Safe Antibiotics During Pregnancy : Amoxicillin Ampicillin Clindamycin Erythromycin Penicillin Gentamicin Ampicillin-Sulbactam Cefoxitin Cefotetan Cefazolin

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

The Food and Drug Administration lists antibiotics in categories based on safety for use during pregnancy. It has established five categories to indicate the evidence and the potential of a drug to cause birth defects if used during pregnancy. The categories are determined by the reliability of documentation and the risk to benefit ratio. They do not take into account any risks from pharmaceutical agents or their metabolites in breast milk. 

The categories are:  The categories are A, B, C, D and X.

CATEGORY DEFINITION COMMENTS A Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities. Drugs that fall under category A have had several well-controlled studies that found no harmful effects or increase in birth defects. These drugs have all had studies conducted in pregnant woman with positive results. Very few drugs fall into this category. Prenatal vitamins receive a category A rating. B Animal studies have revealed no evidence of harm to the fetus, however there are no adequate and well-controlled studies in pregnant women or animal studies have shown an adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus. Drugs assigned a category B rating are not likely to pose a threat to the fetus from the evidence in animal studies, but no well-controlled studies have been performed in pregnant women. However, a drug may also receive a category B rating if animal studies have shown evidence of fetus damage but the same drug tested on pregnant women posed no threat. C

Animal studies have shown an adverse effect and there are no adequate and well-controlled studies in pregnant women. Or, no animal studies have been conducted and there are no adequate and well-controlled studies in pregnant women.

A category C rating is given to drugs that have been shown to be harmful in animal studies but no studies have been conducted on pregnant humans. Drugs may also receive a category C rating if the drug was not studied in animals and there isn't enough evidence from studies in pregnant humans. This implies that the drug may or may not be safe to take.

D Studies, adequate well-controlled or observational, in pregnant women have demonstrated a risk to the fetus. However, the benefits of therapy may outweigh the potential risk.

Drugs receive a category D rating when the drugs have been tested in well-controlled or observational (not controlled) studies, which resulted in harm to the unborn baby. In some cases these drugs may still be given if the benefits to the mother outweigh the risks to the baby (for example, cancer treatment).

X

Studies, adequate well-controlled or observational, in animals or pregnant women have demonstrated positive evidence of fetal abnormalities. The use of the product is contraindicated in women who are or may become pregnant.

A Category X rating is assigned to drugs that should never be used during pregnancy, as there are no benefits that would exceed the potential risk.

Using Antibiotics During Pregnancy

According to doctors and researchers, a few guidelines should be followed before prescribing an antibiotic to a pregnant patient. These include:

    Only use antibiotics if no other treatment option will suffice.
    Avoid prescribing antibiotics during the first trimester when possible.
    Choose a safe medication (typically an older antibiotic tested on pregnant women).
    Choose single prescriptions over polypharmacy when possible.
    Dose at the lowest possible amount proven effective.
    Advise patients not to use over the counter medications during antibiotic treatment.

Antibiotics Generally Considered Safe for Use During Pregnancy

Some of the common infections during pregnancy that require antibiotic treatment include urinary tract infection, bladder infection, pyelonephritis and appendicitis. This is not a complete list of infections that require antibiotic treatment.

If your physician prescribes an antibiotic for use during pregnancy, it is extremely likely that the drug falls into either Category A or Category B on the FDA list of approved drugs for use during pregnancy. Some of the antibiotics that may be prescribed safely during pregnancy include:

    Amoxicillin
    Ampicillin
    Clindamycin
    Erythromycin
    Penicillin
    Gentamicin
    Ampicillin-Sulbactam
    Cefoxitin
    Cefotetan
    Cefazolin

Clinical Information and New Antibiotics


There is very little clinical information on the effect of new antibiotics on pregnancy and fetal complication risk. Decades ago, pregnant women were allowed to participate in drug testing so older antibiotics are typically the first prescribed by obstetricians. However, in some cases, despite the lack of formula testing during pregnancy, obstetricians are faced with a risks versus benefits case. If the benefits of prescribing an antibiotic during pregnancy outweigh the potential risks, the antibiotic in question is chosen.

There are several antibiotics safely prescribed during pregnancy. If you have an infection and your obstetrician has prescribed an antibiotic, talk with your doctor about the possible risks of taking the medication. In some cases, as is the case with urinary tract infections, leaving the infection untreated poses a risk to the pregnancy and unborn fetus.

Medicine and Pregnancy

https://www.fda.gov/forconsumers/byaudience/forwomen/ucm118567.htm

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En Español, In Chinese, In French, In French Creole

Are you pregnant and taking medicines?  You are not alone. Many women need to take medicines when they are pregnant. There are about six million pregnancies in the U.S. each year, and 50% of pregnant women say that they take at least one medicine. Some women take medicines for health problems, like diabetes, morning sickness or high blood pressure that can start or get worse when a woman is pregnant. Others take medicines before they realize they are pregnant.

Pregnancy can be an exciting time. However, this time can also make you feel uneasy if you are not sure how your medicines will affect your baby. Not all medicines are safe to take when you are pregnant. Even headache or pain medicine may not be safe during certain times in your pregnancy. 

Here are four (4) tips to help you talk to your healthcare provider about how prescription and over-the-counter medicines might affect you and your baby.

1. Ask Questions

2. Read the Label

3. Be Smart Online

4. Report Problems

Bonus Tip: Help spread the word about pregnancy safety.

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1. Ask Questions.

Always talk to your healthcare provider before you take any medicines, herbs, or vitamins. Don't stop taking your medicines until your healthcare provider says that it is OK.

Use these questions to help you talk to your doctor, nurse, or pharmacist:

• Will I need to change my medicines if I want to get pregnant? Before you get pregnant, work with your healthcare provider to make a plan to help you safely use your medicines.

• How might this medicine affect my baby? Ask about the benefits and risks for you and your baby.

• What medicines and herbs should I avoid? Some drugs can harm your baby during different stages of your pregnancy. At these times, your healthcare provider may have you take something else.

• Will I need to take more or less of my medicine? Your heart and kidneys work harder when you are pregnant. This makes medicines pass through your body faster than usual.

•  Can I keep taking this medicine when I start breastfeeding? Some drugs can get into your breast milk and affect your baby.

• What kind of vitamins should I take? Ask about special vitamins for pregnant women called pre-natal vitamins.

   

Pre-Natal Vitamins

Some dietary supplements may have too much or too little of the vitamins that you need. Talk to your healthcare provider about what kind of pre-natal vitamins you should take.

What is folic acid? Folic acid helps to prevent birth defects of the baby's brain or spine. Ask about how much folic acid you should take before you become pregnant and through the first part of your pregnancy.

 

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2. Read the Label 

 

Check the drug label and other information you get with your medicine to learn about the possible risks for women who are pregnant or breastfeeding. The labeling tells you what is known about how the drugs might affect pregnant women. Your healthcare provider can help you decide if you should take the medicine.

Find information on a specific drug

New Prescription Drug Information

The prescription drug labels are changing. The new labels will replace the old A, B, C, D and X categories with more helpful information about a medicine's risks. The labels will also have more information on whether the medicine gets into breast milk and how it can possibly affect the baby.

 

 

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3. Be Smart Online.

  

Ask your doctor, nurse, or pharmacist about the information you get online. Some websites say that drugs are safe to take during pregnancy, but you should check with your healthcare provider first. Every woman's body is different. It may not be safe for you.

• Do not trust that a product is safe just because it says 'natural'.

• Check with your healthcare provider before you use a product that you heard about in a chat room or group.

 

Online Resources

• CDC - Centers for Disease Control and Prevention

• MotherToBaby

• text4baby

• March of Dimes

   

 

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4. Report Problems.

  

First, tell your healthcare provider about any problems you have with your medicine. Also, tell FDA about any serious problems you have after taking a medicine.

• Call 1-800-FDA-1088 to get a reporting form sent to you by mail.

• Report problems online. 

 

What to Report to FDA

You should report problems like serious side effects, product quality problems and product use errors. Report problems with these products:

• human drugs

• medical devices

• blood products and other biologics (except vaccines)

• medical foods

 Learn more about reporting problems to FDA.

 

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Sign Up for a Pregnancy Registry

Pregnancy Exposure Registries are research studies that get information from women who take prescription medicines or vaccines during pregnancy. Pregnancy registries help women and their doctors learn more about how medicines can be safely used during pregnancy.

• Help other pregnant women. Share your experiences with medicines.

• You will not be asked to take any new medicines.

• You will provide information about your health and your baby's health.

FDA does not run pregnancy registries, but it keeps a list of registries. See if there is a registry for your medicine.

www.fda.gov/pregnancyregistries

 

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Pregnancy Social Media Toolkit

The FDA Office of Women's Health offers resources to help women and healthcare providers get informed about medicines and other products used during pregnancy. Use the Pregnancy Social Media Toolkit to inform pregnant women in your network about medication safety. The toolkit includes resources for pregnant women and health professionals, including sample social media messages and blog posts.

Download and Share: Social Media Toolkit (PDF 166KB)

 

To Learn More

• Get Information about a Specific Drug
• Use of Codeine and Tramadol Products in Breastfeeding Women - Questions and Answers
• Pregnant? Breastfeeding? Better Drug Information Is Coming
• Registries Help Inform Medication Use in Pregnancy
• Pregnancy: A Time for Special Caution
• MotherToBaby - Provides counseling to patients and health care professionals about medicines used during pregnancy and breastfeeding.

Resources for Health Professionals

• Pregnancy and Lactation Labeling Information for Health Professionals
• Pregnancy Registry Information for Health Professionals
• MedWatch
• Treating for Two (CDC)

For Women

Medication Safety for Women ¡Nunca Más! Novelas An Invitation to Collaborate

Free Publications

Take Time to Care Program

Women's Health Topics

Resources for You

• Tips for Pregnant Women
• Get Other FDA Publications for Women
• For Women Homepage
• FDAWomen on Twitter

Page Last Updated: 05/19/2017

Rev Obstet Gynecol.

