Biomedical subjects

R Ammann

Publications and source records attributed to R Ammann.

At least 37 records · Page 2Linked to original sources

PubMed1995

Two methods of authenticating past criminal conduct by psychiatric inpatients: a comparison of clinical chart reports and criminal records.

Clinical chart reports on criminal activity based primarily on the patients' own reports were compared with official criminal records of their convictions in a large group of male inpatients suffering from schizophrenia, affective disorder and alcoholism. In 69% of the cases studied there was uniformity between both methods of ascertaining criminal activity. A considerable proportion (26%) of schizophrenic patients' clinical charts indicated criminal behaviour which was not officially registered in criminal records, whereas a substantial proportion (24%) of alcoholics did not report their criminal activities in their clinical records in spite of these being recorded in their criminal records. The conclusion is that official criminal records provide an incomplete account of infractions of the law by psychiatric, especially schizophrenic patients. The information recorded in official records seems to be less accurate than that in clinical charts in the case of schizophrenics, but more veracious in the case of alcoholics. When investigating the frequency of criminal behaviour by psychiatric patients these findings will therefore have to be taken into consideration.

Adult↗

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

[Chronic pancreatitis and primary hyperparathyroidism].

The frequency of acute or chronic pancreatitis in primary hyperparathyroidism has decreased from the former 5-10% to 1-2% thanks to earlier diagnosis and operative treatment. Chronic pancreatitis, which occurs only in prolonged primary hyperparathyroidism, should therefore virtually disappear. We investigated this topic in a prospective long term study of chronic pancreatitis (1963-1992). Over the last three decades 336 patients with chronic pancreatitis have been studied at regular intervals. 245 suffered from alcohol-induced (84% with calcifications) and 91 from non-alcohol-induced chronic pancreatitis (77% with calcifications). The average period of observation in the group with non-alcohol-induced chronic pancreatitis was 10.6 years. Primary hyperparathyroidism was found in 6 patients (4 male, 2 female), i.e. 6.6% of non-alcohol-induced chronic pancreatitis (100% with calcifications). They were evenly distributed over the 30 years' study period. 3 patients had acute attacks of pancreatitis prior to the diagnosis of chronic calcific pancreatitis (2 months, 3 + 8 years). In 3 patients with primary painless chronic calcific pancreatitis the condition was diagnosed twice incidentally and once because of diabetes mellitus. Chronic pancreatitis was diagnosed 3 times before primary hyperparathyroidism (8.3 +/- 2.1 years), once simultaneously and twice afterwards (2 + 14 years). In three patients chronic pancreatitis was initially misinterpreted as alcohol-induced. Severe exocrine pancreatic insufficiency was present in 4 of 5 patients (no data in one), and diabetes mellitus in 3 of 6 patients. At the time of diagnosis of primary hyperparathyroidism, mean serum calcium was 3.08 +/- 0.43 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗

PubMed1994

[Gastrointestinal hormone profile in medullary thyroid carcinoma].

Medullary thyroid carcinoma (MTC) can be important for gastroenterologists because 20-30% of patients with MTC suffer from chronic diarrhea and the tumor is capable of producing--besides other bioactive substances--a multitude of gastroenteropancreatic hormones. Gastrointestinal hormone profiles of 5 patients with MTC were determined both basally and after intravenous stimulation with secretin and calcium respectively. Diagnosis of MTC was confirmed histologically or cytologically and by demonstration of elevated serum concentration of calcitonin both basally and after calcium stimulation. 4/5 patients had chronic diarrhea. Normal values or only borderline increases were found for the following hormones: vasoactive intestinal polypeptide (VIP), neurotensin, substance P, growth hormone releasing hormone (GRH), glucagon, neurokinin A, peptide YY, and pancreatic polypeptide. Somatostatin was elevated after calcium stimulation in 1/5 patients only. The main findings were increased basal concentrations for GAWK in 5/5 patients and elevated concentrations for gastrin-releasing peptide (GRP, human bombesin) after calcium stimulation in 4/5. Probably as a consequence of the GRP increase, an increase in gastrin occurred in parallel, indicating bioactivity of the GRP released from the tumor. Besides calcitonin as the main tumor marker for MTC, determination of GAWK and GRP seems to provide helpful additional markers in laboratory diagnosis of MTC. GRP determination after i.v. calcium infusion allowed identification of patients with normal basal plasma GRP concentration.

