Socio-demographic and Clinico-epidemiological Study of Scrub Typhus in A Tertiary Care Hospital of Mymensingh, Bangladesh.

Scrub typhus is one of the leading causes of undifferentiated treatable febrile illness in Asia pacific region. It is grossly under diagnosed in many tropical countries of South Asia including Bangladesh, due to wide range of non-specific clinical presentations, low index of suspicion among clinicians, limited awareness and lack of accurate diagnostic facilities. This cross sectional observational study was conducted at department of Microbiology, Mymensingh Medical College, Mymensingh, Bangladesh from March 2019 to February 2020 enrolling 113 diagnosed cases of scrub typhus by Immunochromatographic test (ICT) and / or Nested PCR to characterize the socio-demographic and clinico-epidemiological features of scrub typhus in Mymensingh area. Majority of the scrub typhus cases came from rural areas (63.83%) and there was a slight female predominance (52.21%). The young (32.74%) and the young-adult age group (28.31%) were mostly affected. Most of the scrub typhus cases were housewives (30.98%), followed by farmers (23.89%) and students (21.23%). All the enrolled cases presented with fever. Other findings were myalgia (76.10%), headache (56.63%), cough (30.97%), vomiting (12.38%) and Respiratory distress (9.73%). Typical eschar of scrub typhus was present only in 9(7.96%) cases and 4(3.53%) patients had rashes on their skin. Few cases (3.53%) had jaundice and 15.96% cases were anaemic. Oliguria (7.96%) and neck rigidity (1.76%) were also documented. Most of the Nested PCR positive scrub typhus cases were documented during late rainy season and beginning of winter months. Findings of the study may offer increased awareness about high burden of scrub typhus as well as heightened suspicion among clinicians for early diagnosis, timely treatment and prevention of complications.

Rapid Serologic and Molecular Diagnosis of Scrub Typhus among Suspected Febrile Patients Visiting Mymensingh Medical College Hospital.

Scrub typhus, caused by the bacterium- Orientia tsutsugamushi is one of the leading causes of undifferentiated treatable febrile illness in Asia pacific region. It is grossly under diagnosed in many tropical countries of South Asia including Bangladesh, due to wide range of non-specific clinical presentations, low index of suspicion among clinicians, limited awareness and lack of accurate diagnostic facilities. This cross-sectional descriptive study was conducted at Department of Microbiology, Mymensingh Medical College to diagnose scrub typhus by rapid Immunochromatographic test (ICT) as well as molecular detection of O. tsutsugamushi by Nested PCR and automated nucleotide sequencing among suspected febrile patients in Mymensingh, Bangladesh during 2019-20. Blood samples were collected from 402 febrile patients of suspected Rickettsial illness, referred from inpatient and outpatient departments of Medicine and Pediatrics, Mymensingh Medical College Hospital (MMCH). Among the enrolled 402 patients, 89 samples (22.13%) were seropositive by Immunochromatographic test (ICT) and 65 samples (16.16%) were positive for O. tsutsugamushi DNA by Nested PCR, targeting 47KDa gene. Therefore, 113/402 (28.10%) samples were positive for scrub typhus by PCR and/ or ICT. Highest number of patients was detected positive by nested PCR during the first 5-10 days of fever but only 2 cases were positive after 20 days. In case of ICT, highest positivity for only IgM (8.13%) and both antibodies (2.43%) were documented in first 5-10 days of fever, but IgG positivity was highest (41.66) in >20 days of fever. From 65 PCR positive samples, automated nucleotide sequencing was performed on 20 randomly selected samples and all were genetically confirmed to be O. tsutsugamushi.

Vesicouterine fistula after vacuum delivery and two previous cesarean sections. A case report.

BACKGROUND: Vesicouterine fistulas are associated with cesarean section and more rarely with vaginal birth after cesarean (VBAC). Many surgical approaches exist, including hysterectomy. CASE: A vesicouterine fistula was diagnosed after VBAC in a 34-year-old multipara with two previous cesarean sections. The defect failed to close after four months of bladder drainage. Closure via laparotomy with an omental flap and preservation of the uterus was successful. CONCLUSION: Vesicouterine fistula can occur after VBAC, and failure of conservative therapy can be treated abdominally with preservation of the uterus.

