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Biomedical subjects

E Bierhoff

Publications and source records attributed to E Bierhoff.

At least 37 records · Page 2Linked to original sources
PubMed1996

Elastofibroma and pre-elastofibroma--a biopsy and autopsy study.

Two biopsy cases of elastofibroma--one unilateral and one bilateral--are described. A study of 100 autopsies revealed 13 elderly patients with elastofibroma. Males (n = 10; 16.9%) were more affected than females (n = 3; 7.3%). Pre-elastofibroma-like morphological changes (e.g. few or many degenerated elastic fibres) were observed in 81% of the autopsies. Minor pre-elastofibroma-like changes were seen in males and major changes predominantly in females. In addition to physiological ageing as yet unknown factors, rather than abnormal elastogenesis or degeneration, seem to be involved in this pseudotumour.

Adolescent↗
PubMed1996

[Intramural hematoma of the thoracic aorta: diagnostic imaging and differential diagnosis].

PURPOSE: Aortic wall thickening due to intramural hemorrhage may be the only sign of aortic dissection. The aim of this study was to evaluate the incidence, imaging features and differential diagnoses of intramural hemorrhage (IMH) of the thoracic aorta. METHODS: 98 patients with clinically suspected aortic dissection were investigated via Spiral-CT and MRT. Diagnosis of IMH based on the presence of smooth crescentic or concentric wall thickening over a longer segment of the thoracic aorta without flow visualization and without compression or distortion of the aortic lumen. RESULTS: 69 patients had classic aortic dissections and 7 patients were diagnosed to have IMH of thoracic aorta. One patient with IMH of the ascending aorta died of aortic rupture and subsequent pericardial tamponade 12 hours after onset of symptoms. In one patient with IMH of the descending aorta on initial examination, there was a progression of overt aortic dissection at follow-up after three weeks. In two patients with IMH of the descending aorta, wall thickening decreased in size at follow-up (10-15 weeks), whereas in one patient it remained unchanged. CONCLUSION: IMH of the aorta should be considered a precursor of aortic dissection. At follow-up IMH may decrease in size, rupture or progress to overt aortic dissection.

Adult↗
PubMed1996

Stromal nodules in benign prostatic hyperplasia.

OBJECTIVE: Stromal nodules from benign prostatic hyperplasia (BPH; n = 375 from autopsy, n = 100 from biopsy specimens) were investigated with regard to cytoskeletal components, topography, vascularization, leukocytic infiltrates, and proliferative activity. METHODS: The nature of stromal nodules was studied by histopathology and immunohistochemistry, using antibodies against alpha-actin, desmin, myosin, vimentin, BMA-120, factor VIII, CD3, CD4, CD20, CD34, CD45RO, CD68, PCNA, and MiB1. RESULTS: The findings lead to an extended classification of stromal nodules in BPH: immature mesenchymal (IM; 8.8%), fibroblastic (FB; 65.2), fibromuscular (FM; 21.6), and smooth muscular (SM; 4.4%). The different types occurred in all age decades in a similar distribution (FB > FM > IM > SM). Topographical studies (modified zonal subdivision of McNeal) revealed stromal nodules predominantly in the transitional zone (n = 286), less in the central zone (n = 78), occasionally in the peripheral zone (n = 11), and predominantly in the periurethral (n = 287) and less in the intermediate (n = 84) and subcapsular (n = 4) regions. The different types of nodules presented a distinct vascular pattern. FB, FM, and SM nodules showed significantly increased diffuse infiltrates of T lymphocytes-mainly T helper cells (mean 73%)-and an increase of B lymphocytes. Proliferative activity in the nodules was not observed. Stromal nodules were not observed in normal nonhyperplastic prostates; they only occurred in combination with hyperplastic nodular glandular proliferates. CONCLUSIONS: The findings are suggestive of a maturational sequence of stromal nodules in BPH and of a possible significance of immunocompetent cells in the development of stromal nodules and further suggest that both stroma and epithelium of the prostate respond with nodular hyperplasia to the stimulus, which causes BPH.

