Biomedical subjects

R Flury

Publications and source records attributed to R Flury.

At least 19 recordsLinked to original sources

PubMed1996

[Effectiveness of triple therapy to eradicate H. pylori in patients after failed therapy with omeprazole/amoxicillin].

Helicobacter pylori (H. pylori) eradication rates with omeperazole/amoxicillin range from 0-90%. The best regimen for retreatment after failure of omeprazole/amoxicillin has not been established so far. The aim of this prospective study was to evaluate the efficacy of triple therapy with bismuth, tetracycline and ornidazole in eradicating H. pylori after failure of omeprazole/amoxicillin. 79 duodenal ulcer patients with H. pylori infection were treated with oral omeprazole (40 mg bid) and amoxicillin solute (750 mg tid) for 10 days. Eradication rate was 28/79 (35%) and was distinctly lower in smokers (> 10 cigarettes/day) vs nonsmokers (10/49 [20%] vs 18/30 [60%], p < 0.001). 37 patients with persistent H. pylori infection in whom omeprazole/amoxicillin had failed agreed to retreatment with triple therapy. Persistence of H. pylori was confirmed by histology (3 antral and 2 gastric body biopsies; H&E, Giemsa), urease test (CLO) and/or H. pylori culture. Patients smoking > 10 cigarettes/day were classified as smokers. Retreatment consisted of oral bismuth-subcitrate 4 x 120 mg/d for 28 days (day 1-28), tetracycline 4 x 500 mg/d and ornidazole 3 x 500 mg/d for 10 days (day 1-10). Control endoscopy was done 30 days after the end of treatment. Criteria for H. pylori eradication was negative urease test, culture and histology. 34/37 patients (6 females/28 males; 39 [23-64] years) completed the study (24/34 smokers, 10/34 nonsmokers). 3/37 patients dropped out because of side effects (n = 1) or incompliance (n = 2). H. pylori subcultures for resistance testing were possible in 32/34 patients: H. pylori was metronidazole-sensitive in 11/32 (1 female, 10 males; 38 [24-55] years; 9 smokers, 2 nonsmokers) and metronidazole-resistant (minimal inhibitory concentration for metronidazole > 8 mg/ml) in 21/32 (5 females, 16 males; 40 [23-64] years; 13 smokers, 8 nonsmokers). The overall H. pylori eradication rate of the triple therapy was 27/34 (79%). H. pylori was eradicated in 19/24 (79%) smokers and in 8/10 (80%) nonsmokers. Eradication rate for metronidazole-sensitive H. pylori was 11/11 (100%) vs 14/21 (67%) for metronidazole-resistant H. pylori (p = 0.012). Triple therapy is effective and safe in eradicating H. pylori in patients after failure of omeprazole/amoxicillin. Smoking had no negative effect on the eradication rate of the triple therapy after failure of omeprazole/amoxicillin. Eradication failures were due to metronidazole-resistance.

Adult↗

PubMed1995

[Clinical manifestations and course of cytomegalovirus colitis in AIDS patients].

The clinical findings and course in 10 HIV-positive patients with cytomegalovirus (CMV) colitis were analyzed. Homosexuality was the main risk factor for HIV infection. All patients had markedly reduced CD4 counts (mean 25 x 10(9)/l). Symptoms at presentation were chronic diarrhea, weight loss, fever and abdominal pain. One of the patients had an abdominal mass in the ileocecal region due to inflammation as the leading symptom. Endoscopically the colitis was more often segmental than diffuse. In 2 out of 9 patients who underwent colonoscopy, only the right hemicolon was affected. Concurrent intestinal infections with up to 4 different pathogens were found in 7 patients. 5 patients had chorioretinitis as an extraintestinal CMV symptom (2 before, 3 after the occurrence of CMV-colitis). In only one patient was there a partial response of CMV-colitis to therapy with ganciclovir and foscarnet. Even under therapy CMV colitis was complicated in 2 patients by perforation and inflammatory stenosis respectively. Both needed surgical treatment. Most of the patients died of generalized CMV infection or wasting syndrome.

AIDS-Related Opportunistic Infections↗

PubMed1995

[Does laparoscopic colonic carcinoma surgery satisfy the radicality criteria of open surgery?].

