DERGİ - g20 istanbul 2015

Yorumlar

Transkript

DERGİ - g20 istanbul 2015
Uzm.-Op. Umur Kayabaşı - Nörooftalmoloji
Toplam
A-Puanı
B-Puanı
464,1
294,22
169,88
A - DERGİ
28,5
28,5
0B
A
A- DERGİ
Puan
Puan
Puan
SCI ve SCIExp
dışındaki
2 / 1.
indekslerde
Yazar
yer alan
yurt dışı
dergiler
Kaynakça: Kayabasi AU, Sergott RC. OCT and FAF in the Early Diagnosis of Alzheimer's Disease.
Neurobiology of Aging 2013; 35(4):786-90.
Özet: OCT and FAF in the Early Diagnosis of Alzheimer's Disease A. Umur Kayabasi1, Robert C.
Sergott2, 1Istanbul University, Istanbul, Turkey; 2Thomas Jefferson University, Department of NeuroOphthalmology, Philadelphia, Pensylvania, USA. Objectives. Optical coherence tomography (OCT)
macula- retina exam and fundus autoflorescence (FAF) test give us extremely important clues about
neurodegenerative diseases. Since the retina and optic nerve share similar tissues with the brain, any
defect detected by OCT and FAF may also be related to a disease of the nervous system. It has been
proposed that beta-amyloid, which causes Alzheimer´ s disease (AD) in the brain, may be observed in
different tissues of the eye (lens, retina etc.) many years earlier. Methods. We examined 14 patients
with a family history of AD and all of whom (except 1 patient with no cognitive defect) had only minor
cognitive dysfunction. Results. FAF exam of the retina revealed suspected regions and OCT exam
through these retinal lesions revealed plaque deposition in the ganglion layer of the retina. Many
plaque deposits colocalized with drusen due to age related macular degeneration. Conclusions. We
believe that these deposits can be signs of AD and contain beta-amyloid. They are located in the inner
parts of the retina, mostly the ganglion layer and are different from the localization of drusen alone. It
is our thought that comprehensive retinal exam should be a part of the neurological exam in AD and
similar neurodegenerative diseases . The detection of plaques in the retina may help us with early
diagnosis of AD.
30
30 A 0 B
A- DERGİ
Puan Puan Puan
SCI ve SCIExp
dışındaki
1 / 1.
indekslerde
Yazar
yer alan
yurt dışı
dergiler
Kaynakça: Kayabasi AU. Different optic neuropathies and novel treatments.Journal of Clinical &
Experimental Ophthalmology.Open Access; Published September 23, 2013
Özet: Abstract: The aim of this workshop is to discuss the diagnosis, treatment and follow- up of
different optic neuropathies. Meanwhile, images from the new technology devices like OCT and the
conventional machines like Perimetry will be shown. Also, MR images of the orbit and brain and
images of optic nerve problems will be the subjects of the main topic. There are some new
developments in the treatment of the optic neuropathies and different ideas about novel treatments
will be shared. OPTİC NEUROPATHİES: - Optic neuritis (demyelination of the optic nerve): Acute,
painful vision loss. Occurs mainly in women within the age range of 18-45. Responds well to high dose
intravenous steroids. Approximately 1/3 of the cases are seen with disc edema, 2/3 are retrobulber.
Retrobulber cases progress to multiple sclerosis (MS) more frequently. The possibility of a woman
patient to develop MS after isolated optic neuritis is about 70% in ten years. The progression of optic
neuritis to MS can be detected by OCT. - Anterior ischemic optic neuropathy (non-arteritic): Acute,
painless visual loss due to a stroke on the optic nerve head. Disc edema is present. Patients usually
have hypertension or diabetes. Visual field defect is altitudinal. Cup to disc ratio is small. No definite
treatment. Intravitreal injections (triamcinolone and anti- VEGF) may be tried in acute cases. Traumatic optic neuropathy: Occurs after a direct or indirect trauma to the optic nerve. Steroids are
not recommended if there is head concussion. Surgery of the optic canal to decompress the nerve
may be tried in early stages. There are reports about success with intravenous erythro poietin. - Toxic
optic neuropathy: Central, bilateral visual loss. There is a new report about improvement after
methanol toxicity with the combination of erythropoietin and steroids. - Radiation optic neuropathy:
Bilateral visual loss months or years after radiation therapy of a brain tumor. There are new reports of
improvement of vision with intravenous bevacizumab tharapy. - Leber’s optic neuropathy: Painless,
bilateral visual loss with central scotomas. Inherited by the maternal mitochondrial DNA mutations:
m.11778, m.14484, m.3460. Idebenone treatment in early stage Leber’s disease have been shown to
be beneficial. - Chronic relapsing inflammatory optic neuropathy: Steroid sensitive optic neuropathy
which recurs after steroid withdrawal. Long term steroids or other immunosuppressive agents are
used. There are other optic neuropathies with inflammatory, infectious, etc. etiology which can be
discusses, too.
