Jewish Hospital

About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.

Psychiatric assessment of candidates for hand transplantation.

Abstract: An important part of the pretransplant evaluation of candidates for hand transplantation is a psychiatric assessment to formulate psychological benefits and risks of transplantation and determine any appropriate psychosocial interventions to optimize the patient's candidacy for the procedure and prevent psychiatric morbidity. Screening data are presented from 213 individuals who contacted a national referral center for hand surgery regarding hand transplantation, and from the subsequent detailed psychiatric assessments of 9 individuals considering the procedure. Most of the nine patients undergoing intensive psychiatric assessment were assessed as demonstrating an overall favorable profile of psychological benefits and risks. In addition to providing information regarding the psychological experience of patients with amputations and their motivation for hand transplantation, it is hoped this information, as compared with posttransplant outcome data, will help further refine the assessment of candidates for this procedure and possibly other forms of composite tissue allotransplantation. © 2000 Wiley-Liss, Inc. Microsurgery 20:453–457 2000

Plasminogen activator inhibitor activity, 4G5G polymorphism of the plasminogen activator inhibitor 1 gene, and first-trimester miscarriage in women with polycystic ovary syndrome.

Abstract: We assessed whether hypofibrinolytic plasminogen activator inhibitor 1 (PAI-1 activity) showed an independent association with first-trimester miscarriage in the 430 women with polycystic ovary syndrome (PCOS) who had previous pregnancies (from a cohort of 967 women with PCOS). Prospectively, we hypothesized that Glucophage (Bristol-Myers Squibb, Princeton, NJ) promotes successful live births in women with PCOS by lowering PAI-1 activity before conception and maintaining further reductions of PAI-1 activity during the first trimester of pregnancy. We also assessed whether PAI-1 activity levels were independently related to PAI-1 genotype and to modifiable risk factors body mass index (BMI), insulin, and triglyceride. By stepwise logistic regression, with the dependent variable being previous pregnancy outcomes at 3 levels (live birth pregnancies only [n = 208]; both ≥1 live birth and ≥1 first-trimester miscarriage [n = 111]; or first-trimester miscarriages only [n = 71]) and explanatory variables PAI-1 genotype, PAI-1 activity, insulin, homeostasis model assessment of insulin resistance, BMI, and triglyceride, PAI-1 activity was positively associated with first-trimester miscarriage (P = .004). For each 5 IU/mL increment in PAI-1 activity, the risk being in an adverse first-trimester miscarriage category increased (odds ratio, 1.12; 95% confidence interval, 1.04-1.20). Prospectively, from pretreatment to the last preconception visit on Glucophage, in 30 women who subsequently had live births, PAI-1 activity fell 44%, but rose 19% in 23 women with first-trimester miscarriage (P = .03). In the 30 women with live birth pregnancies, median PAI-1 activity fell continuously from pretreatment through the first trimester (from 16.8 to 6.7 IU/mL), whereas PAI-1 activity was either unchanged or rose in women with first-trimester miscarriage. Of the 921 women with PCOS who had 4G5G data, 718 (78%) had 4G4G-4G5G genotypes vs 87 (69%) of 126 normal female controls (χ2 = 4.95, P = .026). The 4G allele frequency was 53% in women with PCOS vs 46% in controls (χ2 = 4.3, P = .04). Of the 866 women with PCOS who had PAI-1 activity data, by stepwise regression, positive independent determinants of PAI-1 activity included BMI (partial R2 = 10.6%, P

Testosterone therapy, thrombosis, thrombophilia, cardiovascular events.

Abstract: There are similar time intervals between starting testosterone therapy (TT) and development of thrombotic (~4.5 months) or cardiovascular (CVD) events (~3 months) which may, speculatively, reflect a shared pathophysiology. We have described thrombotic events 5 months (median) after starting TT in 38 men and 4 women, including 27 with deep venous thrombosis-pulmonary embolism, 12 with osteonecrosis, 1 with central retinal vein thrombosis, 1 with amaurosis fugax, and 1 with spinal cord infarction. In 8 men whose TT was continued, second thrombotic events occurred despite adequate anticoagulation with Coumadin in 8 men, 3 of whom had a third thrombotic event. Of these 42 cases, 40 had measures of thrombophilia-hypofibrinolysis, and 39 were found to have previously undiagnosed thrombophilia-hypofibrinolysis. Before beginning TT, especially in men with previous history of thrombotic events, we suggest that, at a minimum, measurements be made for the Factor V Leiden and Prothrombin mutations, Factors VIII and XI, and homocysteine, to identify men who should not receive TT. We need prospective data focused on whether there should be pre-TT screening based on history of previous venous thromboembolism or for all subjects for major gene thrombophilias. To better resolve questions about TT and all cause and cardiovascular morbidity and mortality and thrombosis, a long term, prospective, randomized, blinded study following the example of the Women's Health Initiative is needed. While we wait for prospective placebo-controlled TT outcome data, TT should be restricted to men with well-defined androgen deficiency syndromes.

Metformin therapy throughout pregnancy reduces the development of gestational diabetes in women with polycystic ovary syndrome

Abstract: Women with polycystic ovary syndrome (PCOS) characteristically are obese and have insulin resistance and hyperinsulinemia-all risk factors for gestational diabetes. Conversely women who develop gestational diabetes are likely to have polycystic ovaries. The investigators evaluated treatment with metformin, a safe and effective insulin-sensitizing drug, in forestalling the development of gestational diabetes in 72 women with established PCOS. All were nondiabetic before their pregnancies and had had at least one live birth. Thirty-three women conceived while taking metformin in a dose of 2.55 gm daily, and were studied prospectively. All but five of these women took the drug throughout pregnancy, and there were 34 live births. The remaining 39 women with PCOS were studied retrospectively. They had a total of 64 live births, for 60 of which information on gestational diabetes was available. Women in the prospective group were placed on a high-protein, low-carbohydrate diet with 30% calories as fat. Women were screened for gestational diabetes with a 100-gm glucose challenge at 26 to 28 weeks' gestation. Both groups of women were insulin-resistant with high fasting insulin levels and had elevated insulin secretion. Only one woman in the prospective series (3% of pregnancies) developed gestational diabetes, contrasting with 67% of their previous pregnancies in the absence of metformin therapy. Gestational diabetes developed in 23% of pregnancies in the retrospective group. The overall incidence in all live births without metformin therapy was 31%. The odds ratio of gestational diabetes in pregnancies of metformin-treated women compared to those not receiving metformin was 0.115 (95% CI, 0.014-0.938). Women taking metformin throughout their pregnancies had decreases in body weight and body mass index. At the same time, insulin levels and insulin resistance both declined and did not change significantly during the rest of pregnancy. No woman taking metformin developed lactic acidosis. Intermittent diarrhea or gastritis was common in the first 3 weeks of treatment, but subsequently resolved spontaneously. None of 34 live-born infants were hypoglycemic or had major malformations. A substantial reduction in risk of gestational diabetes is observed when women with PCOS take metformin throughout pregnancy. The drop in insulin resistance and insulin secretion decreases the secretory demands placed on the pancreatic beta cells.