PMCID: PMC2760892

Antibiotics in Pregnancy: Are They Safe?

Errol R Norwitz, MD, PhD^* and James A Greenberg, MD^†

^*Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT

^†Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Division of Gynecology, Faulkner Hospital, and Department of Obstetrics, Gynecology, and Reproductive Biology, Harvard Medical School, Boston, MA

Author information ▼ Copyright and License information ►

The question of whether to prescribe a course of antibiotics to a pregnant woman is a dilemma faced by obstetrics-gynecology (ob-gyn) care providers on a daily basis. In appropriate circumstances-such as the treatment of asymptomatic bacteriuria to prevent ascending infection and pyelonephritis-related adverse pregnancy outcomes-antibiotic therapy can be both effective and life saving. As with the administration of other medications, the potential benefits need to be weighed against the risk to the fetus. Some antibiotics are known to be teratogenic and should be avoided entirely during pregnancy. These include streptomycin and kanamycin (which may cause hearing loss) and tetracycline (which can lead to weakening, hypoplasia, and discoloration of long bones and teeth). How about other antibiotics? Are they safe? Can they be given with impunity?

A decade ago, a number of well-designed clinical trials^1,2 and systematic reviews³ concluded that broad-spectrum antibiotics can prolong the latency period (interval to delivery) and improve short-term perinatal outcome in pregnancies complicated by preterm premature rupture of membranes (pPROM) prior to 34 weeks of gestation, but not in women with preterm labor and intact membranes. Seven-year follow-up of the fetuses exposed to these antibiotics was recently published.^4,5 Reassuringly, broad-spectrum antibiotics given to fetuses in the setting of pPROM were not associated with any long-term disadvantage, although it is concerning to note that the short-term benefits in perinatal outcome described in the original report¹ did not appear to persist to age 7.⁴ Even more concerning, however, was the observation that fetuses exposed to broad-spectrum antibiotics in the setting of intact membranes were at significantly higher risk of cerebral palsy at age 7 (erythromycin, odds ratio [OR] 1.93; 95% confidence interval [CI], 1.21–3.09; co-amoxiclav, OR 1.69; 95% CI, 1.07–2.67).⁵ The risk was even higher when both antibiotics were given together (4.55% incidence of cerebral palsy compared with 1.97% for co-amoxiclav alone, 2.29% for erythromycin alone, and 1.63% for placebo).⁵ Exposure to co-amoxiclav was also associated with an increased risk of necrotizing enterocolitis.⁵

The mechanism of injury is not clear. The most likely explanation is an antibiotic-mediated suppression of infection and preterm birth, thereby causing the fetus to remain in a hostile proinflammatory intrauterine environment for a longer period of time. However, a direct injurious effect of the antibiotic itself cannot be excluded. Indeed, 1 reason why a significant association between antibiotics and cerebral palsy was observed with intact membranes but not in the setting of pPROM may have to do with the dose and/or duration of antibiotic exposure. Because the vast majority of women in the preterm labor and intact membrane study did not deliver within 48 hours (89.9%) or 7 days (84.6%) of enrollment, their fetuses were more likely to be exposed to the full 10-day course of antibiotic therapy.² In contrast, 30% to 40% of women in the pPROM study delivered within 48 hours and 55% to 60% within 7 days. As such, these fetuses were exposed to antibiotics for a far shorter period of time.¹ An additional adverse effect of the increased use of broad-spectrum antibiotics in the setting of pPROM is an increase in antibiotic resistance, especially erythromycin-resistant Group B β-hemolytic streptococcus (GBS).

The debate about the efficacy and safety of antibiotics in pregnancy must be seen in a larger context. It highlights the philosophical difference between 2 distinct groups of obgyn care providers: those who believe that everything possible should be offered in a given clinical setting in the hope that something will help (also known as the we don't have all the information we need or the might as well give it, it won't do any harm group) and those who hold out against popular opinion until there is consistent and compelling scientific evidence that an individual course of action is beneficial and has a favorable risk-to-benefit ratio (the so-called therapeutic nihilists). As protagonists of the latter camp, we offer the following suggestions to ob-gyn care providers faced with the dilemma of whether to prescribe a medication to a pregnant woman:

• Use medications only if absolutely indicated. For antibiotics, this includes treatment of confirmed infection (urinary tract infection, pyelonephritis, appendicitis, cholecystitis, chorioamnionitis), prevention of ascending infection (asymptomatic bacteriuria), and prevention of early-onset neonatal GBS sepsis.
• If possible, avoid initiating therapy during the first trimester. This is the period of fetal structural development and therefore the highest risk for iatrogenic teratogenicity.
• Select a safe medication, which often means an older drug with a proven track record in pregnancy. Certain antibiotics (streptomycin, kanamycin, tetracycline) are best avoided entirely in pregnancy because of their teratogenicity.
• Wherever possible, single-agent therapy is preferred over polypharmacy. Moreover, narrow-spectrum antibiotics are preferred over those with a broad spectrum for the treatment of established infection and intrapartum GBS chemoprophylaxis. The exception is the use of empiric broad-spectrum antibiotics to prolong latency in the setting of pPROM remote from term (discussed above).
• Use the lowest effective dose.
• Discourage the use of over-the-counter drugs, which may interfere with the efficacy and/or metabolism of prescription medications.

Go to:

References

1. Kenyon SL, Taylor DJ, Tarnow-Mordi W ORACLE Collaborative Group, authors. Broad-spectrum antibiotics for preterm, prelabour rupture of fetal membranes: the ORACLE I randomised trial. ORACLE Collaborative Group. Lancet. 2001;357:979–988. [PubMed]

2. Kenyon SL, Taylor DJ, Tarnow-Mordi W ORACLE Collaborative Group, authors. Broad-spectrum antibiotics for spontaneous preterm labour: the ORACLE II randomised trial. ORACLE Collaborative Group. Lancet. 2001;357:989–994. [PubMed]

3. Kenyon S, Boulvain M. Antibiotics for preterm premature rupture of membranes. Cochrane Database Syst Rev. 2000;2 CD001058. [PubMed]

4. Kenyon S, Pike K, Jones DR, et al. Childhood outcomes after prescription of antibiotics to pregnant women with preterm rupture of the membranes: 7-year follow-up of the ORACLE I trial. Lancet. 2008;372:1310–1318. [PubMed]

5. Kenyon S, Pike K, Jones DR, et al. Childhood outcomes after prescription of antibiotics to pregnant women with spontaneous preterm labour: 7-year follow-up of the ORACLE II trial. Lancet. 2008;372:1319–1327. [PubMed]

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Articles from Reviews in Obstetrics and Gynecology are provided here courtesy of MedReviews, LLC

Flu-like illness, fever, malaise and chills, followed by severe nonpleuritic chest pain and shortness of breath

Chronic migraine headache and acute shortness of breath associated with nausea, vomiting, diaphoresis and increasing retrosternal chest pain..Increased frequency of his migraine headaches associated with vague retrosternal chest pain and epigastric pain...................................................................................................................Flu-like illness, fever, malaise and chills, followed by severe nonpleuritic chest pain and shortness of breath................................................................................Palpitations, fatigue, vague chest discomfort, and cardiomegaly and pulmonary congestion visible on chest radiograph. He had developed a flu-like illness with low-grade fever, chills, myalgia and headache a week earlier. There had been no preceding cough, hemoptysis, orthopnea, paroxysmal nocturnal dyspnea or ankle edema. .....................................................................................................................................Eosinophilic myocarditis (EM)........................................................................................................Therapeutic effect of anti-IL-5 on eosinophilic myocarditis with large pericardial effusion

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

PROPIONIBACTERIUM ACNES AND CHRONIC DISEASES : P. acnes is an opportunistic pathogen, causing a range of postoperative and device-related infections e.g., surgery,post-neurosurgical infection,joint prostheses, shunts and prosthetic heart valves. P. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer,SAPHO (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis) syndrome, sarcoidosis and sciatica.

http://otorhinolaryngology-crete.blogspot.com/2017/05/propionibacterium-acnes-and-chronic.html

P. acnes bacteria live deep within follicles and pores, away from the surface of the skin. In these follicles, P. acnes bacteria use sebum, cellular debris and metabolic byproducts from the surrounding skin tissue as their primary sources of energy and nutrients. Elevated production of sebum by hyperactive sebaceous glands (sebaceous hyperplasia) or blockage of the follicle can cause P. acnes bacteria to grow and multiply.[6]

P. acnes bacteria secrete many proteins, including several digestive enzymes.[7] These enzymes are involved in the digestion of sebum and the acquisition of other nutrients. They can also destabilize the layers of cells that form the walls of the follicle. The cellular damage, metabolic byproducts and bacterial debris produced by the rapid growth of P. acnes in follicles can trigger inflammation.[8] This inflammation can lead to the symptoms associated with some common skin disorders, such as folliculitis and acne vulgaris.[9][10][11]

The damage caused by P. acnes and the associated inflammation make the affected tissue more susceptible to colonization by opportunistic bacteria, such as Staphylococcus aureus. Preliminary research shows healthy pores are only colonized by P. acnes, while unhealthy ones universally include the nonpore-resident Staphylococcus epidermidis, amongst other bacterial contaminants. Whether this is a root causality, just opportunistic and a side effect, or a more complex pathological duality between P. acnes and this particular Staphylococcus species is not known.[12]

P. acnes has also been found in corneal ulcers, and is a common cause of chronic endophthalmitis following cataract surgery. Rarely, it infects heart valves leading to endocarditis, and infections of joints (septic arthritis) have been reported.[5] Furthermore, Propionibacterium species have been found in ventriculostomy insertion sites, and areas subcutaneous to suture sites in patients who have undergone craniotomy. It is a common contaminant in blood and cerebrospinal fluid cultures.