19
19 A 0 B
A- DERGİ
Puan Puan Puan
SCI ve SCIExp
dışındaki
2 / 1.
indekslerde
Yazar
yer alan
yurt dışı
dergiler
Kaynakça: Kayabasi AU, Sergott RC. Immunosuppressive therapy in GCA.Int J Biol Med Res.2013;Vol
4,Issue 4:3656-61.
Özet: Review Immunosuppressive therapy in giant cell arteritis Umur A. Kayabasi1 , Robert C
Sergott2 World Eye Hospital, Istanbul, Turkey Accepted 31 October, 2013 Giant cell arteritis (GCA) is
a granulomatous vasculitis of large vessels mostly seen in patients over fifty years of age. Altough
GCA causes blindness , stroke and myocardial infarction if left untreated, it has not been clearly shown
that life expectancy decreases with it , but for sure the quality of life decreases because of long term
use and side effects of drugs, especially steroids. We tried to discuss the treatment of the disease with
other drugs, particularly methotrexate to increase the quality of life in patients. Keywords:
Methotrexate, Giant cell arteritis, Steroids, Immunosuppression IINTRODUCTION Giant cell arteritis
(GCA) is a vasculitis of large vessels generally seen in patients over fifty years of age. The incidence of
GCA has been reported as 15-25 / 100.000 and the prevalence as 1/133 over age fifty. After
seventyeighty years of age, the incidence increases 20-folds and male / female ratio of patients
becomes 2-4 / 1 respectively GCA is more common in white population,who lives in high altitudes and
frequently seen in patients with Scandinavian descent. (Beyer et al., 2011) Altough GCA causes
blindness , stroke and myocardial infarction if left untreated, it has not been clearly shown that life
expectancy decreases with it (Bhatia et al., 2005; Bley et al., 2005). There have been major
developments in the diagnosis, treatment and life quality of the patients in the recent years.
Methotrexate and other immunosuppressives had been either added to the classical steroid treatment
or used alone after a course of steroid treatment (Bhatia et al., 2005). *Corresponding Author E-mail:
[email protected] Tel: 90 532 6129050 Clinical presentation
20
20 A 0 B
A- DERGİ
Puan Puan Puan
SCI ve SCIExp
dışındaki
1 / 1.
indekslerde
Yazar
yer alan
yurt dışı
dergiler
Kaynakça: Kayabasi UA. Genetics and treatment of LHON. Comprehensive Research Journal of
Medicine and Medical Sciences. October 2013 1(2):18-23
Özet: Genetics and treatment of Leber' s hereditary optic neuropathy (LHON) Umur Ali Kayabasi
World Eye Hospital, Istanbul, 34778 Turkey. E-mail: [email protected] Article History ABSTRACT
Received 09 October, 2013 Received in revised form 17 October, 2013 Accepted 14 November, 2013
Key words: Leber's Hereditary Optic Neuropathy, Mitochondria, Genetics. Article Type: Review The
current concepts about Leber's hereditary optic neuropathy (LHON) and mitochondrial connection are
very difficult to understand completely. Even after twenty years of clinical studies, it is still difficult to
completely explain how LHON mutations cause damage to the optic nerve or why particularly the optic
nerve is at risk, and the information about mitochondria, the mitochondrial genome, the metabolism
of the optic nerve and the phenotypic variability of LHON are still being discussed. We cannot fully
explain the incomplete penetrance or the male predominance of LHON, the typical onset in young
adults or the bilaterality of visual loss. Evidence points to abnormalities of the mitochondria as the
direct or indirect cause of LHON. Primary LHON mutations definitely are not present in every family
with the LHON phenotype and multigenerational maternal inheritance. They may be present in only a
minority of patients with LHON phenotype without a clear family history. Therefore, the mitochondriaLHON connection needs to be examined more closely and understood better. This is a review that will
attempt to provide an update on different aspects of LHON and current novel treatment options.
