scholarly journals PREGNANCY IN CONGENITAL SEPTATE UTERUS

2018 ◽  
Vol 1 (1) ◽  
pp. 5-6
Author(s):  
Mihai Cristian Dumitrașcu ◽  
Cătălin-George Nenciu ◽  
Adina-Elena Nenciu
Keyword(s):  
Normal Values ◽  
Clomiphene Citrate ◽  
Normal Range ◽  
Septate Uterus ◽  
Normal Limits ◽  
Increased Risk ◽  
History Of Pathology ◽  
History Of ◽  
Uterine Malformations ◽  
Exploratory Laparoscopy

Congenital uterine malformations can be found in low percentage in the general population due to the defect of joining the paramezonephrotic ducts and  often causes infertility [1]. In the case of malformed uterine pregnancy we encounter increased  risk of spontaneous abortion, premature birth and fetal dystocia [2]. We present the case of a 24 year patience, without a personal history of pathology and  primary infertility for two years .The blood test reveal  normal values with hormonal analyzes within normal limits. The clinically examination it is in normal range. The ultrasound revealed partial septate uterus. The diagnosis was confirmed in histerosalpingography. The  exploratory laparoscopy  shown permeability for both fallopian tubes.After ovarian stimulation with Clomiphene Citrate two months in a row a pregnancy was obtain. The patient delivered at term, without complication during pregnancy.  

scholarly journals Pregnancy in bicornuate uterus

2017 ◽  
Vol 7 (1) ◽  
pp. 346
Author(s):  
D. Borgohain ◽  
Shubhi Srivastava
Keyword(s):  
Successful Outcome ◽  
Septate Uterus ◽  
Bicornuate Uterus ◽  
Unicornuate Uterus ◽  
Mesonephric Duct ◽  
Embryonic Life ◽  
History Of ◽  
Uterine Malformations ◽  
The Subject ◽  
Growth Restrictions

The incidence of the uterine malformations is estimated to be 3% to 5% in the general population. Abnormal fusion of the mesonephric duct (Mullerian duct) during embryonic life results in a variety of congenital uterine malformations like septate uterus, unicornuate uterus, and bicornuate uterus. Fertility and evolution of pregnancy depends on the type of uterine anomaly. Many of them are asymptomatic but it is important to consider this diagnosis in recurrent miscarriages, preterm labours, malpresentations, and intrauterine growth restrictions. We are presenting a 22-years-old pregnant woman with a history of abortion. The patient was not diagnosed with a bicornuate uterus in her first pregnancy. However, she was diagnosed with a bicornuate uterus based on the findings of ultrasound in the present pregnancy. A successful caesarean section was performed on the subject in the 39th week of gestation. According to the results, successful outcome could be achieved in patients with bicornuate uterus.

scholarly journals Assessment of red cell sodium transport in essential hypertension

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 439-442
Author(s):  
JR Mahoney ◽  
NL Etkin ◽  
JD McSwigan ◽  
JW Eaton
Keyword(s):  
Essential Hypertension ◽  
Secondary Hypertension ◽  
Transport Processes ◽  
Red Cell ◽  
Na Transport ◽  
Normal Range ◽  
Normal Limits ◽  
Direct Technique ◽  
History Of ◽  
22Na Uptake

Abnormal erythrocyte Na+ transport has been reported in patients with essential hypertension and some first-degree relatives. The two major techniques now employed for estimating Na+ transport--Na+/Li+ countertransport and Na+/K+ cotransport--are rather intricate and time consuming. Furthermore, the precise nature of the transport processes being measured is not clear. We have developed a simpler, more direct technique based on measurement of 22Na+ accumulation by erythrocytes. 22Na+ uptake by red cells from patients with essential hypertension averages twice normal. Indeed, of 21 patients with essential hypertension, only 2 patients had values within the upper end of the normal range. In 12 patients with secondary hypertension and no family history of essential hypertension, erythrocyte 22Na+ accumulation was within normal limits. Control experiments indicate that our technique for estimating red cell 22Na+ uptake is highly reproducible and shows little day-to-day variation. This procedure for the assessment of erythrocyte Na+ transport should be useful in differential diagnosis and the presymptomatic identification of individuals genetically prone to essential hypertension.

