Recurrent Acute Pancreatitis and Therapy for Ulcerative Colitis.

Drugs are a rare cause of pancreatitis. Whereas some drugs are well known to induce an attack of pancreatitis, some people may be more prone to develop pancreatitis because of personal susceptibility. We describe a recurrent case of acute pancreatitis after administration of several drugs in a patient with intestinal inflammatory bowel disease that needed to be treated with subsequent antiinflammatory agents. Genetic mutation in the CFTR gene was found in the patient that led us to postulate that CFTR was a trigger for drug-induced acute pancreatitis. In conclusion, genetic analysis should be advised in case of recurrent pancreatitis in patient with intestinal inflammatory bowel disease.

Hemobilia, a rare cause of acute pancreatitis after percutaneous liver biopsy: diagnosis and treatment by endoscopic retrograde cholangiopancreatography.

We here report the case history of a 75-yr-old woman who developed pancreatitis and recurrent symptomatic, cholestasis-induced hemobilia after percutaneous liver biopsy. An endoscopic sphincterotomy with clot extraction led to relief of symptoms. The risk of hemobilia after percutaneous liver biopsy is less than one per 1000 procedures, and only two cases of acute pancreatitis after percutaneous liver biopsy have previously been reported. To our knowledge, this is the first case in which endoscopic retrograde cholangiopancreatography was used to both diagnostic and therapeutic ends.

Anti-TNF Therapy in the Treatment of Psoriasis in a Patient with Acute-on-Chronic Pancreatitis.

Background: Psoriasis is accepted as a multisystemic disease with several important systemic manifestations. Thus, underlying comorbidities have to be taken into account in the choice of treatment. Objective: To explore the role of anti-TNF therapy in the treatment of psoriasis in a patient with acute-on-chronic pancreatitis. Methods: Here, we present the case of a 75-year-old patient with severe psoriasis also suffering from chronic alcohol-induced pancreatitis with recurrent acute flares. A recent life-threatening episode of acute pancreatitis and ischemic liver precluded the reintroduction of methotrexate. Cyclosporine was also excluded as it has been reported to induce acute pancreatitis. Thus, an anti-TNF treatment was initiated in close collaboration with a gastroenterologist. Results: A year after starting anti-TNF therapy the patient continues to show complete clinical remission of his psoriasis. No side effects, particularly no bacterial infections, were reported. No relapses of the patient's underlying chronic pancreatitis were observed throughout the entire treatment with regular clinical and laboratory monitoring, suggesting that chronic pancreatitis is not per se a contraindication for anti-TNF therapy. Conclusion: This case study opens the way for further questioning on the role of TNF in the pathogenesis of chronic and acute pancreatitis and the use of anti-TNF therapy in its treatment. © 2013 S. Karger AG, Basel.

Pancréatite aiguë clinique après chimio-embolisation sélective d'un carcinome hépatocellulaire [Acute clinical pancreatitis following selective transcatheter arterial chemoembolization of hepatocellular carcinoma]

Acute pancreatitis can complicate non-selective transcatheter arterial embolization of hepatocellular carcinoma with an incidence ranging from 1,7% (acute clinical pancreatitis) to 40% (biological pancreatitis). This complication is thought to be related to embolization of extrahepatic arterial collaterals.We report herein a case of acute clinical pancreatitis developing within 24 hours after a second course of selective transcatheter arterial chemo-embolization into the proper hepatic artery. Neither anatomical arterial variation nor particular risk factor for acute pancreatitis could be identified. This complication is unusual after selective arterial embolization. Because it may clinically mimick a postembolization syndrome, dosage of serum pancreatic enzymes should be performed systematically in case of abdominal pain following chemoembolization.