P. acnes has been found in herniated discs.[13] The propionic acid which it secretes creates micro-fractures of the surrounding bone. These micro-fractures are sensitive and it has been found that antibiotics have been helpful in resolving this type of low back pain.[14]

P. acnes can be found in bronchoalveolar lavage of approximately 70% of patients with sarcoidosis and is associated with disease activity, but it can be also found in 23% of controls.[15][16] The subspecies of P. acnes that cause these infections of otherwise sterile tissues (prior to medical procedures), however, are the same subspecies found on the skin of individuals who do not have acne-prone skin, so are likely local contaminants. Moderate to severe acne vulgaris appears to be more often associated with virulent strains.[17]

P. acnes is an opportunistic pathogen, causing a range of postoperative and device-related infections e.g., surgery,[18] post-neurosurgical infection,[19] joint prostheses, shunts and prosthetic heart valves. P. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer,[20] SAPHO (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis) syndrome, sarcoidosis and sciatica.[21]

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Dichotic Listening Deficit Associated With Solvent Exposure.Due to their lipophilic nature, solvents can adversely affect large white matter tracks such as the corpus callosum. Previous investigations reveal that long-term workplace exposure to solvents is also deleterious to various auditory processes.

http://otorhinolaryngology-crete.blogspot.com/2017/05/dichotic-listening-deficit-associated.html

Dichotic Listening Deficit Associated With Solvent Exposure.

από Landry, Simon P.; Fuente, Adrian στο Otology & Neurotology Published Ahead-of-Print

Μετάφραση άρθρου

Hypothesis: A significant left ear deficit can be observed in solvent-exposed individuals using the dichotic digit test. Background: Solvents are ubiquitous in global industrial processes. Due to their lipophilic nature, solvents can adversely affect large white matter tracks such as the corpus callosum. Previous investigations reveal that long-term workplace exposure to solvents is also deleterious to various auditory processes. Investigations in exposed populations suggest a decreased performance for dichotic listening. Methods: In this present study, we examined the lateralization of a dichotic digit test score for 49 solvent-exposed individuals along with 49 age- and sex-matched controls. We evaluated group differences between test scores and the right ear advantage using a laterality index (LI). Results: Individual ear results suggest that long-term workplace solvent exposure is associated with a significantly lower dichotic listening score for the left ear. A binaural compound score analysis using a laterality index supports this left-ear deficit. Conclusion: These results provide an insight on the effects of solvent exposure on dichotic listening abilities. Further research should investigate the importance of using dichotic listening tasks to screen for solvent-induced auditory dysfunction in exposed individuals. Copyright (C) 2017 by Otology & Neurotology, Inc. Image copyright (C) 2010 Wolters Kluwer Health/Anatomical Chart Company

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Epstein-Barr virus, human endogenous retroviruses (HERVs) and human herpesvirus 6 (HHV-6) but also less common viruses such as Saffold and measles viruses are associated with multiple sclerosis

http://otorhinolaryngology-crete.blogspot.com/2017/05/epstein-barr-virus-human-endogenous.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Airway management during induction of anaesthesia, spontaneous ventilation (SV) and controlled mechanical ventilation (CMV), using an endotracheal tube (ETT), laryngeal mask (LM), rabbit-specific supraglottic airway device (v-gel) or facemask (FM).

Experimental evaluation of four airway devices in anaesthetized New Zealand White rabbits.

Vet Anaesth Analg. 2017 ;

Authors: Wenger S, Müllhaupt D, Ohlerth S, Prasse S, Klein K, da Silva Valente B, Mosing M

Abstract

OBJECTIVE: To compare airway management during induction of anaesthesia, spontaneous ventilation (SV) and controlled mechanical ventilation (CMV), using an endotracheal tube (ETT), laryngeal mask (LM), rabbit-specific supraglottic airway device (v-gel) or facemask (FM).

STUDY DESIGN: Prospective randomized crossover experiment.

ANIMALS: Ten New Zealand White rabbits.

METHODS: After premedication, rabbits were randomly allocated to four groups: 1) ETT; 2) LM; 3) v-gel or 4) FM. The required dose of propofol, duration and number of attempts to place an airway device and leakage during SV and CMV at different peak inspiratory pressures (6, 10, 12, 14 and 16 cmH2O) were recorded. Computed tomography (CT) of the head, neck and abdomen were performed before and after CMV.

RESULTS: Significantly less propofol and time [2.0±0.5 mg kg(-1), 82±34 seconds, p<0.001] were needed to place the FM compared to the three other groups [v-gel 5.1±2.1 mg kg(-1), 302±124 seconds; LM 4.8±1.2 mg kg(-1), 275±89 seconds; ETT 5.5±1.4 mg kg(-1), 315±147 seconds]. A leak > 25% of the tidal volume occurred at the lowest pressure in FM [median (range), 6 (6-8) cmH2O], which was significantly lower than with v-gel [16 (6-no leak at 16) cmH2O], LM [>16 (6-no leak at 16)] or ETT [>16 (no leak at 16) cmH2O] (p<0.001). On CT images, the height and width of the larynx were significantly smaller with v-gel in comparison to FM and LM (p=0.004). A significant increase in the amount of gas in the stomach (p=0.007), but not gastric volume, was detected in FM and LM.

CONCLUSIONS AND CLINICAL RELEVANCE: The v-gel is a practical alternative to LM and ETT for airway management and CMV, but can compress the larynx. The FM is easily placed, but significant leakage occurs during CMV.

PMID: 28528760 [PubMed - as supplied by publisher]

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Curcumin attenuates lipopolysaccharide/d-galactosamine-induced acute liver injury

Curcumin attenuates lipopolysaccharide/d-galactosamine-induced acute liver injury by activating Nrf2 nuclear translocation and inhibiting NF-kB activation

στο Biomedicine & Pharmacotherapy

Μετάφραση άρθρου

Publication date: July 2017

Source:Biomedicine & Pharmacotherapy, Volume 91

Author(s): Yi-Lian Xie, Jin-Guo Chu, Xiao-Min Jian, Jin-Zhong Dong, Li-Ping Wang, Guo-Xiang Li, Nai-Bin Yang

Curcumin, a polyphenol in curry spice isolated from the rhizome of turmeric, has been reported to possess versatile biological properties including anti-inflammatory, anti-oxidant, antifibrotic, and anticancer activities. In this study, the hepatoprotective effect of curcumin was investigated in lipopolysaccharide (LPS)/d-galactosamine (d-GalN)-induced acute liver injury (ALI) in rats. Experimental ALI was induced with an intraperitoneal (ip) injection of sterile 0.9% sodium chloride (NaCl) solution containing 8μg LPS and 800mg/kg d-GalN. Curcumin was administered once daily starting three days prior to LPS/d-GalN treatment. Results indicated that curcumin could attenuate hepatic pathological damage, decrease serum ALT and AST levels, and reduce malondialdehyde (MDA) content in experimental ALI rats. Moreover, higher dosages of curcumin pretreatment inhibited NF-κB activation and reduced serum TNF-α and liver TNF-α levels induced by LPS/d-GalN ip injection. Furthermore, we found that curcumin up-regulated the expression of nuclear Nrf2 and Nrf2-dependent antioxidant defense genes including heme oxygenase-1 (HO-1), glutamate-cysteine ligase (GCLC), NAD(P)H dehydrogenase, and quinone (NQO-1) in a dose-dependent manner. Our results showed that curcumin protected experimental animals against LPS/d-GalN-induced ALI through activation of Nrf2 nuclear translocation and inhibition of NF-κB activation.

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Bottom of an iceberg: undiagnosed aortic aneurysm masquerading as vocal cord palsy

http://otorhinolaryngology-crete.blogspot.com/2017/05/undiagnosed-aortic-aneurysm.html

 από Rao, V. U. S., Chatterjee, S., Swamy, S. S. στο BMJ Case Reports Last 6 Issues Μετάφραση άρθρου Description A previously healthy woman aged 60 years was referred to a tertiary referral cancer centre with change of voice for 1 week suspecting neoplastic aetiology on account of her tobacco chewing habit of more than 20 years. No history of voice abuse, fever or cough was there preceding the onset of the change of voice. She did not have any previous history of hospitalisation or diagnosed comorbidities. On clinical examination, her pulse rate was 82 bpm; blood pressure was 130/90 mm Hg and respiratory rate was 12/min.  Video laryngoscopy examination revealed left vocal cord palsy with no obvious lesion. A whole-body F18 FDG PET–CT scan revealed the presence of 6.6x4.8x6.7 cm lobulated sacullar aneurysm arising from the aortic arch between the origins of the left common carotid and subclavian arteries (figures 1 and 2). The likely mycotic aneurysm caused significant surrounding metabolically active inflammatory changes (figure 3).

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Scarlet Fever

http://otorhinolaryngology-crete.blogspot.com/2017/05/scarlet-fever.html

A 20-year-old man presented to his primary care physician with a 3-day history of swollen tonsils, sore throat, fevers, chills, and rash. The nonpruritic rash had started on his abdomen, spread to his chest and back, and then appeared on his arms, legs, and face. He had no known allergies or exposures to new medications and had no history of similar rash. Examination revealed exudative tonsillitis (Panel A), strawberry tongue, and cervical adenopathy with tenderness. Skin examination revealed diffuse blanching erythema with punctate papules that caused the skin on his chest, abdomen, back, arms, and legs to have a sandpaper-like quality (Panel B shows the left side of his abdomen). His neck and right flank had linear petechial patches. A rapid test for streptococcal pharyngitis was positive. The finding of acute streptococcal pharyngitis along with the diffuse rash led to a diagnosis of scarlet fever. The rash of scarlet fever is a delayed-type hypersensitivity to an exotoxin and therefore occurs in persons who have had a previous exposure to Streptococcus pyogenes. The rash classically manifests with linear petechial confluences that are known as Pastia's lines, which were seen in this patient. The patient was treated with antibiotic agents and had complete resolution of his symptoms within 3 days.

Alyson Brinker, M.D.

Navy Hospital Guam, Yigo, Guam 

Alexandros Sfakianakis
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Pediatric nasal surgery prior to puberty is not only safe, but may prevent facial deformity in certain patients.

http://alexandrossfa.blogspot.com/2017/05/pediatric-nasal-surgery-prior-to.html

Pediatric nasal surgery: timing and technique.

