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PubMed1984

Electrocardiographic abnormalities in apparently healthy men and the risk of sudden death.

Identification of individuals at increased risk of sudden cardiac death is an important but difficult problem, especially in persons without clinically apparent heart disease. The ability of the electrocardiogram (ECG) to predict sudden death was determined in a study of 3983 men who were 30.8 years of age (mean) at entry and who had been followed with regular examinations, including ECGs. During the 30-year observation period, 70 cases of sudden death occurred in men without previous clinical manifestations of heart disease. Electrocardiographic abnormalities were detected before sudden death in 71.4% of cases. The abnormalities were, in decreasing order of frequency, ST segment and T-wave abnormalities, ventricular extrasystoles, left ventricular hypertrophy, complete left bundle branch block, and pronounced left axis deviation. When these electrocardiographic findings in men without clinical manifestations of heart disease were related prospectively to the incidence of sudden death, ST segment and T-wave abnormalities, ventricular extra-systoles, left ventricular hypertrophy and complete left bundle branch block were significant predictors of sudden death, while left axis deviation and right bundle branch block were not significant predictors of sudden death. Increased severity of primary T-wave abnormalities and the association of ST segment and T-wave abnormalities with increased QRS voltage further increased the sudden death risk. The combination of ventricular extrasystoles with either ST-T abnormalities or left ventricular hypertrophy considerably increased the risk of sudden death. Thus, these data indicate that electrocardiographic abnormalities detected on routine examination in men without clinical evidence of heart disease identify men at an increased risk of sudden death.

Adult↗
PubMed2006

Abnormalities on MRI of the subscapularis tendon in the presence of a full-thickness supraspinatus tendon tear.

OBJECTIVE: Our objective was to determine the association between size and chronicity of full-thickness supraspinatus tendon tears with subscapularis tendon abnormalities on MRI. MATERIALS AND METHODS: One hundred forty-two MRI examinations with full-thickness supraspinatus tendon tears were categorized on the basis of the supraspinatus muscle (SS): normal muscle (SS(normal)), suggesting a recent or small tear; reduced muscle bulk without fatty atrophy (SS(volume loss)); and those with fatty atrophy, suggesting a large or chronic tear (SS(fatty atrophy)). Subscapularis tendon abnormalities, the subcoracoid interval, and subcortical bone marrow edema in the lesser tuberosity and coracoid process were recorded. RESULTS: The mean size of supraspinatus tendon tears in the SS(normal) (n = 45) group was 8.5 mm, 16.6 mm in SS(volume loss) (n = 53), and 29 mm in the SS(fatty atrophy) group (n = 44). Subscapularis tendon abnormality was identified in 22% of SS(normal) patients, 61% of SS(volume loss), and 86% of the SS(fatty atrophy) group (p < 0.001). There was moderate correlation between chronicity of supraspinatus tendon tears and subscapularis tendon abnormality (r = 0.47; p < 0.0001), with no correlation between the subcoracoid interval and abnormalities of the subscapularis tendon. There was moderate correlation between chronicity of supraspinatus tendon tears and bone marrow changes in the lesser tuberosity (r = 0.44; p < 0.0001). CONCLUSION: Subscapularis tendon abnormality is related to chronicity of supraspinatus tendon tears. Bone marrow edema in the lesser tuberosity with a subscapularis tendon abnormality suggests increased stress at the subscapularis tendon insertion with chronicity of full-thickness supraspinatus tendon tears. Lack of correlation with the subcoracoid interval indicates that anterior instability may be a more important contributing factor to subscapularis tendon abnormalities than static subcoracoid impingement in the setting of a full-thickness supraspinatus tendon tear.

Adult↗
PubMed2001

Sulcal hyperintensity on fluid-attenuated inversion recovery mr images in patients without apparent cerebrospinal fluid abnormality.