Minimal invasive surgery is applicable to almost all colorectal operations, with major benefit for the patient. Technically even cancer operations can be performed. However, in laparoscopic assisted colorectal surgery the question of radicality outweighs that of performability and patient comfort. From a prospective series of 88 laparoscopic colorectal operations, 36 were for carcinoma. 34 patients who underwent conventional surgery were matched with regard to age, sex, type of operation and tumor stage (TNM, grading) to compare the two techniques. The two interventions followed exactly the same guidelines. We compared the length of the fixed specimens, the number of resected lymph nodes and the need for blood transfusions. Postoperative complications were noted and follow-up was 3-12 months. The data obtained showed no difference between the two treatment groups, with a slight trend towards laparoscopic surgery with regard to number of resected lymph nodes. A portside metastasis was observed 9 months after an initial tumor stage T4N1M1. The close relation between the portside and infiltration of the adenocarcinoma into the abdominal wall together with a drain placed through this whole was suspected to be the cause of this complication. We conclude that laparoscopic assisted colorectal surgery for cancer is equal to open operation regarding radicality of resection. Long term results are mandatory to determine the value of minimal invasive surgery in the field of oncology.

Adult↗

PubMed1995

[Acute liver failure following tetrabamate].

Tetrabamate (Atrium), a composite preparation of phenobarbital, difebarbamate and febarbamate, is widely used to reduce ethanol withdrawal symptoms such as tremor, agitation and anxiety. Generally this drug is well tolerated and a few cases of reversible hepatitis as well as clinically mild symptoms of asthenia have been described. We report on a 28-year-old female patient admitted to hospital with acute liver failure after treatment with tetrabamate because of alcohol withdrawal symptoms. Liver biopsy revealed a drug-induced toxic alteration with extensive panlobular necrosis without signs of alcoholic hepatitis. Under supportive therapy liver parameters normalized in 3 months. In view of this potentially lethal adverse effect of tetrabamate, it should not be used for ethanol withdrawal symptoms.

Adult↗

PubMed1995

Local Fas/APO-1 (CD95) ligand-mediated tumor cell killing in vivo.

Fas/APO-1 (CD95) is a cell surface receptor which mediates apoptosis when ligated by specific antibodies or by its recently cloned natural ligand, FasL. We have studied the cytotoxic potential of FasL in vivo using Fas/APO-1-expressing Yac-1 cells as targets. Supernatant harvested from Neuro-2a cells transfected with the murine FasL cDNA contains FasL and transduces a potent apoptotic signal to Yac-1 cells in vitro. Specificity of FasL-mediated cytotoxicity was confirmed by competition assays using soluble Fas or anti-Fas/APO-1 F(ab')2 fragments which specifically interfere with FasL-Fas/APO-1 interactions. Intraperitoneal injection of FasL-containing supernatant efficiently killed Yac-1 target cells which had been implanted in capsules into the peritoneal cavity of mice. Analysis of the target cells revealed DNA fragmentation and nuclear changes typical of apoptosis. As previously shown, intraperitoneal injection of anti-Fas/APO-1 antibodies caused liver failure (Ogasawara, J., Watanabe, F.R., Adachi, M., Matsuzawa, A., Kasugai, T., Kitamura, Y., Itoh, N., Suda, T. and Nagata, S., Nature 1993. 364:806) and was observed at doses which did not reduce Yac-1 cell viability. In contrast, FasL did not induce histopathology in the liver when applied intraperitoneally at doses cytotoxic for Yac-1 cells. However, intravenous administration of FasL induced lethal liver hemorrhages and hepatocyte apoptosis. Thus, locally applied FasL kills tumor cells very efficiently without systemic toxicity and may therefore represent a candidate for local tumor treatment.

Animals↗

PubMed1995

[Expression of CD44 isoforms in normal human liver and also in regenerative and neoplastic liver changes].