Effect of feedback on obstetrics and gynecology residents' teaching performance and attitudes.

OBJECTIVE: To evaluate obstetrics and gynecology residents' teaching performance, perception of the importance of teaching and satisfaction with their evaluations after the institution of an oral or written medical student feedback and award system. STUDY DESIGN: Residents at a single, university-based obstetrics and gynecology program were assigned to receive either oral, written or no medical student feedback on their teaching skills in a prospective, randomized, controlled trial. Students rated resident performance in seven teaching categories. Residents' scores per six-week block were evaluated for one year. Questionnaires addressing resident attitudes toward feedback were collected at baseline and at 6 and 12 months. All residents then received written feedback and public awards for high scores for an additional year. RESULTS: After 12 months of feedback there were trends toward improvement in several of the teaching categories and overall evaluations. None of the controls, 29% of residents receiving oral feedback and 50% of residents receiving written feedback rated teaching as more important than before. None of the controls, 57% of those receiving oral feedback (P = NS) and 88% of those receiving written feedback (P = .009), for a total of 73% of residents receiving any feedback (P = .001), thought that the amount of feedback was adequate at 12 months. Follow-up of 15 residents after one year of written feedback with an award for high evaluations showed that 60% improved their overall scores. The mean overall group score improved. CONCLUSION: A feedback and award system can lead to improved resident teaching performance as well as enhanced perception of residents' role as teachers and greater resident satisfaction.

Video vs. CD-ROM for teaching pelvic anatomy to third-year medical students. A comparison.

OBJECTIVE: To compare the effectiveness and student acceptance of video and CD-ROM review of pelvic anatomy in third-year obstetrics and gynecology students. STUDY DESIGN: A 34-item pretest was administered on the first day of the clerkship. Students were then randomized to watch a 45-minute video or use an interactive CD-ROM at home. All students took a posttest identical to the pretest. Examination scores were compared by paired and unpaired t test. Students completed a questionnaire on each method's ease, appropriateness, organization, appeal and time spent and whether they would recommend the method to others. RESULTS: One hundred seventy-six students were randomized, 88 to CD and 88 to video. There was 100% compliance, although not all questionnaire items were completed. The mean pretest score for both groups was 50%. The posttest CD mean score was significantly different from the posttest video mean (64% vs. 70%). Both groups significantly improved after the intervention. The video group noted ease of use, but only 49% recommended it for the future. The CD-ROM was recommended by 80%. Student comments favored the CD-ROM. CONCLUSION: Use of video review resulted in short-term significantly higher test scores, but students preferred an interactive CD-ROM. This method should be made available to all students during the rotation.

Stimulation of macrophages by retinal proteins: production of reactive nitrogen and oxygen metabolites.

PURPOSE: In previous work, it has been shown that in experimental autoimmune uveitis, the peroxynitrite-mediated protein nitration product nitrotyrosine was localized in the degenerating photoreceptors. Subsequently, phagocyte-generated inducible nitric oxide synthase (iNOS) was also found to localize, primarily in the outer retina and to a lesser extent in the anterior segments. This study was intended to determine whether retinal soluble proteins such as S-antigen and interphotoreceptor retinoid-binding protein (IRBP) play a role in the induction of *NO and superoxide by a macrophage cell line and by rat and rabbit peritoneal macrophages. METHODS: Cells from the murine macrophage cell line RAW 264.7 and rat and rabbit peritoneal macrophages were incubated in the presence of retinal soluble proteins. The nitrite level in the cultured supernatant was evaluated for *NO production using the Griess reaction. Activation of nuclear transcription factor kappaB (NF-kappaB) was determined by electrophoretic mobility shift assay. Superoxide production was measured by superoxide dismutase-inhibitable reduction of cytochrome C. RESULTS: Both S-antigen and IRBP induced significant, dose-dependent nitrite production in RAW 264.7 and rat peritoneal macrophages. Induction of iNOS by retinal proteins was inhibited by the iNOS-specific inhibitor aminoguanidine and the tyrosine kinase inhibitor genistein. This iNOS induction was accompanied by the activation of NF-kappaB. S-antigen also induced superoxide production in rabbit peritoneal macrophages, but not in RAW 264.7. CONCLUSIONS: These results show that soluble retinal proteins significantly induce *NO and superoxide production by macrophages. Increased production of reactive oxygen species by macrophages in the presence of these soluble retinal proteins in vivo may accelerate photoreceptor degeneration in uveitis.