OBJECTIVE: Failure to suppress cerebrospinal fluid (CSF) signal intensity (sulcal hyperintensity) on fluid-attenuated inversion recovery (FLAIR) images has been reported in patients with abnormal CSF, such as those with meningitis and subarachnoid hemorrhage. Our study investigates the clinical history and MR findings associated with sulcal hyperintensity on FLAIR images in patients without apparent CSF abnormality. SUBJECTS AND METHODS: Three hundred consecutive MR imaging examinations were prospectively screened for patients with sulcal hyperintensity on FLAIR images. Nine patients with clinical, CT, or laboratory evidence suggesting abnormal CSF were excluded. The distribution of sulcal hyperintensity on FLAIR images and associated abnormal enhancement were evaluated. The presence of the "dirty CSF" sign (mild increase in CSF signal on unenhanced T1-weighted images or mild decrease on T2-weighted images) in the corresponding hyperintense sulcus was also assessed. RESULTS: Twenty-six (8.9%) of the 291 patients had sulcal hyperintensity (16 focal, 10 diffuse) associated with 18 masses (6.1%) and eight vascular abnormalities (2.7%). Sulcal hyperintensity was frequently associated with the dirty CSF sign (69.2%) and abnormal contrast enhancement (overall, 96.2%; 88.5%, leptomeningeal; 53.8%, vascular enhancement). CONCLUSION: Our study shows that sulcal hyperintensity on FLAIR imaging can occur in patients without apparent CSF abnormality. Its frequent association with mass effect, vascular disease, abnormal vascular enhancement, and dirty CSF sign suggests that an increase in blood pool, a small amount of protein leakage, and the "flow-entering" phenomenon of the congested blood may contribute to sulcal hyperintensity on FLAIR images.

Adolescent↗
PubMed2005

Metabolic syndrome and risk of isolated ST-T abnormalities and type 2 diabetes in Japanese male office workers.

Using a modified National Cholesterol Education Program (NCEP) definition of the metabolic syndrome (MS) with body mass index instead of waist circumference, we examined the associations of the MS with the risk of developing ST-T abnormalities in 3405 Japanese men aged 35-59 yr who did not have a history of cardiovascular disease or ST-T abnormalities. Of 3405 participants, 3166 men without type 2 diabetes (as diagnosed with the revised criteria of American Diabetes Association) also constituted a non-diabetic cohort. Examinations including electrocardiogram and fasting plasma glucose were repeated annually for 7 subsequent years. The subjects were classified as having ST-T abnormalities or type 2 diabetes when evidence of either of these disorders was found during at least 2 consecutive annual examinations. After adjustment for potential risk factors, the relative risks of ST-T abnormalities were 1.0 (referent), 2.66, 3.07, 4.27, and 8.40 for the presence of 0, 1, 2, 3, and > or =24 components of the MS, respectively (P for trend <0.001). The corresponding results for the risk of type 2 diabetes were 1.0 (referent), 3.49, 7.45, 15.00, and 24.04 (P for trend <0.001). The estimated incident rates for men in the low-WBC count (<7.3 x 10(9) cells/L)/no MS, high-WBC count (> or =7.3 x 10(9) cells/L)/no MS, low-WBC count/yes MS, and high-WBC count/yes MS were 3.4%, 4.6%, 7.4%, and 13.1% for ST-T abnormalities, respectively and were 3.6%, 7.1%, 18.0%, and 27.2% for type 2 diabetes, respectively. The respective multivariate-adjusted relative risks were 1.0 (referent), 1.26, 2.07, and 3.45 for ST-T abnormalities and were 1.0 (referent), 1.75, 5.14, and 6.90 for type 2 diabetes. A modified NCEP MS definition predicts ST-T abnormalities and type 2 diabetes. WBC count adds clinically important information to new-onset ST-T abnormalities and type 2 diabetes.

Arrhythmias, Cardiac↗
PubMed1997

Maternal cerebral circulation in normal and abnormal pregnancies.