από Gary, Celeste C. στο Current Opinion in Otolaryngology & Head and Neck Surgery - Published Ahead-of-Print

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Purpose of review: Timing of pediatric nasal surgery has always been a controversial topic. Concern over disrupting growing parts of the face and causing permanent facial deformity has led to a primarily conservative approach. Many surgeons feel that it is prudent to wait until the patient has completed nasal growth after puberty to pursue nasal surgery. Recent findings: Recently, this attitude has been challenged with evidence that not only is nasal surgery in the pediatric age group not a detriment to facial growth, but failure to correct significant nasal deformity may actually cause dysmorphic facial growth secondary to obligate mouth breathing. Because of this, recent studies have focused on determining safe surgical techniques for pediatric nasal surgery, including inferior turbinate reduction, septoplasty and rhinoplasty. Research focus on this topic has also been expanded to include quality-of-life measures after nasal surgery. Summary: Pediatric nasal surgery prior to puberty is not only safe, but may prevent facial deformity in certain patients. Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved.

Alexandros Sfakianakis
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A rounded opacity silhouetting the left heart border and hilum

Pericardial incidentaloma: benign pericardial cyst

από Lin, A. N., Lin, S., Lin, K., Raju, F. στο BMJ Case Reports Last 6 Issues

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Description

A 73-year-old woman with hypertension and atrial fibrillation presented with head and neck injury after mechanical fall. During workup, chest X-ray anteroposterior view (figure 1) revealed a rounded opacity silhouetting the left heart border and hilum. Subsequent contrast-enhanced CT of the chest showed single, 6.4 cm, rounded, well-defined, thin-walled, non-enhanced, low attenuated (–20 and 20 Hounsfield Unit) and homogenous cyst-like structure at the left mediastinum connected to pericardial recesses and not attached to adjacent structures (figure 2A–C). Transthoracic echocardiogram ruled out left ventricular aneurysm, aortic aneurysm, solid tumour and outflow tracts obstruction. Although bronchogenic cyst, oesophageal duplication cyst, thymic tumour and mediastinal lymphoma were considered as possible differentials, radiological features such as CT appearance, homogenous attenuation, unrelated to the underlying structures favoured pericardial cyst. Since patient was asymptomatic, patient and family member were unwilling to undergo surgical removal and pathological confirmation. Follow-up with non-enhanced CT of...

Alexandros Sfakianakis
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Transient hemiparaesthesias and dysarthria

Mitral Stenosis

από Oehler, A. C., Sullivan, P. D., Mansoor, A. M. στο BMJ Case Reports Last 6 Issues

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Description

A previously healthy 29-year-old Mexican woman presented to an emergency department with transient hemiparaesthesias and dysarthria. There was no evidence of stroke on cross-sectional imaging of the head, and she was discharged without a clear diagnosis. Two days later, she returned with acute abdominal pain. Abdominal imaging revealed complete occlusion of the right renal artery, prompting emergency embolectomy. Following the procedure, she developed acute haemoptysis, dyspnoea and hypoxaemia. Chest imaging demonstrated evidence of pulmonary venous hypertension. Cardiac auscultation revealed an opening snap followed by a diastolic murmur with presystolic accentuation. These sounds were better appreciated in combination with phonocardiography, a technique supplanted by echocardiography in the 1970s1 that visualised heart sounds (video 1). An echocardiogram confirmed the presence of mitral stenosis (MS), unifying the syndrome of embolic phenomena, haemoptysis and pulmonary hypertension. She underwent successful mitral valve replacement and has since returned to normal...

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

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Management of Massive Hemoptysis with Oren Friedman

http://sfaki.blogspot.com/2017/05/management-of-massive-hemoptysis-with.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

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Mismatch repair cancer syndrome (MMRCS) : Multiple hyperpigmented and hypopigmented skin areas, brain malformations, pilomatricomas, a second childhood malignancy, a Lynch syndrome (LS)-associated tumour in a relative and parental consanguinity.

http://sfaki.blogspot.com/2017/05/mismatch-repair-cancer-syndrome-mmrcs.html

Haematologica. 2010 May; 95(5): 699–701.

doi:  10.3324/haematol.2009.021626

PMCID: PMC2864372

Constitutional mismatch repair-deficiency syndrome

Katharina Wimmer1 and Christian P. Kratz2

1 Division of Human Genetics, Medical University Innsbruck, Innsbruck, Austria

2 Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20852, USA. E-mail: ta.ca.dem-i@remmiw.anirahtak

Katharina Wimmer, PhD, is Associate Professor at the Department for Medical Genetics, Molecular and Clinical Pharmacology, Medical University Innsbruck. She is supervising the onco-genetic laboratory for the diagnostics of cancer predisposition syndromes which are also her main research interest. Christian P. Kratz, M.D. is an investigator in the Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics at the National Cancer Institute, National Institutes of Health. His research focuses on individuals with inherited cancer predispositions.

Author information ▼ Copyright and License information ►

See "Constitutional mismatch repair deficiency and childhood leukemia/lymphoma – report on a novel biallelic MSH6 mutation" on page 841.

This article has been cited by other articles in PMC.

The mismatch repair (MMR) machinery contributes to genome integrity and the MLH1, MSH2, MSH6 and PMS2 genes play a crucial role in this process. MMR corrects single base-pair mismatches and small insertion-deletion loops that arise during replication. Moreover, the MMR system is involved in the cellular response to a variety of agents that damage DNA1 and in immunoglobulin class switch recombination.2 Heterozygous germline mutations in MLH1, MSH2, MSH6 and PMS2 cause Lynch syndrome (LS), an autosomal dominant cancer syndrome associated with hereditary non-polyposis colorectal cancer (HNPCC), endometrium carcinoma and other malignancies, occurring on average in the fourth and fifth decade of life. Notably, LS associated tumors display somatic loss of the remaining wild type MLH1, MSH2, MSH6 or PMS2 allele and evidence of microsatellite instability (for review see 3).

In contrast to individuals with LS who harbor a heterozygous mutant MMR gene allele, rare cases with biallelic deleterious germline mutations in MMR genes leading to constitutional mismatch repair-deficiency (CMMR-D) have been recognized since 1999.4,5 This cancer syndrome is characterized by a broad spectrum of early-onset malignancies and a phenotype that resembles neurofibromatosis type 1. In this issue of Haematologica, Ripperger and colleagues report on a patient with CMMR-D caused by a novel MSH6 mutation leading to a T-cell lymphoma and colonic adenocarcinoma at six and 13 years of age, respectively. In addition, they review 26 leukemia and/or lymphoma cases reported previously.6

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The clinical presentation and tumor spectrum of CMMR-D

Our knowledge of the CMMR-D syndrome originates primarily from the medical literature; consequently, potential publication bias must be kept in mind as we interpret these reports. Table 1 summarizes the malignancies observed in 89 reported6–11 and 3 unreported cases of CMMR-D. Neoplasms can be divided into four groups: (1) hematologic malignancies (reviewed in 6); (2) brain tumors; (3) LS-associated tumors; and (4) other malignancies. Notably, 31 out of the known 92 CMMR-D patients developed more than one malignancy, and in 19 cases the second or third neoplasm was an LS-associated tumor.

Table 1.

List of malignancies in 92 CMMR-D patients.

In some cases of CMMR-D, areas of skin hypo-pigmentation have been reported.12–15 However, signs reminiscent of neurofibromatosis type 1 (NF1), in particular café-aulait macules (CALMs), are much more common and were observed in the majority of the reported cases (63/92). There are only 2 patients explicitly reported to lack CALMs or other signs of NF1.9,13 Interestingly, several reports stress that CALMs in patients with CMMR-D differ from typical NF1-associated CALMs in that they vary in their degree of pigmentation, have irregular borders, and may display a segmental distribution. Other features of NF1 found in CMMR-D patients include skinfold freckling, Lisch nodules, neurofibromas and tibial pseudarthrosis. Hence, it is not surprising that a number of CMMR-D cases were initially diagnosed as having NF1. It has been speculated that the NF1-like clinical features in CMMR-D result from germline mosaicism arising early during embryonic development. The identification of a truncating NF1 mutation in the blood of one patient16 and data supporting the notion that the NF1 gene is a mutational target of MMR deficiency17 are in line with this assumption. However, extensive mutation analysis in other CMMR-D patients has not confirmed this theory (see 8,12,18 and papers cited therein).

Péron et al.2 have shown in 3 CMMR-D patients that constitutional PMS2 deficiency leads to impaired immunoglobulin class switch recombination characterized by increased serum IgM concomitant with decrease or absence of IgG2, IgG4, and IgA. Of note, one CMMR-D patient initially presented with a primary immunodeficiency,2 and patients with biallelic MSH2 and MSH6 mutations also show IgG2 and/or IgA deficiency 15,19,20. It remains to be seen whether defective IgA and IgG production is a common feature of CMMR-D. Fortunately, severe bacterial infections have not been reported to occur at high frequencies in persons with CMMR-D.

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Genotype-phenotype correlation of CMMR-D

A review of the literature suggests that the clinical features in patients with biallelic germline mutations of MLH1 or MSH2 differ from those with biallelic germline mutations of MSH6 or PMS2 (Table 2). Hematologic malignancies appear to occur more frequently in patients with MLH1 or MSH2 mutations than in patients with mutations of MSH6 or PMS2. In contrast, the latter group appears to have a higher prevalence of brain tumors. Furthermore, tumors tend to develop earlier in MLH1 or MSH2 mutation carriers than in patients with a mutation of MSH6 or PMS2. Patients with biallelic mutations in MSH6 or PMS2 are more likely to survive their first tumors and develop a second malignancy. Overall, the prevalence of LS-associated tumors is higher in patients with biallelic MSH6 or PMS2 mutations than in biallelic MLH1 or MSH2 mutation-positive individuals (Table 2). These factors facilitate the clinical diagnosis of CMMR-D in patients with mutations of MSH6 or PMS2 and may at least partly explain the preponderance of PMS2 mutations in published cases.