Cobalt chloride-induced signaling in endothelium leading to the augmented adherence of sickle red blood cells and transendothelial migration of monocyte-like HL-60 cells is blocked by PAF-receptor antagonist.

In response to hypoxia, sickle red blood cells (SS RBC) and leukocytes exhibit increased adherence to the vascular endothelium, while diapedesis of leukocytes through the blood vessel increases. However, the cellular signaling pathway(s) caused by hypoxia is poorly understood. We utilized CoCl2 as a mimetic molecule for hypoxia to study cellular signaling pathways. We found that in human umbilical vein endothelial cells (HUVEC), CoCl2 at 2 mM concentration induced the surface expression of a subset of CAMs (VCAM-1) and activation of transcription factor NF-kappaB in the nuclear extracts of HUVEC. Furthermore, CoCl2 also caused time-dependent tyrosine phosphorylation of mitogen-activated protein (MAP) kinase isoform ERK2 without significantly affecting ERK1, indicating ERK2 is the preferred substrate for upstream kinase of the MAPK pathway. Inhibitors of MAP kinase (PD98059) or platelet-activating factor (PAF)- receptor antagonist (CV3988) inhibited the CoCl2-induced NF-kappaB activation and VCAM-1 expression. Augmented expression of VCAM-1 led to increased SS RBC adhesion, inhibitable by a VCAM-1 antibody. Additionally, CoCl2 caused a two- to threefold increase in the rate of transendothelial migration of monocyte-like HL-60 cells and a twentyfold increase in phosphorylation of platelet endothelial cell adhesion molecules (PECAM-1). The transendothelial migration of monocytes was inhibited by an antibody to PECAM-1. Both phosphorylation of PECAM-1 and transendothelial migration of monocytes in response to CoCl2 were inhibited by protein kinase inhibitor (GF109203X) and augmented by protein phosphatase inhibitor (Calyculin A). Our data suggests that CoCl2-induced cellular signals directing increased expression of VCAM-1 in HUVEC involve downstream activation of MAP kinase and NF-kappaB, while the phosphorylation of PECAM-1 occurs as a result of activation of PKC. We conclude that PAF-receptor antagonist inhibits the CoCl2- or hypoxia-induced increase in the adhesion of SS RBC, PECAM-1 phosphorylation, and the concomitant transendothelial migration of monocytes.

Interaction of sickle erythrocytes with endothelial cells in the presence of endothelial cell conditioned medium induces oxidant stress leading to transendothelial migration of monocytes.

The abnormal adherence of sickle red blood cells (SS RBC) to endothelial cells has been thought to contribute to vascular occlusion, a major cause of morbidity in sickle cell disease (SCD). We determined whether the interaction of SS RBC with cultured endothelial cells induced cellular oxidant stress that would culminate in expression of cell adhesion molecules (CAMs) involved in the adhesion and diapedesis of monocytes and the adherence of SS reticulocytes. We showed that the interaction of SS RBC at 2% concentration in the presence of multimers of von Willebrand factor (vWf), derived from endothelial cell-derived conditioned medium (E-CM) with cultured human umbilical vein endothelial cells (HUVEC), resulted in a fivefold increased formation of thiobarbituric acid-reactive substances (TBARS) and activation of the transcription factor NF-kB, both indicators of cellular oxidant stress. Normal RBC show none of these phenomena. The oxidant stress-induced signaling resulted in an increased surface expression of a subset of CAMs, ICAM-1, E-selectin, and VCAM-1 in HUVEC. The addition of oxygen radical scavenger enzymes (catalase, superoxide dismutase) and antioxidant (probucol) inhibited these events. Additionally, preincubation of HUVEC with a synthetic peptide Arg-Gly-Asp (RGD) that prevents vWf-mediated adhesion of SS RBC reduced the surface expression of VCAM-1 and NF-kB activation. Furthermore, SS RBC-induced oxidant stress resulted in a twofold increase in the transendothelial migration of both monocyte-like HL-60 cells and human peripheral blood monocytes, and approximately a sixfold increase in platelet-endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation, each of which was blocked by protein kinase C inhibitor and antioxidants. These results suggest that the adherence/contact of SS RBC to endothelial cells in large vessel can generate enhanced oxidant stress leading to increased adhesion and diapedesis of monocytes, as well as heightened adherence of SS reticulocytes, indicating that injury/activation of endothelium can contribute to vaso-occlusion in SCD.