BACKGROUND: Abnormal pregnancies are usually associated with an impairment of maternal cerebral circulation which is mainly a consequence of generalized vasospasm and cerebral edema. The pathogenesis of vasospasm has still been a matter of controversy. The aim of this study was to evaluate maternal cerebral blood flow velocity (CBFV) changes in normal and abnormal pregnancies, and to correlate CBFV findings with the severity of symptoms in abnormal pregnancies. METHODS: A group of 40 gravidas (aged between 25 and 32 years) with pre-eclampsia were analyzed by Transcranial Doppler (TCD), Color Doppler Flow Imaging of carotid arteries and Transcranial Color Coded System once a week, starting from 32nd week of pregnancy and followed 2 months after delivery. The study was performed from the January 1996 to June 1996. RESULTS: The results showed 70% of abnormal pregnancies to have impaired TCD findings, mostly increased CBFV. The degree of toxemia measured by Goecke's index significantly correlated with abnormal CBFV Nine gravidas with increased CBFV on the first examination developed vasospasm during 34 to 36 weeks of gravidity. No statistically significant difference of the M1 segment of MCA diameters was found between normal (3.8 +/- 0.7 mm) and abnormal pregnancies (4.1 +/- 0.9 mm). CONCLUSIONS: The increase in the maternal CBFV was the most frequent observation in abnormal pregnancies. It was progressive during late pregnancy, when vasospasm may develop, although the presence of vasospasm is still the matter of controversy. The most important observation was that significant changes in CBFV preceded neurologic symptoms, emphasizing the predictive role of TCD in abnormal pregnancies.

Cerebrovascular Circulation↗
PubMed1986

Abnormal axonemes in sperm of fertile men.

Sperm of 20 men aged 20-44 years was analyzed for motility and tail deformities in a Makler chamber and for axoneme abnormalities by transmission electron microscopy. In the quantitative analyses, 12.5 +/- 5.5% deformed tails at the light microscopic level and 24.4 +/- 7.7% abnormal axonemes in the principal piece. This high incidence of abnormalities in the sperm of fertile men indicated that micrographs of abnormal axonemes alone could not be used to imply the pathogenesis of infertility or sperm immotility without statistical comparison with a control group. Axoneme abnormalities were subdivided into three types. There was an asymmetry of abnormal axoneme types along the length of the sperm tail. Based on this asymmetry and on images of longitudinally sectioned sperm, the different types of abnormal axonemes most likely represented a single process of doublet microtubule detachment and foldback. Correlation of electron and light microscopy suggested that axoneme foldback progressed to focal tail defects and subsequent collapse. The presence of these abnormalities in fertile donors indicated that they were part of a normal process of axoneme instability in human sperm.

Adult↗
PubMed1986

Ultrastructure of abnormal collagen in human tumors.

Abnormal collagen fibrils were identified by transmission electron microscopy in 22 human tumors of differing histogenesis. They were found in a review of 1400 electron microscopy cases. Abnormal collagen fibrils, described by others as amianthoid fibers, composite collagen, collagen flowers and intrafibrillar collagen dysplasia, have been found only rarely in human tumors but commonly in certain connective tissue diseases such as pseudoxanthoma elasticum, Ehlers-Danlos syndromes, Marfan's syndrome, osteoarthritic cartilage, and emphysematous lung among others. Abnormalities in the cases described here included thickened fibrils, fibrillar degeneration of fibrils and irregular external contours. Proposed mechanisms for their formation have included degeneration possibly due to hypoxia or collagenase activity, abnormal collagen biosynthesis, and abnormal tissue levels of glycosaminoglycans. The finding of abnormal collagen fibrils in these 22 human tumors shows that their occurrence is more common than is indicated by previous published reports. Most of the tumors containing abnormal collagen fibrils were mesenchymal or soft tissue tumors. Four neuroendocrine neoplasms had abnormal collagen fibrils.

Adolescent↗
PubMed2000

Glandular abnormalities on cervical smear: a study to compare the accuracy of cytological diagnosis with underlying pathology.