Table 2.

Differences in the overall tumor spectrum and age of malignancy onset between carriers of biallelic MLH1/MSH2 and MSH6/PMS2 mutations, respectively.

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Strategies for clinical and subsequent molecular diagnosis of CMMR-D

In view of the wide tumor spectrum that overlaps with Lynch and Turcot syndrome but also includes hematologic malignancies and embryonic tumors such as neuroblastoma, Wilms tumor and rhabdomyosarcoma (Table 1), CMMR-D should be considered in the differential diagnosis in all patients with malignancies (except clearly NF1-associated tumors) who show one or more of the following features: (1) CALMs and/or other signs of NF1 and/or hypo-pigmented skin lesions; (2) consanguineous parents; (3) family history of LS-associated tumors; (4) second malignancy; and (5) sibling with childhood cancer. It is important to note that especially in patients with PMS2 mutations, the family history will often not fulfill the Amsterdam or revised Bethesda criteria for LS.

Typically, confirmation of the diagnosis involves the analysis of microsatellite instability (MSI) and/or immunohistochemistry (IHC), followed by mutation analysis. MSI analysis follows current protocols used for LS-screening; however, this analysis may be unreliable in CMMR-D related brain tumors.7,11,21 IHC is a useful technique employed in patients with CMMR-D associated neoplasms including brain tumors and guides subsequent mutation analysis in the four MMR-genes. In general, a truncating mutation in PMS2 or MSH6 will result in isolated loss of these proteins, whereas a mutation in MLH1 or MSH2 will lead to concurrent loss of MLH1/PMS2 or MSH2/MSH6, respectively, since MLH1 and MSH2 are the obligatory partners in the formation of MLH1/PMS2 and MSH2/MSH6 heterodimers. Notably, in the case of an underlying missense mutation, IHC may show normal results. As CMMR-D patients constitutively lack the expression of one of the MMR genes, IHC detects loss in both neoplastic and non-neoplastic tissues. Conveniently, expression loss of one of the MMR genes can be demonstrated in blood lymphocytes (e.g. by Western blot 2). Similarly, it has been shown that MSI can be determined in normal non-neoplastic tissue of CMMR-D patients by analyzing DNA samples that are diluted to approximately 0–3 genome equivalents per PCR-reaction.22 Nonetheless, standardized procedures for the detection of MMR expression loss and MSI in non-neoplastic tissue from CMMR-D patients have not been developed to date. The diagnosis of CMMR-D should be confirmed by gene-specific mutation analysis. Reliable methods for all four MMR genes including PMS2 are now available.12 Mutation analysis will facilitate identification and surveillance of heterozygous and homozygous individuals in the wider family, and allow for informed decision-making about prenatal or pre-implantation genetic diagnosis.

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Treatment and surveillance of the patient and counseling of relatives

Genetic counseling should be offered to the parents prior to testing of the affected child, and should include information on the potential 25% recurrence risk and on the clinical consequences of a possible heterozygous mutation in both parents. Predictive testing following the established interdisciplinary counseling guidelines should be offered to all family members once a mutation has been identified. Heterozygous family members should be followed according to current LS-guidelines.23

Because of the wide spectrum of malignancies in CMMR-D patients, defining recommendations for surveillance of affected patients remains a challenge. Early diagnosis of CMMR-D and subsequent cancer screening at regular intervals may increase the likelihood of detecting associated cancers, such as colon cancer or brain tumors, at an operable stage. In theory, this screening could include regular exams such as: (1) clinical evaluation; (2) blood tests with full blood count and carcinoembryonic antigen (CEA); (3) magnetic resonance imaging of the brain; (4) endoscopic examination of the gastrointestinal tract; and (5) endometrial sampling and transvaginal ultrasound for endometrial and ovarian cancer. However, these recommendations rest only on clinical judgment and do not represent a standard of care. To date there is no available evidence to support any of these recommendations or to provide guidance on the optimal frequency of such tests. Likewise, there is currently no information available regarding the optimal treatment of CMMR-D patients. Several reports stress that careful attention should be given to the possibly increased cyto-toxicity and reduced efficacy of chemotherapeutic agents due to constitutionally impaired mutation repair, and the high risk of a second malignancy 6,8,14,15.

Reports such as the article by Ripperger and colleagues are valuable in increasing awareness and knowledge of the syndrome in the clinical community. Nevertheless, systematic studies are needed in order to better define the phenotype of MMR-D. Data related to cancer screening, treatment and outcome should be collected and evaluated systematically to provide a basis for recommendations on how to manage patients with CMMR-D.

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Footnotes

( Related Original Article on page 841)

We thank Drs. Anne Durandy and Johannes Zschocke for their helpful comments on the manuscript. Dr. Kratz's work was supported by the Intramural Research Program of the US National Cancer Institute.

No potential conflict of interest relevant to this article was reported.

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References

1. Jiricny J. The multifaceted mismatch-repair system. Nat Rev Mol Cell Biol. 2006;7(5):335–46. [PubMed]

2. Peron S, Metin A, Gardes P, Alyanakian MA, Sheridan E, Kratz CP, et al. Human PMS2 deficiency is associated with impaired immunoglobulin class switch recombination. J Exp Med. 2008;205(11):2465–72. [PMC free article] [PubMed]

3. Peltomaki P. Role of DNA mismatch repair defects in the pathogenesis of human cancer. J Clin Oncol. 2003;21(6):1174–9. [PubMed]

4. Ricciardone MD, Ozcelik T, Cevher B, Ozdag H, Tuncer M, Gurgey A, et al. Human MLH1 deficiency predisposes to hematological malignancy and neurofibromatosis type 1. Cancer Res. 1999;59(2):290–3. [PubMed]

5. Wang Q, Lasset C, Desseigne F, Frappaz D, Bergeron C, Navarro C, et al. Neurofibromatosis and early onset of cancers in hMLH1-deficient children. Cancer Res. 1999;59(2):294–7. [PubMed]

6. Ripperger T, Beger C, Rahner N, Sykora KW, Bockmeyer CL, Lehmann U, et al. Constitutional mismatch repair deficiency and childhood leukemia/lymphoma - report on a novel biallelic MSH6 mutation. Haematologica. 2009 Dec 16; [Epub ahead of print] [PMC free article] [PubMed]

7. Giunti L, Cetica V, Ricci U, Giglio S, Sardi I, Paglierani M, et al. Type A microsatellite instability in pediatric gliomas as an indicator of Turcot syndrome. Eur J Hum Genet. 2009;17(7):919–27. [PMC free article] [PubMed]

8. Peters A, Born H, Ettinger R, Levonian P, Jedele KB. Compound heterozygosity for MSH6 mutations in a pediatric lymphoma patient. J Pediatr Hematol Oncol. 2009;31(2):113–5. [PubMed]

9. Sjursen W, Bjornevoll I, Engebretsen LF, Fjelland K, Halvorsen T, Myrvold HE. A homozygote splice site PMS2 mutation as cause of Turcot syndrome gives rise to two different abnormal transcripts. Fam Cancer. 2009;8(3):179–86. [PubMed]

10. Toledano H, Goldberg Y, Kedar-Barnes I, Baris H, Porat RM, Shochat C, et al. Homozygosity of MSH2 c.1906G-->C germline mutation is associated with childhood colon cancer, astrocytoma and signs of Neurofibromatosis type I. Fam Cancer. 2009;8(3):187–94. [PubMed]

11. Wimmer K, Etzler J. Constitutional mismatch repair-deficiency syndrome: have we so far seen only the tip of an iceberg? Hum Genet. 2008;124(2):105–22. [PubMed]

12. Etzler J, Peyrl A, Zatkova A, Schildhaus HU, Ficek A, Merkelbach-Bruse S, et al. RNA-based mutation analysis identifies an unusual MSH6 splicing defect and circumvents PMS2 pseudogene interference. Human Mut. 2008;29(2):299–305. [PubMed]

13. Rahner N, Hoefler G, Hogenauer C, Lackner C, Steinke V, Sengteller M, et al. Compound heterozygosity for two MSH6 mutations in a patient with early onset colorectal cancer, vitiligo and systemic lupus erythematosus. Am J Med Genet A. 2008;146A(10):1314–9. [PubMed]

14. Scott RH, Homfray T, Huxter NL, Mitton SG, Nash R, Potter MN, et al. Familial T-cell non-Hodgkin lymphoma caused by biallelic MSH2 mutations. J Med Genet. 2007;44(7):e83. [PMC free article] [PubMed]

15. Scott RH, Mansour S, Pritchard-Jones K, Kumar D, MacSweeney F, Rahman N. Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations. Nat Clin Pract Oncol. 2007;4(2):130–4. [PubMed]

16. Alotaibi H, Ricciardone MD, Ozturk M. Homozygosity at variant MLH1 can lead to secondary mutation in NF1, neurofibromatosis type I and early onset leukemia. Mutat Res. 2008;637(1–2):209–14. [PubMed]

17. Wang Q, Montmain G, Ruano E, Upadhyaya M, Dudley S, Liskay RM, et al. Neurofibromatosis type 1 gene as a mutational target in a mismatch repair-deficient cell type. Hum Genet. 2003;112(2):117–23. [PubMed]

18. Auclair J, Leroux D, Desseigne F, Lasset C, Saurin JC, Joly MO, et al. Novel biallelic mutations in MSH6 and PMS2 genes: gene conversion as a likely cause of PMS2 gene inactivation. Hum Mutat. 2007;28(11):1084–90. [PubMed]

19. Ostergaard JR, Sunde L, Okkels H. Neurofibromatosis von Recklinghausen type I phenotype and early onset of cancers in siblings compound heterozygous for mutations in MSH6. Am J Med Genet A. 2005;139:96–105. discussion 96. [PubMed]

20. Whiteside D, McLeod R, Graham G, Steckley JL, Booth K, Somerville MJ, et al. A homozygous germ-line mutation in the human MSH2 gene predisposes to hematological malignancy and multiple cafe-aulait spots. Cancer Res. 2002;62(2):359–62. [PubMed]