©2013 BluePen Journals Ltd. All rights reserved INTRODUCTION German ophthalmologist, Theodore
Leber (1840-1917), described Leber' s hereditary optic neuropathy (LHON) for the first time (Puomila
et al., 2007). LHON is one of the most common inherited optic neuropathies, with an approximate
disease prevalence of 1 in 30,000 (Man et al., 2003). LHON is mostly detected between 15 and 35
years of age, but the range of onset can vary between childhood and over 60 years (Nikoskelanien et
al., 1996; Howell, 1997). The age of onset is slightly higher in females (19-55 years, average being
31.3 years) than males (15-53 years, average being 24.3) (Leber, 1871; Howell, 1997). LHON affects
mostly males, 80% of patients being male (Spruijt et al., 2007). There may be differences in male to
female ratio between mutations: 3:1 for m.3460G>A, 6:1 for m.11778G>A and 8:1 for m.14484T>C.
The cause of this predominance is still undetermined. Almost one in three cases have no definite
family history (Man et al., 2003). Patients present with painless visual loss and both eyes become
affected either simultaneously (25% of patients) or sequentially (75
36
36 A 0 B
A- DERGİ
Puan Puan Puan
SCI ve SCIExp
3 / 1.
kapsamındaki Yazar
dergiler
Kaynakça: Curr Opin Ophthalmol. 2012 Nov;23(6):477-84. doi: 10.1097/ICU.0b013e328358c7a6
Özet: Curr Opin Ophthalmol. 2012 Nov;23(6):477-84. doi: 10.1097/ICU.0b013e328358c7a6. Different
ophthalmologic manifestations of sarcoidosis. Umur KA, Tayfun B, Oguzhan O. Author information
Abstract PURPOSE OF REVIEW: Sarcoidosis can manifest with different ocular findings. Three different
cases have been presented, each of which showed different ocular problems. The literature has also
been reviewed as to find out other eye signs and treatment strategies of the disease. The diagnosis
may be difficult and the treatment may include combination of different immunosuppressors. RECENT
FINDINGS: Recent findings include a genetic basis, and certain human leukocyte antigens may affect
the course of the disease. Sarcoidosis can influence the eye and the optic nerves in the beginning,
and biopsy of the involved tissue may be necessary for the diagnosis. Laboratory investigation may be
unyielding. Once the diagnosis is made, steroids are generally started. Other than the classical
corticosteroid treatment, other immunosuppressive agents show promise in the atypical cases.
SUMMARY: Our cases show different manifestations of the disease like bilateral optic neuropathy,
Horner's syndrome, pars planitis, and anterior and posterior uveitis. Patients recovered with steroid
treatment, but especially in young patients other agents like methotrexate were needed because of
the sideeffects of steroids. PMID: 23014267 [PubMed - indexed for MEDLINE]
ALZHEIMER’S DISEASE and LIPOFUSCIN HYPOTHESIS – Accepted for publication in the
Next Section of ‘ La Prensa Medica Journal ‘. Summer 2014.
Umur Kayabasi, MD
World Eye Hospital - Istanbul
kayabasi at yahoo.com
Professor Robert C. Sergott, MD
Wills Eye Hospital -Philadelphia
rcs220 at comcast.net
Key Words: Curcumin ; FAF ; OCT; Alzheimer’s Disease
ABSTRACT:
Objective: To demonstrate curcumin’s affinity for AD plaques in retina.
Methods: We examined 40 patients with a family history of AD and/or mild cognitive
defects. In the patients in whom we found hyper or hypofluorescent lesions on FAF, OCT was
performed through these regions to reveal depositions in the retina. Drusen like spots- dots were
noticed in different parts of the retina. All the patients were given curcumin
to check for the changes in FAF and OCT. Also, 20 age matched healthy controls were examined.
Results: In 32 patiens, we were able to find abnormal deposits in different retinal layers. We
believe that these plaque-like lesions are related to neuro- degenerative disease (AD). Curcumin caused
patchy hypofluorescent FAF to occur and spots seemed brighter on OCT.
Conclusion: We proved that curcumin binds to plaques in retina. This finding may be very important for the early
diagnosis of AD. The effects of curcumin on AD plaques need to be examined in detail to find out whether it can shrink
these plaques.