The interpretation of glandular abnormalities detected by cervical smear provides a diagnostic dilemma. This study aims to compare the accuracy of cytological diagnosis with underlying pathology so that guidelines for the investigation and management of abnormal glandular smears may be formulated. A retrospective review of 150 women with glandular abnormalities reported on cervical smear collected over 12 months from 1996 in a University hospital was performed. Smears were graded by the initial report into 3 groups, dependent on the severity of abnormality. Investigation, treatment and subsequent 3-year follow-up were recorded. The accuracy of prediction for a significant neoplastic or preneoplastic glandular pathology only was 0% with mild, 9% (3/35) with moderate, and 24% (9/38) with severe abnormalities. When squamous lesions were included, the chance of finding any dysplastic squamous or glandular abnormality was 16% (12/77), 51% (18/35) and 82% (31/38), respectively, following a smear showing a suspected glandular abnormality only. Our results highlight the poor specificity of predicting glandular neoplasia or preneoplasia from cervical smears, with a final diagnosis of high grade CIN in 35% (17/49) of patients with dyskaryotic glandular cytological changes only and 83% (20/24) where concomitant squamous dyskaryosis was reported. The reporting of reactive or minor changes in endocervical cells was of no diagnostic value. Management protocols for moderate and severe glandular abnormalities should include visualisation and biopsy of the uterine cavity to exclude endometrial neoplasia.

Carcinoma, Squamous Cell↗
PubMed2000

[Cytogenetics and clinical studies of hematologic malignancies with 11q23 abnormalities in China].

OBJECTIVE: To evaluate the association between 11q23 abnormalities and the clinical, hematologic, prognostic aspects of hematologic malignancies. METHODS: A total of 6000 cases of hematologic malignancies from our hospital and near regions in China were investigated between October 1985 and November 1998. Chromosome preparations were made on bone marrow cells by using direct method and/or unstimulated short-term cultures. Karyotypes were analyzed by R-banding technique and expressed according to ISCN(1995). RESULTS: 11q23 abnormalities were found in 28 of 6000 cases with hematologic malignancies(0.47%). It may be separated into seven cytonetic categories: t(4;11)(q21;q23)(ten cases), t(11;19)(q23;p13)(five cases), t(9;11)(p12;q23)(two cases), t(10;11)(p15;q23)(two cases), t(6;11)(q27;q23) (one case), del(11)(q23)(seven cases), and t(11;?)(q23;?)(one case). The diagnoses included acute myeloid leukemia in 14 cases (M(2a), three; M(4), two; M(5a), one; M(5b), eight), acute lymphoblastic leukemia(ALL) in 10 cases, myelodysplastic syndrome in three cases and malignant histiocytosis in one case. All 10 cases with t(4;11) anomaly were ALL. Follow-up data were available for 22 of them. Their median survival was 113 days. The patients may be grouped according to the presence or absence of additional abnormalities and/or normal karyotype. The median survival was 75 days for five patients with 11q23 anomaly only, 18 days for two patients with 11q23 and additional abnormalities, 135 days for 10 patients with 11q23 anomaly, additional abnormalities and normal karyotype, and 150 days for 5 patients with 11q23 anomaly and normal karyotype. CONCLUSION: 11q23 abnormalities were mainly seen in ALL and acute monocytic leukemia. Their prognosis was very poor. Both additional abnormalities and lack of normal karyotype had adverse effects on the survival of patients. Thus, they represent a unique clinical-cytogenetic association. 11q23 abnormality; hematologic malignancy; acute monocytic leukemia; acute lymphoblastic leukemia; prognosis

Adolescent↗
PubMed2000

Prognostic significance of cytogenetic abnormalities of chromosome arm 12p in childhood acute lymphoblastic leukemia: a report from the Children's Cancer Group.