Relationship between a Mild α1 Proteinase Inhibitor Deficiency and Respiratory Symptoms in a Family

1995 ◽  
Vol 32 (6) ◽  
pp. 545-549 ◽  
Author(s):  
Guillemette Huet-Duvillier ◽  
Malika Balduyck ◽  
Yves Watrigant ◽  
Richard Sesboue ◽  
Carole Thiebaut ◽  
...  
Keyword(s):  
Proteinase Inhibitor ◽  
Respiratory Symptoms ◽  
Normal Limit ◽  
Normal Range ◽  
Pancreatic Elastase ◽  
Inhibitory Capacity ◽  
Normal Limits ◽  
The Family ◽  
History Of ◽  
Pi Deficiency

A 34-year-old man with pulmonary emphysema was found to have a mild α1 proteinase inhibitor (α1 PI) deficiency. α1 PI status was investigated in this patient and in 35 members of his family. The α1 PI investigations included α1 PI concentration and phenotype and serum inhibitory capacity for trypsin and pancreatic elastase. Fifteen members of the family had α1 PI concentration and inhibitory capacities below the lower normal limit. Five of these members were characterized by the heterozygous MP phenotype and the 10 others by an apparently homozygous M phenotype, in which the M allele may be associated with another unidentified deficiency allele. Two members of the family had α1 PI concentration and elastase inhibitory capacity below the lower normal limits and trypsin inhibitory capacity within the normal range. They were both characterized by the MP phenotype. Six of these 17 members (three of PI type M and three of PI type MP) showed chronic pulmonary symptoms, whereas among the 19 α1 PI non deficient members, no member had a history of significant pulmonary symptoms.

Indium-111–Antimyosin Scintigraphy in the Early Detection of Heart Damage After Anthracycline Therapy in Children

1999 ◽  
Vol 17 (4) ◽  
pp. 1208-1208 ◽  
Author(s):  
L.C.M. Kremer ◽  
M.M.C. Tiel-van Buul ◽  
M.C. Ubbink ◽  
M. Offringa ◽  
J. Ottenkamp ◽  
...  
Keyword(s):  
Early Detection ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Normal Range ◽  
Normal Limits ◽  
Increased Risk ◽  
Early Increase ◽  
Indium 111 ◽  
Myocyte Damage ◽  
Fractional Shortening

PURPOSE: To determine the value of indium-111–antimyosin (111In-AM) scintigraphy in the early detection of myocardial damage in children treated with doxorubicin. PATIENTS AND METHODS: Twelve planar scintigrams were made of eight patients (seven children and one young adult; mean age, 12 years). Three scans were obtained before doxorubicin therapy in three patients, and nine scans were obtained during doxorubicin therapy in seven patients. The heart-to-lung ratio (HLR) was calculated. Left ventricular function was assessed by echocardiography before and during therapy by measuring the fractional shortening (FS). RESULTS: The HLR of the three baseline scans was below 1.5, within the normal range for adults. Six of the seven patients whose scans were obtained during chemotherapy had abnormal HLR values (> 1.5). One patient had severe myocyte damage and showed an early increase in the HLR (2.3) after a cumulative doxorubicin dose of 150 mg/m2. The FS measured by echocardiography was normal throughout therapy, and the final cumulative dose of doxorubicin was 450 mg/m2. This patient developed fatal clinical heart failure 3 months after completion of chemotherapy. In one patient, who was pretreated with the cardioprotective agent dexrazoxane, the HLR remained within normal limits during therapy. CONCLUSION: 111In-AM scintigraphy seems to be suitable to detect early myocardial damage after a cumulative doxorubicin dose of 150 mg/m2 in children and may be useful for identifying children who are at increased risk of developing cardiac sequelae.