CD44 is a transmembrane glycoprotein of which a large number of isoforms exist. There is evidence, mostly from experimental systems, that isoforms of CD44 generated by alternative splicing of ten variant exons are involved in tumor invasion and metastasis formation. We have evaluated the expression of CD44 standard (CD44s) and variant exons (CD44v) encoded gene products in formalin-fixed and paraffin-embedded human liver specimens, using an immunohistochemical protocol with microwave-based antigen-retrieval and signal amplification. Tissue sections from normal, regenerative and neoplastic liver were studied. Our results indicate that: 1. in normal liver, both, hepatocytes and bile duct epithelia lacked detectable CD44s and CD44v containing isoforms; 2. most cirrhotic liver specimens were unreactive. Some regenerative nodules showed a focal weak positivity for CD44v5 and v9. Most proliferating bile ductules were weakly stained for CD44v9 and some of them also for v5 and v6; 3. most hepatocellular carcinomas displayed a heterogeneous staining of varying intensity for CD44v5, v6, v9 and CD44s. In a few tumors a weak staining for CD44v3 and v4 was also present. Furthermore, there was a tendency to an increased staining intensity of CD44 isoforms with decreasing differentiation; 4. cholangiocarcinomas showed a high expression of CD44s, v3, v5, v6 and v9 containing isoforms. We conclude that neoplastic transformation of hepatocytes and bile duct epithelia is associated with qualitative and quantitative changes in the expression of some CD44 variant exons encoded products. The clinical implications of these findings remain to be determined in a large series of patients.

Adenoma↗

PubMed1994

[Addison crisis due to bilateral adrenal gland histoplasmosis].

A 44-year-old man was admitted with symptoms compatible with Addison crisis. Abdominal computer tomography revealed extensive bilateral adrenal abscesses. Histoplasma capsulatum was cultured from a needle aspirate. The patient was HIV-seronegative and had no underlying malignancy. He may have acquired the infection during several stays in endemic areas in the United States, South America and Asia. The case was also remarkable for moderate brain atrophy, thrombosis of the portal and splenic veins and liver cirrhosis caused by alpha-1-antitrypsin deficiency (phenotype MZ). The patient recovered fully under substitution of adrenal hormones and antifungal treatment. He received intravenous amphotericin B (75 mg q24h) for 10 days, followed subsequently by oral treatment with itraconazole (400 mg q24h) over several months. Radiologic follow-up 9 and 18 months later showed a pronounced decrease of the inflammatory adrenal lesions.

Abscess↗

PubMed1994

[Neuroendocrine tumors of the stomach (stomach carcinoid)].

We report about two patients with gastric neuroendocrine tumours (carcinoids) and chronic atrophic gastritis. A 68-year-old woman presented with nonspecific dyspeptic complaints. Gastroscopy revealed a single neuroendocrine tumour of the corpus. 33 months after endoscopic therapy she is free of detectable tumour. As cause of an upper gastrointestinal bleeding in a 75-year-old woman, a small ulcerated fundic neuroendocrine tumour was found together with other multiple tumours. Repeated endoscopic removals of these and further developing similar tumours were necessary during a follow-up of 25 months. Neuroendocrine tumours of the stomach are rare and are potentially malignant. According to their clinical context they can be divided into three subtypes: 1. tumours in chronic atrophic gastritis, 2. tumours in multiple endocrine neoplasia type I, 3. sporadic tumours, not associated with particular diseases. The first two types may be gastrin-promoted; they occur often multifocal only in the nonantral mucosa and seem to behave relatively benign. Metastasis limited to regional lymph nodes has not been described often. The very rare third type appears solitary in the whole stomach and seems to have a higher malignant potential with frequent distant metastasis to the liver. Therapy should be mainly guided by subtype and tumour size.

Aged↗

PubMed1994

[Eradication of metronidazole-resistant Helicobacter pylori: is omeprazole/amoxicillin a therapeutic alternative?].

Recommended therapies with the highest eradication rates for Helicobacter pylori (HP) are triple therapies comprising bismuth salts, nitroimidazole and amoxicillin or tetracycline. Primary and secondary resistance of HP to nitroimidazole, however, represents a major problem of this treatment since it is the main cause of eradication failure. In these cases therapeutic regimes without nitroimidazole could prove more successful. High dose omeprazole/amoxicillin has been suggested as a simple and effective therapy with few side effects. The effectiveness of this combination in eradicating metronidazole resistant HP has not been established so far. The aim of this study was to evaluate high dose omeprazole/amoxicillin in eradicating metronidazole resistant HP in our population. 33 patients (6 women, 27 men, mean age 39 [range 21-68]) with recurrent duodenal ulcer and gastric colonization by metronidazole resistant HP were examined. Smokers were defined as patients currently smoking > 10 cigarettes/day. Exclusion criteria were: gastric surgery or intake of antibiotics, omeprazole bismuth salts and NSAIDs within four weeks before study entry endoscopy. Biopsy specimens were obtained in a standardized manner: 5 from the gastric antrum (1 CLO, 1 culture, 3 histology: H & E, Giemsa) and 2 from the gastric body (histology). Resistance testing for penicillin, amoxicillin and metronidazole was performed using a disk diffusion test (E-test, AB Biodisk, Sweden). Metronidazole resistance was defined as a minimal inhibitory concentration (MIC) of metronidazole of > 8 micrograms/ml. Eradication therapy consisted of oral omeprazole (40 mg bid) and amoxicillin solute (750 mg tid) for 10 days. Subsequently, for ulcer treatment, patients were given omeprazole (20 mg per day) for 20 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[Omeprazole/amoxicillin: improved eradication of Helicobacter pylori in smokers because of N-acetylcysteine].