BACKGROUND: The authors have determined the prognostic significance of cytogenetically detectable 12p abnormalities, which are frequent in children with acute lymphoblastic leukemia (ALL), in a large cohort of patients treated on risk-adjusted protocols of the Children's Cancer Group (CCG). METHODS: The presence of an abnormal 12p was identified among 1880 children with newly diagnosed ALL; outcome was assessed by standard life table methods. RESULTS: A total of 174 cases (9%) had cytogenetically detectable 12p abnormalities; the majority of cases had a balanced translocation, a del(12p), or an add(12p). In the overall cohort, event free survival (EFS) at 6 years was similar for patients with or without a 12p abnormality (76%, SD = 6%, vs. 75%, SD = 2%, respectively; P = 0.60). Among patients with pseudodiploidy, an abnormal 12p conferred improved outcome (P = 0.008; relative risk = 0.51; 95% confidence interval [CI], 0.31-0.85). There was a trend for improved EFS for those with abnormalities in both chromosome 12 homologues (P = 0.16; relative risk = 0.39; 95% CI, 0.10-1.55) and those with low hyperdiploidy (P = 0.07; relative risk = 0.44; 95% CI, 0.18-1.09). Among T-lineage ALL patients, there was a trend for worse outcome for abnormal versus normal 12p (P = 0.14; relative risk = 1.97; 95% CI, 0.78-4.93). There was no difference in EFS for the 12 patients with a dic(9;12) compared with patients lacking an abnormal 12p. CONCLUSIONS: These data suggest that although a cytogenetically detectable 12p aberration is a favorable risk factor for children with ALL and pseudodiploidy, it is not prognostic for the overall group of pediatric ALL patients treated with contemporary therapies of the CCG.

Adolescent↗
PubMed2001

Characterization of complex chromosomal abnormalities in uveal melanoma by fluorescence in situ hybridization, spectral karyotyping, and comparative genomic hybridization.

Several nonrandom recurrent chromosomal changes are observed in uveal melanoma. Some of these abnormalities, e.g., loss of chromosome 3, gain of the q arm of chromosome 8, and chromosome 6 abnormalities, are of prognostic value. Cytogenetic analysis and/or fluorescence in situ hybridization (FISH) are used to detect these changes. In some cases, however, detailed cytogenetic analysis is not possible due to the presence of complex abnormalities. To define more accurately these cytogenetic changes, we have applied comparative genomic hybridization (CGH) and/or spectral karyotyping (SKY) to two uveal melanoma cell lines and five primary uveal melanomas, with partially defined and/or complex abnormalities. SKY provided additional information on 34/39 partially defined aberrant chromosomes and revealed a new abnormality, a der(17)t(7;17)(?;q?), that had not been recognized by conventional cytogenetics. Additionally, using SKY, abnormalities involving chromosome 6 or 8 were found to be twice as common as observed with cytogenetic analysis. CGH was especially useful in assigning the abnormalities identified by SKY to specific chromosomal regions and, in addition, resulted in the detection of a small deletion of chromosome region 3q13 approximately 21. We conclude that SKY and CGH, as methods complementary to cytogenetic and FISH analysis, provide more complete information on the chromosomal abnormalities occurring in uveal melanoma.

Adult↗
PubMed2002

[Abnormal metabolism of glucose as clue for early diagnosing pancreatic cancer].

OBJECTIVE: To investigate the incidence, features, and course of abnormal metabolism of glucose in patients with pancreatic cancer and the possibility of using the abnormal metabolism of glucose as early precursory manifestation of pancreatic cancer. METHODS: Fasting plasma-sugar (FPG), plasma insulin and C peptide were examined in 98 patients with pancreatic cancer diagnosed by B mode ultrasonography, CT, endoscopy, and pathological examination. The family history of DM was collected. The body mass index (BMI) was calculated. The relation between abnormal metabolism of glucose and diagnosis of pancreatic cancer was analyzed. One hundred and fifteen patients with advanced gastric cancer (AGC), 87 patients with colon cancer, and 146 patients with type 2 diabetes mellitus (DM) were used as controls. RESULTS: Abnormality of FPG, insulin and C peptide was found in 17 out of the 98 patients with pancreatic cancer, with an incidence rate of 17.4%, significantly higher than that in patients with AGC (1/115, 1.7%, P < 0.05), and patients with colon cancer (5/87, 5.8%, P < 0.025). Thirty eight patients with type 2 DM (39.0%) had their BMI > 24, while no pancreatic cancer patients with abnormality of metabolism of glucose had his BMI > 24 (0/17, 0%, P < 0.05). The duration between the discovery of abnormal metabolism of glucose and the diagnosis of cancer in the 17 patients was 10.8 +/- 7.4 months, and was < 2 years in 15 of them (88.2%), significantly longer than the duration between the appearance of symptoms and the diagnosis in the 146 type 2 DM patients (21/146, 14.4%, P < 0.05). The proportion of positive DM family history was 1/17 in patients with pancreatic cancer, significantly lower than in patients with type 2 DM (97/146, 66.4%, P < 0.05). However, the values of FPG, insulin, and C peptide between the groups with and without pancreatic cancer were not significantly different. CONCLUSION: Clinical manifestations of abnormal metabolism of glucose appear prior to the discovery of space occupying lesions in pancreas in about 17% patients with pancreatic cancer. Newly appearing abnormalities in metabolism of glucose in patients without DM family history and without symptom of obesity should be regarded as important clues for early diagnosing pancreatic cancer.

