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D Bastian

Publications and source records attributed to D Bastian.

At least 19 recordsLinked to original sources
PubMed2002

[Recurrent hemoptysis as initial symptom of a thoracic angiomatosis in an adult patient].

HISTORY: A 24-year-old man presented with recurrent hemoptysis and decreased exercise capacity. DIAGNOSTIC FINDINGS: The chest radiograph demonstrated multiple disseminated pulmonary nodules. In addition the patient developed a hematopericardium with tamponade. The further diagnostic approach revealed an extensive thoracic angiomatosis affecting the lung and the heart. TREATMENT AND COURSE: Tumor resection could not be performed. A therapy with Interferon alpha-2a was initiated. After 3 month a significant regression of the pulmonary angiomatosis was documented. On the other hand the cardiac tumor showed no therapeutic response. CONCLUSION: Thoracic angiomatosis should be considered in the differential diagnosis of otherwise unclear hemoptysis or hematopericardium. Diagnosis intra vitamin requires an aggressive and invasive approach. Interferon alpha-2a is effective in palliative treatment of diffuse angiomatous diseases. But not all angiomatous processes respond to that therapy.

Adult↗
PubMed1999

Malignant fibrous histiocytoma of the pancreas: a case report with genetic analysis.

BACKGROUND: Malignant fibrous histiocytoma (MFH) is the most common type of soft tissue sarcoma in adults; it occurs frequently in the extremities, the trunk, or retroperitoneal tissues. MFH rarely is detected in digestive organs, such as the liver or stomach. METHODS: The authors report a patient with MFH of the pancreas who was treated with surgery alone. The tumor was studied for genetic alterations in the p53, p16ink4a, and DPC4 tumor suppressor genes as well as the K-ras oncogene by immunohistochemistry, single strand conformation variant (SSCV) analysis, and direct DNA sequencing. RESULTS: The authors believe that this is the 13th report of primary pancreatic MFH in the world literature and the first genetic analysis of this rare tumor. The patient is alive with no evidence of recurrence 34 months after surgery. Immunohistochemistry revealed no abnormal accumulation of the p53 protein and normal nuclear p16 expression. Mutation analysis of the p53, p16, DPC4, and K-ras genes showed only a polymorphism at codon 72 of the p53 gene and no mutations in any of the genes. CONCLUSIONS: Genotypically, MFH of the pancreas is clearly different from other malignant pancreatic tumors, which further supports the hypothesis that this tumor is a rare but distinct entity.

Aged↗
PubMed1999

Higher frequency of DPC4/Smad4 alterations in pancreatic cancer cell lines than in primary pancreatic adenocarcinomas.

The tumor suppressor gene DPC4/Smad4 at 18q21.1 is inactive in about 50% of pancreatic carcinoma xenografts and cell lines. However, the role of DPC4 in the multistep carcinogenesis of primary pancreatic adenocarcinomas remains uncertain. Therefore, we examined 45 primary human pancreatic adenocarcinomas and 12 pancreatic cancer cell lines for DPC4 alterations by single-strand conformational variant (SSCV) analysis and a PCR-based deletion assay. DPC4 was inactivated by either homozygous deletion or point mutation in 6 of 12 cell lines (50%). None of the primary pancreatic carcinomas carried a DPC4 mutation, although 66% revealed LOH of 18q21 sequences. These findings suggest that inactivation of DPC4 occurs more frequently in tumor-derived cell lines than in primary pancreatic adenocarcinomas. In addition, another, yet unidentified, tumor suppressor gene(s) may be linked with the frequent LOH of 18q21 in primary pancreatic adenocarcinomas.

Adenocarcinoma↗
PubMed1999

Mutations of the DPC4/Smad4 gene in neuroendocrine pancreatic tumors.

Tumors of the endocrine pancreas are extremely rare, and molecular mechanisms leading to their development are not well understood. A candidate tumor suppressor gene, DPC4, located at 18q21, has recently been shown to be inactivated in half of pancreatic adenocarcinoma xenografts. The close anatomical relationship of the exocrine and endocrine pancreas prompted us to determine the role of DPC4 in the tumorigenesis of 25 pancreatic islet cell tumors (11 insulinomas, nine non-functioning endocrine carcinomas, three gastrinomas, two vipomas). A mutation screening of the highly conserved COOH-terminal domain of DPC4 (exons 8-11) was performed by single-strand conformational variant (SSCP) analysis and a PCR-based deletion assay. Five of nine (55%) non-functioning endocrine pancreatic carcinomas revealed either point mutations, small intragenic deletions or homozygous deletion of DPC4 sequences compared to none of the insulinomas, gastrinomas or vipomas. These results suggest that DPC4 is an important target gene promoting tumorigenesis of non-functioning neuroendocrine pancreatic carcinomas.

