol measurements. Afterwards, a short corticotrophin hormone
test (250 ?g Synacthen) was performed and samples were obtained at 30 and 60 min. We compared HPA response in TBI patients
presenting with and without ECT and investigate potential mechanisms underlying this response.
Results One hundred and eight patients presented with isolated TBI, whereas 57 patients presented associated ECT. Both groups were
comparable. Overall, 23.6% of patients fulfilled adrenal insufficiency (AI) criteria. Patients with plasma ACTH <9 pg/ml and
patients presenting with hemorrhagic shock were more likely to present adrenal impairment. Variables associated with mortality
were Injury Severity Score, Glasgow Coma Scale, Traumatic Coma Data Bank classification different than type II, need of second
level measures to control intracranial pressure and plasma ACTH >9 pg/ml.
Conclusion Patients with TBI presenting with or without associated ECT present similar acute HPA response. AI is present in 23.6% of
patients. Risk is increased in patients with low plasma ACTH levels and in patients with hemorrhagic shock. Both primary and
secondary mechanisms of HPA failure were found. However, AI did not affect outcome.
Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s12028-008-9115-6Authors
Juan A. Llompart-Pou, Hospital Universitario Son Dureta Servicio de Medicina Intensiva c/ Andrea Doria n 55. 07014, Palma de Mallorca Illes Balears SpainJoan M. Raurich, Hospital Universitario Son Dureta Servicio de Medicina Intensiva c/ Andrea Doria n 55. 07014, Palma de Mallorca Illes Balears SpainJon Pérez-Bárcena, Hospital Universitario Son Dureta Servicio de Medicina Intensiva c/ Andrea Doria n 55. 07014, Palma de Mallorca Illes Balears SpainAntonia Barceló, Hospital Universitario Son Dureta Análisis Clínicos Illes Balears SpainJordi Ibáñez, Hospital Universitario Son Dureta Servicio de Medicina Intensiva c/ Andrea Doria n 55. 07014, Palma de Mallorca Illes Balears SpainJosé I. Ayestarán, Hospital Universitario Son Dureta Servicio de Medicina Intensiva c/ Andrea Doria n 55. 07014, Palma de Mallorca Illes Balears Spain
Journal Neurocritical CareOnline ISSN 1556-0961Print ISSN 1541-6933 (Source: Neurocritical Care) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Clinical and molecular genetic findings in a 6-year-old bosnian boy with triple a syndrome
Abstract The triple A syndrome is a rare autosomal recessive disease that is characterised by the triad of adrenocorticotropin (ACTH)-resistant
adrenal insufficiency, achalasia and alacrima. In most patients, neurological and dermatological abnormalities are associated
features. We report on the first Bosnian patient with triple A syndrome. Endocrine investigation confirmed primary adrenal
insufficiency at the age of 5.8 years. Two months lather, achalasia was diagnosed, and in the presence of alacrima, the patient
satisfies the diagnostic criteria of triple A syndrome. In addition, a large number of associated neurological and dermatological
features were present in this patient. Moreover, he has dysmorphic facial features, which have not been previously described
in triple A syndrome. Triple A syndrome was confirmed by molecular analysis, revealing a nonsense mutation p.W84X in the AAAS gene. The parents are both heterozygous carriers of the mutation. The affected twin brother unfortunately died from hypoglycaemic
shock, despite a normal cortisol rise in an ACTH stimulation test. Further, triple A syndrome patients carrying the identical
homozygous p.W84X mutation have to be studied to assess a genotype?phenotype relationship for this mutation.
Content Type Journal ArticleCategory Original PaperDOI 10.1007/s00431-008-0758-2Authors
Alma Toromanovic, University Clinical Center Department of Pediatrics Trnovac bb 75000 Tuzla Bosnia and HerzegovinaHusref Tahirovic, University Clinical Center Department of Pediatrics Trnovac bb 75000 Tuzla Bosnia and HerzegovinaTatjana Milenkovic, Mother and Child Health Care Institute of Serbia ?Dr Vukan ?upi?? Department of Endocrinology Radoja Daki?a b 8 11070 Belgrade SerbiaKatrin Koehler, Technical University Children?s Hospital Fetscherstrasse 74 01307 Dresden GermanyBarbara Kind, Technical University Children?s Hospital Fetscherstrasse 74 01307 Dresden GermanyDragan Zdravkovic, Mother and Child Health Care Institute of Serbia ?Dr Vukan ?upi?? Department of Endocrinology Radoja Daki?a b 8 11070 Belgrade SerbiaMensuda Hasanhodzic, University Clinical Center Department of Pediatrics Trnovac bb 75000 Tuzla Bosnia and HerzegovinaAngela Huebner, Technical University Children?s Hospital Fetscherstrasse 74 01307 Dresden Germany
Journal European Journal of PediatricsOnline ISSN 1432-1076Print ISSN 0340-6199 (Source: European Journal of Pediatrics)
Ten-year experience of free flaps in head and neck surgery. how necessary is a second venous anastomosis?
