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Biomedical subjects

A Lavy

Publications and source records attributed to A Lavy.

13 recordsLinked to original sources
PubMed1992

Diseases of the intestine mimicking Crohn's disease.

We describe five patients who were initially thought to have Crohn's disease and were treated accordingly. The original diagnosis was based upon clinical presentation, roentgenograms, and histological examination, but subsequent follow-up showed that diagnosis to be in error. The following diagnoses were established instead: tuberculosis, Actinomyces Israeli infection, reaction to gold therapy, metastatic cancer, and linitis plastica. We stress the importance of considering conditions that can mimic Crohn's disease.

Actinomycosis↗
PubMed1992

Mycobacterium xenopi, a potential human pathogen.

Mycobacterium xenopi is infrequently recognized as a cause of pulmonary disease. During a 12-year survey (1978-89),. 108 strains of this Mycobacterium were isolated from 90 persons and 6 hot water samples. From 87 patients 89 occasional strains of M. xenopi were isolated, and 3 patients were diagnosed as having pulmonary mycobacteriosis caused by it. The treatment and the response in these three cases were variable, depending on clinical conditions and sensitivity to drugs. Most of the strains isolated came from patients hospitalized at the Barzilai Hospital, Ashkelon, therefore a local environmental contamination was suspected. The suspicion was confirmed by the isolation of this thermophile organism from the hot water samples of the above hospital.

Aged↗
PubMed1991

Enhanced in vitro oxidation of plasma lipoproteins derived from hypercholesterolemic patients.

In vitro oxidation of plasma lipoproteins, derived from either normolipidemic or hypercholesterolemic subjects, was performed in the presence of copper ions. Following this procedure, hypercholesterolemic low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), and high-density lipoprotein (HDL) demonstrated greater propensity for oxidation than the corresponding normocholesterolemic lipoproteins. The oxidation was determined by the concentration of thiobarbituric acid-reactive substances (TBARS), which was 44%, 71%, and 54% greater in the patients' VLDL, LDL, and HDL in comparison to the normocholesterolemic lipoproteins, respectively. An associated reduction in trinitrobenzensulfonic acid (TNBS) reactivity in the patients' lipoproteins was noted. These changes were consistent whether expressed per lipoprotein protein or per concentration. Macrophage cholesterol esterification induced by oxidized LDL was substantially increased (up to 59%) when patients' lipoproteins were used, in comparison to control lipoproteins. A positive correlation was present between the LDL cholesterol to protein ratio, the extent of lipoprotein oxidation, and macrophage uptake of the oxidized lipoproteins. The lipoprotein content of pro-oxidant and antioxidant constituents was also analyzed. No measurable ferric or copper ions could be found in association with any of the lipoproteins. However, arachidonic acid content of the patients' LDL was 10.1% +/- 1.0% in comparison to 6.2% +/- 0.8% of total lipoprotein fatty acids in the control group (n = 5). Antioxidants such as vitamin E and carotenoids were significantly reduced in all patients' lipoproteins compared with those of controls. Thus, we suggest that increased cholesterol and arachidonic acid content and reduced concentration of antioxidants in lipoproteins of hypercholesterolemic patients may be responsible for the enhanced propensity for oxidation observed in these lipoproteins.

Dose-Response Relationship, Drug↗
PubMed1990

[Actinomycosis imitating acute appendicitis].

Actinomycosis is a rare infection which can attack most parts of the body, even in normal individuals. In the gastrointestinal tract it may imitate acute appendicitis, Crohn's disease or tumors. We present a young soldier with appendiceal involvement who was mistakenly operated on. Because of its very good response to antibiotics, this infection should be recognized early and treated, to prevent prolonged, unnecessary suffering.

Actinomycosis↗
PubMed1990

Mycobacterium avium-intracellulare in clinical specimens: etiological factor or contaminant?

The Mycobacterium avium-intracellulare (MAI) group comprised 10.5% of all nontuberculous mycobacteria isolated in the Mycobacterium Reference Laboratory, Tel Aviv, in an 11-year study period. From the Buirej Chest Hospital in Gaza, alone, 273 strains were isolated, representing 12.1% of the specimens from that hospital, while 149 strains (0.24% of all specimens) were isolated from all other institutions. Pulmonary disease was attributed to this organism in 22 patients, 17 of whom were hospitalized (initially for tuberculosis or another lung disease) in Buirej Hospital. The water was thought to be the source of contamination, since MAI strains, similar to those found in sputum, were isolated from it. In 1985, the water system was renovated and the MAI incidence in sputum from this hospital consequently declined.

Cross Infection↗
PubMed1989

Right heart failure as the sole presentation of carcinoid syndrome.