Journal of Functional Foods in Health and Disease , May 2014
CURCUMIN AS A BIOACTIVE COMPOUND IN ALZHEIMER’S
DISEASE
Umur Kayabasi, MD
World Eye Hospital - Istanbul
kayabasi at yahoo.com
Professor Robert C. Sergott, MD
Wills Eye Hospital -Philadelphia
rcs220 at comcast.net
Key Words: Curcumin ; FAF ; OCT; Alzheimer’s Disease
European Journal of Neurology : Congress abstracts, June, 2014
Retinal plaques in Alzheimer’s disease
U.A. Kayabasi1, R.C. Sergott2
1Neuro-Ophthalmology, Dunya Goz Hospital, Istanbul,
Turkey, 2Neuro-Ophthalmology, Wills Eye Institute,
Philadelphia, PA, United States
Objectives: To evaluate the existence of pathologic retinal
deposits in patients with possible Alzheimer’s Disease
(AD).
Methods: We examined 20 patients with mild cognitive
impairment, 10 of whom had family history of AD. Also, 10
patients with no complaints were examined. The age range
was between 45 and 86. We performed fundus autofluorescence
(FAF) test and optical scanning tomography
(OCT) test on all of them. The retinal regions with
hypofluorescent and hyperfluorescent images were taken
into consideration and OCT was also performed through
these lesions to detect the layer of the abnormality.
Patients with diabetic retinopathy and vascular occlusions
were excluded.
Results: In 16 patients with mild cognitive defects we were
able to find abnormal accumulations in the ganglion layer
and nerve fiber layer. Some of the accumulations were
hypofluorescent and others were hyperfluorescent on FAF.
In the other group of patients who had no complaints , only
drusen on the pigment epithelium layer could be seen.
Conclusions: We believe that abnormal retinal deposits
(possibly containing beta amyloid protein ) can be observed
in the ganglion and retinal fiber layers in patients who have
high risk for AD. Retinal examination can be very helpful
in the evaluation of these patients.
Disclosure: Nothing to disclose.
NeuroTherapeutics – Dilemmas, Debates, Discussions (DDDN) Accepted to be published in
September 2014.
RETINA EXAMINATION WITH CURCUMIN FOR THE DIAGNOSIS OF ALZHEIMER’S DISEASE
Umur A. Kayabasi 1,*Robert C. Sergott 2
1Neuro- ophthalmology, Istanbul Medical Faculty, Istanbul, Turkey, 2Neuro- ophthalmology, Wills Eye,
Philadelphia, United States.
Problem statement: To demonstrate Alzheimer’s (AD) plaques in retina .It has been suggested that Beta amyloid starts
to accumulate in the retina even before it affects the brain. Some studies even showed amyloid depositions in regions
close to age related macular degeneration(AMD) lesions.
Methods: Methods
We examined 25 patients with a family history of AD and/or mild cognitive defects. All the patients were given oral
curcumin for
three days before the exam. In the patients in whom we found hyper or hypofluorescent lesions on fundus
autofluorescence (FAF),
optical coherence tomography (OCT) was performed through these regions to reveal depositions in the ganglion and
nerve fiber
layers. None of thepatients had retinal vascular disease due to hypertension or diabetes mellitus ; only drusen like
spots- dots were
noticed in different parts of the retina. Defects on RPE were not taken into consideration so that AMD lesions
Conclusion: We stress that all the middle- aged patients who have family history of AD should have thorough medical
examinations
and retina investigation may be a part of the exam. This is the first study in which AD plaques were shown in the retinas
of alive AD
patients with FDA approved devices.
Disclosure of Interest: None Declared
B - KİTAP / E-KİTAP
40
Puan
40 A
Puan
0B
Puan
Orjinal, Türkçe
BKİTAP 1 / 1.
/ EYazar
KİTAP
Başlık: OCT ve FAF' ın Nörolojik Hastalıklardaki Önemi.
Özet: DunyaGoz- Medical Tribune ortak yayın.
40
Puan
40 A
Puan
0B
Puan
Orjinal
BKİTAP 1 / 1.
/ EYazar
KİTAP
Başlık: Optik Nöropatiler
Özet: Dunya Goz Yayınları.
25
Puan
25 A
Puan
0B
Puan
Orjinal, Türkçe
BKİTAP 1 / 1.
/ EYazar
KİTAP
Başlık: MS ve optik nöropatiler.
Özet: Dünya Göz: Göz Hastalıkları Nöro-oftalmoloji chapter'ı.
25
Puan
25 A
Puan
0B
Puan
Çeviri
Başlık: Non-organik hastalıklar
Özet: Walsh ve Hoyt Esaslar
SERBEST SUNU KABULLERİ
My Schedule
Friday - 12 September 2014 Free paper
BKİTAP 1 / 1.
/ EYazar
KİTAP
Session
ID
Title
Room
Start
Time
End
Time
Main
Session
Start
Main
Session
End
FP2751
Retina examination with
examination with curcumin for
the diagnosis of Alzheimer's
disease
Boulevard
C.