Successful free flap surgery in the head and neck is dependent on the successful anastomosis of both artery and vein. The success of all free flaps was analyzed to determine the necessity for performing 2 venous anastomoses.We retrospectively analyzed a single surgeon's 10-year experience (August 1993-August 2003) in free flap reconstruction for malignant tumors of the head and neck. Four hundred ninety-two free flaps were primary reconstructions that did not require a vein graft, vein loop, or cephalic turnover procedure. Three hundred forty-five flaps had 1 venous anastomosis, and 147 flaps had 2 venous anastomoses.Overall, flap success was 468 of 492 (95.1%). Successful flap reconstruction in patients undergoing 2 venous anastomoses was 145 of 147 (98.6%) compared with 323 of 345 (93.6%) in patients undergoing 1 anastomosis (p < .05).Where possible, a second venous anastomosis should be performed in head and neck free flap reconstruction. © 2008 Wiley Periodicals, Inc. Head Neck, 2008 (Source: Head)
Use of a low-dose acth stimulation test for diagnosis of hypoadrenocorticism in dogs.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18537878">Related Articles</a></td></tr></table>
<p><b>Use of a Low-Dose ACTH Stimulation Test for Diagnosis of Hypoadrenocorticism in Dogs.</b></p>
<p>J Vet Intern Med. 2008 Jun 3;</p>
<p>Authors: Lathan P, Moore GE, Zambon S, Scott-Moncrieff JC</p>
<p>Background: Although definitive diagnosis of hypoadrenocorticism usually is made by an adrenocorticotrophic hormone (ACTH) stimulation test using 250 mug/dog of synthetic ACTH (cosyntropin/tetracosactrin), increased costs have prompted a search for less-expensive diagnostic methods. Hypothesis: A low-dose ACTH stimulation test (5 mug/kg) will distinguish between dogs with nonadrenal illness and hypoadrenocorticism. Additionally, administration of cosyntropin will not affect the results of another ACTH stimulation test performed 24 hours later. Animals: Eight healthy adult dogs and 29 hospitalized dogs with suspected hypoadrenocorticism. Methods: In this prospective study, each healthy dog received 4 ACTH stimulation tests. Dogs received either 5 mug/kg or 250 mug/dog of cosyntropin on day 1 and the alternate dose on day 2. The opposite dosing sequence was used after a 2-week washout period (days 15 and 16). Dogs with suspected Addison's disease received 2 ACTH stimulation tests, 24 hours apart, using either a dose of 5 mug/kg cosyntropin or 250 mug/dog on the 1st day and the alternate dose on the 2nd day. Results: In healthy dogs, poststimulation cortisol concentrations on days 2 and 16 and days 1 and 15 were equivalent (90% confidence interval [CI]: 86.7-101.2%). In dogs with suspected Addison's disease, mean (+/-SD) cortisol responses to ACTH in the 5 mug/kg dose (16.2+/-7.7 mug/dL) and 250 mug/dog dose (15.9+/-6.3 mug/dL) were statistically equivalent (90% CI: 91.2-105.4%). Conclusions and Clinical Importance: Low-dose ACTH stimulation testing distinguishes between dogs with nonadrenal illness and hypoadrenocorticism. Additionally, the administration of 2 ACTH stimulation tests on consecutive days does not affect results of the second test.</p>
<p>PMID: 18537878 [PubMed - as supplied by publisher]</p> (Source: Journal of Veterinary Internal Medicine)
Comparison of serum cortisol concentrations in preterm infants with or without late-onset circulatory collapse due to adrenal insufficiency of prematurity.