Boerhaave Syndrom: an unusual complication of acute vomiting in a child

Introduction: Boerhaave syndrome (BS) is a spontaneous esophageal perforation, described in aged, alcoholic males, secondary to forceful vomiting. BS has rarely been described in children. Case presentation: The patient is a 7-year-old Nigerian girl. She has a past history of clinical gastro-esophageal reflux (treated conservatively with prokinetics and good evolution), malaria at the age of 3 months and an episode of acute pancreatitis at 5 years. One week prior admission, she had stopped atovaquone-proguanil (AP) prophylaxis after a trip in an endemic area. Two days prior admission, she presented several bouts of isolated acute vomiting, without fever or diarrhea. On admission, she complained of chest pain. Cardiac auscultation revealed crepitus. No subcutaneous emphysema nor respiratory distress was present. Chest radiography and CT-scan confirmed a pneumomediastinum extending to the neck. Esophageal perforation was suspected. An upper gastrointestinal endoscopy was performed and showed a small esophageal tear, grade II-III esophagitis and a single gastric ulcer without any sign of H. Pylori infection. Enteral feeds were stopped and a nasogastric sucking tube inserted. The patient made a full recovery on intravenous antibiotics and conservative treatment. Of note a second episode of subclinical acute pancreatitis, treated conservatively, probably drug-induced. Discussion: BS is a complete rupture of all layers of the esophagus, secondary to an increased intra-abdominal pressure due to incomplete opening of the cricophayngeal sphincter occurring during vomiting or cough. Rarer causes include eosinophilic or Barrett's esophagitis, HIV and caustic ingestion. Esophageal perforation in children is rare, most of time secondary to necrotizing esophagitis in the newborn, medical intervention (endoscopy, sucking, or intubation) or trauma in the older child. Our patient had none of those risk factors and it is still unclear what predisposed her to this complication. However, we believe that preceding forceful vomiting with increased abdominal pressure acting on a weakened oesophagus due to esophagitis might be responsible. We could not find any association in the literature between AP and BS nor between BS and acute pancreatitis. The origin of her recurrent pancreatitis remains unclear, reason for which genetic testing for mutations in the trypsinogen, trypsin inhibitor and CFTR genes will be performed in case of a third episode.

β-Glucan Antigenemia Anticipates Diagnosis of Blood Culture-Negative Intraabdominal Candidiasis.

Rationale: Life-threatening intraabdominal candidiasis (IAC) occurs in 30 to 40% of high-risk surgical intensive care unit (ICU) patients. Although early IAC diagnosis is crucial, blood cultures are negative, and the role of Candida score/colonization indexes is not established. Objectives: The aim of this prospective Fungal Infection Network of Switzerland (FUNGINOS) cohort study was to assess accuracy of 1,3-β-d-glucan (BG) antigenemia for diagnosis of IAC. Methods: Four hundred thirty-four consecutive adults with abdominal surgery or acute pancreatitis and ICU stay 72 hours or longer were screened: 89 (20.5%) at high risk for IAC were studied (68 recurrent gastrointestinal tract perforation, 21 acute necrotizing pancreatitis). Diagnostic accuracy of serum BG (Fungitell), Candida score, and colonization indexes was compared. Measurements and Main Results: Fifty-eight of 89 (65%) patients were colonized by Candida; 29 of 89 (33%) presented IAC (27 of 29 with negative blood cultures). Nine hundred twenty-one sera were analyzed (9/patient): median BG was 253 pg/ml (46-9,557) in IAC versus 99 pg/ml (8-440) in colonization (P < 0.01). Sensitivity and specificity of two consecutive BG measurements greater than or equal to 80 pg/ml were 65 and 78%, respectively. In recurrent gastrointestinal tract perforation it was 75 and 77% versus 90 and 38% (Candida score ≥ 3), 79 and 34% (colonization index ≥ 0.5), and 54 and 63% (corrected colonization index ≥ 0.4), respectively. BG positivity anticipated IAC diagnosis (5 d) and antifungal therapy (6 d). Severe sepsis/septic shock and death occurred in 10 of 11 (91%) and 4 of 11 (36%) patients with BG 400 pg/ml or more versus 5 of 18 (28%, P = 0.002) and 1 of 18 (6%, P = 0.05) with BG measurement less than 400 pg/ml. β-Glucan decreased in IAC responding to therapy and increased in nonresponse. Conclusions: BG antigenemia is superior to Candida score and colonization indexes and anticipates diagnosis of blood culture-negative IAC. This proof-of-concept observation in strictly selected high-risk surgical ICU patients deserves investigation of BG-driven preemptive therapy.

Indicazioni e risultati della laparostomia retroperitoneale nel trattamento della pancreatite acuta necrotizzante infetta [Indications and results of retroperitoneal laparostomy in the treatment of infected acute necrotizing pancreatitis]

The aim of this study is to describe personal experience with retroperitoneal laparostomy in the management of infected acute necrotizing pancreatitis. The presence of an infected phlegmon requires surgical debridement and drainage. The surgical approach can be either an anterior laparotomy with irrigation and drainage (which can be either an open or closed laparotomy) or a posterior laparostomy. Three patients (2 men and 1 woman) presented with an unfavourable course of their acute necrotizing pancreatitis despite the administration of broad spectrum antibiotics. A posterior laparostomy with necrosectomy and drainage was performed. The postoperative course was slowly favorable in all 3 cases. Abdominal CT is the best modality for the detection and follow-up of pancreatic necrosis. CT-guided fine needle aspiration can detect superinfection of areas of necrosis. Posterior laparostomy presents several advantages compared to an anterior approach. There is no contamination of the peritoneal cavity; the integrity of the abdominal wall is respected. The necrosectomy is equally complete and the drainage is better as it is direct and posterior.

