A Laboratory Case Report Of “Hypercoagulation Syndrome” Following Eight Weeks Of Estrogen Replacement Therapy

Mapping Intimacies ◽

10.1055/s-0038-1653089 ◽

1981 ◽

Author(s):

C Palmason ◽

S Shams ◽

C Harris

Keyword(s):

Replacement Therapy ◽

Blood Coagulation ◽

Estrogen Replacement Therapy ◽

Estrogen Therapy ◽

Abdominal Distension ◽

Estrogen Replacement ◽

Laboratory Findings ◽

Coagulation Parameters ◽

Coagulation Function ◽

Patient Reported

A preliminary study was designed to identify if estrogen replacement therapy (E.R.T.) could be correlated with any progressive alterations in blood coagulation function. A total of thirty post menopausal women were assigned to treatment groups and monitored monthly for six months. This presentation relates the laboratory findings of one 55 year old woman who developed significantly altered blood coagulation parameters after two months on conjugated estrogens equine (1.25 mg/day).Routine biochemistry, F.S.H. levels, haematology, and eight standard coagulation tests were done. However, prothrombin time (P.T.), and partial thromboplastin times (P.T.T.), were done on a Coagulation Profiler (T.M.). Assessment of coagulation function was affected through comparison of the patients present P.T. and P.T.T. profiles with pretreatment and reference standard profiles. All aspects of the patient’s coagulation kinetics were altered significantly, in the direction of hyper-coagulation (p< 0.001) with the exception of the P.T. time alone, which was unchanged. Platelet aggregation was impossible, due to spontaneous aggregation during pre-test standing, fibrinogen and euglobulin lysis levels were also raised. The patient reported breast engorgement, abdominal distension and calf tenderness. Two months following E.R.T. discontinuation, the patient’s blood coagulation parameters had all returned to pretreatment levels.The case is discussed within the context of an hypercoagulation syndrome resultant upon an idiosyncratic response to estrogen therapy.

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The Shereshevsky-Turner syndrome: Spontaneous growth and growth-promoting effects of estrogen replacement therapy

Problems of Endocrinology ◽

10.14341/probl12070 ◽

1996 ◽

Vol 42 (4) ◽

pp. 23-27

Author(s):

Ye. В. Koledova ◽

T. V. Semicheva ◽

A. N. Tyulpakov ◽

I. S. Yarovaya ◽

V. A. Peterkova

Keyword(s):

Replacement Therapy ◽

Short Stature ◽

X Chromosome ◽

Growth Retardation ◽

Estrogen Replacement Therapy ◽

Estrogen Therapy ◽

Birth Length ◽

Estrogen Replacement ◽

Spontaneous Growth ◽

Parental Height

Short stature and ovarian failure are typical features of Turner's syndrome (TS). Although growth in TS has been intensively studied, few data are available concerning the influence of different karyotypes and estrogen replacement therapy on the growth of TS patients. This paper presents the first results of studying the growth of TS patients in Russia. Sixty-one girls aged 5 to 17 with TS were examined. Auxological data included parental height (Ht), target Ht, predicted Ht (1), spontaneous Ht, Ht SDS (Tanner), Ht SDS TS (1), birth length, birth length SDS, and Ht SDS for BA before and after estrogen therapy. The diagnosis of TS was confirmed by the identification of the karyotype from peripheral leukocytes. 45,X karyotype was detected in 69%, different types of mosaicism including X chromosome (45,X/46,XX; 45,X/46,X(r)x) in 16%, 46,Xi(q) and deletions of X chromosome in 10%; Y chromosome mosaicism (45,X/46,XY) in 5%. Estrogen replacement (dihydrostilbestrol orally in a daily dose of 1.0 mg) was started at BA11.0 years if no signs of spontaneous puberty were observed. The mean duration of estrogen therapy was 0.960.15 years. A moderate growth delay was seen at birth (0.950.11 Ht SDS). There was no correlation between birth length and parental height (r=0.09 for maternal and r=-0.33 for parental height, respectively). The degree of postnatal growth retardation negatively correlated with CA (r=-0.647; p0.01). Short stature was particularly evident at CA9.0 yrs (-2.460.19 Ht SDS and -3.360.20 Ht SDS, CA9.0 yrs vs. CA9.0 yrs, respectively). The karyotype (45, X or mosaicism) did not influence growth retardation either at birth (49.320.28 cm vs. 48.610.56 cm; p=0.48) or in the postnatal life (p=0.8). Estrogen appreciably accelerated the growth (0.600.14 and 0.800.15 Ht SDS TS, before vs. after estrogen, p=0.006), followed by a decrease of SDS for BA (-1.430.23 vs. -1.800.34, p=0.2). Hence, spontaneous growth in Turner girls in Russia does not appreciably differ from European standards. Short stature progressed with age irrespective of the karyotype (45,X or mosaicism). Low estrogen doses, minimizing the unfavorable effects on BA maturation, are more appropriate for replacement therapy in TS.

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Estrogen Replacement Therapy Increases Plasma Ghrelin Levels

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2004-2016 ◽

2005 ◽

Vol 90 (5) ◽

pp. 2954-2963 ◽

Cited By ~ 44

Author(s):

Eija Kellokoski ◽

Seppo M. Pöykkö ◽

Anna H. Karjalainen ◽

Olavi Ukkola ◽

Jorma Heikkinen ◽

...