Adult↗
PubMed1996

Perforation of the small intestine in a patient with disseminated Pneumocystis carinii infection in AIDS.

Perforation of the small intestine due to a segmental transmural Pneumocystis carinii infiltrate of the whole circumference was found in a surgical resection specimen as the cause of an acute abdomen in a 48-year-old heterosexual male patient suffering from acquired immunodeficiency syndrome. On autopsy, a disseminated Pneumocystis carinii infection was found involving spleen, thyroid gland and lymph nodes. The origin of this disseminated infection was a recurrent and severe Pneumocystis carinii pneumonia, which was first diagnosed two years before death and was treated with success. The hitherto unknown complication of an extrapulmonary Pneumocystis carinii infection described here extends the spectrum of lethal complications of opportunistic infections in acquired immunodeficiency syndrome.

AIDS-Related Opportunistic Infections↗
PubMed1996

Autopsy findings in patients with human immunodeficiency virus infection with emphasis on the risk factor of hemophilia.

The autopsy findings of 80 human immunodeficiency virus (HIV)-infected adults, who died between 1982-1995, are presented with special emphasis on the risk factor of hemophilia. The study included 23 blood product recipients (hemophiliacs n = 21; non-hemophiliacs n = 2), 34 homosexuals, four intravenous drug abusers, and 19 patients with no known risk factor. Nearly all individuals (93%) showed the late stage of acquired immunodeficiency syndrome (AIDS). Blood product recipients had a significantly lower overall frequency of opportunistic infections (p < 0.05). Homosexuality was associated with the highest overall frequency of opportunistic infections and HIV-associated malignancies, such as Kaposi's sarcoma and malignant non-Hodgkin's lymphoma. Exclusive visceral involvement of Kaposi's sarcoma was frequent, and no decrease of Kaposi's sarcoma was observed during the study period. Pneumocystis infections, atypical mycobacteriosis, and non-Hodgkin's lymphoma showed a significant increase during the last five years (1991-1995) of the observation interval. Opportunistic infections and malignancies were the cause of death in approximately one-half of the patients. In blood product recipients, hepatic failure due to posthepatitic cirrhosis and hemorrhage due to hepatic failure with subsequent coagulopathy and in non-blood product recipients, bacterial bronchopneumonia, and diffuse alveolar damage were additional major causes of death. The data suggest a lower risk for HIV-infected blood product recipients, particularly hemophiliacs, to acquire opportunistic infections and malignant neoplasms.

Adult↗
PubMed1996

Malignant mesothelioma arising from a benign mediastinal mesothelial cyst.

A 50-year-old man presented with a cervical lymph node metastasis of malignant tumor and a radiologically documented well-defined tumorous mass in the middle portion of the mediastinum. Under the presumptive diagnosis of an undifferentiated bronchogenic carcinoma, the patient underwent chemotherapy. However, the tumor did not respond to this treatment and showed further progression. The patient died four weeks after the lymph node biopsy. Autopsy revealed a well-defined cystic tumor in the mediastinum with infiltration of the pericardium. The tumor was not attached to the lungs. By histology and immunohistochemistry, a metastasizing malignant biphasic mesothelioma was diagnosed. The tumor had metastasized to intrapulmonary perivascular and peribronchiolar lymph vessels and hilar lymph nodes. Distant metastases were found in the right and left adrenal gland and in the brain. The strictly mediastinal localization and the cystic growth pattern of the tumor strongly suggest that this mesothelioma developed from a primary benign mesothelial cyst of the pericardium with secondary transformation into a malignant mesothelioma.

Humans↗
PubMed1996

Histopathologic findings in chronic hepatitis C.

