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Background: There are rich knowledge and practice in Ethiopian traditional medicine of using plants for the treatment of various ailments, including wounds. Though scholars have been working on documenting the ethnobotanical use of plants, the studies are still ongoing. Objectives: This study systematically reviewed medicinal plants traditionally employed for the treatment of wounds in Ethiopia. Methods: A systematic review of the literature was conducted using PubMed and Google Scholar; a search of grey literature was also carried out as part of the review. Search terms and phrases included 'traditional medicine', 'ethnomedicine', 'ethnobotany' and 'Ethiopia'. Data regarding the scientific name, family, local name, growth form of the plant, mode of administration, and availability of voucher specimen were extracted. Results: Based on the eligibility criteria, 29 studies were retrieved from PubMed, and 25 from Google Scholar and the grey literature. Around 200 medicinal plants which are used to treat wounds in Ethiopian traditional medicine were recorded. Leaves and roots were the most commonly used plant parts to treat wounds, while shrubs and herbs were reported to be the growth forms of most plants. The mode of administration was topical in almost all cases. Conclusions: Medicinal plants have been used extensively to treat wounds in Ethiopia. Nevertheless, the scientific exploration of plants' efficacy and safety is inadequate, and relevant activity studies ought to be conducted to provide scientific evidence to the traditional claims of these plants

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BACKGROUND AND AIMS: A further development of the risk profile for severe postoperative hypocalcaemia after surgery for primary hyperparathyroidism (pHPT) was made with the aim of expanding the group of patients who can be discharged safely after 23 hours. METHODS: Prospective study with 156 consecutive pHPT patients (158 operations) during 2001 and 2002. Risk factors for postoperative severe hypocalcaemia (ionised calcium < 1 mmol/L), were (1) preoperative concentration of parathyroid hormone (PTH) > 35 pmol/L (five times the upper reference value, reference range 1.1 to 6.9), (2) history of previous neck surgery, (3) biopsy/excision of > 2 parathyroid glands or (4) concomitant thyroid surgery. RESULTS: The risk factors showed a sensitivity of 100 % (9/9). In 110 of the operations (70%) no risk factors were identified. Postoperative calcium levels were significantly lower after 48 operations with risk factor(s) identified, as compared to the group without risk factors (p < 0.01). Seven of 17 patients (41%) with PTH > 35 pmol/L developed severe postoperative hypocalcaemia. Two of 31 patients (6%) with PTH < 35 pmol/L in the presence of other risk factor(s) developed severe postoperative hypocalcaemia. CONCLUSION: Patients with no risk factor can safely been discharged from hospital on the first postoperative day. Patients with preoperative concentration of PTH > 35 pmol/ L (five times the upper reference value) should stay in hospital until nadir level of calcium is reached. Patients with concentration of parathyroid hormone less than 35 pmol/ L in the presence of other risk factor(s) may have an early discharge from hospital (second postoperative day) combined with outpatient measurements of calcium levels.

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BACKGROUND AND OBJECTIVES: In patients with breast cancer, planning of the surgical strategy may rely on preoperative tumour size. The optimal method for assessment of small tumours has not been established. We compared findings from preoperative mammography and ultrasonography with histopathological tumour size in patients treated with breast-conserving surgery. MATERIAL AND METHODS: The study was retrospective and the setting a single institution clinic with free referral of patients. The patients were examined before the operation with mammography, ultrasonography, and findings were compared with postoperative histopathological tumour size. RESULTS: The study included 131 patients (median age was 59) years with grade I, II, and III cancers in 47, 71 and in 13 patients, respectively. The medium histological tumour size was 14 mm, range 4-45 mm. A wide 95% confidence interval between histopathological tumour size and preoperative mammography (standard deviation 4.8 mm) and ultrasonography (standard deviation 4.8 mm) was found. The combination of mammography and ultrasonography did not improve the results (standard deviation 4.3 mm). Preoperative mammography tended to over estimate the tumour size compared with histological tumour size whereas preoperative ultrasonography tended to underestimate the tumour size. CONCLUSION: In this retrospective study with preoperative evaluation of small breast cancers by mammography and ultrasonography, wide 95% confidence intervals for the methods were found and they should therefore be used with caution in the planning of the surgical strategy.

