[Homozygous form of factor V Leiden mutation as the cause of a myocardial infarction in patient with an unremarkable coronary vascular system?]. / Homozygote Form der Faktor-V-Leiden-Mutation als Ursache eines Myokardinfarktes bei unauffälligem Koronargefässsystem?

HISTORY AND ADMISSION FINDINGS: A 32-year-old smoker was referred to our hospital for the evaluation of acute chest pain. 9 years earlier he had had a non Q-wave myocardial infarction. At that time, angiography showed widely patent coronary arteries without atherosclerotic lesions. INVESTIGATIONS: Electrocardiographic as well as creatine kinase patterns were consistent with an acute transmural myocardial infarction. Cholesterol, triglyceride und homocysteine levels were normal. The patient was homozygous for the factor V Leiden mutation. TREATMENT AND COURSE: Thrombolysis was performed with streptokinase followed by coronary angiography showing a patent left coronary system and a non-occlusive thrombosis in the distal part of the right coronary artery. Body weight adapted abciximab infusion was started immediately. 9 weeks later coronary angiography was repeated. Now, in the distal part of the right coronary artery a minor dissection was seen followed by a not flow-limiting stenosis. CONCLUSION: On the evidence of this case history, we think it possible that the pronounced thrombophilia created by the homozygous factor V Leiden mutation may provoke myocardial infarction even if the atherosclerotic lesions are still too trivial to be detected by angiography.

[Helicobacter pylori and coronary heart diseases--hypotheses and facts]. / Helicobacter pylori und koronare Herzkrankheit--Hypothesen und Fakten.

In 1994 Mendall et al. (9) have suggested that there might be a correlation between Helicobacter pylori (HP) infection and coronary heart disease (CHD), mediated by a chronic low-grade acute phase reaction with mildly raised serum or plasma concentrations of C-reactive protein and fibrinogen. According to this hypothesis, a gastric HP colonization might be an additional risk factor for CHD. In the meantime, 35 studies have examined whether HP seropositivity is associated with CHD occurrence. However, in 8 publications only CHD was definitively proven (in CHD+ patients) or excluded (in the corresponding control groups) by coronary artery angiography, and in only 2 of them (1 abstract, 1 full-length publication) a significant association between HP positivity (serologically proven) and CHD was ascertained. Additionally, a metaanalysis of 18 studies including 10,000 patients could not demonstrate any correlations between HP seropositivity and different acute phase proteins (66). Thus, a positive correlation between gastric HP colonization and CHD is far from being proven. Further proposed links between HP infection and CHD such as hyperhomocysteinemia (67) or autoimmune mechanisms (71) due to cross-reacting antibodies to HP HSP60/65 (heat shock protein) with human endothel-derived HSP60/65 need further confirmation.

[Pica in Germany--amylophagia as the etiology of iron deficiency anemia]. / Pica in Deutschland--Amylophagie als Ursache einer Eisenmangelanämie.

Pica (pica = magpie) is an eating disorder that is manifested by a craving for oral ingestion of a given substance that is unusual in kind (nonfood items) or quantity (food items). Pica has been described as a world wide phenomenon, but there are more frequent occurrences of selected substances among selected groups--especially young children and black pregnant and nonpregnant women in the southern part of the USA. In Central Europe and Germany this syndrome has not been described in the moderne literature. For this reason, we report a case of pica for starch associated with severe iron deficiency anemia in Germany. Iron deficiency anemia and--less often-potassium and zinc deficiency are the main complications of an excessive starch or clay ingestion, followed by gastrointestinal obstructions due to gastroliths or impaction. Additionally, naphtalene poisoning (in pica for toilet air-freshener blocks), phosphorus poisoning (in matches pica), mercury poisoning (in paper pica), and lead poisoning (in dried paint pica) have been described.

Ion transport in the experimental short bowel syndrome of the rat.

The adaptational changes of epithelial ion transport in the short bowel syndrome were studied. Ileal remnants of rats were investigated 8 weeks after 70% proximal small intestinal resection. Pure epithelial resistance measured by impedance analysis decreased from 27 +/- 1 to 21 +/- 1 omega.cm2, and polyethylene glycol 4000 fluxes increased from 2.5 +/- 0.3 to 3.6 +/- 0.3 nmol.h-1.cm-2, indicating increased permeability of the short bowel. Unidirectional flux measurements in control ileum showed absorptive net fluxes of Na+ and Cl- that were assigned to electroneutral NaCl absorption and a short-circuit current that was accounted for by the residual flux (HCO3- secretion). Neither NaCl absorption nor HCO3- secretion were altered in the short bowel. Also, electrogenic Cl- secretion, defined after maximal stimulation by theophylline and prostaglandin E1 was not changed in the short bowel. In contrast, electrogenic Na+/glucose cotransport increased in Vmax from 2.0 +/- 0.3 in controls to 5.0 +/- 1.0 mumol.h-1.cm-2 in the short bowel. Tight junction structure was studied by freeze-fracture electron microscopy. The number of horizontal strands was unchanged, whereas tight junction depth was slightly increased in the short bowel. Microvillus area of short bowels was increased by 20% in villus regions. Under the light microscope, villus height was increased by 30%. In conclusion, the short bowel mucosa undergoes adaptive responses to reduced overall absorptive area by increasing glucose-dependent electrogenic Na+ absorption to 250%, which is partly caused by increased villus and microvillus surface area. Electrogenic Cl- and HCO3- secretion and electroneutral NaCl absorption remained unchanged. The decreased epithelial resistance is caused by mucosal surface amplification.