An episode mimicking a versive seizure in acute bilateral pontine stroke.

Pontine ischemia usually results in focal deficits such as hemiparesis, facial palsy, dysarthria, disorders of eye movements or vertigo. Although rarely described, involuntary abnormal movements and "convulsions" due to pontine lesions can also occur. Here we describe a 67-year-old woman with hypertension who presented with a tonic movement mimicking a versive seizure in the acute phase of bilateral pontine ischemia. Post-stroke movement disorders are well known. They are usually associated with supratentorial lesions and rarely occur in the acute phase, but "seizure-like" episodes can be seen in pontine ischemia. Awareness of this rare phenomenon is useful for the management of acute stroke patients.

Diarrhées aiguës: propositions de prise en charge ambulatoire [Acute diarrhea: proposal for outpatient management]

Dans la majorité des cas, les diarrhées aiguës sont bénignes et d'évolution spontanément favorable. Il faut cependant savoir reconnaître les situations pouvant mener à des complications, en l'occurrence identifier les diarrhées invasives, inflammatoires, caractérisées par la présence de fièvre, de douleurs abdominales, de ténesmes, de mucus et, ou de sang dans les selles. Celles-ci sont à distinguer des diarrhées sécrétoires, non invasives, non inflammatoires, sans fièvre, généralement aqueuses et volumineuses. En cas de doute diagnostique, l'identification de leucocytes par microscopie ou test à la lactoferrine dans les selles permet d'évoquer une gastroentérite invasive. Les indications à une antibiothérapie empirique dans l'attente du résultat de la coproculture sont la présence d'un syndrome dysentérique (T > 38°C, > 6 selles/24 heures, douleurs abdominales, diarrhées mucopurulentes), l'âge avancé, des comorbidités significatives, une immunosuppression et la présence d'une prothèse endovasculaire. In the majority of the cases, an acute diarrhea is mild and of spontaneously favorable evolution. It is however necessary to know how to recognize the situations being able to lead to complications, in particular to identify the invasive, inflammatory diarrheas, characterized by the presence of fever, abdominal pains, mucus and\or blood. The identification of leukocytes by microscopy or lactoferrine test is helpful. Empiric quinolones treatment is recommended in the presence of dysenteric syndrome (T > 38 degrees C, > 6 stods/24 h 00, abdominal pain muco-purulent diarrhea), advanced age, significant comorbidities, immunosuppression or presence of an endovascular prothesis

Acute flare induced by the calcific tendonitis of the rotator cuff: inhibition of IL-1 a potential therapeutic target?

Introduction: Calcific tendonitis of rotator cuff is observed on plainradiographs in 10% of adults, but remains asymptomatic in half thesecases. Sometimes, these calcifications induce acute flares withmassive inflammation similar to gout or CPPD crisis. Analgesics/anti-inflammatory medications are usually not sufficient to controlssymptoms in these situations. Local steroid infiltration with or withoutremoval of the calcific deposition with a needle aspiration may beuseful. A new approach could be IL-1 inhibitors. Indeed, basic calciumphosphate crystals are capable of stimulating the release of activeIL-1β in vitro. These crystals trigger IL-1β release, in an analogousmanner to MSU crystals in acute gout, suggesting that IL-1β blockademay be clinically useful.Case presentation: This report describes a 70-year old woman withacute rest pain of the right shoulder since 48 hours. On examination,we found massive limitations of active and passive movements. Thepatient evaluated, on the visual scale, her symptoms at 10/10 the nightand 5/10 the day. The radiography and showed a rounded, 8 mmcalcification in the subscapularis tendon. The ultrasound aspectrevealed a heterogeneous calcification partially non solid, surroundedby massive inflammation on Doppler. C-reactive protein anderythrocyte sedimentation rate were high (74 mg/ml, 54 mm/hour).The patient received subcutaneous injections of anakinra: 100 mgdaily for 3 days (D1-D3). We evaluated the patient in our consult at dayD1, D2, D3, D7, D16 and by phone at D70.This treatment rapidly relieved the inflammatory symptoms (within afew hours with no relapse). The mobility of the shoulder, the biologicsparameters improved and the size of the calcification as well thedegree of inflammation regressed on ultrasound after 3 days.Conclusion: This is the first report of a woman with an acute flareinduced by calcific tendonitis who received anakinra. IL-1 inhibitionmay be a therapeutic target in calcific tendonitis. To analyse thisresponse more precisely and elaborate definitive conclusions, aprospective pilot study is on-going in our ambulatory institute.

