Jurnal translet

Mrs. TA, 28 year old and married since 1 year, was anxious to
conceive due to her irregular cycles as a result of PCOS. Her age at
menarche was 12 years, with menstrual cycles being irregular for 1-2
days every 35-45 days. She also had a history of premenstrual pain,
and tension and spotting with dysmenorrhea. She had undergone
ureteroscopy for renal calculi twice. She also had a family history of
hemophilia with two of her brothers being affected and her mother
was a carrier. Her three maternal uncles also had hemophilia.
She was obese with moderate hirsutism. Clinically, her uterus was
normal sized, firm, and mobile with al I fornices being clear. At her
baseline ultrasound, the uterine size was 70.6/ 33.2/42.2 mm;
endometrial thickness was 6.1 mm; both ovaries were enlarged with
multiple follicles and increased stroma.
Her baseline hormone levels on day 2 of the cycle were as follows:
follicle stimulating hormone (FSH)-5.6 mIU/ml, luteinizing hormone
(LH)-5.3

mIU/ml,

dehydroepiandro

sulfate

(DHEAS)-780

ng/ml,

androstenidione-2.7 ng/ ml, estradiol (E2)-20.73 pg,/ml, progesterone

(P4)-3.68 ng/ml, thyroid stimulating hormone (TSH)-9.4 uRJ/ml, free
T4 (FT4)-1.25, fasting insulin (FI)-15.8 uU/mI. Fasting Insulin levels
were repeated after 3 months of Metformin (500 mg twice a day)
which were 3.1 Semen analysis done was normal.
In view of the family history of haemophilia, she was evaluated to rule
out a carrier state. Her prothrombin time (PT) was 13.2 s (control 12
s), activated part ialthromboplas tin time (aPTT) 33 s (control 30 s),
factor VIII c activity S6% (60-150), factor IX c assay - 60% (60-150),
and factor XIII screening showed stable clot. Her results for PCR for
carrier state revealed that she was not a carrier for hemophilia. Her
hysterosalphingography (HSG) showed a normal uterine cavity with a
good filling of both tubes with the bilateral spill. The right tube was
morphologically normal with mild dilatation and clumping of the distal
end of the left tube. Tubal pressures were low.
She was started on 511 )1g of tablet eltroxin and tablet metrofin 50(1
mg BD. Metformin was discontinued after 2 months due to
gastrointestinal side effects.
11w first cycle was monitored without 01 drugs, with no ovulation

documented after monitoring till day 21 of the cycle. In the second

cycle, clomiphene citrate (CC) 100 mg was given from days 2 to 6,
and ovulation was documented on day 22.1n the next two cycles, the
dose of CC was increased to 150 mg. Ovulation was documented on
days 15 and 17. In the next three cycles letnyzole 5 mg was given
from days 3 to 7, and ovulation was documented on day 14 or 15 of
the cycle. As there was no pregnancy even with letrazole, CC was
given again in the seventh cycle. She had three mature follicles on
day 12, when KC 5000 IL was given intramuscular, and ovulation was
documented on days 14 and 15. Micronized progesterone vaginal
pessaries were given for In teal support. A total at 20 days alter
ovulation, Il-hUG dune on November 19, 2007, was 410 mil:init. 111)CG was repeated again on November 22, 2007, which had
increased to 1085 militia USG revealed a single intrauterine (I U) sac
with a gestational sac diameter (C,SD) of 4.4 mm (5 weeks 1 day).
On November 26, 2007, a repeat TVS did not show any increase in
GSD (5.13 mm - 5 weeks 2 days). No yolk sac or fetal pole was seen.
Repeat TVS after a week on December 3, 2007, documented a
gestational sac of 8.4 net (5 weeks 4 days) with no yolk sac or fetal
pole seen. There was minimal tenderness in the right fomix, but no
ectopic gestational sac (GS) seen in either fomix. The 13-KG level on
that day was 9515 which was too high for an anembryonic pregnancy
it-hce was repeated on December 6, 2C07, and WAS 11342 mfUltrd;
WS documented a GS of 10.5 nun (5 weeks 6 days) with no fetal pole
or yolk sac seen. There was another small GS seen measuring 4 mm .
There were also two small sacs measuring 4 and 6 mm, seen in the
right adenexa, the left adenexa appearing normal with no free fluid in
POD. There was no abdominal tenderness or guarding or tenderness
in all fornices. On December 8, 2007, the p-hCG was 12947 mIU/ ml
with IU GS of 10.5 mm (5 weeks 6 days) with no fetal pole or yolk sac
The two sacs in the right adenexa had increased in size to 8 and 6
mm, respectively. There was no free fluid in POD. The patient was
clinically asymptomatic and stable so a decision to start medical
therapy was taken. Inj MTX 1 mg/kg was given IM with inj. leucovorine
0.1/kg given IM on alternate days.
The patient was followed up on a regular basis clinically and by TVS.