Endotoxin-induced migration of monocytes and PECAM-1 phosphorylation are abrogated by PAF receptor antagonists.

The trafficking of monocytes across the endothelial lining of the blood vessel increases in response to bacterial infection at sites of inflammation. However, the molecular events involved in the diapedesis of monocytes in response to endotoxin are not completely understood. Our studies revealed that signaling by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC) resulted in a threefold increase in the transendothelial migration of monocyte-like HL-60 cells and a sevenfold increase in the phosphorylation of platelet endothelial cell adhesion molecule-1 (PECAM-1). The transmigration induced by LPS was inhibited by an antibody to PECAM-1. Both the phosphorylation of PECAM-1 and transendothelial migration of monocytes were inhibited by a platelet-activating factor (PAF) receptor antagonist, indicating the autocrine effect of PAF in these events. Treatment of HUVEC with LPS caused a fourfold increase in PAF receptor mRNA expression that was completely blocked by the PAF receptor antagonist. We conclude that PAF, generated by HUVEC in response to LPS or gram-negative bacterial infection, acts in an autocrine manner, causing PECAM-1 phosphorylation and thus the transendothelial migration of monocytes.

Oxidant stress-induced transendothelial migration of monocytes is linked to phosphorylation of PECAM-1.

Reactive oxygen species (ROS) are believed to cause vascular injury in the pathophysiology of atherosclerosis, diabetes, and vasoocclusion in sickle cell disease. Studies have shown that ROS causes increased adhesion of monocytes and neutrophils to the endothelium. We investigated the effects of tert-butylhydroperoxide (t-BuOOH), an inducer of oxidant stress, to determine the cellular signaling pathway leading to the transendothelial migration of polymorphonuclear leukocytes. Our studies revealed that signaling by t-BuOOH in human umbilical vein endothelial cells (HUVECs) causes a twofold increase in the transendothelial migration of monocyte-like HL-60 cells and a fivefold increase in platelet endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation. The transmigration induced by t-BuOOH was inhibited by an antibody to PECAM-1. These events were inhibited by antioxidants and inhibitors of protein kinase C, p21ras and glutathione synthesis. However, treatment of HUVECs with the phosphatase inhibitor calyculin A augmented the t-BuOOH-mediated transendothelial migration of monocytes and PECAM-1 phosphorylation. Our results suggest that oxidative stress can induce the transendothelial migration of monocytes as a result of phosphorylation of PECAM-1, a crucial event in the diapedesis of leukocytes during pathophysiology of vascular diseases.

Diabetic RBC-induced oxidant stress leads to transendothelial migration of monocyte-like HL-60 cells.

Red blood cells (RBC) from patients with diabetes mellitus exhibit an increased propensity to adhere to cultured human umbilical vein endothelial cells (HUVEC) as a result of interaction of advanced glycation end products with their counter receptors, contributing to the pathogenesis of vascular complications. We determined whether the interaction of diabetic RBC with HUVEC induced cellular oxidant stress that would culminate in adherence and diapedesis of monocytes, these being initiating events in endothelial injury and atherogenesis. We show that the adherence of diabetic RBC (2% hematocrit), but not normal RBC, to HUVEC results in a fourfold increase in the production of lipid peroxides. Furthermore, diabetic RBC-induced oxidant stress causes a sixfold increase in platelet endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation and doubles transendothelial migration of monocyte-like HL-60 cells; both are blocked by antioxidants and protein kinase C (PKC) inhibitors. Our results show that the adherence of diabetic RBC to endothelial cells initiates a cascade of cellular events resulting in PKC activation, causing PECAM-1 phosphorylation and concomitant transendothelial migration of monocytes. The increased diapedesis of monocytes, brought about by the interaction of diabetic RBC across vascular endothelium, may play an important role in accelerated atherosclerosis and cardiovascular disease in diabetics.

Morbidity and mortality of incontinence surgery in elderly women: an analysis of Medicare data.