Adult↗

PubMed1994

[Eosinophilia in primary biliary cirrhosis: regression under therapy with ursodeoxycholic acid].

Eosinophilia can be observed in up to 40% of patients with primary biliary cirrhosis (PBC). Eosinophilia is transient, tends to occur in the early stages of the disease and seems to be associated with episodes of florid bile duct destruction [42-45]. 14 Patients with PBC were examined before and during treatment with ursodeoxycholic acid (UDCA) (10 mg/kg/d) for episodes of eosinophilia and the number of eosinophilic granulocytes in differential white blood cell counts. Group A consisted of 5 patients with one or several episodes of eosinophilia before the start of UDCA. Group B included 9 patients without known episodes of eosinophilia. Observation time before and after start of treatment for group A was 3-96 (mean 25) months and 6-24 (mean 14) months, and for group B 3-108 (mean 34) months and 6-27 (mean 19) months respectively. During treatment with UDCA the mean counts of eosinophilic granulocytes decreased in both groups from 309 +/- 47/mm3 to 135 +/- 14/mm3 (p < 0.001). In group A there was a decrease from 529 +/- 89/mm3 to 157 +/- 17/mm3 (p < 0.001) and in group B from 151 +/- 15/mm3 to 128 +/- 15/mm3 B (n.s.). In group A 9/18 differential white blood cell counts showed eosinophilia before UDCA medication (3 x relative [> or = 6%], 6 x absolute [> or = 500/mm3]) and 0/24 after the onset of UDCA (p < 0.001). In group B 0/25 differential white blood cell counts showed eosinophilia before UDCA and 2/72 after start of the therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[Parietal cell antibodies in primary biliary cirrhosis: pathogenetic or diagnostic significance?].

24 patients with primary biliary cirrhosis (21 female, 3 male; mean age 51 years) were examined for the occurrence of autoantibodies to gastric parietal cells (APA). APA-titers were correlated with several hematological, chemical and immunological parameters. The results of upper GI-endoscopy were available from 12 patients. APA were positive in 24/24 PBC patients. None of the endoscopies revealed evidence for type A gastritis. No pathological decrease in serum vitamin B12 was found (n = 21). Hemoglobin was either normal (n = 18) or the anemia was microcytic with low serum ferritin (n = 6). Erythrocyte MCV was < or = 97 fl in all patients. No positive correlation was found between APA and erythrocyte sedimentation rate (r = 0.13, n = 24) or the titer of antinuclear antibodies (r = -0.18, n = 24) by linear regression. Correlation coefficient between APA and total serum-Ig was 0.67 (n = 24), 0.74 between APA and serum IgM (n = 24) and 0.13 between total serum-Ig minus IgM (n = 24), indicating that APA found in PBC patients belong to the IgM-isotype. Correlation between APA and anti-M2 was 0.65 (n = 21) and between APA and antimitochondrial antibodies (AMA) 0.96 (n = 24), suggesting recognition of identical epitope(s) by APA and AMA in PBC patients. APA were consistently negative in a control group of 40 patients with various forms of chronic liver disease. We conclude that parietal cell antibodies (APA) in PBC patients seem to be of diagnostic rather than pathogenic importance. Sensitivity for PBC appears comparable to that of AMA.(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

[Dilatation of the common bile duct: what does endoscopic sonography contribute?].

In a prospective study 20 patients (14 women, 6 men; mean age 62 [31-81] years) with extrahepatic obstructive jaundice (n = 15) or common bile duct dilatation (CBD) without cholestasis (n = 5) were investigated by endoscopic ultrasound (EUS). All these patients underwent negative transabdominal ultrasonography (US) (n = 20) and computed tomography (CT) (n = 16). Inclusion criterion was a dilatation of the CBD of > 7 mm or > 10 mm in patients with previous cholecystectomy. The definitive diagnosis of a tumor (n = 8), choledocholithiasis (n = 7), stone migration (n = 1), choledochocele (n = 2) or slight dilatation of the CBD without obstruction (n = 2) was confirmed by endoscopic retrograde cholangiopancreatography (ERCP) (n = 13), percutaneous transhepatic cholangiography (PTC) (n = 2), intraoperative cholangiography (n = 1) and follow up (n = 4; mean 21 [3-36] mo.). Dilatation of the CBD could be demonstrated in all cases by EUS. Common bile duct stones (2-15 mm) were demonstrated by EUS in every case. CBD dilatation without underlying obstruction was correctly identified by EUS in all patients and confirmed by further clinical and laboratory findings as well as EUS and ERCP (n = 1). EUS correctly described the localization of a malignant obstruction (n = 8) as confirmed by ERCP/PTC. All tumors (pancreatic head carcinoma n = 3, periampullary tumor (n = 5) could be visualized by EUS. The diagnosis was confirmed by surgery (n = 5) or ultrasound guided fine needle puncture (FNP) after a bile duct prosthesis had been placed (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

[Sulindac in familial adenomatous polyposis coli--preliminary findings of a prospective study].

