Abnormal bile duct epithelium in liver biopsies with histological signs of viral hepatitis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Poulsen.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a controlled clinical trial in 488 patients with chronic liver disease treated with prednisone or placebo, survival data were analyzed using Cox's proportional hazards model. A total of 162 variables were screened separately for prognostic and/or therapeutic effect by log-rank analyses, whereby 46 clinical, biochemical, serological, and histological variables were isolated. Another five variables traditionally found to be important in patients with liver disease were included. After extensively checking the assumptions of the model, the 51 variables were, by a step-wise procedure, reduced to a final model. It comprised, besides a treatment indicator, 12 variables with significant (p less than 0.05) prognostic or therapeutic effect. The following eight variables had a significant prognostic effect: sex, age, prothrombin, acetylcholinesterase, eosinophil leucocytes in liver parenchyma, liver cell necrosis, inflammation in liver connective tissue, and efferent veins in parenchymal nodules. A prognostic index based on the final model is formed allowing calculation of 5 years survival probability. The usefulness of the prognostic index was tested by a cross-validation method, and no statistical significant difference was found between the estimated and observed survivorship functions.
The conversion from micro- to macronodular cirrhosis is claimed to be a general phenomenon. In this study, the conversion was quantitated by means of liver needle follow-up biopsies and autopsy in 156 patients followed in a controlled clinical trial of prednisone treatment in cirrhosis. In the initial biopsy, 75 patients were classified as micronodular cirrhosis, and of them, 68 had macronodular cirrhosis at autopsy indicating a conversion ratio of about 0.9 in 10 years. This may overestimate the true conversion ratio slightly since conversion in many cases only was demonstrated at autopsy where the diagnosis of macronodular cirrhosis is made with greater certainty than from a needle biopsy. The median time interval between the diagnosis of micro- and macronodular cirrhosis was 2.25 years which is a maximum estimate of the conversion time due to irregular spacing between biopsies (or biopsy and autopsy). No significant difference was found between the conversion time in females and males. The conversion was faster in patients not drinking alcohol compared to patients drinking alcohol, but the difference was not significant. Prednisone treatment tended to accelerate the conversion, but not significantly.
The Child- Turcotte criteria (CTC) (based on serum bilirubin and albumin, ascites, neurological disorder and nutrition) are established prognostic factors in patients with cirrhosis having portacaval shunt surgery. The objective of this study was to evaluate the prognostic value of CTC in conservatively treated cirrhosis. Patients (n = 245) with histologically verified cirrhosis from a control group of a controlled clinical trial were studied. Data at entry into the trial were used to classify patients according to CTC. Survival curves for up to 16 years were made, and survival rates were compared using the log-rank test. Survival decreased significantly with increasing degree of abnormality (A----B----C) of albumin (p less than 0.001), ascites (p less than 0.001), bilirubin (p = 0.02) and nutritional status (p = 0.03). Survival was insignificantly influenced by neurological status (p = 0.11) probably because none of the patients had hepatic coma at entry into the trial. The five variables in CTC were combined to a score. With increasing score, the median survival time decreased from 6.4 years (score 5) to 2 months (scores 12 or more). Furthermore, the mortality from hepatic failure, gastrointestinal bleeding or hepatocellular carcinoma increased significantly with increasing score. CTC provide valuable and easily obtainable prognostic information in cirrhosis. However, CTC are inferior to a prognostic index based on multivariate analysis of prognostic factors.
The time change of laboratory variables in cirrhosis was studied by analysis of data from 488 patients with cirrhosis included in a controlled clinical trial of long-term prednisone vs. placebo. In the placebo group, a marked regression towards normal was seen within 3 months of entry into the trial (increase in serum albumin, acetylcholinesterase, cholesterol, hemoglobin and decrease in erythrocyte sedimentation rate). The subsequent course did not show a clear pattern, except for a slight increase in serum bilirubin and decrease in albumin. When studied in relation to the time of death in patients dying from a "hepatic" cause, marked increase in bilirubin and decrease in prothrombin index, albumin and cholesterol were seen in the year prior to death with little change before that time. In the prednisone group, a more marked decrease in bilirubin, SGOT, alkaline phosphatase, gamma-globulin, sulfobromophthalein retention, erythrocyte sedimentation rate and increase in leukocytes, prothrombin index and cholesterol were seen during the first 3 months. In relation to time of death from a "hepatic" cause, similar changes were seen as in the placebo group except that alkaline phosphatase increased and cholesterol did not decrease. A beneficial effect of prednisone on survival, as expressed by a previously developed therapeutic index, was associated with decrease in SGOT, alkaline phosphatase and gamma-globulin within the first 3 months. An increase in SGOT during prednisone seemed to be associated with harmful effects of therapy.
Surgical specimens from 62 patients with vulvar dysplasia and carcinoma in situ were morphologically investigated. Lesions were classified according to WHO (mild, moderate, severe dysplasia and carcinoma in situ) and according to Toki et al. (1991) (warty, basaloid, combined warty/basaloid or basaloid/warty types or mixed (warty, basaloid and simple) forms). Following the WHO classification, moderate dysplasia was shown in 4 cases, severe dysplasia in 47 and carcinoma in situ in 11 cases. Pure warty type was shown in 2 cases (both biopsy specimens). One case revealed pure simple dysplasia whereas no case of pure basaloid type was found. Various combinations of warty and basaloid types were shown in 52 cases and mixed forms in 7 cases. The results indicate that pure forms of warty and basaloid types probably do not exist. HPV DNA was detected by PCR in 51/58 cases (88%) (45 with HPV type 16 and 6 with HPV type 33) evenly distributed in all age groups and in all types of lesions (WHO and Toki et al. 1991). By ISH HPV was detected in 24/62 cases (39%) (21 with HPV type 16/18 and 3 with HPV type 31/33), nearly always in warty areas. All these cases were positive for the same virus type by PCR. No case revealed more than one type of HPV. HPV type 6, 11, 18, and 31 were not detected by PCR. The results indicate a correlation between HPV type 16 and 33 and dysplasia/carcinoma in situ in the vulva.
Explore the source record for details and available documents.
The aim of the present study was to describe and pathologically evaluate an apparently unreported craniofacial malformation, based on comparison of the cranial midsagittal components with similar components under normal developmental conditions. A severely malformed fetus with a gestational age of about 17 weeks underwent whole body and special craniofacial radiography. Following autopsy dissection, the midsagittal segment of the cranial base, including the eyes, was radiographed in different projections. Midsagittal tissue blocks were serially sectioned for microscopy. Routine stains and immunohistochemical stains were applied. The face was characterized by hypertelorism, absence of external nose but with open shell-like cavities medio-cranially to the eyes, and by a palate fused in the midline and with extensive bony ridges laterally. There was absence of normal nasal cavities, presence of nasal septum and vomer, normal eyes, and nasal ducts covered with nasal mucosa ending blindly in the cartilage. No olfactory bulbs were found. The palatal ridges consisted of bony tissue. The pituitary gland was severely malformed and consisted solely of adenopituitary gland tissue, located in its full extent in the pharyngeal mucosa. There was no sella turcica. From a pathogenetic point of view, it is suggested that the neural crest cells in the frontonasal region of the crest were reduced in amount or late in migration to the midfacial region compared to the neural crest cells to the maxillary region. Therefore, we believe that the malformations observed in the nasal placodes and in the pituitary placode, combined with abnormal migration or abnormal timing of neural crest cells during the craniofacial development, are important factors behind this disorder.