OBJECTIVE: Our purpose was to examine length of hospital stay, complications, morbidity, and mortality associated with surgery for urinary incontinence in women > 65 years old. STUDY DESIGN: Data obtained from Medicare billing forms (HCFA form 1450, UB-82, UB-92) in the Medicare Provider Analysis and Review Record database for surgical procedures done for incontinence (international Classification of Diseases, Ninth Revision, codes 59.3 to 59.79) from 1984 to 1991 were reviewed. Comorbidities and reasons for readmission were extracted from secondary diagnosis codes. RESULTS: There wee 66,478 patients in the cohort. The mean and median ages were 71 years. The 30-day surgical mortality was 0.33%. Length of stay and mortality increased linearly with age. Acute events associated with death were myocardial infarction (14.2% of deaths), cerebrovascular accident (stroke) (14.6%), pulmonary embolism or deep vein thrombosis (9.7%), and pneumonia (2.7%). Patients who died had higher rates of diabetes and heart failure but not of hypertension. The 30-day readmission rate was 4.8% with higher rates in patients > 80 years old. Urinary tract infection (12.2%), hypertension (16%), and unspecified complications (9%) were the most frequent diagnoses on readmissions. Myocardial infarction, pulmonary embolism, cerebrovascular accident, deep vein thrombosis, and pneumonia each occurred in only 1%. CONCLUSION: Incontinence surgery is safe in the "young elderly." Those > 80 years old and with certain chronic illness should be counseled about increased risks.

Hypoxia induces PECAM-1 phosphorylation and transendothelial migration of monocytes.

Polymorphonuclear neutrophils (PMN) adhere to the vascular endothelium under hypoxic conditions, causing microvascular injury. The molecular mechanism of hypoxia-induced adhesion of PMN to and diapedesis through the vascular endothelium is poorly understood. We examined the effects of hypoxia on the transendothelial migration of monocytes. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in Transwell chambers under low oxygen tension (3% O2 compared with 21% O2) resulted in an increased rate of migration of both monocyte-like HL-60 cells and human peripheral blood monocytes. Migration was inhibited by addition of an antibody to platelet endothelial cell adhesion molecule-1 (PECAM-1), a protein kinase C (PKC) inhibitor, or a platelet-activating factor (PAF)-receptor antagonist. In HUVEC, hypoxic conditions (1, 3, 5, and 14% O2) increased the phosphorylation of PECAM-1. The extent of phosphorylation of PECAM-1 was inversely related to the concentration of oxygen to which HUVEC were exposed. Hypoxia-induced phosphorylation of PECAM-1 was inhibited by either a PKC inhibitor or a PAF-receptor antagonist, indicating the involvement of hypoxia-induced release of PAF in both PKC activation and the concomitant phosphorylation of PECAM-1. These results were substantiated by the findings that treatment of HUVEC with 100 nM PAF under normoxic conditions augmented 11.8-fold the phosphorylation of PECAM-1 and twofold increase in the transendothelial migration of monocyte-like HL-60 cells. We conclude that PAF, produced by cultured endothelial cells in response to hypoxia, acts in an autocrine fashion to activate PKC, causing PECAM-1 phosphorylation and thus the transendothelial migration of monocytes.

Glucose-induced transmigration of monocytes is linked to phosphorylation of PECAM-1 in cultured endothelial cells.

The adherence of circulating monocytes to the endothelium, their migration into the subendothelium, and the subsequent formation of foam cells are initial events in the pathogenesis of atherosclerosis. However, the effect of hyperglycemia on the transendothelial migration of monocytes is not known. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in a Transwell chamber to 25 mM D-glucose (a concentration representing a hyperglycemic state) for 2 h resulted in a twofold increase in the migration of vitamin D3-differentiated monocyte-like HL-60 cells. The migration was inhibited by addition of either an antibody to platelet-endothelial cell adhesion molecule-1 (PECAM-1) or a protein kinase C inhibitor, GF-109203X. In HUVEC, high concentrations of D-glucose (25 mM), but not of other sugars such as L-glucose, 2-deoxyglucose, D-galactose, or D-mannitol, caused a sevenfold increase in the phosphorylation of PECAM-1 as a result of activation of protein kinase C. The 25 mM D-glucose-induced PECAM-1 phosphorylation and transmigration of monocyte-like HL-60 cells were further increased by treatment of HUVEC with the phosphatase inhibitor calyculin A. These results suggest that direct phosphorylation of PECAM-1 in response to elevated glucose promotes transendothelial migration of monocytes, contributing to accelerated atherogenesis in diabetics.