She was also closely monitored for -hCG, hemoglobin (HB), complete
blood count (CBC), liver function test (LFT), and peripheral smears.
The (3-hCG levels after MTX injection were as follows:
December 12, 2007, 11,967 mIU/ml
December 14, 2007, 10,164 mIU/m1
December 17, 2007, 6292 mIU/m1
December 20, 2007, 3232 mIU/ml
December 22, 2007, 1088 mIU/ml
December 24, 2007, 791 mIU/m1
December 28, 2007, 90 mIU/m1
January 2, 2008, 9 mIU/ml.
Serial TVS done showed regression of intrauterine and right adenexal
sacs. Once the hCG levels were less than 1000 mIU/ml, the patient
had per vaginal bleeding. TVS showed the products in the cervical
canal which were then removed under aseptic precautions.
A total of six injections of MTX were given. All her blood parameters
were normal throughout the treatment.
Once j3-hCG was below 10 mIU/ml, she was advised not to conceive
for 6 months, with follow-up of p-hCG after 1 and
2 months which was normal.
After 6 months, she was again given CC for OI, and ovulation was
documented on day 15. She conceived in the second treatment cycle
with timed intercourse. Her -hCG 20 days after ovulation was 3571
mIU/ml with an IU GS of 9 mm corresponding to 5 weeks 3 days seen
on TVS. Corpus luteum was seen on the right side with no other
adenexal pathology. Repeat -hCG after 1 week was 15,000 mIU/m1.
A gestational sac with yolk sac and fetal pole corresponding to 6
weeks and 5 days was seen. Fetal heart was also documented. She
had a normal vaginal delivery at 39 weeks of gestation. She delivered
a female baby weighing 3.4 kg.
Case 2
Mrs SS presented with secondary infertility for 6 months. She had a
full-term normal delivery female baby aged 4.5 years alive and
health); after which she used harrier contraception fur 3 years and
IUCD for 1.5 years for spacing. 1-15G done outside on February 7,
2007, showed right tubal block with the left tube filling poorly.

Cannulation was done under fluoroscopic guidance, after which both

the

tubes

showed

free

spill.

Endometrium

was

positive

Ibr

tuberculosis PCR. She had undergone four cycles of ovulation

induction, two citrate and two with gonad otrophias. She ovulated in
all the cycles but her endometrium was thin and lesser than 7.5 mm
in all four cycles.
Her first scan done at our clinic was on day 19 of the menstrual cycle.
The uterus was normal, but the endometrium was only 7.R nun thick.
Both ovaries were normal with a volume of 4.96 and 4.20 cm and an
antral follicle count (AFC} of seven. With this history and investigation
report, the patient was planned for 01 with RH. Two cycles of Ur were
performed with tablet I .Ct razolc 5 mg, given from days 3-7. The
dermal application of EstroGel was done once the follicles were 16
mm for the treatment of thin endometrium. The ovulation occurred on
days 13 and 15. The endometrial thickness on the day of 1111 was
12.8 and 12.3 mm. We did two inure cycles of 1U1 with gonad ot
rophins. Ovulation was documented on days 11 and 14 of the cycle
and the endometrial thickness was 11.6 and 11.1 mm. As there was
no pregnancy, the patient was counselled for in vitro teriilizatinn
([VF). Hysteroscopy was done prior to JIFF, which revealed adhesions
at the &MILLS and both cornu. The codonwtrium was fibrotic and
pearly white in color except for a small portion oil the :Interior wall. he
cavity was stnaller Ohm Hun mat in size. Adhesiolysis was done and
the patient was put on conjugated estrogen (Premarin) 1.25 mg twice
a day for 25 days with medrosyprogesterone 10 mg twice a day for
the last ID days. This hormone replacement therapy (I IRT) was given
for 3 months. A repeat hysteroscopy done after 3 months revealed
reformation of adhesions at the IlunduS which were rut using scissors
and Fifa given again for 3 months. Before IVF, hysteroscopy did not
show any adhesions but the endometrium was thin and fibrotic on the
posterior wall.
The protocol used fur IVF was long luteal down-regulation from day 21
with gunadotrophins started on day 3 of the gels when the cstradiol
was 18 pg/MI and progesterone was 1.15 ng/ml. She was started on
urinary FSH 30U 1U and as the estradiol level on day 8 of the cycle
was 6 pg/ nil and the tollicular size was 8-12 mm, the dose was