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The activity of platelet-activating factor (PAF) acetylhydrolase in biopsy specimens of intestinal mucosa was compared in patients with Crohn's disease (n = 11) and controls (n = 6). In addition, PAF acetylhydrolase activity was determined in the plasma of Crohn patients (n = 30) and healthy subjects (n = 35). The activity of PAF acetylhydrolase in mucosal samples from the distal ileum was significantly lower in Crohn patients than in control patients (p < 0.02), whereas there was no difference in PAF acetylhydrolase activity of colonic or jejunal samples between Crohn patients and controls. The PAF acetylhydrolase activity in the plasma of Crohn patients was significantly decreased as compared to healthy subjects. Crohn patients with high disease activity (symptomatic index > 150) had a significantly lower PAF acetylhydrolase activity in plasma, as compared to patients in clinical remission (symptomatic index < 150; p < 0.02), and as compared to healthy subjects (p < 0.001). PAF acetylhydrolase activity in plasma increased within 4 months after bowel resection (p < 0.05). These findings indicate that the PAF acetylhydrolase activity is decreased in the ileal mucosa of patients with Crohn's disease and that PAF acetylhydrolase activity in plasma is inversely related to disease activity in Crohn's disease. The possibility that PAF acetylhydrolase is one factor of importance for protecting the intestinal mucosa against PAF-mediated inflammation is inferred.

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OBJECTIVE: To find out if concentrations of platelet activating factor (PAF), which has been proposed as a mediator in the pathogenesis of ulcerative colitis and Crohn's disease, are increased in the rectal mucosa of patients with ulcerative colitis. DESIGN: Open study. SETTING: University hospital, Sweden. SUBJECTS: 45 Patients with ulcerative colitis (19 with active disease and 26 in remission), and 6 control patients and 11 healthy volunteers who acted as controls. INTERVENTIONS: Rectal biopsy. MAIN OUTCOME MEASURE: PAF content of rectal biopsy specimens. RESULTS: There were no differences between the PAF content of rectal mucosa in patients with active disease (median 47 pmol/g wet weight), patients in remission (47 pmol/g), and controls (51 pmol/g). There was no correlation between PAF content and inflammation seen endoscopically or histologically. 13 Patients who had active disease were investigated on a second occasion 9 weeks later (range 7-17), when in remission having received steroids but steroid-free at that time. There was a slight but not significant trend towards lower concentrations of PAF (median 33 pmol/g) compared with their previous results, possibly as a result of treatment. PAF concentrations were significantly lower than those of a group of patients in clinically stable remission of longer duration (p < 0.05). CONCLUSIONS: We did not find high concentrations of PAF in the rectal mucosa of patients with active ulcerative colitis compared with patients in remission or controls. We therefore have no evidence that PAF has an important role as a mediator in the inflammation of ulcerative colitis.

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OBJECTIVE: To study blood and bronchoalveolar lavage (BAL) fluid levels of platelet activating factor (PAF-acether) and phospholipase A2 (PLA2) in patients with septic shock or following severe trauma. DESIGN: Prospective controlled clinical study. SETTING: An intensive care unit (ICU) of a university hospital. PATIENTS AND PARTICIPANTS: The study comprised 12 patients, 8 with septic shock and 4 with trauma, consecutively admitted to the ICU. Healthy volunteers were used as controls. MEASUREMENTS AND RESULTS: Blood PAF-acether and plasma PLA2 levels were measured within 24 h after the patients arrival to the ICU. The Apache II score and outcome were registered. Median values for PAF-acether and PLA2 in the septic shock patients were 10.5 x 10(-10) M and 5300 units/ml, respectively, whereas corresponding values in the trauma patients were 1.3 x 10(-10) M and 770 units/ml. Normal healthy individuals had no detectable PAF-acether in the circulating blood (< 0.5 x 10(-10) M), and normal plasma PLA2 activity was < 300 units/ml. Moreover, both PLA2 and PAF-acether levels correlated well with the severity of the disease as assessed by the Apache II scoring system (p < 0.01 for PLA2 and p < 0.05 for PAF-acether). In addition, PAF-acether and PLA2 were determined in BAL fluid of patients with septic shock (n = 5) and trauma (n = 3); increased PAF-acether levels were found in four patients with septic shock and one patient with trauma. CONCLUSION: These results demonstrate a significant increase of both PLA2 and PAF-acether in the circulation of trauma patients, and a further increase in septic shock patients. It is possible that PAF-acether and PLA2 can be used as markers for the severity of the disease in septic shock and following severe trauma.

