Israel Medical Association Journal

Objective: To investigate whether cigarette smoking has an additive effect on the clinical presentation and course of disease in Helicobacter pylori-positive dyspeptic patients.

Patients and Methods: The study group comprised 596 consecutive H. pylori-positive dyspeptic patients (334 males and 262 females, mean age 50.6, range 12--81 years). Following upper gastrointestinal endoscopy, patients were subdivided by diagnosis as follows: Non-ulcer patient group (n=312: gastritis 193, duodenitis 119), gastric ulcer (n=19), and duodenal ulcer (n=265). H. pylori infection was confirmed by histology and/or rapid urease test. In addition, 244 patients had a positive 14C-urea breath test prior to antimicrobial treatment. The patients' medical history and smoking habits were obtained using a detailed questionnaire completed by the patients and their referring physicians.

Results: There were 337 non-smoking patients, 148 current smokers and 111 past smokers. Gastric and duodenal ulcers were significantly less prevalent in non-smokers than in current or past smokers (gastric 1.8%, 4.1%, 6.3%; duodenal 39.8%, 50%, 51.4%, respectively) (P0.05). The incidence of gastrointestinal bleeding was significantly lower in non-smokers than in current or past smokers (7.1%, 8.1% and 20.7%, respectively) (P0.05). Bacterial density, as assessed by the UBT value in 244 patients, was higher in non-smokers (mean 352.3273 units) than in past smokers (mean 320.8199) or current-smokers (mean 229.9162) (P0.05). Logistic regression analysis revealed that male gender, current smoking, and immigration from developing countries were all significant independent risks for developing duodenal ulcer, while only past smoking was associated with a higher rate of upper gastrointestinal bleeding in the past.

Conclusions: In H. pylori-positive dyspeptic patients, current smoking as well as male gender and immigration from developing countries are associated with an increased risk for duodenal ulcer. This effect does not seem to be related to the bacterial density or increased urease activity of H. pylori organisms.

Objective: To investigate the clinical, laboratory and radiological findings of the disease.

Methods: During the years 1995-88 five patients with primary epiploic appendigitis were diagnosed at our institution. The clinical, laboratory and imaging results were summarized and compared to previously reported series. Emphasis was placed on the computed tomography findings, which are the gold standard for diagnosis.

Results: All our patients (two males and three females, mean age 47 years) presented with left lower quadrant abdominal pain. CT proved to be the imaging modality of choice in all patients by showing a pericolic fatty mass with an increased attenuation as compared to normal abdominal fat. In all cases the mass was surrounded by a high attenuation rim, and focal stranding of the fat was observed. In no case was there thickening of the adjacent bowel wall. This serves as an important, and previously unreported, clue for diagnosis.

Conclusion: Primary epiploic appendagitis is a relatively rare condition that may be clinically misdiagnosed, resulting in unnecessary surgical intervention. Judicious interpretation of CT may lead to early diagnosis and ensure proper conservative treatment.

Background: Tumor necrosis factor is associated with various local and systemic inflammatory sequelae following snakebite. Xanthine oxidase is a principal mediator of remote tissue injury (e.g., lungs, heart, liver).

Objective: To investigate in a snakebite-like animal model the as yet unexplored role of TNF and XO in mediating organ damage following snakebite.

Methods: Sprague-Dawley rats were injected intramuscularly with a non-lethal 500 g/kg dose of Vipera aspis venom (n=10) or saline (n=10). Blood pressure and heart rate were continuously monitored, TNF- was measured in the blood, and total XO + xanthine dehydrogenase activity was assessed in various tissues. Lung histology and permeability indices were analyzed.

Results: Venom injection caused a significant (P0.05) reduction in both heart rate and invasive arterial pressure. The blood circulating TNF levels were significantly higher in the intoxicated group (P0.05 vs. saline group), with changes seen at 30 minutes from intoxication in both groups. Total XO + XDH activity in the kidney, lung and liver of the venom-injected group was significantly (P0.05) higher than in the saline group, while the activity in the heart was similar.

Conclusions: The mediation of remote organ and hemodynamic changes following intramuscular injection of a non-lethal dose of Vipera aspis venom can be attributed partly to TNF and partly to XO. More research is needed to better understand the role of either compound and the time frame of their activity before specific antagonists can be introduced for snakebite management.
 

There is increasing evidence to suggest that aspirin and other non-steroidal anti-inflammatory drugs reduce the risk of colorectal cancer. This observation is supported by animal studies that show fewer tumors per animal and fewer animals with tumors after administration of several different NSAIDs. Intervention data in familial adenomatous polyposis have established that the effect is exerted on the process of human colonic adenoma formation. Supportive evidence in sporadic colorectal neoplasia, derived from 22 of 24 studies (both case-control and cohort), found a reduced risk in men and women for cancers of the colon and the rectum and for both aspirin and the other NSAIDs. Earlier detection of lesions as a result of drug-induced bleeding does not seem to account for these findings. Although the molecular mechanism responsible for the chemopreventive action of this class of drugs is not yet completely understood, the protection may affect several pathways including both cell cycle arrest and induction of apoptosis.

In the third millennium the question is not if but how. Based on the consistency of epidemiological, clinical and experimental data, the association between regular long-term aspirin or NSAIDs intake and a decreased death rate from colorectal cancer is sound and there is no need for further placebo trials. At the same time, despite this consistency there is no clear data on the dose, duration or frequency of use for cancer-preventive activity.