increased by 75 Hi and continued till day 13. On day 14, Rec. hCG 250
meg will; given subcutaneously when there were SIX follicles 16-18
mm in d iameter. On the day tit heG, estradiol was 3265 pg/ml and
progesterone was 2.8 ng/ml. Oocyte retrieval was done 35 h later.
Luteal phase support was given with intramuscular inj. Gestone 100
mg (Ferring Pharmaceuticals, India). The luteal phase was monitored
for ovarian hyperstimulation syndrome (OHSS). Ten days after ET, hCG was 53 mIU/m1 and a repeat level after 7 days was 1030 mIU/ml.
At that time, a single gestational sac was seen with a mean
gestational sac diameter (MGSD) of 4.5 mm corresponding to 5 weeks
and 1 day. Two days later, the patient complained of minimal bleeding
per vaginum. The -hCG level was 1258 mIU/ml, the MGSD was 4.6
mm and both adenexa showed multiple corpora lutea. No gestational
sac was seen in the adenexa. One week later, the MGSD had
increased to 8.5 mm which corresponded to 5 weeks and 5 days, but
no fetal pole was seen and the bleeding had stopped. Despite the
increase in the MGSD, there was no corresponding increase in the pHCG levels which were 1567 mIU/ml. Two days later, the patient had
three syncopal attacks. On examination, the vitals were normal but
there was tenderness in the right iliac fossa and fornix. On TVS, the IU
sac with yolk sac was seen, but there was also a complex mass of 90
x 70 mm in the right adenexa with free fluid in POD, which was turbid.
Diagnosis of right EP with coexisting IU pregnancy was made. In view
of an IU pregnancy and right adenexal mass, the decision for
laparoscopy was taken. At laproscopy, right partial salpingectomy for
ruptured EP was done. One week later, the TVS showed a irregular
gestational sac with MGSD of 5.8 min and the p-hCG level was 820
mIU/ml. The repeat hCG level after 5 days was 418 mIU/m1 and the
gestational sac had not increased in size. Decision for a curettage was
taken. One week later, the p-hCG level was 5 mIU/ml. A frozen
embryo transfer was done in a natural cycle, and a biochemical
pregnancy was documented with the 3-hCG level going to 378
mIU/ml.
VM, seorang wanita 34 tahun menikah sejak 14 tahun, disajikan
kepada kita pada tahun 2004 dengan infertilitas primer. Siklus nya

adalah dari 7-15 hari setiap 45-60 hari. HSG nya dilakukan pada tahun
1994

adalah

normal.