Adenoma, Islet Cell↗
PubMed1998

Localization, malignant potential, and surgical management of gastrinomas.

Between 1987 and 1996 a total of 25 patients with proved Zollinger-Ellison syndrome (ZES) have been treated in our department. If preoperative imaging studies did not show diffuse metastatic disease, patients were scheduled for operation with a standardized surgical approach including thorough exploration and intraoperative ultrasonography (IOUS) of the pancreas and a longitudinal duodenotomy, with separate palpation of the anterior and posterior walls. Postoperatively, patients were followed up by physical examination, fasting gastrin levels, and the secretin stimulation test. Altogether 10 patients had duodenal wall gastrinoma, 14 patients pancreatic gastrinoma, and the tumor was not found in 1 patient. Only 15 tumors (60%) (2 duodenal wall and 13 pancreatic gastrinomas) could be visualized preoperatively. Intraoperatively, 24 of 25 primary gastrinomas were localized. The mean size of duodenal wall gastrinomas (9.6 mm) was significantly smaller than that of pancreatic gastrinomas (28.7 mm) (p < 0.05). At the time of surgical exploration, five duodenal and seven pancreatic gastrinomas had metastasized. The incidence of lymph node metastases was similar for both tumor sites, whereas patients with pancreatic gastrinomas more frequently had liver metastases. The presence of liver metastases was the most important determinant for survival. Four patients (40%) with duodenal and seven with pancreatic (50%) gastrinomas (mean follow-up 5.2 years) were biochemically cured by operation. Of the remaining patients, eight are still alive with recurrent disease. Our results suggest that preoperative localization of gastrinomas often fails despite all modern imaging methods. Therefore a standardized surgical exploration of the pancreas including IOUS and a duodenal exploration should be performed to achieve optimal results. Preoperative diagnostic imaging tests should include computed tomography, ultrasonography, and somatostatin receptor scintigraphy to exclude diffuse metastases. In contrast to liver metastases, lymph node metastases do not have a significant influence on survival.

Diagnostic Imaging↗
PubMed1998

K-ras oncogene mutations indicate malignancy in cystic tumors of the pancreas.

OBJECTIVE: To evaluate clinical parameters, presurgical diagnostic tests, histologic findings, and the presence of K-ras oncogene mutations in cystic tumors of the pancreas to determine which best predict malignancy. SUMMARY BACKGROUND DATA: Because presurgical, intraoperative, and final pathologic differentiation is difficult in cystic tumors of the pancreas, it would be a major benefit to identify markers that accurately predict malignancy in these rare tumors. The role of K-ras oncogene mutations as an indicator of malignancy has not been determined in these tumors. METHODS: Nineteen patients with cystic tumors of the pancreas were evaluated, including K-ras mutation analysis based on polymerase chain reaction and restriction digestion assays and direct DNA sequencing, to screen for parameters that accurately predict malignancy. RESULTS: All malignant cystic pancreatic tumors (five cystadenocarcinomas and three mucin-producing adenocarcinomas) harbored K-ras mutations at codon 12 or 13. K-ras mutations were also detected in the percutaneous fine-needle aspirates of two of these patients. In contrast, none of nine benign cystadenomas or the solid-papillary neoplasm had K-ras mutations. None of the patients with a benign tumor carrying K-ras wild-type sequences developed recurrent disease after a mean follow-up of 50 months. Seven of the 8 malignant cystic pancreatic tumors, but none of the 11 benign tumors, showed dilatation of the main pancreatic duct on computed tomography or endoscopic retrograde cholangiopancreatography. CONCLUSIONS: K-ras mutation analysis seems to be a powerful tool to determine the malignant potential of cystic pancreatic tumors before and after surgery. Dilatation of the main pancreatic duct on computed tomography or endoscopic retrograde cholangiopancreatography is highly suggestive for malignancy in these rare tumors.

Adult↗
PubMed1998

[Detection of hepatic micrometastasis in ductal pancreatic carcinoma by K-ras mutation analysis and determination of clinical relevance].

In this prospective study we evaluated the presence and importance of hepatic micrometastases at the time of operation in patients with resectable pancreatic carcinoma. In 13 patients with pancreatic carcinoma and 5 patients with chronic pancreatitis Truecut-Needle biopsies of the liver were obtained during operation. K-ras mutation analysis was done by the PCR/restriction digestion assay with HphI, followed by an ultrasound of the liver in 3 monthly intervals. Four of 13 (30%) pancreatic cancer patients had K-ras gene mutations in the liver and had a mean survival of 6 months after resection. All chronic pancreatitis patients and 8 of the 9 remaining pancreatic cancer patients without K-ras mutations in the liver biopsies are alive without evidence of liver metastases after a mean follow-up of 9 months. Detection of micrometastases in the liver by K-ras mutation analysis might be a powerful tool to identify occult clinical relevant liver metastases.

