A, Jadus M. Growth factors: new 'endogenous drugs' for ulcer healing. Scand J Gastroenterol 1995;30 Background: The pathogenesis of gastroduodenal ulceration has been investigated mostly from the point of view of aggressive factors; the therapeutic interventions affected the healing process only indirectly. With the discovery of the potent healing capacity of growth factors, direct treatment of ulcers is now possible regardless of HCI and pepsin secretion. We review our recent data on how growth factors (e.g., bFGF, PDGF in comparison with EGF) can promote ulcer healing. Resulcs: Treatment of rats with bFGF, PDGF accelerated the healing of experimental chronic duodenal and gastric ulcers without suppressing gastric acid secretion and resulted in superior quality of ulcers healed. We also detected additive or synergistic action between bFGF and cimetidine or bFGF and sucralfate in the healing of chemically induced chronic duodenal ulcers and chronic erosive gastritis. Conclusions: We conclude that growth factors such as bFGF, PDGF can promote ulcer healing without the need to neutralize gastric secretion and may lead to a direct and efficient therapeutic regime.

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The most effective resuscitative procedure in choking by foreign bodies is the Heimlich maneuver, described for the first time by Henry Heimlich (1974) and recognized by the US Surgeon General (1985) as the "only method that should be used for the treatment of choking from foreign body airway obstruction." If performed correctly, this lifesaving maneuver is associated with rare complications, of which the most frequent are rib fractures and gastric or esophagus perforations. Other rare traumatic injuries such as pneumomediastinum, aortic valve cusp rupture, diaphragmatic herniation, jejunum perforation, hepatic rupture, or mesenteric laceration have been described.However, we are unaware of previous reports of splenic rupture after Heimlich maneuver. We present an interesting case of fatal hemoperitoneum due to a hilar laceration of the spleen following a correctly performed Heimlich maneuver.

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Since recent studies suggest an imbalance between cathepsin B and its tissue protease inhibitors (PI) in the pathogenesis of acute and chronic diseases, we tested the hypothesis that release of activated cysteine proteases (P) such as cathepsins B, H, and L might play a role in the pathogenesis of gastric hemorrhagic mucosal lesions (HML) induced by ethanol (E) or ammonia (A). Anesthetized rats received 1 ml of 50% E or 1% A solution intragastrically for 1 min during in situ gastric luminal perfusion. Rapid activation and release of cathepsins B, L, and H into the luminal perfusate preceded the formation of HML quantified by planimetry. Mucosal presence and activity of cysteine PI and cathepsin B have also been investigated in the pathogenesis of chemically induced HML. We extracted and partially isolated acid and thermostable inhibitors of cathepsin B in the gastric mucosa, and found rapid inactivation of PI and activation of cathepsin B in the early phase of E-or A-induced HML. Negative correlations were found between P and PI activities by E or A solutions. Both the activation of cathepsins B, L, and H and the development of E-induced HML were prevented by pretreatment with the sulfhydryl alkylator N -ethylmaleimide. These results suggest that cysteine P may be activated in the rat stomach after E or A exposure, and cysteine P may have a role in the pathogenesis of E-or A-induced gastric HML. Endogenous PI may also participate in the mechanisms of gastric mucosal lesions and gastroprotection. ( J. Clin. Invest. 1996. 98:1047-1054.)