17:42
17:50
16:30
18:00
© 2014 EURETINA
Rome - December 12 -13, 2014
International Congress on "En Face" OCT imaging
New Developments in OCT, OCT Angiography
13.30 – 14.30 LUNCH BREAK
Audrey Giocanti (Paris, France) - Predictive value of outer retina “En face” OCT imaging in geographic
atrophy progression
Anita Leys (Leuven, Belgium) - “En face” OCT in familial pattern dystrophy
Thomas Jouffroy (Paris, France) - "En face" imaging in retinal detachment
Andrea Sodi (Florence, Italy) - “En face” OCT in Stargardt disease
Claire Scemama(Paris, France) - OCT “En face” in choroidal focal folds
Amani Fawzi (Chicago, USA) - “En face” to predict vision after recovery in uveitic CME
Umur A. Kayabasi (Istanbul, Turkey), Robert C. Sergott (Philadelphia, USA) - Differential diagnosis of Alzheimer’s
disease by OCT-FAF
Ioannis Theocharis (Athens, Greece) – “En face” 3D-SDOCT images and the saltmarshes sign
C - EĞİTİM VE DİPLOMALAR
50
Puan
10 A
Puan
0B
Puan
C- EĞİTİM VE DİPLOMALAR
Wills Eye.
2005
C- EĞİTİM VE DİPLOMALAR
Michigan State
University
1995
Detay: Fellowship
Başlık: Adjustable sutures.
50
Puan
10 A
Puan
0B
Puan
Detay: NO Clinical Fellowship
Başlık: MRI in NO.
ESKİ YAYINLAR: Yurtdışı :
Eggenberger E, Kayabaşı AU. Hering’ s law for the
Neurology: November, 1996 ; 55 ( 11 ) : 1105- 08.
eyelids.
Manrique C, Kayabaşı U, Varadarajan J et al. MRI enhancement of
the optic nerve. Journal of N- O, December 1997 ; 17 ( 4 ) : 240- 2.
Kayabaşı U, Eggenberger E. Lid signs in Miller- Fisher syndrome.
Neurology, 2000 ; 54 : 2039- 2042.
Yurtiçi yayınlar:
Kayabaşı U, Kaufman D. Temporal kresent defekti. Türk oftalmoloji
gazetesi 2003; 33 ( 5 ) : 682- 685.
Kayabaşı U, Kandemir B, Doğan ÖK . Tolosa- Hunt sendromu. Türk
oftalmoloji gazetesi 2004 ; 34 (4 ) : 413- 416.
1997-2012 arasında, Türk oftalmoloji derneği kongre
toplantılarında, poster sunumları ve panel konuşmaları.
ve
D2 – TOPLANTILARDA BİLİMSEL FAALİYETLER
3,6
Puan
0,72 A 2,88 B - Sözel
Dunyagoz Noro-oftalmoloji 2012
Puan Puan sunum
1 / 1.
Yazar
Başlık: Non-organik gorme kaybı
Özet: www.dunyagoz.com
Oturum
Başkanı
1,5
0,3 A 1,2 B
(Konferans Dunyagoz Noro-oftalmoloji
Puan Puan Puan
ve bildiri
seansları)
/ 0.
Yazar
Başlık: Diplopi
Özet: www.dunyagoz.com
11,4
Puan
2,28 A 9,12 B - Sözel
1.retina gunleri Aralık 2013
Puan Puan sunum
2 / 1.
Yazar
Başlık: Alzheimer H.da FAF ve OCT
Özet: www.todnet.org
17,1
Puan
3,42 A 13,68 - Sözel
International OCT en face, Rome
Puan B Puan sunum
Başlık: OCT in AD.
Özet: www.symposiacongressi.eu
2 / 1.
Yazar
E - ÖDÜLLER
20
Puan
4A
Puan
16 B
Puan
E- ÖDÜLLER
Kızılay Dernegi odulu
1997
Detay: 1997 Kızılay Uluslararası NO Kongresi
Adres: www.kizilay.com.tr
Akademik Unvan: Klinik Nöro-oftalmoloji Fellowship - Michigan State UniversityWills Eye Hospital.
Ameliyat tecrübesi: Intravitreal Enjeksiyon ( 5 yıldır yapılıyor. )
Extraorbital kas Botox Enjek. ( 3 yıldır yapılıyor )
DGH çalışma süresi: 4 yıl

Benzer belgeler