Carcinoma, Pancreatic Ductal↗
PubMed1996

[Diagnostic localization of insulinoma. Experiences with 25 patients with solitary tumors].

OBJECTIVE: The most effective way to localize the mostly small ( < 2 cm), benign and solitary insulinomas is still under discussion. Especially the evaluation of the different preoperative localization methods is not clarified. The aim of our study was to support the ongoing discussion in that matter. PATIENTS AND METHODS: In total 25 patients have been included in our study since 1987. All showed sporadic insulinomas and underwent surgery. The following preoperative localization methods had been used: ultrasonography (US): 25 patients, computed tomography (CT): 23 patients, somatostatin receptor scintigraphy (SRS): four patients since 1990, angiography: six patients, endosonography (ES): five patients since 1995, selective portal venous sampling (PVS): two patients, magnetic resonance imaging (MRI): four patients since 1993. All 25 patients underwent a bidigital palpation in combination with intraoperative ultrasonography (IOUS). Four of the 25 patients were reoperated and had a prior unsuccessful operation elsewhere. RESULTS: Preoperatively 19 of 25 insulinomas were localized (76%). The following sensitivity rates had been found: ultrasonography: 56%, computed tomography: 43%, endosonography: 100%, angiography: 66%, magnetic resonance imaging: 25%, selective portal venous sampling: 100%, somatostatin receptor scintigraphy: 0%. All 25 insulinomas were detected during operation, 100% by palpation in combination with intraoperative ultrasonography and 92% by palpation on its own. CONCLUSION: After an insulinoma is biochemically proven and after exclusion of a malignant metastasizing tumor by ultrasonography, all patients should be operated on. Intraoperative ultrasonography should be performed in any case. As other preoperative localization methods did not prove a convincing cost-utility-relation, one should not consider the usage of these methods before the initial operations. Before re-operations one should consider the use of costly pre-operative methods to localize insulinomas. Here endosonography and selective portal venous sampling are recommended as the first procedures of choice.

Adolescent↗
PubMed1996

[Structural MRI study of the Achilles tendon. Correlation with microanatomy and histology].

On T1 and T2 weighted MR Imaging, normal Achilles tendon is generally described as a homogeneous low signal structure. However, punctuate and/or short linear high signal foci are often seen, especially on the anterior part of axial sections. These images are not artifacts. The aim of this study was to correlate MR images of 20 normal Achilles tendons with micro-anatomic and histologic studies of 2 cadaver tendons. Intratendinous vessels were found in connective tissue septa called mesotenon. Foci of high signals result from this mesotenon. On T1 weighted images, a normal Achilles tendon can present high signal images without any disease process.

Achilles Tendon↗
PubMed1991

Anatomical basis of a new naso-labial island flap.

We describe a nasolabial island flap with a proximal base. This anatomical study confirms the interest of a proximal base especially with regard to venous return. As opposed to classical naso-labial flaps with subcutaneous pedicle, it has a vascularization of musculo-cutaneous type which allows a greater degree of mobility and reliability. This flap is an effective therapeutic option in surgery for skin defects of the face.

Arteries↗
PubMed1989

[Magnetic resonance imaging of the knee menisci. Normal aspects. Misleading images. Meniscus degeneration. Anatomic correlations].

The authors report the result of a study on 5 knees of fresh corpses explored with magnetic resonance imaging, including 1 examined before and after intraarticular contrast injection, and on 15 asymptomatic subjects examined with the same procedure. A very thorough study of the menisci and of their attachment, ie. The tibial insertion of the menisceal horns, the transverse ligament, and the meniscofemoral ligament, is possible with T1-weighted MR sequences. The T2-weighted sequences, either following intraarticular contrast injection or in cases of articular effusion, allow analyzing the capsular attachments of the posterior horn of the lateral meniscus and its relationships with the tendon of the popliteal muscle. Five misleading images must be known for the exploration of the menisci, in order to avoid a number of interpretation problems. Images of type I and II initial meniscus degeneration are observed in 47% of all cases (control group). One case of menisceal cyst developing in the anterior horn of the lateral meniscus, with anatomical correlation, is also reported.

Adult↗
PubMed1985

Immune response to nucleic acid antigens and native DNA by human peripheral blood lymphocytes in vitro.