Aged↗
PubMed2002

[Management of abnormal fetal heart rate in the second stage of labor].

OBJECTIVE: We investigated the correlations between abnormal fetal heart rate (FHR) during the second stage of labor and delivery types and intrapartum maternal complications and fetal outcome. METHODS: The data of 232 nulliparas with single vertex in the second stage of labor (111 cases with normal FHR, 121 cases with abnormal FHR) were analyzed retrospectively. RESULTS: The incidence of abnormal FHR in the second stage of labor was 52.2% (121/232). The patterns of abnormal FHR included: 81 (66.9%) cases with moderate and/or severe variable deceleration (VD), 27 (22.3%) cases with scattered late deceleration (LD), only one with continuous LD, 4 (3.3%) cases prolonged deceleration (PD), 2 (1.7%) cases with VD and LD, 3 (2.5%) cases with VD and PD, 4 (3.3%) cases with diminished baseline variability. There were 13 (11.7%) among the cases with normal FHR and 35 (28.9%) among the cases with abnormal FHR underwent assistant delivery operations (forceps or/and vaccum), respectively (P < 0.05). Furthermore 29 of 35 (82.9%) cases underwent assistant operations for vagina delivery due to abnormal FHR, the others underwent assistant operations for vagina delivery due to weak expulsive force or malpositioning of fetal head. There was one case of complicated vaginal laceration in the group with abnormal FHR. There was no difference of newborns with low Apgar score between two groups. CONCLUSIONS: There was a very high incidence of abnormal FHR during the second stage of labor, however, the most cases were response to parasympathetic stimulation due to umbilical cord or fetal head compression by mothers over push and descent of fetal head, or temporal diminishing of uterine placenta blood flow. It suggests that it is unnecessary to interfere immediately, unless truly fetal distress.

Adult↗
PubMed2002

[Relationship between abnormal expression of beta-catenin in gastric carcinoma and survival].

BACKGROUND & OBJECTIVE: Altered cell adhesion has a critical role in the development of epithelial cancers. E-cadherin act on the maintenance of cell-cell adhesion and its function was thought to be regulated by associated cytoplasmic proteins, such as alpha-catenin and beta-catenin. This study was designed to examine the expression of beta-catenin in gastric carcinoma and to determine the relationship between tumor characteristics and survival. METHODS: Immunohistochemical staining of beta-catenin and E-cadherin was performed in 148 patients with gastric carcinoma. RESULTS: Abnormal expression of beta-catenin and E-cadherin was performed in 148 patients with gastric carcinoma. RESULTS: Abnormal expression of beta-catenin and E-cadherin was demonstrated in 43.2% and 44.6% of tumors respectively. Up to 63% of tumors stained abnormally for one or two components of the cadherin-catenin complex (beta-catenin, E-cadherin). Abnormal beta-catenin and E-cadherin staining occurred more frequently in poor differentiated tumor than in good differentiated tumors (P < 0.005, respectively). There was a significant correlation between abnormal beta-catenin expression and depth of invasion(P < 0.025). Moreover, abnormal beta-catenin expression was more frequent in tumors with positive lymph node metastasis (45/84, 53.6%) and distance metastasis(21/31, 67.7%) than in tumors without lymph node metastasis (19/64, 29.7%) (P < 0.005) and distance metastasis (43/117, 36.8%) (P < 0.005). A survival advantage was noted in tumors retaining normal membranous expression of beta-catenin, independent of type, grade, or stage (P < 0.005). CONCLUSIONS: Abnormal expression of the E-cadherin-catenin complex occurs frequently in gastric carcinoma. The close correlation with poor survival suggests that abnormal beta-catenin may be a useful prognostic marker.