<table border="0" width="100%"><tr><td align="left"/></tr></table>
<p><b>Comparison of Serum Cortisol Concentrations in Preterm Infants With or Without Late-Onset Circulatory Collapse due to Adrenal Insufficiency of Prematurity.</b></p>
<p>Pediatr Res. 2008 Jun;63(6):686-690</p>
<p>Authors: Masumoto K, Kusuda S, Aoyagi H, Tamura Y, Obonai T, Yamasaki C, Sakuma I, Uchiyama A, Nishida H, Oda S, Fukumura K, Tagawa N, Kobayashi Y</p>
<p>A recent survey found that approximately 4% of very low birth weight infants in Japan were treated with glucocorticoids postnatally for circulatory collapse thought to be caused by late-onset adrenal insufficiency. We identified 11 preterm infants with clinical signs compatible with this diagnosis (hypotension, oliguria, hyponatremia, lung edema, and increased demand for oxygen treatment) and matched them for gestational age with 11 infants without such signs. Blood samples were obtained for cortisol and its precursors from the patient group before the administration of hydrocortisone, and from the control group during the same postnatal week. All samples were analyzed using a gas chromatography-mass spectrometry system. Cortisol concentrations did not differ between the two groups (6.6 +/- 4.5 vs 3.4 +/- 2.7 mug/dL); however, the total concentration of precursors in the pathway to cortisol production was significantly higher in the patient group (72.2 +/- 50.3 vs 25.0 +/- 28.5 mug/dL; p < 0.05). We conclude that the clinical picture of late-onset adrenal insufficiency in preterm infants is not a result of an absolute deficiency of cortisol production, but may be a result of a limited ability to synthesize sufficient cortisol for the degree of clinical stress. ABBREVIATIONS::</p>
<p>PMID: 18520332 [PubMed - as supplied by publisher]</p> (Source: Pediatric Research)
Successful autologous peripheral blood stem cell transplantation for a patient with primary adrenal lymphoma with hemophagocytic syndrome.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18650184">Related Articles</a></td></tr></table>
<p><b>Successful autologous peripheral blood stem cell transplantation for a patient with primary adrenal lymphoma with hemophagocytic syndrome.</b></p>
<p>Clin Lymphoma Myeloma. 2008 Jun;8(3):184-7</p>
<p>Authors: Uehara T, Yokota A, Onoda M, Yamamoto K, Terano T</p>
<p>The adrenal glands are often an affected extranodal site in advanced non-Hodgkin lymphoma, but primary adrenal lymphoma (PAL) is extremely rare. Histologic examination of adrenal glands from patients with PAL reveals predominantly diffuse large B-cell lymphoma. Adrenal insufficiency is observed in about two thirds of patients. The prognosis of patients with PAL is poor: > 90% of patients die within 1 year of diagnosis, and long-term survivors are few. Effective therapeutic management of the condition has not been established. Herein, we report a 57-year-old man with PAL of diffuse large B-cell type that was later accompanied by hemophagocytic syndrome. He was initially treated with combination chemotherapy (1 cycle of CHOP [cyclophosphamide/doxorubicin/vincristine/prednisone] and 4 cycles of rituximab plus CHOP) and subsequently underwent autologous peripheral blood stem cell transplantation (auto-PBSCT) in his first complete remission. He has been well and disease free for 39 months since undergoing auto-PBSCT. The successful outcome of using auto-PBSCT in the treatment of a patient with PAL suggests that this therapeutic approach has value in treating this poor-prognostic disease.</p>
<p>PMID: 18650184 [PubMed - in process]</p> (Source: Clinical Lymphoma and Myeloma) <p> </p><p><b><i>MedWorm Sponsored Message:</i></b> Find out how you can <a href="http://www.medworm.com/rss/medicalsponsorship.php" target="_self">get your message across here</a> by sponsoring this MedWorm news feed.</p>
Evaluation of serum cortisol in the postmortem diagnosis of acute adrenal insufficiency.
Page: 181DOI: 10.1097/PAF.0b013e318174e7c8Authors: Clapper, Adam MD; Nashelsky, Marcus MD; Dailey, Morris MD, PhD (Source: The American Journal of Forensic Medicine and Pathology)
Endocrine issues in the pediatric intensive care unit.
<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=PubMed_PubMed&from_uid=18501767">Related Articles</a></td></tr></table>
<p><b>Endocrine Issues in the Pediatric Intensive Care Unit.</b></p>
<p>Pediatr Clin North Am. 2008 Jun;55(3):805-833</p>
<p>Authors: Clark L, Preissig C, Rigby MR, Bowyer F</p>
<p>This article reviews selected issues of endocrine concerns in the pediatric intensive care unit, exclusive of diabetic ketoacidosis. The sympathoadrenergic arm of the neuroendocrine stress response is described, followed by discussions of two topics of particular current concern: critical illness hyperglycemia and relative adrenal insufficiency. A selected set of common scenarios encountered in the daily practice of intensive care follows.</p>
<p>PMID: 18501767 [PubMed - as supplied by publisher]</p> (Source: Pediatric Clinics of North America)
Compartment syndrome after closure of the anterolateral thigh flap donor site: a report of two cases.
Page: 635DOI: 10.1097/SAP.0b013e3181453b7aAuthors: Addison, Patrick D. MD, MB, ChB, FRCS (Plast); Lannon, Declan MSc, FRCSI; Neligan, Peter C. MD, FRCS, FACS (Source: Annals of Plastic Surgery)
Dickson launches drug temperature monitor
Dickson of Addison, IL, has launched its Dickson Drug Recorder, which allows radiology department and diagnostic lab managers to track temperatures in drug storage units, the company announced. (Source: AuntMinnie.com Headlines)
|
|