The immunogenicity of DNA fragments (either oligonucleotide (oligo) or total DNA digest) covalently linked to keyhole limpet hemocyanin (oligo-KLH or DNA-KLH) was tested with peripheral blood lymphocytes (PBL) from 63 systemic lupus erythematosus patients (SLE) in vitro. PBL from 10 normal individuals and 11 rheumatoid arthritis (RA) patients served as controls. Antibodies to three nucleic acid antigens (oligo, denatured DNA (d-DNA), and native DNA (n-DNA] were assayed in supernatants of cultured lymphoid cells by a sensitive solid-phase radioimmunoassay. More than 50% of SLE and RA patient lymphoid cells formed spontaneous antibodies to one or several nucleic acid antigens. In contrast, only two normals did. After in vitro challenge with oligo-KLH or DNA-KLH, cultured lymphocytes of more than 50% of SLE patients formed antibodies to one or several nucleic acid antigens. Similar results were obtained in PBL from RA patients. In SLE patients, the response to both antigens was either monospecific or polyspecific, but DNA-KLH appeared to raise a greater proportion of antibody to n-DNA than oligo-KLH. A greater proportion of patients with active disease responded in vitro compared with those with inactive disease. A mixture of oligo together with KLH was not immunogenic in vitro. Oligo-KLH or DNA-KLH did not raise antibody to an irrelevant antigen, ovalbumin. Of particular interest, PBL from seven of 10 normal subjects formed antibody to n-DNA after challenge in vitro with oligo-KLH. The data support the view that DNA fragments could be an important immunogen in SLE. Furthermore, this study provides an in vitro model to test the tolerogenicity of similar fragments of DNA linked to self carrier molecules such as gamma-globulin.

Antibody Formation↗
PubMed1981

Mechanism of stimulation of prostaglandin synthesis by a factor from rheumatoid synovial tissue.

Rheumatoid synovial cell monolayers, with [1-14C]arachidonic acid ([1-14C]AA) incorporated into cell lipids, are stimulated by a factor (RSF) produced by explant cultures of rheumatoid synovial tissue to produce up to 50-fold increases in [1-14C]prostaglandin E2 and [1-14C]prostaglandin I2. In contrast, levels of free [1-14C]AA released from RSF-stimulated cells are generally lower than [1-14C]AA levels in cultures of untreated cells. These observations are inconsistent with a mechanism of prostaglandin stimulation consisting of an increase in phospholipase activity, because this mechanism would increase free AA levels as well as prostaglandins. A mechanism is proposed in which free AA is maintained at low steady-state levels by reacylation of free AA into phospholipids at a rate more rapid than its reaction with cyclooxygenase to form prostaglandins. In this mechanism, stimulation of the rate of the cyclooxygenase step by RSF accounts for increased prostaglandin synthesis as well as the decreased release of AA. On the basis of data previously reported by others, it is suggested that this mechanism may also be applicable to the stimulation of prostaglandin synthesis by several other agents. Preliminary characterization of the RSF indicates that it is a protein, and molecular seive chromatography indicates that its molecular weight is about 18,000. The production of RSF by rheumatoid synovial tissue is suppressed to undetectable levels by 1 microM dexamethasone.

Arachidonic Acid↗
PubMed1979

[Malignant plasma cell lymphoma of the stomach. Two cases and review of the literature (author's transl)].

Malignant plasma cell lymphomas have rarely been studied in the literature. We report two personal cases, the first survived 9 years, in the second case, histo-immunofluorescence revealed the presence of IgA kappa immunoglobulin. 59 cases have until now been reported to the best of our knowledge. They were reported under the term plasmocytoma. Analysis of data in the literature shows that plamocytomas resemble clinically and in prognosis, non-Hodgkin malignant lymphomas, of which Lukes and Lennert have recently given a new classification. Histo-immunofluorescence will permit in the future better understanding of the immunoglobulins secreted. Treatment is not yet standard. Three methods are used, depending on the spread of the tumour (surgery, radiotherapy and chemotherapy).

Female↗
PubMed1978

The effects of anti-inflammatory drugs on prostaglandin production by rheumatoid synovial tissue.

The effect of anti-inflammatory drugs on prostaglandin production by rheumatoid synovial tissue has been investigated. Synovial explants were maintained in tissue culture for periods up to six days and PGE2 concentrations in culture were determined by radioimmunoassay. The more potent nonsteroidal inhibitors of PGE2 production and their IC50 (micrometer) values were indomethacin 0.005, flufenamic acid 0.2, flurbiprofen 0.6, ibuprofen 2.0 , naproxen 6.0, phenylbutazone 10.0, and aspirin 20.0. Drugs with weak or insignificant effects were hydroxychloroquin, acetaminophen, azathioprine, chloroquin, penicillamine, gold Na thiomalate, and Na salicylate. Glucocorticoids were potent inhibitors; dexamethasone 0.003, prednisolone 0.01, hydrocortisone 0.03; while mineralocorticoids deoxycorticosterone and aldosterone were inactive at 1.0 micrometer. There is a reasonably good correlation between the IC50 concentrations of the nonsteroidal inhibitors and their peak free plasma concentration achieved during therapy in man. Inhibition of prostaglandin synthesis may contribute to the effects of many but not all anti-inflammatory drugs.

Adrenal Cortex Hormones↗