Lipoxygenase metabolites induced expression of adhesion molecules and transendothelial migration of monocyte-like HL-60 cells is linked to protein kinase C activation.

Studies have shown that, among lipoxygenase metabolites examined, 15(S)-hydroperoxy-5,8,11,13-eicosa-tetraenoic acid (15[S]-HPETE), at micromolar concentrations, selectively causes injury to cultured endothelial cells. We investigated whether physiologically relevant concentrations of lipoxygenase metabolites affected the expression of cell adhesion molecules (CAMs) involved in the adhesion of leukocytes and/or the accumulation of leukocytes in the vascular endothelium, these being the initial events in endothelial cell injury. Among lipoxygenase metabolites, 15(S)-HPETE and 12(S)-HETE, at nanomolar concentrations, induced surface expression of a subset of cell adhesion molecules (CAM), ICAM-1, ELAM-1, and VCAM-1, in human umbilical vein endothelial cells (HUVEC), which is associated with an increased binding activity of the transcription factor, NF-kappa B, to the consensus motif common to the CAM genes in the HUVEC nuclear extracts. Furthermore, 15(S)-HPETE (1 nM) caused a threefold increase in the rate of transendothelial migration of vitamin D3-differentiated HL-60 monocyte-like cells and showed a thirtyfold increase in the phosphorylation of PECAM-1, an adhesion molecule involved in endothelial cell-cell adhesion. Both an antibody to PECAM-1 and the protein kinase C inhibitor, GF 109203X, reduced 15(S)-HPETE-induced transmigration of monocyte-like HL-60 cells by approximately 75% and 85%, respectively. Treatment of HUVEC with a phosphatase inhibitor, calyculin A, augmented both the phosphorylation of PECAM-1 and transmigration of monocyte-like HL-60 cells induced by 15(S)-HPETE. Our results show that 15(S)-HPETE, at physiological concentrations, induced activation of protein kinase C in HUVEC and leads to the phosphorylation of PECAM-1, thus facilitating the migration of monocyte-like HL-60 cells across the endothelial cell monolayer. It is suggested that phosphorylation/dephosphorylation events in PECAM-1 are important in regulating the trafficking of monocytes across the endothelial cell monolayer.

Cigarette smoke condensate-induced adhesion molecule expression and transendothelial migration of monocytes.

Cigarette smoking is clearly linked with increased incidence of atherosclerosis and cardiovascular disease. The adherence of blood monocytes to the endothelium, followed by their migration beneath the endothelium, are initiating events in the formation of foam cells, promoting atherogenesis. We show that cigarette smoke condensate (CSC)-induced surface expression of a subset of cell adhesion molecules (CAM) [intercellular adhesion molecule 1 (ICAM-1), endothelial leukocyte adhesion molecule 1 (ELAM-1), and vascular cell adhesion molecule 1 (VCAM-1)] in human umbilical vein endothelial cells (HUVEC) is associated with an increase in the binding activity of nuclear transcription factor NF-kappa B to the consensus motif common to the CAM genes. Furthermore, CSC (25 microgram/ml) both increases the rate of transendothelial migration of vitamin D3-differentiated monocyte-like cells across the HUVEC monolayer by 200% and causes an approximately 10-fold increases in the phosphorylation of platelet endothelial CAM (PECAM-1), an adhesion molecule located at intercellular junctions and involved in endothelial cell-cell adhesion. Our results show that CSC-induced activation of protein kinase C in endothelial cells initiates a signaling pathways, leading to heightened binding of NF-kappa B to specific DNA sequences, which in turn increases surface expression of the subset of CAMs. Furthermore, our studies demonstrate a link between the phosphorylation of PECAM-1 and the migration of blood monocytes across vascular endothelium.

Laparoscopy vs. laparotomy for gynecologic procedures. Impact on resident training.