Masa

lalu

analisis

semen

Suaminya

menunjukkan oligoasthenospermia berat dengan hitungan 6 juta dan

motilitas 22%. Pemeriksaan panggul normal dan pada TVS, rahim
adalah 78 x 43 x 58 mm; kedua ovarium normal dengan jumlah folikel
antral dari 5. Kanan adenexa mengungkapkan hidrosalping a.
Keputusan untuk hysterolaparoscopy diambil. Pada histeroskopi, ada
polip di dinding lateral kiri yang dipotong. Ostia, kornu, fundus,
rongga, dan enciometrium normal. Pada laparoskopi, rahim, tabung,
dan ovarium yang normal. Tabung yang tepat memiliki kista paratubal
besar yang mensimulasikan hidrosalping di TVS. Pada hari 2, tes
hormon dilakukan dengan hasil sebagai berikut: FSH-3.5 m1U / m1;
LH-2.2 mIU / m1; prolaktin -21,4 ng / ml; TSH-3.3 uIU / ml. Pasien
diinginkan dua siklus IUI, yang dilakukan dengan CC 150 mg dari hari
2 sampai 6 dari MC.
Dia mengembangkan satu folikel dominan, di sebelah kanan pada
siklus I, dan di sebelah kiri pada siklus kedua. Saat ia gagal untuk
hamil, ICSI direncanakan. Pada hari 2, estradiol (U) adalah 36,6 pg /
ml dan progesteron 1,4 mg / ml. Stimulasi ovarium terkontrol (COS)
dimulai dengan FSH 150 IU dan 75 IU IINIC. Pada hari ke-5, tingkat E2
adalah 33.6 dan hanya satu folikel dari enam '. 8.3 mm WAS Remaja
di sisi kiri. The IIMG dosis ditingkatkan menjadi 150 Ill. Pada hari 10
dari COS, hanya ada satu folikel 10,5 mm ukuran dan tingkat E2
adalah 34 pg / mI. Keputusan untuk membatalkan siklus itu diambil
dan darah untuk AMR dikirim. Nilai-nilai AMH adalah 0.04 / lib ml. 1
dia keputusan untuk sumbangan oosit diambil sebagai cadangan
ovarium miskin. Sumbangan Oocote adalah klon dalam GnRH agonis
protokol panjang siklus HRT. Tiga kelas 1 embrio dua 10-sel dan satu
dipindahkan. Pertama tingkat p-ICG 14 hari setelah ET adalah 68
mIU / ml. Delapan hari kemudian, tingkat-b hcg adalah 9781 mIU / m1
dan kantung kehamilan berukuran 4 x 3,3 mm 3,8 sesuai dengan 5
minggu 2 hari terlihat, tapi kantung ditempatkan di bagian bawah
rongga rahim (kehamilan serviks) . Lima hari kemudian, ', ia datang
dengan bercak; yang MUSD adalah 6,6 mm, dengan yolk sac dilihat
tapi tidak ada tiang janin. 'The (4-110: tingkat adalah 11,875 mIU /
m1 yang dikurangi menjadi 9.781 setelah 2 hari, dan un TVS, kantung

di bagian bawah rahim memperluas ke leher rahim tidak teratur

dalam ukuran Mengingat kehamilan serviks,. bergantian dengan
leucovorin diberikan. Butuh waktu hampir 2 bulan untuk fi-ha; tingkat
mencapai 10 colt / ml. "Siklus kedua donasi oosit lagi-lagi dune 10
bulan

kemudian

dalam

siklus

IIZT

sebagai

pasien

sedang

menstruasi. Kali ini kami melakukan hari 5 Transfer dan dua blastosis
diperluas kelas 4 AA dipindahkan. Yang pertama ii-nya, tingkat setelah
1,0 hari adalah 134 mIU / m1 dan .second satu 7 hari kemudian
adalah 1168 int U / ml. Meskipun ha beta: makhluk> 1000 mIU / ml,
ada kantung intrauterine terlihat. Lima hari kemudian, dia datang
dengan rasa sakit di perut bagian bawah, pusing, dan muntah.
Parameter penting nya yang normal, dan tidak ada 'nyeri tekan
abdomen dan kekakuan. Di TVS, ketebalan endometrium adalah 20
mm tanpa kantung kehamilan; kantung kecil divisualisasikan dalam
adenexa yang tepat, meskipun tidak ada pemeriksaan nyeri. The-b
hCG tingkat itu adalah 5664 mIU / ml. Keputusan untuk terapi medis
diambil dan dia sudah memulai MTX 1 mg / kg bolak dengan
leucovorin. Sebanyak empat dosis diberikan. Kali ini juga, butuh 50
hari untuk tingkat menjadi negatif. Lima bulan kemudian, siklus lain
dari sumbangan oosit dilakukan dalam siklus I IRT. Dua kelas 1
delapan sel bendung embrio yang ditransfer. Kali ini juga, leer
pertama tingkat-b hCG positif, dan 1 minggu kemudian, meningkat
menjadi 1.359, dan kantung kehamilan IU sesuai dengan S minggu
dan 3 hari divisualisasikan. Sayangnya dia punya aborsi terjawab
pada 7 minggu kehamilan dengan jantung janin pertama menjadi
lambat selama 2 hari, dan yang kemudian berhenti. Sebuah aborsi
medis dilakukan. Pada Juni 2011, tingkat FSH-nya pada hari 2 adalah
0.44 dan LH adalah 0,01; satu siklus lebih dari COH dengan FSH150
TU + hMG 300 IU diadili. Tidak ada pertumbuhan folikel terlihat
setelah 10 hari dengan tingkat E2 dari 24 pg / ml; sehingga siklus itu
dibatalkan. Setelah satu bulan, satu lagi siklus