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The mechanisms by which phospholipase C from Clostridium perfringens stimulates the formation of platelet-activating factor (PAF-acether) in cultured intestinal epithelial cells (INT 407) were investigated. Although stimulation with phospholipase C caused a significant formation of PAF-acether, there was no significant increase in the cellular levels of lysoPAF-acether after stimulation. Moreover, when cells prelabeled with 3H-1-O-alkyl-2-acyl-sn-glycerophosphocholine were stimulated with phospholipase C, the 3H-lysoPAF-acether content was not increased in stimulated cells as compared with unstimulated cells. When cells were preincubated with the calmodulin inhibitor trifluoperazine (TFPA), the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), or the combined phospholipase A2-inhibitor and lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) before stimulation with phospholipase C, the PAF-acether formation was significantly decreased. The phospholipase A2 inhibitor 4-bromophenacyl bromide (BPB), on the other hand, had no significant effect on the PAF-acether formation. Preincubation with NDGA also decreased the levels of lysoPAF-acether, whereas BPB, H7, or TFPA had no such effect. These findings indicate that stimulation of acetyltransferase activity with increased acetylation of lysoPAF-acether may be one way by which phospholipase C from C. perfringens stimulates formation of PAF-acether in INT 407 cells.

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This study demonstrates the formation of platelet-activating factor (PAF) in rats with acute experimental pancreatitis (AEP). The AEP was induced by infusing sodium taurodeoxycholate and trypsin into the bile-pancreatic duct. The PAF content was increased in blood samples and in pulmonary and pancreatic tissue as compared with control animals. Significant amounts of PAF were also found in peritoneal fluid. The PAF content did increase in blood samples and in pulmonary tissue after administration of endotoxin intravenously. The effects of intraperitoneal PAF administration were also studied and showed an increase of polymorphonuclear cells in blood samples. These findings suggest that acute pancreatitis might generate and release PAF. Whether PAF release is associated with the pathophysiology of complications in acute pancreatitis remains to be elucidated.

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Tumor necrosis factor-alpha (TNF-alpha), a known pro-inflammatory cytokine, has been suggested to play a role in the pathogenesis of inflammatory bowel disease (IBD) by mediating damage to the intestinal epithelial cells. The present study demonstrates that TNF-alpha potentiates release and metabolism of 14C-labeled arachidonic acid (14C-AA) in cultured intestinal epithelial cells (INT 407). Although TNF-alpha on its own was but a weak stimulator of cellular 14C-AA turnover, it significantly potentiated the release of 14C-AA and 14C-labeled prostaglandin E2(14C-PGE2) after stimulation with three known phospholipase A2 activators: phospholipase. C from Clostridium perfringens, the calcium ionophore A23187, and the phorbol ester 4-beta-phorbol-12-myristate-13-acetate (PMA). The phospholipase A2 inhibitor quinacrine significantly reduced both AA and PGE2 release after combined stimulation with phospholipase C and TNF-alpha. In contrast to its effect on the AA turnover, TNF-alpha did not affect the phospholipase C-stimulated production of platelet-activating factor (PAF-acether). Taken together, these findings indicate that a) TNF-alpha potentiates phospholipase A2-stimulated AA release from cultured intestinal epithelial cells; b) TNF-alpha may stimulate phospholipase A2-dependent AA release without affecting the formation of PAF-acether and c) pretreatment with TNF-alpha potentiates the formation of PGE2 after stimulation with phospholipase A2 activators. In summary, the present investigation points to the possibility that TNF-alpha may stimulate intestinal epithelial cells to produce biologically active AA metabolites and that this stimulation may be modulated by components of the intestinal luminal content, like bacterial toxins.