OBJECTIVE: To compare laparoscopic approaches to traditional ones for operative procedures. STUDY DESIGN: Operating residents collected data on all abdominal, vaginal and laparoscopic vaginal hysterectomies, myomectomies, cystectomies/oophorectomies and ectopics between December 1, 1992, and July 31, 1993. Statistical analysis included Student's t test for interval data and chi (2)/Fisher's exact test for categorical data. RESULTS: Leiomyomas were the major indications for all three types of hysterectomy. Patients selected for vaginal hysterectomy had significantly higher parity and older age than those scheduled for abdominal hysterectomy or laparoscopically assisted vaginal hysterectomy (LAVH). Abdominal hysterectomy uteri were larger than those using vaginal or LAVH procedures. LAVH procedures were significantly longer when failed laparoscopic procedures were excluded. Abdominal hysterectomy patients used twice as much morphine as vaginal and LAVH patients, and the length of stay was longer. LAVH was significantly more expensive than vaginal hysterectomy. There was no difference in operating time for nonhysterectomy cases, but the cost and length of stay were less for laparoscopy. CONCLUSION: Laparoscopy can be advantageous for certain procedures but has little advantage for hysterectomy and may make fewer vaginal hysterectomies available for resident education since the patients selected for LAVH and total vaginal hysterectomy are more similar to each other than to patients selected for total abdominal hysterectomy.

Urethral closure pressure and leak-point pressure in incontinent women.

OBJECTIVE: To examine the association between maximum urethral closure pressure and Valsalva leak-point pressure in women with genuine stress incontinence (GSI). METHODS: Fifty-six women with GSI were evaluated in a urodynamics laboratory. Maximum urethral closure pressure and vesical leak-point pressure were measured with multichannel urodynamic testing. The correlation coefficient and regression line were calculated. RESULTS: Forty subjects demonstrated a leak on Valsalva maneuver and, in these women, maximum urethral closure pressure and leak-point pressures were related significantly (r = 0.62, P < .001). The relationship was strongest between leak-point pressure up to 120 cm H2O and absolute vesical pressure with Valsalva rather than with a change in vesical pressure. The sensitivity of leak-point pressure for predicting low urethral pressure was 100%. CONCLUSION: There is a correlation between maximum urethral closure pressure and leak-point pressure that can provide useful information about incontinence in women.

Estrogen and urinary incontinence in women.

OBJECTIVE: The purpose of this study was to review the efficacy of estrogen therapy for urinary incontinence by examining published trials and to review the epidemiologic and physiologic evidence for its action. DATA SOURCES: Controlled and uncontrolled trials of estrogen therapy in the English literature were collected. Eight controlled and 14 uncontrolled trials were identified. METHODS OF STUDY SELECTION: Trials were selected if they were prospective. All types of estrogen treatment were included. All types of outcome measurements were included. DATA EXTRACTION AND SYNTHESIS: Trials were categorized by type of estrogen used; outcome variables (subjective improvement vs objective urodynamic data); and cure/improvement rates. CONCLUSIONS: Published trials do not support estrogen replacement as efficacious therapy for stress urinary incontinence. It may be useful for incontinence associated with urgency and frequency. Adequately large controlled trials that evaluate estrogen replacement regimens used in the USA remain to be done.

Outcome of laparoscopic versus traditional surgery for ectopic pregnancies.

OBJECTIVE: To compare pregnancy rates after three surgical procedures for ectopic pregnancy (EP) over a 9-year period for normal and infertility patients. DESIGN: In a retrospective analysis, we examined crude pregnancy rates and life-table analysis of cumulative pregnancy rates. A proportional hazard regression model was used to examine relative risk of type of surgery and fertility rates. PATIENTS, PARTICIPANTS: One hundred twenty-six cases of EPs were reviewed at the Cleveland Clinic Foundation, a tertiary institution. MAIN OUTCOME MEASURES: Comparisons of rates of viable term deliveries were calculated between three types of surgery and were stratified according to the status of infertility. Confidence intervals for relative risk of surgery and fertility status on future pregnancy were calculated. RESULTS: No difference in pregnancy rates was observed after the three procedures (P = 0.08). Normals had a significantly higher (4 times higher) pregnancy rate than infertility patients, independent of surgical procedure. CONCLUSION: Successful pregnancy after EP is related to history of infertility rather than type of surgery to treat ectopic event. More randomized study is needed to examine laparoscopic salpingostomy, especially in patients with other infertility problems.