Tight junction regulation during impaired ion transport in blind loops of rat jejunum.

Epithelial cell tight junction structure in self-filling blind loops of rat jejunum, a model for blind loop syndrome in humans, was analyzed morphometrically along the crypt-villus axis. In control jejunum, the number of strands and junctional depth, including meshwork depth, decreased from crypt to villus tip. In the blind loop, aberrant strands appeared below the meshwork, particularly in crypt cells. Consequently, total junctional depth was greater than in controls. Furthermore, strand number and junctional meshwork depth were increased in blind loops at the villus tip. It is that site along the crypt-villus axis which showed the most shallow junction in control jejunum. This structural change is paralleled by a three-fold increase in epithelial resistance as previously measured by alternating current impedance analysis. Relative Na over Cl permeability (PNa:Cl) was obtained from dilution potential measurements. PNa:Cl was 1.50:1 in control jejunum and 1.35:1 in the blind loop (n.s.). Considering the cation selectivity of the tight junction, the increase in epithelial resistance in blind loops cannot be attributed to a collapse of the lateral intercellular space but is due to changes in tight junctional permeability resulting from structural alteration. The blind loop syndrome represents a further example of diminished epithelial ion transport and concomitant decrease in tight junction permeability, thus supporting the general concept of regulation of the tight junction in response to active transport activity.

Adaptation of epithelial ion transport in the short bowel syndrome.

Ileal remnants 8 weeks after 70% proximal small intestinal resection were used as a model for the short bowel syndrome in man. For comparing active ion transport between control ileum and short bowel with the Ussing technique, the relative contribution of the subepithelial resistance has to be considered. Epithelial/subepithelial voltage divider ratios were determined in the Ussing chamber by positioning the tip of a microelectrode just below the epithelium. In control ileum, the ratio of total to epithelial voltage deflection was 1:0.56 +/- 0.03 (n = 48) and decreased to 1:0.42 +/- 0.01 (n = 67; p less than 0.001) under the short bowel condition. Thus, the factors by which a measured short-circuit current (Isc) underestimates the true electrogenic transport was 1.78 +/- 0.09 (n = 48) in control ileum and 2.36 +/- 0.08 (n = 67; p less than 0.001) in the short bowel. Glucose-dependent electrogenic Na absorption was defined using bathing media containing 48 mM 3-o-methyl-glucose as the decrease in Isc (delta Isc) after addition of 0.5 mM phlorizin. After correction for the respective contributions of the subepithelial resistance, delta Isc was -1.4 +/- 0.2 microEq.h-1.cm-2 (n = 13) in control ileum and -3.2 +/- 0.7 microEq.h-1.cm-2 (n = 11; p less than 0.01) in the short bowel. We conclude that the mucosa in the short bowel syndrome is characterized by an increase in glucose-dependent electrogenic Na absorption, probably as an adaptive response to the reduced overall absorptive area of the remaining intestine.

The role of gut-glucagon-like immunoreactants in the control of gastrointestinal epithelial cell renewal.

In vitro and in vivo studies have provided considerable information on the possible physiologic function of circulating gastrointestinal hormones as well as locally acting regulatory peptides in the multifactorial control of adaptive gastrointestinal epithelial cell proliferation and cell renewal. It has been suggested by circumstantial evidences that enteroglucagon (EG; G-GLI I) may act as a trophic factor on the intestinal mucosa which may account for adaptive changes of the small intestine following various stimuli. However, we have shown that there are experimental conditions (germ-free rats after conventionalisation; jejunal self-filling blind loops) in which intestinal hyperplasia does not correspond to an increase in the concentrations of enteroglucagon in plasma or intestinal mucosa. Furthermore, despite a continuous immunoneutralisation of circulating endogenous enteroglucagon by monoclonal antibodies there was an adaptive, hyperplastic response of the ileal remnants after a 70% proximal small bowel resection which was of the same magnitude as in the control group but was even greater considering the increased number of mitoses per crypt. In order to gain additional insight into the putative role of enteroglucagon as an enterotrophic regulatory peptide, an in vitro model was used to investigate the effect of highly purified rat G-GLI I on the proliferative response of primary small intestinal epithelial cells of fetal rats. Whereas there was a well known growth-promoting action of EGF, the proliferation of rat fetal intestinal epithelial cells was inhibited by the addition of purified G-GLI I. These results indicate that enteroglucagon does not act as an enterotrophic factor but provide the first direct evidence consistent with an antitrophic role of enteroglucagon in the small intestine.

