Effect of bromhexine hydrochloride therapy for alcoholic chronic pancreatitis.

BACKGROUND: Abstinence is a prerequisite for the treatment of alcoholic chronic pancreatitis, but there are patients who have repeated attacks because of their inability to abstain and the consequent congestive effects of the continued alcohol intake on pancreatic juice. Bromhexine hydrochloride, a bronchial mucolytic, has an affinity for acinar cells and causes them to secrete pancreatic juice of low viscosity. METHODS: Twelve patients with alcoholic chronic pancreatitis, who were unable to abstain from drinking, were administered bromhexine hydrochloride for 6 months to assess its therapeutic efficacy. RESULTS: Of 12 patients administered bromhexine, 8 (67%) reported symptomatic improvement, and all patients showed improvement in the levels of pancreatic enzymes. Pancreatic exocrine function also tended to improve, but no improvement of pancreatic endocrine function was detected. Although none of the pancreatic stones present in some patients disappeared, a protein plug present in one patient disappeared, accompanied by improvement in the irregular outline of the lumen of the main pancreatic duct. CONCLUSION: Bromhexine hydrochloride may be a new for the morbidity of chronic pancreatitis, in which there is increased viscosity of the pancreatic juice and formation of a protein plug.

Decreased activity of plasma ADAMTS13 may contribute to the development of liver disturbance and multiorgan failure in patients with alcoholic hepatitis.

BACKGROUND: The pathogenesis of alcoholic hepatitis (AH) remains unclear and the prognosis of severe alcoholic hepatitis (SAH) is very poor. Deficiency of von Willebrand factor (VWF)-cleaving protease (VWF-CP/ADAMTS13) results in an increase of the plasma unusually large VWF multimer and leads to platelet clumping, which causes microcirculatory disturbance and finally multiorgan failure. The aim of this study was to explore the potential role of ADAMTS13 on the development of liver disturbance and multiorgan failure in AH. METHODS: The activity of plasma ADAMTS13 and its clinical correlation were determined in 14 patients with AH, 4 with SAH (Maddrey score, mean 62), and 10 with alcoholic liver cirrhosis (LC). RESULTS: The activity of the plasma ADAMTS13 significantly decreased in patients with AH (mean 59%, p < 0.001), SAH (17%, p < 0.001) and LC (76%, p < 0.02) as compared with the healthy subjects (102%, n = 60). The activity was markedly lower in SAH than in AH (p < 0.02) and LC (p < 0.02). In three nonsurvivors with SAH who had multiorgan failure, it was extremely low (4.5%, 5.0%, and 16.0%, respectively), but in a survivor with SAH it remained mild decrease (44%). In AH, the protease activity increased at the recovery stage (42% --> 75%, p < 0.05). In the univariate analysis, the activity correlated with 10 clinical variables including functional liver capacity, inflammation signs, renal function, and platelet count in patients with AH and SAH. Among these, multivariate analysis showed that serum total bilirubin and C-reactive protein independently correlated with the protease activity. CONCLUSION: The activity of plasma ADAMTS13 markedly decreased in SAH in addition to AH. The activity was closely related to hyperbilirubinemia and inflammation signs, and was extremely low in nonsurvivors with SAH and multiorgan failure. The marked decrease of plasma ADAMTS13 may, in part, contribute to not only the progression of liver disturbance in AH, but also the development of multiorgan failure in SAH through microcirculatory disturbance.

Mediastinal pancreatic pseudocyst caused by obstruction of the pancreatic duct was eliminated by bromhexine hydrochloride.

A 49-year-old man, who had a 30-year history of drinking the equivalent of 80 g of ethanol per day, underwent a detailed medical examination for cough and dyspnea. Chest-abdominal computed tomography and endoscopic retrograde pancreatography led to the diagnosis of a mediastinal pancreatic pseudocyst resulting from obstruction of the pancreatic duct by a protein plug. The pseudocyst rapidly improved with conservative treatment with camostat mesilate, H2-receptor antagonist and digestive enzymes. Although the patient abstained from alcohol for approximately 6 months, he resumed drinking, leading to recurrent attacks of pancreatitis. Bromhexine hydrochloride was then administered for 6 months, with the expectation that it would have a mucolytic effect on the pancreatic juice, resulting in improvement in the clinical symptoms, pancreatic enzymes and pancreatic exocrine function, as well as elimination of the protein plug. Bromhexine hydrochloride may be a new therapy for pathological states, such as alcoholic chronic pancreatitis, in which there is increased viscosity of the pancreatic juice because of elevated protein concentration, leading to protein plug formation and temporary blockage of the pancreatic duct.