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We report the presence of platelet-activating factor (PAF-acether; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in small-intestinal and colonic mucosa of neonatal rats. The PAF-acether content was higher in the colon than in the small intestine, and was lower in the small intestine of 30-day-old animals than in 14-day-old animals. We also report that cultured intestinal epithelial cells (INT 407) produce PAF-acether when stimulated with the calcium ionophore A23187, and that homogenized INT 407 cells can degrade PAF-acether with the formation of lysoPAF-acether. These findings suggest that intestinal epithelial cells are able to produce and metabolize PAF-acether, a potent mediator of inflammation. The authors propose that this might contribute to the pathophysiology of inflammatory bowel disease.

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This study demonstrates the ability of phospholipase C from Clostridium perfringens to stimulate the generation of platelet-activating factor (PAF-acether) in cultured intestinal epithelial cells (INT 407). Cells were exposed to phospholipase C for up to 60 min, and the content of PAF-acether within the cells and in the extracellular medium was determined. Phospholipase C caused a time-dependent formation of PAF-acether within the cells and also release of PAF-acether to the medium. In contrast, phospholipase C did not affect the cellular acetylhydrolase activity or the ability of the cells to metabolize extracellularly added 14C-PAF-acether. These findings suggest the possibility that intestinal epithelial cells, when stimulated with a naturally occurring intestinal bacterial toxin, generate and release PAF-acether. The possibility that this might contribute to the pathophysiology of inflammatory bowel disease is discussed.

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Intestinal mucosal content of platelet-activating factor (PAF-acether) was investigated in Crohn's disease. The PAF-acether content was determined in mucosal biopsies from the ileum and colon in Crohn patients (n = 13), and in normal mucosa of control patients (n = 11). PAF-acether was found in both groups and was raised in Crohn patients, both in the ileum (6.3 +/- 4.7 vs. 0.6 +/- 0.4 pmol/g; p less than 0.01) and colon (6.2 +/- 4.2 vs. 0.7 +/- 0.4 pmol/g; p less than 0.01). Colonic PAF-acether content was raised irrespective of the presence of colonic inflammation as judged macroscopically. These findings add further support to the importance of bioactive lipids in inflammatory bowel disease and suggest a possible role for PAF-acether in Crohn's disease.

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Good results from endoscopic sphincterotomy (EST) for removing choledochal stones following cholecystectomy, have led to increasing use of the method when the gallbladder is in situ. The need for cholecystectomy after successful EST has been questioned. As cholecystectomy in elderly patients involves substantial risk, we routinely defer cholecystectomy in such patients while they remain asymptomatic. Experience of 40 cases is reported. Thirty-four were discharged without cholecystectomy and one underwent elective cholecystectomy at his own request. The remaining 33 patients were followed up for 6-53 (mean 21.5) months. Four died from causes unrelated to gallstone disease. Symptoms requiring cholecystectomy arose in two cases (6%). We found no problems due to refraining from routine elective cholecystectomy following EST for common bile duct stones. The rarity of later symptoms appears to justify a "wait and see" attitude to post-EST cholecystectomy.

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During the period February 1981--February 1986 101 poor-risk patients with common bile duct stones were treated with EST (endoscopic sphincterotomy). 51 of the patients had no previous gallbladder surgery. The first year 7 complications occurred among 11 patients, including 3 deaths. The following four years we had a total of 8 complications among 90 patients, including 1 death. The complications consisted of: Bleeding needing transfusion (n = 5), pancreatitis (n = 5), cholangitis (n = 2), perforation (n = 2), impaction of the Dormia basket (n = 1). Fourty-five patients were discharged without cholecystectomy. Two patients later underwent elective cholecystectomy. Four patients developed symptoms requiring cholecystectomy. The remaining 39 patients have not required any further treatment for their gallstone disease. This study demonstrates that EST in experienced hands is a safe and effective method even in extremely poor-risk patients and that EST might be used as the sole treatment of common bile duct stones in this type of patients without previous cholecystectomy. The few complications are mostly mild and can be managed conservatively.

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