Evaluation of liver biopsies in hepatitis C is aimed at confirming the clinical and serologic diagnosis, grading of necroinflammatory activity, staging of consecutive fibrosis, ruling out or confirming liver diseases of different etiology, and assessment of therapeutic effects. Usually, the course of chronic hepatitis C virus (HCV) infection is slow, with mild inflammatory changes. Nevertheless, even in mild asymptomatic chronic hepatitis C episodes of higher inflammatory activity associated with extensive piecemeal necrosis and porto-central bridging, necrosis can accelerate the course of the disease. For this reason, the traditional, morphologically based classification of chronic hepatitis and the term "chronic persistent hepatitis" have lost their predictive usefulness, especially in hepatitis C. Chronic hepatitis should be characterized by etiologic designation as well as grade and stage of the disease. Portal lymphoid aggregates, some inflammatory bile duct damage and mild steatosis are the most characteristic features by which hepatitis C can be differentiated from other progressive inflammatory liver diseases. Antibodies directed against HCV antigens allow identification of viral proteins by immunohistochemistry. Immunostaining for hepatitis B antigens, for alpha-1-antitrypsin and copper staining are helpful in detecting hepatitis B and congenital liver diseases (Wilson's disease, alpha-1-antitrypsin deficiency) as possible causes of chronic progressive inflammatory liver disease. Centrilobular Mallory's hyalin, identified by immunostaining for ubiquitin in combination with perivenular fibrosis, is helpful in diagnosing concomitant alcoholic liver disease. In our own biopsy material (n = 100) and autopsy material (n = 58), HIV/HCV-coinfected patients have a significantly higher rate of fibrosis and cirrhosis than HIV patients without HCV infection. Hepatitis C can apparently aggravate the course of HIV infection. Our morphologic findings support the clinical observation that chronic HCV infection seems to be the main cause of liver failure, especially in the risk group of HCV/HIV-coinfected hemophiliacs.

Chronic Disease↗
PubMed1996

Immunosuppression may lead to progression of hepatitis C virus-associated liver disease in hemophiliacs coinfected with HIV.

OBJECTIVE: The aim of this study was to examine the interaction between HIV and hepatitis C virus (HCV) in hemophiliacs coinfected with the viruses and to investigate the possible relationship between immunosuppression and liver failure. METHODS: To identify risk factors for impending liver failure in hemophiliacs coinfected with HIV and HCV, we analyzed clinical and laboratory parameters, including CD4 count, aminotransferases (ALT, AST), cholinesterase, alkaline phosphatase, bilirubin, and gamma-glutamyltransferase, during 3 yr of follow-up (1990-1993) in four groups of patients: hemophiliacs with progressive immunodeficiency who were coinfected with HCV and HIV (group A, n = 49); hemophiliacs with stable immune function who were seropositive for HIV and HCV (group B, n = 95); hemophiliacs who were infected with HCV but not HIV (group C, n = 72); and homosexuals with progressive immunodeficiency who were infected with HIV but not HCV (group D, n = 24). RESULTS: Univariate analysis of data for group A showed a significant rise in gamma-glutamyltransferase and alkaline phosphatase (p < 0.01) that was not seen in groups B, C, and D. In a multivariate Cox regression analysis, age (odds ratio, 1.054 per yr; 95% confidence interval, 1.014-1.096 per yr), decline in CD4 count (odds ratio, 1.063 per cell/microl; 95% confidence interval, 1.037-1.091 per cell/microl), and alkaline phosphatase level (odds ratio, 1.012 per U/L; 95% confidence interval, 1.002-1.021 per U/L) emerged as independent determinants of death. CONCLUSIONS: Our data suggest that progressive immune dysfunction in hemophiliacs coinfected with HIV and HCV may influence progression of liver failure. In these patients cholestasis is an additional prognostic marker for survival that may reflect both exhausted immunity and impaired liver function.

Acquired Immunodeficiency Syndrome↗
PubMed1995

[Detection of genetic alterations in sporadic breast tumors].