21. Bougeard G, Charbonnier F, Moerman A, Martin C, Ruchoux MM, Drouot N, et al. Early onset brain tumor and lymphoma in MSH2-deficient children. Am J Hum Genet. 2003;72(1):213–6. [PMC free article] [PubMed]

22. Felton KE, Gilchrist DM, Andrew SE. Constitutive deficiency in DNA mismatch repair. Clin Genet. 2007;71(6):483–98. [PubMed]

23. Vasen HF, Moslein G, Alonso A, Bernstein I, Bertario L, Blanco I, et al. Guidelines for the clinical management of Lynch syndrome (hereditary non-polyposis cancer) J Med Genet. 2007;44(6):353–62. [PMC free article] [PubMed]

Articles from Haematologica are provided here courtesy of Ferrata Storti Foundation

Alexandros Sfakianakis
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2841026182

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Current FDA-approved injection pattern versus targeted peripheral nerve–directed injection pattern. The current FDA-approved injection pattern includes chemodenervation of 7 head and neck muscle groups (A–C). The total units of BOTOX injected for each site bilaterally include: corrugators 10U, procerus 5U, frontalis 20U (A), temporalis 40U (B), occipitalis 30U, cervical paraspinal 20U, and trapezius 30U (C). By comparison, peripheral nerve–directed BOTOX injection targets fewer sites with a smaller total quantity of BOTOX (D–F). The total units of BOTOX injected for each site bilaterally include: supraorbital nerve/supratrochlear nerve 25U (D), zygomaticotemporal nerve 37.5U (E), and greater occipital nerve 50U (F). Source Targeted Peripheral Nerve-directed Onabotulinumtoxin A Injection for Effective Long-term Therapy for Migraine Headache

http://otorhinolaryngology-crete.blogspot.com/2017/05/current-fda-approved-injection-pattern.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Autologous Platelet-rich Plasma Glue : Seroma and hematoma formations are the most common complications after plastic surgery. The aim of this study was to assess the efficacy of autologous platelet-rich plasma (A-PRP) glue to reduce postoperative wound complications and improve surgical outcomes.

http://otorhinolaryngology-crete.blogspot.com/2017/05/autologous-platelet-rich-plasma-glue.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Thanks

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Heavy mite exposure in the environment can induce allergic systemic reactions.

http://alexsfakianakis.blogspot.com/2017/05/mite-hypersensitivity.html

Anaphylaxis

Anaphylaxis is an acute emergency that is potentially fatal and commonly related to an allergic and immunologic trigger requiring immediate effective life-saving treatment [151]. Heavy mite exposure in the environment can induce allergic systemic reactions. More recently, the induction of anaphylaxis through ingestion of mite-contaminated foods has been described [152].

Pancake anaphylaxis, also called oral mite anaphylaxis (OMA), is a relatively new syndrome characterized by severe allergic symptoms occurring immediately after eating foods, especially containing flours, contaminated with mites. These cooked foods contain thermoresistant mite allergens and contaminated wheat flour used to make pancakes is its most common presentation [152]. A variant clinical picture is provoked by physical exercise and is called dust mite ingestion-associated exercise-induced anaphylaxis [153]. OMA is more prevalent in tropical and subtropical areas of the globe where mites grow easily in their warm and humid environments [154]. There are reports in the literature of two fatalities associated with the ingestion of foods contaminated with mites [155, 156]. Mites responsible for OMA include domestic and storage species and can be present in any type of flours. There is an intriguing association of OMA and hypersensitivity to aspirin and nonsteroidal anti-inflammatory drugs (NSAIDS) for which there is no good explanation yet and it is more prevalent in patients with house dust mite allergic rhinitis and/or asthma [157]. The higher the contaminated mite ingestion the greater the risk for anaphylaxis. OMA confirmation requires the microscopic documentation and identification of mites in the suspected flour. Alternatively the immunoassay for demonstration of the presence of mite allergens in the suspected flour can be used. It is imperative to try to prevent the worldwide OMA delineating predisposing genetic factors and determining if mite immunotherapy might be efficacious modifying the clinical course of this important variety of food anaphylaxis [152, 158].

Co-sensitization to cockroaches, some crustaceans (shrimp, crab, lobster), shellfish (clams, mussels), and mollusks (snails) is often described and likely due to the presence of allergens in the tropomyosins family, present in some crustaceans (major allergen of shrimp: Pen 1), insects (some flies, mosquitoes, cockroaches), gastropods and mites (Der f 10) [122].

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

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Prevention of Dust Mite and Dust Mite Allergen Exposure

http://alexsfakianakis.blogspot.com/2017/05/mite-hypersensitivity.html

Justification for Dust Mite Exposure Control

The decision to initiate environmental controls to reduce dust mite exposure can be complex. Total prevention of exposure to mite allergenic material to prevent IgE sensitization to mite allergens in genetically susceptible individuals requires strict, continuous avoidance of mite exposure, which is practically all but impossible [199]. Furthermore, to curtail development of all cross-reacting specific IgE, avoidance of all arthropods would probably be required [200]. The majority of the world's population lives on seacoasts [201] or along rivers [202] and these areas typically have adequate humidity to support growth of dust mites and storage mites during all parts of the year.

Much research has been conducted to determine if it is possible to reduce development of mite-specific IgE-mediated sensitization (primary prevention). Several studies comparing dust mite sensitization rates in children from areas endemically low and areas endemically high in dust mite allergen indicated that the prevalence and degree of sensitization to dust mite was strongly associated with the amount of exposure to mite allergens [203, 204]. A prospective study of mite allergen avoidance in Manchester, UK, [205, 206] using a combination of interventions, decreased Der p 1 from mattresses by 97% to the nanogram range during pregnancy and 12 months after birth in the active group [205]. However, with all possible dust mite exposures at homes of friends and family, on public transportation and in public places and at schools and day care centers, primary prevention of dust mite sensitization by mite allergen avoidance may not be possible [207, 208, 209].

Secondary prevention, or the attempt to reduce the risk of asthma in dust mite sensitized children has also received much attention. The link between asthma and dust mite exposure is one of the most extensively studied relationships between environmental exposure and disease development [210, 211, 212, 213]. In all climates conducive to the growth of dust mites, mite exposure may be one of the factors contributing to the development of asthma [112, 214]. Secondary prevention has also been the goal for many children with allergic rhinitis who are at risk of the subsequent development of asthma. However, to date there is no evidence-based information as to whether mite avoidance may be effective as a secondary preventive measure to prevent/delay asthma development among mite-sensitized individuals, or those with allergic rhinitis.

The relation of dust mite allergen exposure and the worsening of allergic respiratory symptoms is well documented [215]. In one study of 311 subjects both sensitized and exposed to high levels of indoor allergen including dust mite allergen there was significantly lower FEV1% predicted values (mean, 83.7% vs 89.3%; mean difference, 5.6%; 95% CI, 0.6%-10.6%; P = .03), higher eNO values (geometric mean [GM], 12.8 vs 8.7 ppb; GM ratio, 0.7; 95% CI, 0.5-0.8; P = .001), and more severe airways reactivity (PD20 GM, 0.25 vs 0.73 mg; GM ratio, 2.9; 95% CI, 1.6-5.0; P < .001) as compared with subjects not sensitized and exposed [216]. Adults in a 4-year study who were both sensitized and exposed to high levels of dust mite allergens had increased bronchial hyper-responsiveness [217]. Many additional links between dust mite exposure and allergic disease are documented in the recent environmental practice parameter on dust mites [198]. A reduction in the symptoms experienced by those with atopic dermatitis has also been linked to house dust-mite allergen avoidance [218].

Facilitative factors and Allergen Reservoirs

Controlling factors that facilitate the growth and reproduction of dust mites has been an often sought goal in exposure control. The dependence of dust mites on the water content of the air has been extensively documented [219, 220]. Arid climates have an intrinsically low abundance of dust mites, and the most effective method of controlling dust mite exposure is to live in a very dry climate such as the high desert of New Mexico in the US or the Altiplano or Bolivian Plateau, in west-central South America [202]. Since this is not a practical solution, mimicking these conditions in the home environment as much as possible provides an opportunity to control mite population growth.

Humidity control should be the mainstay of any mite control efforts. The most important factor facilitating dust mite growth, reproduction and allergen production is the availability of water in the surrounding environment [220]. Mites absorb moisture directly from their surroundings under conditions of high moisture and lose water when moisture is low. The mite moisture equilibrium therefore is not directly relative humidity dependent. It is instead dependent of the moisture situation of the local microenvironment and the moisture retention ability of the mite's immediate surroundings such as carpet dust reservoirs or bedding. A simple measurement of relative humidity may not assure an environment free of dust mite activity. Microenvironments that exist in bedding, in carpet next to concrete or in pet lounging areas may provide adequate moisture for mite survival in climates not expected to have a mite presence. A mite surrounded by a hygroscopic microenvironment as moist bedding can survive much dryer conditions than would be expected. Of note, exposure to a moisture rich environment for only a short period can provide enough moisture for growth and metabolism [221].

Although directly linked to water content of the air in the calculation of relative humidity, temperature is also a factor in dust mite survival. Conditions at the extreme ends of the temperature spectrum, either to cold or to hot can impact mite survival although elevated temperature conditions tend to be more lethal than freezing. Mites and their eggs survive poorly when exposed to hot water and clothes dryers but survive during short periods of freezing conditions. The exposure to direct sunlight is an often forgotten factor in the destruction of dust mites [222].

It is not enough to address mite factors facilitating mite population growth. Reservoirs of mite allergen must also be eliminated. House dust mites can be found in any area of the home, however they are most often associated with certain indoor environments including the bedroom carpet, mattresses and bedding, frequently occupied upholstered furniture and in pet lounging areas [223, 224]. Recent investigations have questioned the traditional concepts of the location of dust mite reservoirs indicating that significant exposure can occur in public transportation conveyances and associated with work environments as well as clothing [207].