Colonization of Helicobacter pylori (HP) beneath the protective film of gastric mucus enables the organism to survive in the hostile environment of the gastric mucosa. N-acetylcysteine (NAC), a sulfhydryl compound with potent mucolytic activity, induces a reduction of gastric barrier mucus thickness of about 75% and reduces mucus viscoelasticity. We therefore tested the hypothesis whether better eradication results could be achieved by addition of NAC to omeprazole/amoxicillin (OME/AMOX). 34 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included in an ongoing, prospective, randomized trial. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids or NSAIDs within 4 weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from gastric antrum and 2 from gastric body; H&E, Giemsa) and at least positive rapid urease test or culture. All 34 patients underwent ulcer therapy with OME (20 mg per day) for 20 days (d 1-20). Group A: in 17 patients (5 females, 12 males, mean age 46 [29-74] years; 8 smokers, 9 nonsmokers) the subsequent eradication therapy, consisting of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days, was combined with NAC solute (2 x 600 mg bid (d 21-30). Group B: 17 patients (2 females, 15 males, mean age 39 [19-70] years; 11 smokers, 6 nonsmokers) underwent eradication therapy without NAC (d 21-30). Control endoscopy was done after a minimal interval of 30 days from the end of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗

PubMed1994

[Omeprazole/amoxicillin: impaired eradication of Helicobacter pylori in smoking but not in premedication with omeprazole].

The efficacy of high dose omeprazole/amoxicillin (OME/AMOX) for eradication of Helicobacter pylori (HP) is controversial. Reported eradication rates range from 0% to 90%. Different therapy schedules and unknown factors may be crucial; in particular, pretreatment with OME has been thought to endanger HP eradication by subsequent OME/AMOX. Preliminary findings suggested that smoking may impair eradication with OME/AMOX. The aims of this study were (1) to establish whether HP eradication rates differ depending on whether eradication with OME/AMOX was performed before or after ulcer therapy with OME, (2) to determine whether smoking impairs HP eradication by OME/AMOX and (3) to evaluate the efficacy of OME/AMOX in our population. 52 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids and NSAIDs within four weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from the gastric antrum and 2 from the gastric body; H&E, Giemsa) and at least positive rapid urease test (CLO) or culture. Eradication therapy consisted of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days (OME/AMOX). This therapy preceded (group A) or followed (group B) ulcer therapy with OME (20 mg per day for 20 days). In group A 17 patients (2 females, 15 males, mean age 39 [19-70]; 11 smokers, 6 nonsmokers) underwent ulcer therapy with OME (d 1-20) before OME/AMOX d 21-30).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[Duodenal ulcer disease: a defect in the secretory immune response to Helicobacter pylori?].

In a prospective study we examined 20 Helicobacter pylori (HP)-positive duodenal ulcer patients (5 female, 15 male; age 26-70 [mean 43] years), 20 HP-positive patients with non-ulcer dyspepsia (10 female, 10 male; age 26-79 [mean 48] years) and 10 HP-negative patients with non-ulcer dyspepsia (5 female, 5 male; age 21-76 [mean 45] years) during upper GI-endoscopy. HP was detected by histology (H&E, Giemsa), rapid urease test (CLO) and serology (Cobas Core Anti-H. pylori EIA). IgA anti-HP in gastric juice was determined by ELISA. HP-positivity included positivity in all methods, and HP-negativity failure to detect HP-infection by all methods used. Of the 20 duodenal ulcer patients, 10 patients (2 female, 8 male; age 26-70 [mean 42] years) had an endoscopically documented duodenal ulcer at an earlier endoscopy with no current ulcer, 10 patients had florid duodenal ulcer disease at the time of examination. Duodenal ulcer patients compared with non-ulcer dyspepsia patients were tended to have higher serum IgG anti-HP (551 +/- 240 vs. 338 +/- 159 U/ml) and significantly higher gastric juice IgA anti-HP (50.0 +/- 7.3 vs. 26.5 +/- 4.3 relative units). Concentrations of both serum IgG anti-HP and gastric juice IgA anti-HP tended to be higher in patients with positive ulcer history but no present ulcer compared with patients with florid ulcer disease (934 +/- 456 vs. 170 +/- 63 U/ml and 60.0 +/- 8.6 vs. 40.8 +/- 10.4 relative units).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[Suppression of Helicobacter pylori by local secretory immune response?].