Adult↗
PubMed2003

Transvaginal sonography combined with saline contrast sonohysterography to evaluate the uterine cavity in patients with abnormal uterine bleeding and postmenopausal endometrium more than 5 mm.

OBJECTIVES: To determine whether saline contrast sonohysterography (SCSH) gives additional information to that obtained by transvaginal sonography (TVS) for predicting endometrial abnormality in premenopausal, menopausal and postmenopausal patients with abnormal uterine bleeding and postmenopausal patients with endometrial thickness > 5 mm. METHODS: This was a prospective study at the Ege University Obstetrics and Gynecology Clinic in Izmir, Turkey. Patients presenting with abnormal bleeding related to uterine pathologies, postmenopausal patients with endometrial thickness more than 5 mm and scheduled for surgical treatment were prospectively included in our study conducted between 1 July, 2000 and 31 January, 2002. The uterine cavity was first evaluated with TVS in 53 premenopausal, menopausal, postmenopausal patients with abnormal uterine bleeding and postmenopausal patients whose endometrial thickness was > 5 mm measured by conventional ultrasound examination. SCSH was carried out later with the intention of establishing further surgical management (hysterectomy). Twenty of the patients had operative hysterectomy within the 1.5 year period of time. The presence of focally growing lesions and the type of lesion (endometrial polyp, submucous myoma, malignancy or unclear focal lesion) were noted at ultrasound examination and at hysteroscopy, and then hysterectomy material was examined by Ege University's Pathology Department which provided a detailed evaluation of the uterine cavity. RESULTS: Based on normal endometrial morphology alone, the results for detection of an abnormal uterine cavity were as follows: sensitivity of TVS 0.94, SCSH 0.97; specificity of TVS 0.56, SCSH 0.62; positive predictive value of TVS 0.79, SCSH 0.81; negative predictive value of TVS 0.83, SCSH 0.93. Transvaginal sonography combined with SCSH was superior to TVS for detection of intracavitary abnormalities. When normal endometrial morphology was combined with an endometrial thickness of < 12 mm for evaluation of all abnormalities including hyperplasia, the diagnostic potential of TVS or SCSH was almost unchanged. Transvaginal sonography missed 24% of the polyps. CONCLUSIONS: Sonohysterography was a sensitive tool and was superior to TVS used alone for evaluation of the uterine cavity in patients who underwent operative surgery for abnormal uterine bleeding.

Adult↗
PubMed2003

Incidence of anal cytological abnormalities in a cohort of human immunodeficiency virus-infected women.

Little is known about the natural history of anal human papillomavirus (HPV) infection in HIV-infected women because, to date, no longitudinal studies have been reported in the scientific literature. This article estimates the incidence of anal cytological abnormalities in a cohort of HIV-infected women. It also examines potential risk factors for the development of an anal cytological abnormality. A cohort of HIV-infected women underwent interview, anal cytology, and anogenital HPV DNA testing. Women with a normal baseline anal cytology were followed for the development of an anal cytological abnormality. The incidence of an abnormality was calculated. Survival analyses were performed to examine risk factors for the development of an abnormality. Fourteen of 100 HIV-infected women had an abnormal anal cytology at baseline. Among the 86 women with a normal baseline cytology, the incidence of an abnormality was 22 [95% confidence interval (CI), 14-33] per 100 person-years. In a multivariate analysis, women were at increased risk if, at baseline, they had a CD4+ T-cell count of <500 cells/mm(3) [relative hazard (RH) = 4.11; 95% CI, 1.18-14.25], high-risk type anal HPV infection (RH = 2.54; 95% CI, 0.91-7.14) or were cigarette smokers (RH = 3.88; 95% CI, 1.12-13.42). The incidence of anal cytological abnormalities was high among this cohort of HIV-infected women, indicating that they are at high risk of anal squamous intraepithelial lesions. HIV-infected women are likely to be at higher risk than their HIV-uninfected counterparts because immune suppression conferred substantially increased risk. Continued research on the association between smoking and the development of squamous intraepithelial lesions in HIV-infected women is warranted.