Climate Factors

Although residents of cold and arid climates are less likely to be exposed to house dust mites, the large majority of the world population is exposed to house dust mites. Nearly half of the people in the world live within 200 km of the coast where humidity levels are typically higher. The rate of population growth in coastal areas is accelerating. In China alone over 400 million live in coastal cities. Dust mite exposures and the allergic problems related to those exposures are likely to increase [201].

Although many climates are naturally conducive to mite growth and allergen production, the artificial control of indoor climates is increasing. Even though it is energy intensive, the use of forced air heating and air conditioning is growing around the world and especially in more affluent economies. Dust mite allergen exposure control is therefore a viable option for large numbers of persons. In many areas seasonal heating requirements result in very dry indoor environments and subsequently dust mite exposure is a seasonal phenomenon. Low humidity conditions can also be obtained through use of air conditioning and dehumidification. Yet, in many areas of the world ambient humidity levels are high enough that producing low humidity levels sufficient to preclude dust mite growth is not practically achievable. The recent Cochrane study on dehumidification alone indicates that evidence of clinical benefits of dehumidification using mechanical ventilation with dehumidifiers is scanty [225]. Indeed, the meta-analysis of multiple dust mite control studies would lead the reader to believe that there is nothing that can be physically done to control dust mites and improve health. Yet, this conclusion is disputed by many experts in the field of allergy [226]. Furthermore, the nature of single source exposure control studies may preclude successful clinical improvement because allergen sensitization is typically to multiple agents.

A significant amount of work has been done on removal of mites and mite allergens through cleaning. It goes without saying that efforts to control mite infestations of the skin and remove mite infestations from clothing are essential in the maintenance of overall health [227]. Humans have been living with dust mites for generations and they might even be described as among our "old friends" [228]. But no physician would advocate for wearing mite infested clothing or sleeping in mite infested bedding. Mite sensitization is likely to occur in genetically susceptible individuals, therefore efforts to reduce instances of elevated mite exposure and thus reduce allergic symptoms are only prudent [229].

Since mite allergens are located in known areas of a typical house [229, 230] removing mite allergen reservoirs is a very effective way to reduce mite allergen exposure. Efforts to remove carpets, drapes, upholstered furniture and any other fabric covered objects from the living environment can effectively reduce mite allergen exposure. The extent to which these items are removed will ultimately be a matter of personal preference. Since mite allergens are known to be heavy and not aerodynamically suited for airborne disbursal [34] and high humidity microenvironments are known to exist in bedding it is logical to focus dust mite reduction efforts on bedding. Efforts to enclose mattresses, box springs and pillows in mite-impermeable covers are known to be very effective [231]. However, it is important to mention that the efficacy of allergen avoidance in patients with already established rhinitis or asthma is a matter of debate [232, 233, 234, 235].

Washing bedding in hot water and even with bleach and drying bedding in very hot conditions or even in direct sunlight are known to reduce both the presence of mite allergen and the mites themselves [236, 237]. Washing bedding and clothing removes mite allergens and kills mites. Most of the killing is through drowning, although washing in hotter water kills more mites. The temperature used to wash bedding has become an issue. Elevated temperatures are more energy intensive and hotter water is a scalding hazard. Experts agree that washing is better than not washing and washing with water that is 48° Celsius provides optimum mite killing and home safety [199].

Heat treatment can be effective in killing mites and their eggs. Treatment of cloth at 95° Celsius killed all mites present [238]. However, treatment at 40 °C under dry and wet conditions allowed approximately 80% of all mite eggs to survive. Under dry heat at 50 °C, the thermal death point of dust mite eggs occurred at 5 h and at 60 °C death occurred almost instantaneously [239]. Presumably the eggs survive heat better than the mites themselves. Homes treated with heat-steam over a period of months showed a sustained reduction of Der p 1 and Der p 2 compared to sham treated homes [240] However, mite allergens have been demonstrated to be stable even at elevated temperatures [241].

Although the practice has fallen into senescence in the modern world of appliances, there was a time when frequently placing bedding in direct sunlight for several hours was practiced in many cultures. It has been demonstrated that ultraviolet irradiation is lethal to many organisms including dust mites [242, 243].

Many harsh chemicals are known to kill dust mites or denature mite allergens in industrial and household settings. Agents like tannic acid, Benzyl benzoate, Disodium octaborate tetrahydrate, tri-n-butyl tin maleate, pirimiphos methyl and even "essential oils" like methyl eugenol have been described in the literature to effectively kill mites [244, 245, 246, 247, 248]. However, they are all dangerous at some concentration and cannot be recommended for use by patients or homeowners [199].

It has been suggested that freezing can be effective in killing dust mites and the recommendation to place small cloth items like stuffed animals in the freezer compartment of house hold refrigerators has been frequently given out by allergists. However, there is little evidence that this is effective. There may be some mite death due to desiccation in the dry environment of a household freezer. But, dust mite eggs have been shown to resist freezing at temperatures above −70° Celsius [222]. And, freezing is not effective in removing dust mite allergen from reservoirs because dust mite allergen is stable at low temperatures for extended periods of time [239].

Air conditioning would have a twofold impact on dust mite populations. The cool temperatures will slow mite metabolism and reproduction and reduce moisture need for mite survival. Microenvironments or increased humidity can be reduced using a dehumidifier and/or air conditioning. The absence of air conditioning has been shown to be a factor contributing to increased mite allergen levels in US homes [249]. Air conditioners must be operated for a long time to remove sufficient moisture from the air to effectively decrease room humidity. Mechanical ventilation heat pump recovery units in the UK failed to achieve the desired mite reduction results [250].

Evidence on clinical benefits of dehumidification using mechanical ventilation with dehumidifiers remains scanty [225]. Although dehumidification and air conditioning doubtlessly reduce overall dust mite exposure [251], the difficulty in using dehumidification alone in damp environments to decrease dust mite antigen exposure has been described in a recent Cochrane review [225].

Summary of current recommendations

Most publications on allergy and dust mite control would agree that a comprehensive program of personal hygiene, bed hygiene, properly fitted allergen-impermeable covers, cleaning, dehumidification or air conditioning and appropriate food storage in very damp climates can reduce exposure to house dust mite allergens. It is a stretch further to conclude that the above steps can improve symptoms in those already allergic to dust mites. However, depending on the sensitivity and life style of the allergic person, prudent efforts over an extended period of time are likely to result in gradual improvement in health. The fact that current studies do not provide sufficient evidence for critical reviews to conclude there is unequivocal benefit is no reason to abandon logical and prudent efforts to reduce mite exposure.

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Mite Allergy Research The authors view the following as currently unmet needs in mite allergy research: Since mites constitute the most important allergen source worldwide the information contained in this document needs to be disseminated to all ranks of the medical establishment for educational purposes and to stimulate research Increased knowledge on the cellular basis of the immune responses to mites A better understanding of the link between mite sensitization and allergic diseases Better insights into the genetic influences controlling IgE responses to mite allergens. Effects of epigenetic factors Improved mite allergen standardization Development of purified mite allergens with defined clinically relevant epitopes for molecular diagnosis and evaluation of the response to immunotherapy Development of objective methods to assess allergen exposure and environmental control outcomes Better strategies for immunotherapy and immunoprophylaxis of mite allergy: recombinant allergens, h

http://alexsfakianakis.blogspot.com/2017/05/mite-hypersensitivity.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Rick factors for medical and allergic events during air travel An increase of passenger’s age Flight stress and anxiety, including increased security procedures Disruption of routine Changes in the cabin environment (temperature, humidity, air pressure) Decreased seat space Flight delays Alcohol/drug intake Longer flights Altered circadian rhythm Jet lag Pre-existing medical conditions

http://alexsfakianakis.blogspot.com/2017/05/in-flight-allergic-emergencies.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

In-flight treatment of allergic emergencies and asthma Treating medical emergencies during flight is a major challenge and air travel is an important concern for subjects with asthma and a history of a SAR. The resources to treat allergic emergencies are somewhat limited. In the United States, the Federal Aviation Administration requires the inclusion of epinephrine in medical kits carried on board [18]. These emergency medical kits typically contain the following medications [19]: Aqueous epinephrine (adrenaline) 1:10000 and 1:1000 dilution. Albuterol (salbutamol) for nebulization. Bronchodilator aerosol inhaler. Cortisol (hydrocortisone). Antihistamines tablets and injectable (commonly diphenhydramine). A recommendation from this World Allergy Organization (WAO) expert group for in-flight treatment of a SAR and AE is: a) For AE, inhaled bronchodilator and oxygen. Consider an oral, intramuscular or intravenous corticosteroid for moderate to severe symptoms and intramuscular epinephr

http://alexsfakianakis.blogspot.com/2017/05/in-flight-allergic-emergencies.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Measures that reduce the risk of an in-flight reaction to peanut and tree nuts 1. Passengers requesting any kind of special accommodation (e.g., peanut/tree nut snacks not be distributed, announcement to not eat items with peanut/tree nut, request special peanut/tree nut-free meal, buffer zone, pre-board, request to sit in a certain seat/zone). 2. Peanut/tree nut-free meals. 3. Wiping of tray tables 4. Avoidance of airline pillows or blankets 5. Buffer zones around which peanut or nut products cannot be consumed 6. Request other passengers not to consume peanut/tree nut-containing products 7. Announcement that passengers do not eat peanut/tree nut containing goods 8. Not consuming airline-provided food

http://alexsfakianakis.blogspot.com/2017/05/in-flight-allergic-emergencies.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Recommendations to prevent and manage in-flight allergic events • Promote the prevention of allergic diseases via passenger education • Medical consultation for high-risk passengers before traveling • Train and re-train aircrews • Promote general preventive measures during the flight: hydration, food allergen avoidance (especially peanuts, tree nuts, other foods, as necessary) • Provide an appropriate place for furry pets away from subjects with pet allergy • Provide for sufficient quantities of appropriate medications: epinephrine (adrenaline), β2 agonists for inhalation and nebulization, oral and injectable corticosteroids and antihistamines • Oxygen

http://alexsfakianakis.blogspot.com/2017/05/in-flight-allergic-emergencies.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