Several authors have reported regression of rectal polyps after administration of sulindac in patients with familial adenomatous polyposis (FAP) and subtotal colectomy. However, only a few reports have been published about the effect of sulindac in the intact colon of FAP-patients. 12 patients (FAP n = 10, Lynch-I-syndrome n = 1, juvenile polyposis n = 1/patient with intact colon n = 6, ileorectal anastomosis n = 4, right-sided hemicolectomy n = 2) have been treated with sulindac (3 x 100 mg/d orally) for 4 months. In all patients colonoscopy (if postcolectomy, rectoscopy) with videotape documentation was performed before and after sulindac therapy. Some polyps were excised for histology. In 11/12 patients a regression of the number and size of polyps occurred. In addition, in patients with intact colon no polyps were observed proximal to the sigmoid colon. In one patient sulindac had to be discontinued after 4 weeks' course because of abdominal pain. A control colonoscopy revealed only slight reduction in polyps. In 3/12 patients no polyps remained after sulindac. In a further 3/12 patients with initial tubulous adenomatous polyps, only microadenomas were observed after treatment. We therefore conclude that sulindac is effective in FAP-patients (and very probably in other hereditary polyposis syndromes) with intact colon as well as after (hemi-)colectomy in reducing the number and size of polyps. Long term studies are needed to clarify the optimal dosage, treatment time period, and long term potential for development of carcinoma under sulindac treatment.

Adenomatous Polyposis Coli↗

PubMed1994

Mutational analysis of the first 14 exons of the adenomatous polyposis coli (APC) gene.

In the present study, the polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) technique has been applied to the mutation analysis of the adenomatous polyposis coli (APC) gene. We examined the first 14 exons of the APC gene in 46 polyposis coli patients. Five germline mutations were observed, including a single-nucleotide substitution and small (1-4 bp) deletions leading, in 4 cases, to a stop codon. A missense mutation in exon 3 and a 1 bp deletion in exon 4 of the APC gene were observed in patients presenting with the attenuated form of FAP.

Adenomatous Polyposis Coli↗

PubMed1994

Detection of Septata intestinalis in stool specimens and coprodiagnostic monitoring of successful treatment with albendazole.

We describe two patients with AIDS and chronic diarrhea in whom the microsporidian Septata intestinalis was detected with use of light and electron microscopic coprodiagnostic techniques. The ultrastructure of the microsporidian spores found in their stool specimens was distinctly different from that of Enterocytozoon bieneusi, another intestinal microsporidian found in patients infected with human immunodeficiency virus. Electron microscopic examination of duodenal biopsy specimens available from one of the patients enabled identification of S. intestinalis and confirmed the similarity of spores found in feces and in duodenal tissue. Both patients' diarrhea stopped when they were treated with albendazole. Coprodiagnostic monitoring indicated disappearance of the parasites and allowed the diagnosis of a relapse in one patient, who responded well to a second course of treatment.

AIDS-Related Opportunistic Infections↗

PubMed1993

[Transient eosinophilia in primary biliary cirrhosis].

We reviewed 144 differential white blood cell counts from 23 patients with primary biliary cirrhosis (PBC, 21 females, 2 males) for occurrence of eosinophilia. Over an average observation time of 43 +/- 9 months, 9/23 (39%, 9 female) patients were found to have transient absolute (> 500/mm3, n = 5) or relative (> or = 6%, n = 4) blood eosinophilia. The maximum value of eosinophilic granulocytes observed was 1385/mm3 (19%). Other causes of eosinophilia had been ruled out. Eosinophilia was transient, disappearing without treatment. Significantly younger patients with eosinophilia also had a tendency to prognostically more favourable values for serum albumin, prothrombin time, bilirubin and galactose elimination capacity. None had edema, compared to two patients with edema in the group without eosinophilia. Two patients died during the observation period; both were from the group without eosinophilia. The average 5- and 7-year survival probability, calculated on the Mayo survival model, tended to be higher for patients with eosinophilia (92% and 87%) compared to patients without eosinophilia (79% and 72%). In patients with eosinophilia, disease stage I (5/6 vs 1/9) and epitheloid cell granuloma (4/6 vs 1/9) were significantly more frequent. Blood eosinophilia in PBC seems to be an indicator of an early disease state with florid bile duct lesions. Primary biliary cirrhosis should therefore be considered--with other hepatopathies--as a possible cause of eosinophilia of otherwise unknown origin. These observations could be of importance for future therapeutic concepts, at least for patients in early disease states.