Keyword(s):

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Low Density Lipoprotein ◽

Estrogen Therapy ◽

Density Lipoprotein ◽

Very Low Density Lipoprotein ◽

Low Density ◽

Estrogen Replacement ◽

Low Density Lipoprotein Cholesterol ◽

Transdermal Estrogen

Ghrelin is a novel peptide hormone that has GH releasing activity and also other endocrine and metabolic functions. The purpose of this study was to investigate the effects of estrogen replacement therapy on plasma active ghrelin levels in 64 hysterectomized postmenopausal women receiving peroral estrogen (PE) or transdermal estrogen therapy for 6 months. Active ghrelin was measured using commercial RIA. Estrogen therapy increased plasma active ghrelin from 479 ± 118 to 521 ± 123 pg/ml (P = 0.002) among all the study subjects. PE therapy increased plasma ghrelin levels from 465 ± 99 to 536 ± 104 pg/ml (P = 0.001). Transdermal estrogen therapy did not increase plasma ghrelin levels significantly (from 491 ± 132 to 509 ± 138 pg/ml; P = 0.332). The relative changes in plasma ghrelin levels were associated with the relative changes in serum estradiol concentrations (r = 0.299; P = 0.017). During the estrogen therapy, negative associations were found between plasma active ghrelin levels and several plasma lipids (total cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total triglycerides, and very low-density lipoprotein triglycerides). As a conclusion, estrogen replacement therapy increased active plasma ghrelin levels, particularly PE therapy. Additional studies are needed to determine the possible underlying mechanisms.

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Angiogenesis Changes in Ovariectomized Rats with Osteoporosis Treated with Estrogen Replacement Therapy

BioMed Research International ◽

10.1155/2019/1283717 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Yige Zhang ◽

Fei Hua ◽

Kai Ding ◽

Haifeng Chen ◽

Chenyang Xu ◽

...

Keyword(s):

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Bone Microarchitecture ◽

Estrogen Therapy ◽

Ovariectomized Rats ◽

Sham Operation ◽

Dependent Manner ◽

Estrogen Replacement ◽

Sham Operation Group ◽

Menopausal Osteoporosis

To investigate whether angiogenesis changes in early menopausal osteoporosis treated with estrogen replacement therapy, 120 rats were randomly divided into five groups: sham operation group (SHAM), ovariectomy group (OVX), and ovariectomy plus three different estrogen doses replacement therapy groups (OVX + E2). We detected the bone microarchitecture and measured the expression levels of estrogen receptor beta (ERβ), vascular endothelial growth factor (VEGF), osteoprotegerin (OPG), and receptor activator of NF-κB ligand (RANKL). CD31 immunofluorescence and silica gel perfusion imaging were used to analyze the vascular distribution. We confirmed that the femur BMD of ovariectomized rats was significantly lower than SHAM group and OVX+E2 groups. After estrogen therapy, the local microvascular formation increased after estrogen treatment in a dose dependent manner. ERβ was downregulated and VEGF was upregulated, positively correlated with estrogen dosage. We successfully constructed an osteoporosis model of ovariectomized rats with estrogen replacement therapy. We also found angiogenesis changed in early menopausal osteoporosis treated with estrogen replacement therapy. We indicated that estrogen replacement therapy increased angiogenesis through VEGF upregulation. However, we observed that, at the highest doses of estrogen studied, increased angiogenesis was associated with a decrease in BMD, the underlying mechanisms of which remain unclear.

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Menopause and Estrogen Replacement Therapy

Psychiatric Clinics of North America ◽

10.1016/s0193-953x(18)30456-8 ◽

1989 ◽

Vol 12 (1) ◽

pp. 133-152 ◽

Cited By ~ 6

Author(s):

Cynthia A. Stuenkel

Keyword(s):

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Estrogen Replacement

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The Effects of Transdermal Estradiol and Oral Conjugated Estrogens on Haemostasis Variables

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642453 ◽

1994 ◽

Vol 71 (04) ◽

pp. 420-423 ◽

Cited By ~ 100

Author(s):

Ulla-Beth Kroon ◽

G Silfverstolpe ◽

L Tengborn

Keyword(s):

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Hormone Replacement ◽

Plasminogen Activator Inhibitor ◽

Estrogen Replacement ◽

Transdermal Administration ◽

Conjugated Estrogens ◽

Transdermal Estradiol ◽

Estrogen Administration ◽

Activator Inhibitor

SummaryThe effects of oral and transdermal administration of estrogen replacement therapy (ERT) have been fairly well investigated regarding lipoprotein and carbohydrate metabolism, while the effects of different modes of estrogen administration on the haemostatic system have been less well studied.To delineate and compare the effects of perorally administered conjugated estrogens (CE) and transdermally administered estradiol (E2) in doses needed for hormone replacement therapy (HRT) on haemostasis parameters, 23 postmenopausal women were engaged in a study with an open cross-over design. The doses compared (0.625 mg CE and 50 μg E2/24h) are the lowest which, with few exceptions, eliminate climacteric symptoms. Both CE and E2 increased factor VII:C, factor VII:Ag, and the prothrombin fragment1+2. The increase in factor VII:Ag, however, was significantly higher after treatment with CE. These changes were all towards a state of hypercoagulability. Furthermore, CE decreased plasminogen activator inhibitor (PAI) and the thrombin-antithrombin complexes (TAT), as well as antithrombin (ATIII).

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