I strongly recommend that all practicing physicians consider such a list, and review it occasionally. I wish for the judgement to know what is best for my patients and to weigh the merits of interventions; surgically, medically, and radiotherapeutically. I wish that I can master the complexities of the practice of medicine and be worthwhile as a physician. I wish for the honesty and integrity to objectively assess my competencies and fallibilities. I wish for the intellectual drive to maintain currency of knowledge. I wish for the wisdom to assess and maintain appropriate costs for medical care. I wish for the integrity to avoid marketing my skills and accomplishments unrealistically and erroneously. I wish for the compassion that allows me to separate my personal problems from the needs of the patients that I serve. I wish for the courage to challenge the wisdom of those that create policies and regulations that fail to consider the full dimension and scope of medical care. Please p

Brazilian Journal of Otorhinolaryngology

Print version ISSN 1808-8694

On-line version ISSN 1808-8686

Braz. j. otorhinolaryngol. vol.83 no.2 São Paulo 

http://dx.doi.org/10.1016/j.bjorl.2017.01.001 

EDITORIAL

Ethics in the twenty first century otolaryngology☆

Charles W. Cummings1 

1Johns Hopkins University, Baltimore, USA. E-mail: ccumming@jhmi.edu

In the United States, the climate of the practice of Medicine is in transition and under siege by policy revisionists and governmental/political opportunists. Regulatory and legislative hubris has enshrouded the medical arena through formulaic dictums and onerous regulations oft times constructed by individuals who have no clinical experience or knowledge. The art of Medicine is being dismantled by emphasis on outcomes based solely on statistical evidence, with no concern for the human variables. Objective analysis is not inherently bad provided the personal and social factors are properly emphasized in the analysis. Freedom to make clinical decisions MUST be preserved for optimal care.

This phenomenon exerts undue pressure on the clinician leading to professional frustration and anemia of job satisfaction. Also, the environment which enables the best of care is further challenged and compromised.

Never the less, we, as physicians, must continue to acknowledge our calling and respond to the gifts of our profession. It seems appropriate to review the commitments that we have made to ourselves and our patients. Over the years, I have created a wish list concerning the way I want to conduct myself to satisfy my professional goals. What follows are those wishes. I strongly recommend that all practicing physicians consider such a list, and review it occasionally.

I wish for the judgement to know what is best for my patients and to weigh the merits of interventions; surgically, medically, and radiotherapeutically.

I wish that I can master the complexities of the practice of medicine and be worthwhile as a physician.

I wish for the honesty and integrity to objectively assess my competencies and fallibilities.

I wish for the intellectual drive to maintain currency of knowledge.

I wish for the wisdom to assess and maintain appropriate costs for medical care.

I wish for the integrity to avoid marketing my skills and accomplishments unrealistically and erroneously.

I wish for the compassion that allows me to separate my personal problems from the needs of the patients that I serve.

I wish for the courage to challenge the wisdom of those that create policies and regulations that fail to consider the full dimension and scope of medical care.

Please preserve the art of Medicine. We must steward our wonderful calling.

☆Please cite this article as: Cummings CW. Ethics in the twenty first century otolaryngology. Braz J Otorhinolaryngol. 2017;83:119.2

Conflicts of interest

The author declares no conflicts of interest.

© 2017 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier Editora Ltda.

 This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

 

Sede da Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico Facial

Av. Indianópolia, 1287

04063-002 São Paulo/SP Brasil

Tel.: (0xx11) 5053-7500

Fax: (0xx11) 5053-7512

revista@aborlccf.org.br

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Dietary Guidelines for Vitamin D : A vitamin D intake requirement of 14 µg/day would maintain 97.5% of 25(OH)D >50 nmol/L.

http://alexandrossfa.blogspot.com/2017/05/dietary-guidelines-for-vitamin-d.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Endocrine Emergencies : 1. THYROID STORM, 2. MYXEDEMA COMA, 3. DIABETIC KETOACIDOSIS, 4. ACUTE ADRENAL CRISIS

http://alexandrossfa.blogspot.com/2017/05/endocrine-emergencies-1-thyroid-storm-2.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Hypersensitivity pneumonitis (HP) : Dyspnea and cough

http://alexandrossfa.blogspot.com/2017/05/hypersensitivity-pneumonitis-hp-dyspnea.html

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com

Nasal ala reconstruction: Tunnelled island pedicle melolabial flap; jigsaw puzzle advancement flap; spiral flap; dog-ear island pedicle flap and banner melolabial transposition flap.

http://sfaki.blogspot.gr/2017/04/nasal-ala-reconstruction-surgical.html

Skin tumours of the nasal ala are common and surgery is the treatment
of choice. Nasal ala reconstruction is challenging due to the reduced
mobility and unique features of its thick and sebaceous skin. The
natural arc of the ala and its boundary with the cheek are difficult
features to reproduce. One should bear in mind the functional and
cosmetic risks of nasal ala reconstruction. A distorted nasal contour
may impair the nasal valve; the alar rim may notch or elevate; facial
symmetry may be disrupted by blunting of the alar crease, trapdooring,
bridging of the nasofacial sulcus and poor colour and texture match.

Our aim is to review and compare the functional and cosmetic results
of different local flaps used to correct intermediate-thickness
defects on the nasal ala after surgical excision of cutaneous tumours.
We present representative patients who were treated at our
Dermatological Surgery Unit from June 2015 to September 2016.

The choice of the flap was adapted to the patients' physiognomy and
the defects' size: tunnelled island pedicle melolabial flap [Figure
1]; jigsaw puzzle advancement flap [Figure 2]; spiral flap [Figure 3];
dog-ear island pedicle flap [Figure 4] and banner melolabial
transposition flap [Figure 5]. Surgery was performed under
loco-regional anaesthesia, in an outpatient basis, followed by
prophylactic antibiotic therapy. There were neither immediate
complications nor subsequent flap necrosis. The tumours were
completely excised.
Figure 1: Female, 86-year-old, nodular ulcerated basal cell carcinoma
in the nasal ala: tunnelled island pedicle melolabial flap. (a)
Surgical plan, (b) primary defect, (c) secondary defect after
tunnelling of the flap, (d) immediate post-operative, (e and f) result
after healing (10 months after surgery).

Click here to view
Figure 2: Male, 76-year-old, nodular basal cell carcinoma on the nasal
ala: jigsaw puzzle advancement flap. (a) surgical plan, (b) primary
and secondary defects, (c) anchoring sutures secure the flap in place;
(d) immediate post-operative, (e) result after healing (3 months after
surgery).

Click here to view
Figure 3: Female, 76-year-old, nodular basal cell carcinoma on the
nasal ala: spiral flap, a combination of advancement and rotation. (a)
Surgical plan, (b) immediate post-operative, (c) result after healing
(2 months after surgery).

Click here to view
Figure 4: Female, 76-year-old, basal cell carcinoma on the nasal ala:
dog-ear island flap, combining two flaps: cheek advancement and
rotated island pedicle. (a) Surgical plan, (b) primary defect, (c)
immediate post-operative, (d) day 7 post-operative, (e) result after
healing (1 month after surgery).

Click here to view
Figure 5: Male, 83-year-old, two nodular basal cell carcinomas on the
nasal ala and dorsum: Banner's melolabial transposition flap. (a)
Surgical plan, (b) primary defect, (c) immediate post-operative, (d)
result after healing (7 months after surgery)

Click here to view


Facial symmetry was well preserved by the spiral and jigsaw puzzle
flaps [Figure 2] and [Figure 3]. The nasal sulcus was left intact by
the spiral flap as well as the tunnelled melolabial island flap
[Figure 1] and [Figure 3]. The melolabial flaps and the dog-ear island
flap allowed for the correction of larger defects on the nasal ala
[Figure 1], [Figure 4] and [Figure 5]. The dog-ear island flap [Figure
4] obtained a good result despite the large size of the primary
defect. Banner's melolabial transposition flap [Figure 5] was used to
correct a complex defect involving not only the nasal ala but also the
nasal dorsum and resulted in facial asymmetry due to trapdooring.

The small size of the defects that can be addressed by the spiral and
puzzle flaps may explain their superior cosmetic results.[1],[2] The
tunnelled melolabial island flap, although technically demanding, may
produce excellent results; compared to the cheek-to-nose interpolation
flap, the tunnelling technique offers the advantage of being one-stage
procedure. The dog-ear island flap is an adaptation of the cheek
advancement flap; despite its apparent complexity, it offers a viable
alternative to the melolabial flaps,[3] with a lower risk of trapdoor
effect and with proper preservation of the alar contour. The discussed
flaps are useful alternatives to the bilobed transposition flap and
the skin graft for the surgical reconstruction of the nasal ala.

When planning the surgery, it is important to assess the primary
defect on the nasal ala: size and location (medial or lateral), depth,
involvement of other cosmetic units/subunits and extension to the alar
rim, nasal tip or adjacent cheek. Several techniques have been
developed that are useful for the reconstruction of defects of the
nasal ala. Based on our experience and a review of the literature, we
present an algorithm [Table 1] to optimise the choices in the
reconstruction of intermediate-thickness defects in nasal ala. In
[Table 2], we review the main advantages and caveats of some of the
most useful surgical techniques for nasal ala
reconstruction.[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14]
Table 1: Nasal ala reconstruction: What is the optimal approach
according to the defects' size and location?

Click here to view
Table 2: Nasal ala reconstruction: major advantages and potential
caveats of different surgical techniques

Click here to view


In the nasal ala, given the paucity of surrounding skin and the
importance of minimising nasal ala distortion, flaps that recruit skin
from a distant site should be considered. Mastering different
techniques is essential for a surgeon to optimise treatment for each
patient. At the end of the day, the best choice depends on many
factors and should be adapted on a case-by-case basis and to the
surgeon's expertise.

--
Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182
6948891480
alsfakia@gmail.com

Half knowledge is worse than ignorance....... Imperfect understanding is often more dangerous than ignorance

Alexandros Sfakianakis
Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182

6948891480

alsfakia@gmail.com