Acute pancreatitis after a course of clarithromycin

We present a case of acute pancreatitis after a course of clarithromycin. An 84-year-old woman died of suspected pneumonia and cardiac failure. Autopsy surprisingly revealed acute pancreatitis. Except for the use of clarithromycin no other cause for her acute pancreatitis was obvious. Pancreatitis induced by clarithromycin has been reported twice in the English literature so far. There are, however, a few reports on acute pancreatitis associated with other macrolide antibiotics, such as erythromycin and roxithromycin.     

Acute pancreatitis

Acute pancreatitis is an inflammatory disease of the pancreas. Acute abdominal pain is the most common symptom, and increased concentrations of serum amylase and lipase confirm the diagnosis. Pancreatic injury is mild in 80% of patients, who recover without complications. The remaining patients have a severe disease with local and systemic complications. Gallstone migration into the common bile duct and alcohol abuse are the most frequent causes of pancreatitis in adults. About 15-25% of pancreatitis episodes are of unknown origin. Treatment of mild disease is supportive, but severe episodes need management by a multidisciplinary team including gastroenterologists, interventional radiologists, intensivists, and surgeons. Improved understanding of pathophysiology and better assessments of disease severity should ameliorate the management and outcome of this complex disease.     

Acute pancreatitis

The exocrine pancreas secretes into the gut on demand more than 20 proteins that are indispensable for digestion. In-vivo autodigestion is prevented by an array of natural safeguards. In acute pancreatitis, inappropriate intrapancreatic activation and release of pancreatic hydrolases occur, but the pathogenetic mechanism of autodigestion is unclear. The release of proteases, lipase and colipase, phospholipase A, vasoactive peptides, and other agents probably accounts for the edema, tissue destruction, fat necrosis, metabolic abnormalities, and complications. Ethyl alcohol abuse, gallstones, trauma, and other common and rare conditions can induce pancreatitis. The patient's outcome can be predicted by certain prognostic signs. Ultrasonography and computerized tomography are invaluable diagnostic tools and magnetic resonance imaging appears promising. Hemodynamic monitoring, intensive care with colloid and crystalloid infusions, correction of electrolyte abnormalities, judicious use of antibiotics, peritoneal lavage, drainage of pancreatic exudation fluids, and surgical intervention require a team approach, especially in patients with multiple complications. Additional research is needed into the pathogenetic mechanism of autodigestion and the design of specific therapies.     

Acute pancreatitis

While interstitial acute pancreatitis usually takes a benign course, necrotizing acute pancreatitis takes a severe course, mainly because of severe local and systemic complications. After a quick diagnosis it is necessary to rapidly assess a degree of severity of the disease and thus the prognosis. The clinical picture and the result of imaging procedures do not always correspond. The management basically includes to treat pain as well as to administer fluid, electrolyte, protein and calories. In addition, systemic treatment of complications such as shock or respiratory and renal insufficiency--if occurring--is necessary. In case of pancreatic necrosis, prophylactic administration of pancreas-penetrable antibiotics is recommended to avoid infection. In the severely ill with infected pancreatic necrosis, surgery is the treatment of choice. In approximately 10% of all patients with alcohol-induced pancreatitis, there is a gradual transition to chronic pancreatitis.     

Acute pancreatitis

Acute pancreatitis is an insidious inflammatory disease of the pancreas with its serious form leading to mortality in 20 to 30% of patients. Seemingly good clinical state at the onset of the disease is the cause of underestimation of resuscitation care in first hours of the disease. Whereas a basic prevention of the development of multiorgan dysfunction are an early re-establishing of the microcirculation and supranormal hemodynamic values. Making a differential diagnosis of the mild and the severe form of pancreatitis is possible after several days of intensive resuscitation care. Treatment of complications of acute pancreatitis, especially a long-term inflammatory process in retroperitoneum, require a patient and sometimes several month lasting intensive approach and interdisciplinary co-operation. Too early removal of drainage from the area of a necrotic gland or suppuration in retroperitoneum can be fatal to the patient.     

急性胰腺炎与慢性胰腺炎

随着人们生活水平的提高,胰腺炎的发病率在逐年上升.过去的几年里,虽然胰腺炎的研究取得了很大的进展,但仍存在许多争议的问题.其中急性胰腺炎(AP)与慢性胰腺炎(CP)的关系尤其是AP是否能向CP演变,以及演变的机制等都还不甚清楚.     

急性胰腺炎与慢性胰腺炎

随着人们生活水平的提高,胰腺炎的发病率在逐年上升。过去的几年里,虽然胰腺炎的研究取得了很大的进展,但仍存在许多争议的问题。其中急性胰腺炎(AP)与慢性胰腺炎(CP)的关系尤其是AP是否能向CP演变,以及演变的机制等都还不甚清楚。     

Acute pancreatitis in diabetics

All diabetic patients with acute pancreatitis should be intensively treated and monitored in spite of the fact that 75-80% have mild-to-moderate disease. This is due to difficult diagnosis and problems with standard monitoring due to diabetes and its complications. Especially intensive rehydration and subsequent fluid mobilisation can be difficult. Also glucose control and impaired gut motility can cause difficulties in diabetic patients with acute pancreatitis. Nutrition support should be implemented according to severity of disease and insulin infused to control glycaemia.     

Acute pancreatitis in children

OBJECTIVES: Currently, there is no scoring system for predicting severity in acute pancreatitis in children. Our intent was to evaluate the performance of existing scoring systems in children, to develop a system for children, and to examine the etiology of acute pancreatitis in children. METHODS: A chart review of children with acute pancreatitis was conducted at six centers, three serving as criterion centers and three as validation centers. Ranson and Glasgow scores were calculated for each admission. Additional clinical data were collected, and parameters correlating with severity were incorporated into a new scoring system. Performance characteristics were calculated for each system. RESULTS: A total of 301 admissions were reviewed, 202 in the criterion group and 99 in the validation group. Eight parameters were included in a new scoring system for children. The parameters were as follows: age (<7 yr), weight (<23 kg), admission WBC (>18,500), admission LDH (>2,000), 48-h trough Ca2+ (<8.3 mg/dl), 48-h trough albumin (<2.6 g/dl), 48-h fluid sequestration (>75 ml/ kg/48 h), and 48-h rise in BUN (>5 mg/dl). When the cut-off for predicting a severe outcome was set at 3 criteria, the new system had better sensitivity versus Ranson and Glasgow scores (70% vs 30% and 35%, respectively) and a better negative predictive value (91% vs 85% and 85%). The specificity (79% vs 94% and 94%) and positive predictive value (45% vs 57% and 61%) fell slightly. CONCLUSION: The new scoring system performs better in this group than do existing systems.