54 patients (22 females, 32 males, age 21-79, mean 45 years) referred for upper gastrointestinal endoscopy were investigated. Helicobacter pylori (HP) infection was determined using histology (H&E and Giemsa stain), rapid urease test (CLO) and serology (Cobas Core Anti-H. pylori EIA). Density of HP colonization was determined in gastric antral (3 biopsy specimens) and body mucosa (2 biopsy specimens) and semiquantitatively graded on a scale of 0 to 3. Gastric colonization was obtained by addition of the two scores. IgA anti-HP concentration was determined by ELISA using the same FPLC purified HP-antigen mixture as for serology. Gastric juice IgA anti-HP concentration in HP-positive patients (n = 40) was significantly higher than in HP-negative (n = 14) patients (38.3 +/- 4.6 vs. 5.4 +/- 1.2 relative units, p < 0.001). Comparison of HP-colonization density of gastric mucosa with gastric juice IgA anti-HP concentration of the 54 patients by binominal regression analysis yielded a correlation coefficient of 0.65 (p < 0.01). The biphasic course of the curve suggests a mutual relationship of HP-colonization density and IgA immune response. Increasing colonization densities seemed to induce increasing secretory immune responses. Half-maximal and higher immune responses, however, seemed to suppress further HP colonization in vivo without eradicating the infection.

Adult↗

PubMed1994

[Thoracic pain, shock-inducing gastrointestinal bleeding].

A 65-year-old patient was referred to hospital with suspected myocardial infarction because of left-sided thoracic pain. A paresis of the left recurrent nerve of unknown etiology has been known for three years. Because of shock with anemia, upper gastrointestinal endoscopy was performed. A diverticulum-like lesion in the proximal esophagus was found to be the source of the bleeding. A contrast X-ray examination showed a cavity of approximately 2 x 2 cm originating from the proximal esophagus. Computerized tomography revealed a large mediastinal mass reaching from the thyroid to the diaphragm. An ultrasound-guided fine-needle puncture of this tumor, together with the endoscopical snare biopsies of the esophageal lesion, allowed the diagnosis of an anaplastic thyroid carcinoma with erosion of the esophagus. The patient responded well to palliative radiotherapy. The defect in the proximal esophagus refilled quickly. Nine months after radiotherapy the patient is doing well.

Aged↗

PubMed1994

Chlorpromazine-induced vanishing bile duct syndrome leading to biliary cirrhosis.

We describe a 33-yr-old pregnant woman in whom a primary biliary cirrhosis-like syndrome developed after 2 wk of chlorpromazine therapy. The clinical course was characterized by severe jaundice lasting 22 mo, intense pruritus, fever, steatorrhea, high alkaline phosphatase levels and hypercholesterolemia. Jaundice resolved with initiation of ursodeoxycholic acid therapy, but subclinical cholestasis and low-level inflammatory activity persisted and ultimately evolved into biliary cirrhosis. The pathological substrate of this severe and prolonged cholestatic reaction was found to be the vanishing bile duct syndrome with a marked transient pseudoxanthomatosis.

Adult↗

PubMed1994

Chronic viral hepatitis B and C: an argument against the conventional classification of chronic hepatitis.