OBJECTIVE: Loss of heterozygosity (LOH) indicates the existence of tumor suppressor genes (TSG) in the affected chromosomal loci. In order to uncover the involvement of such genes, we analyzed LOH in different chromosomal regions of sporadic breast carcinomas. MATERIAL AND METHOD: 47 breast cancer patients were screened for LOH with microsatellite markers on 18 different loci. DNA fragments were amplified by PCR from tumor and reference tissue. The PCR products were run on 8% denaturing polyacrylamide gels and visualized by silver straining. RESULTS: The following LOH-rates were found for the different loci: D6S497 (6p21, WAF-Region): 0%, D7S495: 9%, D7S522: 13%, D7S523: 22%, D11S488 (11q24-25): 38%, D13s321 and D13s765 (13q13-14, Rb-Region): 30% and 17%, D13S260 and D13S267 (13q12.3, BRCA2-Region): 28% both, D16S539 (16q22-24, E-Cadherin-Region): 35%, D17S5 (17p13.3): 17%, TP53 (17p13.1): 32% D17S250 (17q11-12): 22%, D17S855 (17q21 within the BRCA1 gene): 25%, D17S579 (17q21 telomer from BRCA1): 13%, D17S846 (centromere from BRCA1): 17%, 17q24 (SSTR 2): 9%, D22S684 (22q12, NF2-Region): 20%. Overall 66% of the tumors exhibited LOH. Lymphnode positive tumors showed significantly higher LOH rates than lymphnode negative tumors. CONCLUSIONS: Highest LOH-rates were found on chromosomes 11, 13, 16 and 17 indicative of relevant TSG's in the examined loci. In addition the findings indicate prognostic relevance of multiple LOH's in breast cancer.

Alleles↗
PubMed1995

[Hepatitis and posthepatic cirrhosis in AIDS].

Liver biopsy (n = 35) and autopsy (n = 71) specimens from HIV infected HCV-positive and HCV-negative haemophiliacs and non-haemophiliacs and liver biopsies (n = 33) from HIV-negative HCV-infected haemophiliacs and non-haemophiliacs were studied by histo- and immunohistochemistry to investigate the influence of HIV-coinfection on chronic C hepatitis (> 10 years duration). Almost all HIV-infected patients had a CD4 cell counts < 200/microns3. In biopsies and autopsies HCV-infection lead to stronger portal, periportal and lobular inflammatory changes independent from HIV-infection and haemophilia. However, HIV-infected patients with HCV-coinfection showed much more granulocytic infiltrates, particularly in the small bile ducts. In biopsies and autopsies HCV infection was associated with a stronger (centrilobular) fibrosis, particularly in HIV-positive haemophiliacs, and significantly stronger compared to HCV-negative patients. In the autopsy group half of the HIV-infected and HCV-positive haemophiliacs (n = 20) had developed posthepatitic liver cirrhosis due to C hepatitis, contrasted by two liver cirrhosis in HCV-infected non-haemophiliacs (n = 6) due to chronic B and C hepatitis and chronic alcohol abuse; no liver cirrhosis was observed in HIV-positive HCV-negative non-haemophiliacs (n = 45). Cholestasis and mild granulocytic cholangiolitis was a predominant feature in HIV/HCV-coinfection and similar distributed in haemophiliacs and non-haemophiliacs. The findings are suggestive that HIV-coinfection aggravates the course of a preceding hepatitis C virus infection, by a more granulocytic inflammatory infiltrate, stronger (centrilobular) fibrosis followed by a high incidence of posthepatitic cirrhosis--particularly in multitransfused haemophiliacs--and by cholestatic hepatopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1994

[Polycystic and cavernous course of pneumocystis carinii pneumonia in AIDS].