Acute Eosinophilic and Neutrophilic Pneumonia following Transarterial Chemoembolization with Drug-Eluting Beads Loaded with Doxorubicin for Hepatocellular Carcinoma: A Case Report.

At an intermediate or advanced stage, i.e. stage B or C, based on the Barcelona Clinic Liver Cancer classification of hepatocellular carcinoma (HCC), transarterial chemoembolization (TACE) may be offered as a treatment of palliative intent. We report the case of a patient suffering from acute respiratory distress syndrome after TACE with drug-eluting beads loaded with doxorubicin for HCC. To our knowledge, this is the first case described where a bronchoalveolar lavage was performed, and where significant levels of alveolar eosinophilia and neutrophilia were evident, attributed to a pulmonary toxicity of doxorubicin following liver chemoembolization. © 2014 S. Karger AG, Basel.

Neuroendocrine, metabolic, and immune functions during the acute phase response of inflammatory stress in monosodium L-glutamate-damaged, hyperadipose male rat.

In rats, neonatal treatment with monosodium L-glutamate (MSG) induces several metabolic and neuroendocrine abnormalities, which result in hyperadiposity. No data exist, however, regarding neuroendocrine, immune and metabolic responses to acute endotoxemia in the MSG-damaged rat. We studied the consequences of MSG treatment during the acute phase response of inflammatory stress. Neonatal male rats were treated with MSG or vehicle (controls, CTR) and studied at age 90 days. Pituitary, adrenal, adipo-insular axis, immune, metabolic and gonadal functions were explored before and up to 5 h after single sub-lethal i.p. injection of bacterial lipopolysaccharide (LPS; 150 microg/kg). Our results showed that, during the acute phase response of inflammatory stress in MSG rats: (1) the corticotrope-adrenal, leptin, insulin and triglyceride responses were higher than in CTR rats, (2) pro-inflammatory (TNFalpha) cytokine response was impaired and anti-inflammatory (IL-10) cytokine response was normal, and (3) changes in peripheral estradiol and testosterone levels after LPS varied as in CTR rats. These data indicate that metabolic and neroendocrine-immune functions are altered in MSG-damaged rats. Our study also suggests that the enhanced corticotrope-corticoadrenal activity in MSG animals could be responsible, at least in part, for the immune and metabolic derangements characterizing hypothalamic obesity.

Bradykinin in blood and cerebrospinal fluid after acute cerebral lesions: correlations with cerebral edema and intracranial pressure.

Abstract Bradykinin (BK) was shown to stimulate the production of physiologically active metabolites, blood-brain barrier disruption, and brain edema. The aim of this prospective study was to measure BK concentrations in blood and cerebrospinal fluid (CSF) of patients with traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), and ischemic stroke and to correlate BK levels with the extent of cerebral edema and intracranial pressure (ICP). Blood and CSF samples of 29 patients suffering from acute cerebral lesions (TBI, 7; SAH,: 10; ICH, 8; ischemic stroke, 4) were collected for up to 8 days after insult. Seven patients with lumbar drainage were used as controls. Edema (5-point scale), ICP, and the GCS (Glasgow Coma Score) at the time of sample withdrawal were correlated with BK concentrations. Though all plasma-BK samples were not significantly elevated, CSF-BK levels of all patients were significantly elevated in overall (n=73) and early (≤72 h) measurements (n=55; 4.3±6.9 and 5.6±8.9 fmol/mL), compared to 1.2±0.7 fmol/mL of controls (p=0.05 and 0.006). Within 72 h after ictus, patients suffering from TBI (p=0.01), ICH (p=0.001), and ischemic stroke (p=0.02) showed significant increases. CSF-BK concentrations correlated with extent of edema formation (r=0.53; p<0.001) and with ICP (r=0.49; p<0.001). Our results demonstrate that acute cerebral lesions are associated with increased CSF-BK levels. Especially after TBI, subarachnoid and intracerebral hemorrhage CSF-BK levels correlate with extent of edema evolution and ICP. BK-blocking agents may turn out to be effective remedies in brain injuries.