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To the EditorWe read the articles by Al-Ghamdi et al. [1] and Zhang et al. [2] referring to some pathophysiological and clinical disorders associated to the inflammatory diseases of the pancreas. These and other articles frequently published in Digestive Diseases Sciences led us to afford some useful information for gastroenterologists and clinicians that might change the point of view about all types of pancreatic disturbances. In this sense, we are obliged to provide information concerning the absolute therapeutic success we have obtained through the administration of small doses of clonidine (an alpha-2 agonist) in 41 consecutive subjects affected by inflammatory disease of the pancreas. We demonstrated in 1962 that clonidine was able to annul the excito-secretory effects of secretin (a gastrointestinal hormone) on the pancreatic juice secretion of dogs whose pancreatic ducts had been previously cannulated [3]. We reported the absolute suppression of pancreatic juice secretion after the intramuscular administration of 0.15 mg of clonidine [3]. These findings were further verified when the clonidine challenge was carried out in gastrectomized dogs [4]. Moreover, we also found that clonidine was able to interfere not only with pancreatic juice secretion, but also with the excito-secretory effects of cholecystokinin on both biliary secretion and motility [5,6]. The above experimental results registered in mammals led us to attempt the use of clonidine to treat patients affected by acute pancreatitis. The rationale for this strategy was based on the pathophysiological knowledge that the inflammatory process should interfere with adequate drainage of the pancreatic juice and would exacerbate the damage at the acinar pancreas level. The absolute success of this neuropharmacological strategy has been reported in [7,8] as well as in other communications [9][10][11]. These successful therapeutic results should be understood according to findings that demonstrated that the sympathetic innervation of the pancreas arises from the Cl(Ad) medullary nuclei, which are located at the rostroventrolateral area of this central nervous system structure [12][13][14][15][16]. These nuclei are responsible for secretion from the adrenal glands, which release 80% of adrenaline (Ad) plus 20% of nor-adrenaline (NA) and dopamine (DA) [15,17]. This anatomical plus physiological information is consistent with our findings showing that patients affected by acute pancreatitis show raised plasma levels of Ad but not NA or DA. Thus, clonidine (an alpha-2 agonist) should act at the hyperactive Cl(Ad) rather than at the hypoactive A5(NA) or A6(NA). The two latter nuclei are also crowded by inhibitory alpha-2 receptors. However, facts showing that these three nuclei interchange inhibitory axons would explain why the predominance of one of them-Cl(Ad)-facilitates the selective effect of clonidine at these latter nuclei [15][16][17].All patients affected by pancreatic inflammatory disorders were improved after the first dose of clonidine. Normalizat...