scholarly journals Assessment of red cell sodium transport in essential hypertension

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 439-442 ◽  
Author(s):  
JR Mahoney ◽  
NL Etkin ◽  
JD McSwigan ◽  
JW Eaton
Keyword(s):  
Essential Hypertension ◽  
Secondary Hypertension ◽  
Transport Processes ◽  
Red Cell ◽  
Na Transport ◽  
Normal Range ◽  
Normal Limits ◽  
Direct Technique ◽  
History Of ◽  
22Na Uptake

Abstract Abnormal erythrocyte Na+ transport has been reported in patients with essential hypertension and some first-degree relatives. The two major techniques now employed for estimating Na+ transport--Na+/Li+ countertransport and Na+/K+ cotransport--are rather intricate and time consuming. Furthermore, the precise nature of the transport processes being measured is not clear. We have developed a simpler, more direct technique based on measurement of 22Na+ accumulation by erythrocytes. 22Na+ uptake by red cells from patients with essential hypertension averages twice normal. Indeed, of 21 patients with essential hypertension, only 2 patients had values within the upper end of the normal range. In 12 patients with secondary hypertension and no family history of essential hypertension, erythrocyte 22Na+ accumulation was within normal limits. Control experiments indicate that our technique for estimating red cell 22Na+ uptake is highly reproducible and shows little day-to-day variation. This procedure for the assessment of erythrocyte Na+ transport should be useful in differential diagnosis and the presymptomatic identification of individuals genetically prone to essential hypertension.

PROS1 genotype phenotype relationships in a large cohort of adults with suspicion of inherited quantitative protein S deficiency

2016 ◽  
Vol 115 (03) ◽  
pp. 570-579 ◽  
Author(s):  
Genevieve Plu-Bureau ◽  
Marie Héléne Horellou ◽  
Antoine Rauch ◽  
Pierre Suchon ◽  
Martine Alhenc-Gelas ◽  
...  
Keyword(s):  
Retrospective Cohort ◽  
Protein S ◽  
Type I ◽  
Type Ii ◽  
Protein S Deficiency ◽  
Normal Range ◽  
Established Risk Factor ◽  
S Deficiency ◽  
Increased Risk ◽  
History Of

SummaryInherited protein S deficiency (PSD) is an established risk factor for venous thromboembolism (VTE). However, data are conflicting concerning risk of VTE associated with decreased free PS level (FPS) and information on PROS1 genotype-phenotype relationship is sparse. In a retrospective cohort of 579 patients with inherited type I/III deficiency suspicion, PROS1 genotyping was performed and the effect of genotype on FPS and on VTE risk was investigated. We found 116 (including 65 novel) detrimental mutations (DM) in 222 (type I/III in 194, type II in 28), PS Heerlen in 74, possibly non DM in 38 and no mutation in 245 subjects. Among DMs, type I/IIIDMs only were found in subjects with FPS<30 %. Prevalence of type I/III DM decreased with increasing FPS level. Risk of VT associated with FPS level and genotype was studied in the 467 subjects with personal or family history of thrombosis. Only type I/IIIDM carriers presented with an increased risk of VTE [1.41 (95%CI (1.05–1.89)] compared to subjects with no mutation. Among the group of type I/IIIDM heterozygotes and subjects with no mutation, the optimal FPS cut-off point for identifying subjects at increased VTE risk was searched for. We found that only subjects with FPS<30% and type I/IIIDM presented with an increased risk [1.48 (95%CI 1.08–2.04)]. Our findings confirm the value of a cut-off FPS level for identifying subjects at increased VTE risk far below the lower limit of the normal range and suggest a place for PROS1 genotyping in PSD diagnosis strategy.