Background: Many medications used for children have not undergone evaluation to assure acceptable standards for optimal dose, safety and efficacy. As a result, the majority of children admitted to hospital wards receive medications outside the terms of their license (off-label) or medications that are not specifically licensed for use in children (unlicensed). The extent of unlicensed and off-label medication use in ambulatory children is unknown.

Objective: To determine the extent of unlicensed and off-label medication use in a general pediatrics ambulatory hospital unit in Israel.

Patients and Methods: We conducted a retrospective analysis of the medical records of 132 outpatient children treated in the General Pediatrics Ambulatory Unit of the Soroka Medical Center, Beer Sheva, in November–December 1998.

Results: The children’s ages ranged from 1 month to 18 years (mean ± SD 50±58 months). Of the 222 prescriptions given to these children, one-third were unlicensed (8%) or unlabeled (26%). Different dose and age were the most common categories of off-label medication use. All 18 cases of unlicensed use were due to modifica-tion of licensed drugs (tablets were crushed to prepare suspensions). Altogether, 42% of children received medicines that were off-label and/or unlicensed.

Conclusions: More off-label than unlicensed medications were used. Further investigations are required to establish the extent of unproved drug use in both hospitalized and ambulatory pediatric patients in Israel. Recommendations recently issued by the Ministry of Health’s National Council for Child Health and Pediatrics constitute a first step in the Israeli contribution to the international effort demanding testing of medications for children.

Background: Childhood poisoning continues to challenge the diagnostic and treatment skills of the pediatrician. Generally, childhood poisoning can be attributed to suboptimal parental supervision and accessibility of products with poisoning potential.

Objective: To evaluate the pattern of acute poisoning in children with relation to different age groupings.

Methods: Pediatric patients hospitalized for acute poisoning at the Soroka Medical Center over a 5 year period (1994-98) were evaluated retrospectively. Special attention was given to poisoning in relation to age groupings.

Results: During the years 1994-98 a total of 1,143 children were admitted for acute poisoning to the Soroka Medical Center. The majority of cases occurred in children aged 2-5 and 14-18 years. Males under 14 had a higher frequency of poisoning, the poisoning usually being unintentional, whereas poisoning in females occurred mostly in the 14-18 age group and was intentional. Drugs were the most common agent of poisoning in infants (0-1 year), in older children (10-13 years), and in adolescents (14-18 years), while in children aged 2-5 and 6-9 years either cleaning products or drugs were the usual agents of poisoning. Most poisonings in children aged 2-13 occurred between 4 and 8 p.m., and for most adolescent patients (14-18 years old) between 4 p.m. and midnight. Poisoning in children aged 2-13 were usually due to accessible home products, and to medicinal errors such as overdose and improper drug administration.

Conclusions: This study defines the characteristic pattern of pediatric poisoning with respect to different age groups and gender. Unintentional childhood poisoning predominated in males and occurred mostly because of accessible home products and suboptimal parental supervision during critical hours of the day. Most adolescent poisoning occurred in females and was intentional. Parental education and intensified child supervision are indicated measures of prevention for unintentional poisoning.

Background: Uterine rupture is a catastrophic obstetric complication, most often associated with a preexisting cesarean section scar. Although a vaginal birth after a cesarean is considered safe in modern obstetrics, it is not known whether repeated VBACs increase the risk of rupture, or whether the first VBAC proves the strength and durability of the scar, predicting further successful and less risky vaginal deliveries.

Objectives: To evaluate the effect of repeated vaginal deliveries on the risk of uterine rupture in women who have previously delivered by cesarean section.

Methods: In this retrospective study, 26 VBAC deliveries complicated by uterine rupture were matched for age, parity, and gravidity with 66 controls who achieved VBAC without rupture. The histories, demography, pregnancy, labor and delivery records, as well as neonatal outcome were compared.

Results: We found that the risk of rupture decreases dramatically in subsequent VBACs. Of the 40 cases of uterine rupture recorded during the 18 year study period, 26 occurred during VBAC deliveries. Of these, 21 were complicated first VBACs. We also found that the use of prostaglandin-estradiol, instrumental deliveries, and oxytocin had been used significantly more often during deliveries complicated with rupture than in VBAC controls.

Conclusions: Once a woman has achieved VBAC the risk of rupture falls dramatically. The use of oxytocin, PGE2 and instrumental deliveries are additional risk factors for rupture, therefore caution should be exerted regarding their application in the presence of a uterine scar, particularly in the first vaginal birth after cesarean.

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VBAC= vaginal birth after cesarean section

PGE2= prostaglandin-estradiol

Objective: To report a unique hereditary, juvenile onset, craniocervical predominant, generalized dystonia and parkinsonism affecting four members of one family.

Family Description: A father and three of his four daughters presented to us over the past 30 years with a similar picture of generalized dystonia, starting in the craniocervical region in the second or third decade of life. They later developed moderate parkinsonism, mainly manifesting bradykinesia, rigidity and abnormal postural reflexes. Biochemical and genetic tests excluded Wilson's disease, Huntington's disease and Oppenheim's dystonia.

Conclusion: This is a new type of familial dystonia-parkinsonism where the craniocervical dystonic symptoms are most prominent in the early stages while parkinsonism becomes the predominant problem later in life. A search for the genetic mutation in this family is underway.