Pharmacological studies on perazine and its primary metabolites.

The study served to answer the question whether metabolites possibly contribute to the clinical actions of the neuroleptic drug perazine. The primary metabolites demethylperazine and perazine sulfoxide were investigated with regard to influences on behavior in mice, to an antiemetic action in dogs, and to a modification of the pressor effect of noradrenaline in rats. In contrast to perazine, none of the metabolites exhibited effects that can be interpreted to indicate neuroleptic or antidepressive properties of the compounds.

Effects of the antiparkinson drug budipine on EEG activity in unrestrained rats.

Rats were stereotactically implanted with electrodes into four brain areas (frontal cortex, hippocampus, striatum, and reticular formation) to allow registration of intracerebral field potentials. Connection of the electrodes to a microplug fixed to the skull of the animals allowed wireless transmission of the signals using a four-channel telemetric device. The potentials were subjected to a frequency analysis in real time, the power spectra obtained were segmented according to previous experience. Even in the low-dose range, budipine affected the power within these frequency bands: at 2 mg/kg i.p. in the hippocampus, at 4 mg/kg in the frontal cortex also. Power increases, observed mainly in the alpha-1 and beta-2 bands, became decreases in several bands when the dosage was raised to 8 mg/kg. Further power decreases, especially in the alpha-1 and beta-1 range, were observed after 12 mg/kg of budipine. It is notable that the reticular formation was affected only at the high dosage. The muscarinic anticholinergics biperiden and scopolamine provoked a pattern of electric brain activity changes which were to some extent similar to those obtained with the low dose of budipine, in terms of power increases the delta, alpha-1 and beta-2 frequencies in the hippocampus and frontal cortex. In the striatum and reticular formation, however, they were essentially different. Here the anticholinergics differed not only from budipine, but also from each other: biperiden caused decreases in theta and alpha-2 power comparable to the action of 2,3,4,5-tetrahydro-1-phenyl-1H-3-benzazepine-7,8-diol, a dopamine D1-agonist. Scopolamine, in contrast, displayed the familiar pattern of delta and alpha-1 increases in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunohistochemical and electron microscopic study of interaction of Yersinia enterocolitica serotype O8 with intestinal mucosa during experimental enteritis.

The experimental infection of mice with Yersinia enterocolitica serotype O8 was investigated in a quantitative and histological study. The course of bacterial penetration and spreading was precisely determined by immunohistochemical staining. After oral administration, the bacteria passed the epithelial barrier of the ileum and spread into the lamina propria. By preference they entered Peyer's patches, which were about 1,000 times more heavily colonized than the surrounding epithelium of a comparable surface area. The bacteria proliferated in the follicles, from which they spread into the lamina propria of the villi. At either site most of the bacteria multiplied extracellularly, with only a small percentage observed to be present within the phagocytes. The bacteria did not appear to be able to pass the intact basement membrane; hence, the integrity of the basement membrane is likely to play a role in determining the route of entry and limit of spread of Y. enterocolitica infection.

[Campylobacter pylori in the stomach, duodenum and colon of gastroenterological patients. An epidemiologic study of 120 subjects]. / Campylobacter pylori in Magen, Duodenum und Kolon gastroenterologischer Patienten. Eine epidemiologische Studie an 120 Personen.

In a prospective study of 120 gastroenterological patients in Berlin, Germany, the prevalence of Campylobacter pylori was determined. When the gastric mucosa was normal, the prevalence was one in 19 patients (5.3%). In 101 patients with chronic gastritis it was cultured in 55 (54.5%). In 31 patients with chronic atrophic gastritis the organism was cultured in 25 (81%); in 60 patients with severe gastritis it was present in 75%, in 35 with moderate or severe chronic active gastritis in 82.8%. The diagnosis of gastric ulcer (9) or duodenal ulcer (12) was associated with the isolation of Campylobacter pylori in 55.6 and 91.7%, respectively. The prevalence of this organism in antral mucosa of this group of patients thus corresponds to that in Australia, England and North America. The organism was also demonstrated in the duodenum of 10 among 25 patients examined. But in none of 25 patients was it demonstrated in the sigmoid colon.