We observed a polycystic and cavitating presentation of Pneumocystis carinii pneumonia as primary manifestation of AIDS in a patient with previously unknown HIV-infection. Pneumocystis carinii was histologically proved by transbronchial biopsy but not by bronchoalveolar lavage. A nearly complete resolution of all pulmonary lesions could be achieved with cotrimoxazole. Pneumocystis carinii must be considered in differential diagnosis of cystic and cavitating pulmonary disease in patients with unknown or positive serology for HIV-infection.

AIDS-Related Opportunistic Infections↗
PubMed1993

[Morphological classification and comparison of the different types of stromal nodules in benign prostatic hyperplasia].

The expression of immunohistochemical markers for cytoskeletal differentiation and that of neuroendocrine- and immunological cells showed in general the same tendency in the 4 types of prostatic stromal nodules: missing or low expression in immature-mesenchymal-, distinct augmentation in fibroblastic-, a maximum in fibro-muscular- and a slight decline in smooth-muscular nodules. These results are in agreement with developmental sequences, revealed by immunohistochemical investigations of fetal prostates, and seem to confirm the hypothesis that the four types of stromal nodules represent successive degrees of maturation, recapitulating ontogenetic processes.

Biomarkers↗
PubMed1992

Sequence analysis of polymerase chain reaction amplified t(14;18) chromosomal breakpoints in formalin fixed, paraffin wax embedded follicular lymphoma.

AIMS: To determine whether junctional sequences of rearranged chromosomes can be amplified by use of the polymerase chain reaction (PCR) and whether direct sequence analysis of the PCR products is possible, using DNA from formalin fixed, paraffin wax embedded biopsy specimens. METHODS: DNA was extracted from paraffin wax embedded, formalin fixed lymphoma specimens, and junctional sequences of rearranged chromosomes were amplified by the PCR. The products were used as templates for asymmetrical PCR. Subsequently, direct sequence analysis was performed using the chain termination method. RESULTS: Formalin fixed, paraffin wax embedded biopsy specimens and PCR amplification could be used to determine the nucleotide sequences of junctional regions of rearranged chromosomes t(14;18) from patients with follicular lymphoma. CONCLUSION: The identification of junctional sequences of the translocation in follicular lymphoma provides a molecular "fingerprint" of t(14;18) of the lymphoma of an individual patient and can be used for the detection of clone specific DNA in any biopsy tissue obtained from the patient. The strategy used for rapid sequence analysis of PCR amplified DNA sequences will be useful in many areas of molecular pathology.

Base Sequence↗
PubMed1992

[Cytomegalovirus infections of the gastrointestinal tract].

Histopathological findings in 8 cases of CMV infections of the gastrointestinal tract including 5 cases with AIDS are presented. The cytomegalic cells were irregularly distributed and were predominantly found in esophagus, small bowel and colon. Viral inclusions were detected in "stromal" cells and in endothelial cells, sometimes associated with lesions of the vascular wall. Cytomegalic smooth muscle cells and glandular epithelia were also observed. No correlation was found between the number of cytomegalic cells per mm2 of tissue and the inflammatory response. Monoclonal CMV antibodies reacted immunohistologically not only with cytomegalic cells but also with a few normally appearing cells. The in-situ-hybridization detected CMV-DNA also in cells which were negative for CMV antigens. Notwithstanding the new immunohistological techniques the searching for cytomegalic cells and their recognition still belong to the most important steps required for the diagnosis of CMV infection.

AIDS-Related Opportunistic Infections↗
PubMed1991

[Progressive cytomegalovirus encephalitis in successful ganciclovir therapy of cytomegalovirus retinitis in an AIDS patient].

We describe a case of an HIV-infected intravenous drug-abuser who died of progressive cytomegalovirus encephalitis despite successful treatment of cytomegalovirus retinitis with ganciclovir. On autopsy, complete remission of retinitis and widespread cytomegalovirus-encephalitis could be demonstrated. Therapeutic failure therefore seems attributable to insufficient CNS-distribution of ganciclovir rather than to ganciclovir-resistant cytomegalovirus strains.

AIDS Dementia Complex↗