Increased Heparin Cofactor II Levels in Women Taking Oral Contraceptives

1990 ◽  
Vol 64 (03) ◽  
pp. 365-368 ◽  
Author(s):  
P Toulon ◽  
J M Bardin ◽  
N M Blumenfeld
Keyword(s):  
Oral Contraceptives ◽  
Antithrombin Iii ◽  
Thrombin Inhibitor ◽  
Control Groups ◽  
Normal Range ◽  
Heparin Cofactor Ii ◽  
Men And Women ◽  
Pooled Data ◽  
Contraceptive Pills ◽  
Increased Risk

SummaryHeparin cofactor II (HCII) is a thrombin inhibitor present in human plasma whose activity is enhanced by heparin. HCII exhibits important homologies with antithrombin III, the main heparin-enhanced thrombin inhibitor. Cases of recurrent thromboembolism have been recently reported in patients with HCII deficiency. Since the use of oral contraceptives (OC) is associated with an increased risk of thrombosis, the study of the plasma levels of HCII was undertaken in women taking contraceptive pills. Plasma HCII levels were found significantly higher in 62 women taking low-estrogen content OC (1.20 ± 0.28 U/ml) than in 62 age matched women not taking OC (0.94 ± 0.16 U/ml) or in 62 men (0.96 ± 0.19 U/ml). Significant correlations between HCII and fibrinogen levels were reported in the three groups. From the pooled data of the two control groups (men and women not taking OC), the normal range for plasma HCII levels was defined to be between 0.60 and 1.30 U/ml (mean ± 2 SD). Two cases of low HCII levels (<0.60 U/ml) were found in the control groups, but none in the group of women taking OC. It is concluded that the use of oral contraceptives is associated with a rise in HCII levels and that the screening for HCII deficiency has to be performed at distance of any OC therapy.

Hereditary Heparin Cofactor II Deficiency and the Risk of Development of Thrombosis

1987 ◽  
Vol 57 (02) ◽  
pp. 196-200 ◽  
Author(s):  
R M Bertina ◽  
I K van der Linden ◽  
L Engesser ◽  
H P Muller ◽  
E J P Brommer
Keyword(s):  
Liver Disease ◽  
Venous Thrombosis ◽  
Healthy Volunteers ◽  
Mean Value ◽  
Age Group ◽  
Normal Range ◽  
Heparin Cofactor Ii ◽  
History Of ◽  
Group 2 ◽  
Hereditary Nature

SummaryHeparin cofactor II (HC II) levels were measured by electroimmunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established.It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.

Spontaneous Haemophilia in a Female

1960 ◽  
Vol 04 (03) ◽  
pp. 369-375 ◽  
Author(s):  
E. H Braun ◽  
David B. Stollar
Keyword(s):  
Family History ◽  
Bleeding Time ◽  
Dental Extraction ◽  
White Girl ◽  
Complete Family ◽  
Normal Limits ◽  
Sex Chromatin ◽  
History Of ◽  
Generation Test

SummaryA case of haemophilia in a young white girl is described. There was a history of bleeding from birth. The thromboplastin generation test was grossly abnormal and A. H. G. levels were below 1%. Bleeding time and capillary morphology was within normal limits. Dental extraction after transfusion caused almost uncontrollable haemorrhage.A complete family history was obtained for four generations. There was no case of a “bleeder” amongst these.The girl’s apparent sex was confirmed by sex chromatin studies.

The Prevalence of Hereditary Antithrombin-III Deficiency in Patients with a History of Venous Thromboembolism

1985 ◽  
Vol 54 (04) ◽  
pp. 744-745 ◽  
Author(s):  
R Vikydal ◽  
C Korninger ◽  
P A Kyrle ◽  
H Niessner ◽  
I Pabinger ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Antithrombin Iii ◽  
Positive Family History ◽  
Normal Range ◽  
The Family ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Recurrent Venous Thrombosis ◽  
Antithrombin Iii Activity ◽  
Slight Deficiency

SummaryAntithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

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