We report the case of a woman with symptomatic right heart failure. Despite lack of the characteristic features of the carcinoid syndrome, echocardiographic and histologic investigations confirmed the diagnosis of carcinoid disease with cardiac involvement.

Carcinoid Heart Disease↗
PubMed1988

Cationic environment and secretin secretion in canine duodenal mucosa in vitro.

We examined the effects of the divalent cation calcium (Ca2+) and the monovalent cations potassium (K+) and sodium (Na+) and different modalities that affect the fluxes of these cations on immunoreactive secretin (IRS) secretion from canine duodenal mucosa in vitro. In the absence of extracellular Ca2+, the basal IRS secretion was inhibited by 29%. Increased uptake of Ca2+ by passive diffusion and facilitated uptake of Ca2+ by ionophore A23187 had no effect on basal IRS secretion. However, Ca2+ channel blocking agents, LaCl3 and verapamil, inhibited basal IRS secretion by 18 and 33% respectively. High concentrations of extracellular K+ caused a dose-dependent but delayed stimulation of IRS secretion. K+-stimulated IRS secretion was not neurally mediated. Similarly, 9-aminoacridine, which blocks K+ exchange, mimicked the effects of K+. Valinomycin (10(-6) M) inhibited both K+-stimulated and 9-aminoacridine-stimulated IRS secretion. In the absence of extracellular Na+, there was a delayed inhibition of both basal and K+-stimulated IRS secretion. These results suggest that changes in cationic environment are associated with alterations in the secretion of IRS. High extracellular K+ concentration is conducive, and the absence of extracellular Na+ and Ca2+ is inhibitory to IRS secretion.

Aminacrine↗
PubMed1986

Neurohormonal regulation of secretin secretion in canine duodenal mucosa in vitro.

We examined the effects of cholinergic, peptidergic and GABAergic agents on secretin secretion from canine duodenal mucosal explants incubated in organ culture media. Carbachol (10(-12) to 10(-4) M), atropine (10(-6) to 10(-4) M), hexamethonium (10(-6) to 10(-4) M), and somatostatin did not alter basal secretion of secretin. Somatostatin (10(-7) to 10(-8) M) inhibited secretin secretion stimulated by pH 4.5. Met, Leu and their D-ala2-analogs inhibited both basal and pH 4.5-stimulated secretin. Naloxone reversed the inhibition caused by met-enkephalin at pH 7.4. GABA (10(-9) to 10(-6) M) stimulated both basal and pH 4.5-stimulated secretin secretion. GABA-stimulated secretin secretion was neuronal in nature, bicuculline sensitive and was mediated via post ganglionic cholinergic neurons. GABA-stimulated secretin secretion was inhibited by both somatostatin and metenkephalin, suggesting that GABA-stimulated secretin secretion may be under the inhibitory control of peptidergic agents as well.

Animals↗
PubMedDate not supplied

The effect of cyclic nucleotides on secretin secretion in canine duodenal mucosa in vitro.

We examined the effects of cyclic nucleotides and calcium on secretin release from canine duodenal mucosal explants incubated in organ culture media. Time course studies revealed that at pH 7.4, 5 and 10 mM dibutyryl cyclic adenosine monophosphate (DBcAMP) increased secretin release progressively, reaching a peak at 2 hours. Two mM of DBcAMP at pH 7.4 did not increase secretin release but at pH 4.5, all 3 doses potentiated secretin release. DBcAMP-stimulated secretin release was not dependent on the influx of extracellular calcium. Graded doses of 3-isobutyl-1-methylxanthine (IBMX) did not stimulate secretin secretion but 1 mM IBMX with 2 mM DBcAMP increased secretin secretion significantly. Dibutyryl cyclic guanosine monophosphate, cholera toxin and 5'-guanylyl-imidodiphosphate (GPP(NH)p) did not stimulate basal secretion release. The release of secretin from our explants incubated at pH 7.4 was not due to specific leakage because all of our viability studies revealed that our explants were functionally intact at the end of 2 hours. Our observations suggest that cyclic nucleotides may participate in the intracellular regulation of secretin secretion.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Topical pharyngeal anesthesia for easing endoscopy: a double-blind, randomized, placebo-controlled study.

The aim of this work was to compare the efficacy of the Cetacaine topical anesthetic spray preparation to placebo. Cetacaine and placebo, from coded but otherwise identically packaged and scented sprays, were administered to 150 consecutive patients. After endoscopy, patients and physicians completed questionnaires evaluating the difficulty of the endoscopy. No statistically significant differences were found between the full formula and placebo-treated patient responses to the amount of cough or gag, or the degree of difficulty of intubation of the endoscope. Analysis of physician responses showed that in the subgroup of patients being endoscoped for the first time, the gastroscope was introduced more easily (p less than 0.05) when the premedication had been full formula rather than placebo.

4-Aminobenzoic Acid↗