Adult↗

PubMed1993

[Hepatosplenic schistosomiasis: case report and clinical review].

Although seen rarely in Switzerland, schistosomiasis is a parasitosis affecting 200 to 250 million people round the world, mainly in tropical and subtropical regions of Africa, Asia, Central and South America. Depending on the parasitic species, the ureters and the bladder (S. haematobium) or the intestine and the liver (S. mansoni, S. japonicum, S. mekongi) are primarily involved. Other organs may be affected (lung, kidneys and central nervous system). Hepatosplenic schistosomiasis represents a special form of chronic infection by S. mansoni, S. japonicum or S. mekongi predominantly occurring in adolescents heavily and repeatedly infected during childhood, together with an additional genetic predisposition for the disease. Hepatosplenic schistosomiasis on a worldwide scale is one of the most prevalent causes of portal hypertension in man. We describe a 33-year-old Portuguese female with mansonian hepatosplenic schistosomiasis 12 years after leaving Africa, who had hepatosplenomegaly, portal hypertension, esophageal varices and hypersplenism. Splenomegaly and slight anemia had been known for years without prompting further work-up. Two months before diagnosis she had been delivered of a normal child after pregnancy without portal-hypertensive complications, namely esophageal hemorrhage. Because of placenta accreta, however, erythrocyte transfusion had been performed after delivery and was possibly responsible for hepatitis C found later on. Pathophysiology, clinical findings and therapy of the disease are discussed.

Adult↗

PubMed1993

[A trial of modified triple therapy for the eradication of H. pylori in recurrent duodenal ulcer].

In a prospective trial we examined the efficacy and acceptability of a modified triple therapy in H. pylori (HP)-positive patients with recurrent duodenal ulcer disease. Oral administration of amoxicillin for two weeks was substituted for one single injection of intramuscular depot penicillin (benzathine penicillin G). Additionally, patients were given ornidazole 500 mg tid for 14 days and 120 mg colloidal bismuth sub-citrate qid for 28 days. The patients were investigated for H. pylori colonization using a rapid urease test (CLO), histology (H&E-, Giemsa stain), culture (including determination of the minimal inhibitory concentrations for metronidazole, penicillin G and amoxicillin) and H. pylori serology (Cobas Core Anti-H. pylori EIA, F. Hoffmann-La Roche). Control endoscopies using the same methods were performed 1 and 6 months after eradication therapy. The eradication rate was 50% and the ulcer healing rate 90% 1 month after therapy. Ulcers recurred in 2/3 of patients with persistent infection vs 0/5 of HP-eradicated patients after 6 months. Both successfully HP-eradicated patients and patients with treatment failure exhibited comparable decreases in mean serum IgG anti-HP concentration within 2 months. Discrimination between the two groups and hence identification of the eradication success by serology was not possible within a time period of 2 months. After 6 months, serum IgG anti-HP concentrations in non-HP-eradicated patients returned to pre-therapy values, in HP-eradicated patients the concentrations further decreased. The above-described modified triple therapy against HP cannot be recommended as a standard therapy, mainly because of the insufficient eradication effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

[Recurrent, life-threatening anaphylaxis as initial manifestation of cystic echinococcosis (granulosus) of the liver].

A 34-year-old, previously healthy Yugoslav developed relapsing generalized anaphylactic reactions associated with life-threatening laryngospasm. After successful life support with volume-replacement, epinephrine, antihistamines and steroids, clinical workup disclosed a slight tenderness in the right upper abdomen and sonography a polycystic tumor with coarse calcification within the wall. The presumptive diagnosis of cystic liver echinococcosis with spontaneous rupture of a hydatid cyst was confirmed surgically and serologically. This case history shows that liver echinococcosis should be considered in otherwise unexplained anaphylaxis.

Adult↗