Tujuan: Profilaksis Asiklovir jangka panjang (ACV) , dianjurkan untuk mencegah

herpes simplex virus berulang Tipe 1 (HSV-1) dapat menimbulrefractory disease karena
resisten ACV. Kami menentukan pengaruh profilaksis ACV pada prevalensi HSV-1
resisten ACV(ACVr) kornea dan konsekuensi klinis
daripadanya pada pasien dengan Keratitis HSV-1 berulang (RHK).

Metode. Frekuensi virus resisten ACV ditentukan pada 169 kornea HSV-1 isolat dari 78
pasien RHK dengan riwayat penyakit stroma. Profil kerentanan ACV isolat berkorelasi
dengan parameter klinis untuk
mengidentifikasi faktor risiko predisposisi dari RHK resisten ACV
Hasil. HSV-1 kornea isolat dengan> 28% virus resisten ACV yang didefinisikan
sebagai ACVr isolat. Empat puluh empat isolat (26%) adalah resisten ACV. Analisis
multivariat mengidentifikasi ACV profilaksis jangka panjang (12 bulan) (rasio odds
[OR] 3,42; 95% confidence interval [CI], 1,32-8,87) dan durasi ulangan45 hari (OR
2.23; 95% CI, 1.02- 4,87), menunjukkan ACVrefractory disease, sebagai faktor risiko
independen untuk ACVr isolat. Selain itu, kornea ACVr Isolat adalah faktor risiko untuk
penyakit ACV-refractory diseasea (OR 2.28; 95% CI, 1,06-4,89).
Kesimpulan. Data menunjukkan bahwa ACV profilaksis jangka panjang merupakan
predisposisi ACV refractory disease karena munculnya HSV-1 kornea resistan ACV.
Pengujian kerentanan ACV dijamin selama follow up pasien RHK.
Herpes simplex virus tipe 1 (HSV-1) adalah human
alpha-herpes virus yang endemik di seluruh dunia. Virus biasanya diperoleh pada masa
anak usia dini melalui rute orofasial, yang mengarah ke pembentukan infeksi laten
seumur hidup neuron yang terletak di dalam ganglia trigeminal. Reactivations
Intermittent menyebabkan virus shedding dan kadang-kadang untuk penyakit berulang [
1 ]. HSV-1 menyebabkan berbagai penyakit, mulai dari
herpes labialis ringan sampai penyakit mata mengancam [ 1 ].
Infeksi HSV-1 pada kornea, disebut sebagai herpes keratitis (HK), adalah penyebab
infeksi umum yang menyebabkan gangguan penglihatan terutama karena sifat berulang
mereka [ 2 , 3 ]. HK
bermanifestasi sebagai keratitis epitel menular (IEK), yang
ditandai dengan replikasi virus dangkal, atau bis
menginfeksi stroma kornea yang mendasari dan menyebabkan herpes
stroma keratitis (HSK) [ 2 ] .Recurrent HSK dapat mengakibatkan kebutaan kornea 4 ].

Permulaan dari keratitis hsv-1 yang berulang didefinisikan sebagai

presentasi dari IEK yang dikarakteristikan dengan ulkus kornea
dendritik dan geograpik atau gejala klinik

yang terkait dengan

patologi HSK, termasuk infiltrasi sel pada stroma kornea atau bilik
mata anterior dan penjarangan stroma kornea, edema, vaskularisasi,
atau cornea pseudoguttata. Akhir dari IEK yang di isolasi didefinisikan
sebagai

waktu

penutupan

komplit

dari

epitelkornea,

setelah

pengobatan ACV topikal dihentikan. Pada HSK yang terkait dengan

kekambuhan, akhir dari kerusakan epitel HSV-1 yang timbul kembali
di