AIDS-Related Opportunistic Infections↗
PubMed2003

Isolated lipid abnormalities in rural and urban normotensive and hypertensive north-west Indians.

BACKGROUND: Lipid abnormalities are common in patients with hypertension. The prevalence of isolated lipid abnormalities is not known in normotensive and hypertensive population of north-west India. METHODS: We studied the prevalence of isolated low high density lipoprotein cholesterol (IL-HDLC), isolated high low density lipoprotein cholesterol (IH-LDLC) and isolated high triglycerides (IH-TG) abnormalities among rural and urban normotensive and hypertensives of north-west India. RESULTS: The prevalence of lipid abnormalities was 47.6% and 51.4% in rural normotensives and hypertensives and 43.8% and 46.8% in urban normotensives and hypertensives respectively. The prevalence of IL-HDLC varied from 3.8% to 23.7% among hypertensives and 19.4% to 30.4% among normotensives. The prevalence of IH-TG abnormalities was 11.8% to 18.8% among hypertensives and 7.0% to 15.4% among hypertensives. The prevalence of isolated high LDLC abnormalities was low (0.8-9.2%). There was no significant difference in these abnormalities in relation to age and sex except IH-LDLC in male hypertensives. CONCLUSION: Isolated low HDLC and isolated high TG were the commonest isolated lipid abnormalities among rural and urban population of north-west India whereas isolated high LDLC was uncommon.

Adult↗
PubMed1992

Nonrandom abnormalities involving chromosome 1 and Harvey-ras-1 alleles in rat mammary tumor progression.

Little is known about the role of chromosomal abnormalities in the widely used models of rat mammary carcinogenesis. In this study, we cytogenetically analyzed nitrosomethylurea-induced rat mammary adenocarcinomas at different time points of development. As tools to study more advanced stages of malignant progression, we also analyzed the cytogenetic progression of tumors transplanted into younger syngeneic hosts, and of tumors that did not regress or that developed after host ovariectomy. Our results indicate that rat mammary adenocarcinomas appear to start development as diploid lesions with cytogenetically "normal" karyotypes. However, upon progression, tumors showed coexistence of normal diploid clones with abnormal clones bearing specific abnormalities affecting mainly chromosomes 1 and 15. Almost every ovary-independent tumor presented stem lines with specific nonrandom chromosomal abnormalities. Numerical chromosomal abnormalities such as specific trisomies started to develop mainly after subsequent in vivo transplantations. The abnormalities affecting chromosome 1 observed in many tumors were: (a) interstitial deletions and breakpoints for translocation in region 1q22; and (b) partial or complete overrepresentation of chromosome 1 in the form of direct duplication of region 1q22q43 or as trisomy 1. Interestingly, Harvey-ras-1 gene maps to rat chromosome 1, and by Southern analysis we observed that 4 of 8 primary tumors and 6 of 9 ovary-independent tumors showed considerable loss of Harvey-ras-1 signal indicating probable allele loss. However, analyses of some tumor transplants in more advanced stages of progression showed, paradoxically, an increased copy number of the Harvey-ras-1 oncogene coinciding with the presence of the direct duplication observed in chromosome 1 or with trisomy 1 as possible mechanisms for gene amplification. Interestingly, rat chromosome 1 is the homologue to human chromosome 11, and in numerous cases of human breast cancer loss of heterozygosity of several genes in chromosome 11p15.5 has been reported. Some of the rat chromosome 1 abnormalities observed may be equivalent to those affecting 11p15 in human tumors. We also observed 8 tumors with abnormalities affecting chromosome 15. At least 3 genes of interest in breast cancer have been previously mapped to that rat chromosome. The similarities observed with human breast cancer may point to common mechanisms of tumor progression in both species.

Adenocarcinoma↗