The classification of chronic hepatitis distinguishing benign chronic persistent hepatitis from severe chronic active hepatitis was constructed without knowledge of well-defined aetiological factors. Better understanding of the different hepatitis-viruses has shed new light on this subject. Chronic viral hepatitis B and C each show typical histological patterns. The validity of the conventional classification has been evaluated by a comparative study of chronic viral hepatitis B and C. 130 biopsies from 110 patients with chronic hepatitis C (CH-C) proven serologically by antibodies (second generation testing) were compared with 105 biopsies from 73 patients with chronic hepatitis B (CH-B). These were scored semi-quantatively. In CH-C, lymphoid follicles and/or aggregates were found in 88.5%, fatty degeneration in 51%, bile duct lesions in 46.2%, and Mallory body-like material in the hepatocytes in 9.2%. The portal lymphocytic infiltration generally predominated over the necro-inflammatory lesions of the parenchyma. Chronic persistent hepatitis (defined by the presence of portal hepatitis) was present exclusively in CH-C. Chronic lobular hepatitis was found exclusively in CH-B. We conclude that the histological criteria described for CH-C are highly suggestive of the diagnosis, that the artificial subdivision of chronic hepatitis into CPH and CAH is obsolete and that the histological assessment of chronic hepatitis should consist of a grading of inflammatory activity (minimal, mild, moderate, severe) and staging of fibrosis (extent of distortion of architecture). The final diagnosis should be based on the demonstration of the aetiological agent.

Chronic Disease↗

PubMed1994

Evaluation of methods for hepatitis C virus detection in archival liver biopsies. Comparison of histology, immunohistochemistry, in-situ hybridization, reverse transcriptase polymerase chain reaction (RT-PCR) and in-situ RT-PCR.

To evaluate reliable methods for detection of hepatitis C virus (HCV) infection in routinely processed liver biopsies we analyzed formaldehyde-fixed and paraffin-embedded liver specimens of 10 patients with serological confirmed HCV infection. We compared (1) conventional histology; (2) indirect immunofluorescence using the mAb TORDJI-22 (Clonatec, Paris, France); (3) RT-PCR using total RNA and Southern blotting with chemiluminescent detection; (4) non-radioactive in-situ hybridization (ISH) with digoxigenin-labeled oligo- and cRNA probes; (5) direct in-situ RT-PCR with incorporation of labeled nucleotides into PCR-products, and (6) indirect in-situ RT-PCR using subsequent ISH for the visualization of intracellular PCR-products. Our results indicate that: (1) using the histological criteria described by Lefkowitch et al. [Gastroenerology 1993;104:595] together with clinical data, most chronic HCV infections can be diagnosed by conventional histology, if liver biopsies specimens are adequate; (2) the commercially available mAb TORDJI-22 appears to crossreact with non-HCV epitopes, resulting in false positives; (3) molecular methods performed on routinely fixed and processed liver biopsies frequently yield false negative results due to sampling problems, low viral copy number and RNA degradation in infected cells; (4) analysis of HCV-RNA by RT-PCR of extracted total RNA is more sensitive than indirect in-situ RT-PCR or ISH; and (5) direct in-situ RT-PCR is not reliable despite the use of modifications such as DNase pretreatment and hot-start procedures. It is concluded, that several molecular methods for HCV detection must await further improvements of protocols to be suitable for routine diagnostics on paraffin-embedded liver biopsies.

Base Sequence↗

PubMed1994

Childhood stroke at three years of age with transient protein C deficiency, familial antiphospholipid antibodies and F. XII deficiency--a family study.

The unusual case of a boy with a stroke occurring at three years of age, transient reduction in protein C activity and high concentrations of antiphospholipid antibodies (APA) is described. APA or Lupus Anticoagulant (LA) were found in 7 of 11 relatives studied out of three different generations. In addition, antigenic Factor (F) XII deficiencies or borderline values were found in the propositus and 2 relatives. Evidence for F. XII inhibitors was found in the propositus, one of his brothers and both of his parents. Whether F. XII inhibitors in patients with APA and/or LA are pathophysiologically relevant in vivo or if they are only an in vitro phenomenon remains to be elucidated. It is reasonable to believe that the main laboratory pathology (APA and/or LA activity) in antiphospholipid syndrome is related to the clinical picture of a hypercoagulable state. There is evidence from the literature that deficiency or inhibition of F. XII might contribute to a prothrombotic state through impairment of the fibrinolytic system. There is also evidence that APA are able to reduce protein C activation. From a clinical point of view, it seems that hypercoagulability in our patient was controlled by low-dose aspirin therapy (75 mg/d). In conclusion, this case seems to support the idea of a genetic predisposition for the development of APA and/or LA. The related disturbances of the coagulatory, anticoagulatory and fibrinolytic systems might contribute in different ways to the prothrombotic state seen in patients with "antiphospholipid syndrome", eventually resulting in possible venous thrombosis or arterial thrombosis with corresponding ischaemic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antiphospholipid↗