Purulent Pericarditis Due to Pneumococcal Bacteremia Caused by Acupuncture: An Autopsy Case Report.

Purulent pericarditis is an infection of the pericardial cavity that produces purulent fluid and is commonly caused by Streptococcus pneumoniae. We herein report an autopsy case that is unique in two respects: the patient had pneumococcal bacteremia from a skin and soft tissue infection associated with acupuncture as well as purulent pericarditis from pneumococcal bacteremia. This case suggests that bloodstream infection should be included in the differential diagnosis on observing pneumococcal pericarditis. Furthermore, it is necessary to recognize that S. pneumoniae may be the organism responsible for skin and soft tissue infections caused by trauma in immunosuppressed patients.

Termination of Atrial Flutter and Fibrillation by K201's Metabolite M-II: Studies in the Canine Sterile Pericarditis Model.

INTRODUCTION: K201, a 1,4-benzodiazepine derivative, acts on multiple cardiac ion channels and the ryanodine receptor. We tested whether administration of M-II, the main metabolite of K201, would terminate induced atrial flutter (AFL) or atrial fibrillation (AF) in the canine sterile pericarditis model. METHODS: In 6 dogs, electrophysiologic studies were performed at baseline and after drug administration, measuring atrial effective refractory period (AERP), and conduction time from 3 sites during pacing at cycle lengths (400, 300, and 200 milliseconds) on postoperative days 1-4. In 12 induced episodes of sustained AF/AFL (2/10, respectively), M-II was administered intravenously to test efficacy. Five of the AFL episodes were studied in the open chest state during simultaneous multisite atrial mapping. RESULTS: M-II terminated 2/2 AF and 8/10 AFL episodes, prolonged AERP (P < 0.05), significantly increased atrial pacing capture thresholds but did not significantly change atrial conduction time. AFL CL prolongation was largely explained by prolonged conduction in an area of slow conduction in the reentrant circuit. AFL terminated with block in the area of slow conduction. CONCLUSIONS: M-II was very effective in terminating AFL/AF in the canine sterile pericarditis model. AFL terminated due to block in the area of slow conduction of the reentrant circuit.

Oral vanoxerine prevents reinduction of atrial tachyarrhythmias: preliminary results.

BACKGROUND: Vanoxerine is a promising, new, investigational antiarrhythmic drug. The purpose of this study was to test the hypothesis that oral dosing of vanoxerine would first terminate induced atrial flutter (AFL) and atrial fibrillation (AF), and then prevent their reinduction. METHODS: In 5 dogs with sterile pericarditis, on the fourth day after creating the pericarditis, we performed electrophysiologic (EP) studies at baseline, measuring atrial excitability, refractoriness (AERP), and conduction time (CT) when pacing from the right atrial appendage, Bachmann's bundle (BB), and the posteroinferior left atrium at cycle lengths (CLs) of 400, 300, and 200 ms. Then, after induction of AFL or AF, all dogs received hourly oral doses of vanoxerine: 90 mg, followed by 180 mg and 270 mg. Blood was obtained to determine plasma vanoxerine concentrations at baseline, every 30 minutes, when neither AFL nor AF were inducible, and, finally, 1 hour after the 270 mg dose. Then we repeated the baseline EP studies. RESULTS: Four dogs had inducible, sustained AFL, and 1 dog only had induced, nonsustained AF. In 4 AFL episodes, oral vanoxerine terminated the AFL and then rendered it noninducible after an average of 111 minutes (range 75-180 minutes) after the first dose was administered. The mean vanoxerine plasma level at the point of noninducibility was 84 ng/mL, with a narrow range of 76-99 ng/mL. In the dog with induced, nonsustained AF, it was no longer inducible at a drug level of 75 ng/mL. Vanoxerine did not significantly (1) prolong the AERP except at BB, and then only at the faster pacing CLs; (2) change atrial excitability thresholds; (3) prolong atrial conduction time, the PR interval, the QRS complex or the QT interval. CONCLUSIONS: Orally administered vanoxerine effectively terminated AFL and rendered it noninducible. It also suppressed inducibility of nonsustained AF. These effects occurred at consistent plasma drug levels. Vanoxerine's insignificant or minimal effects on measured electrophysiologic parameters are consistent with little proarrhythmic risk.

Fatal acute hepatitis after sequential treatment with levofloxacin, doxycycline, and naproxen in a patient presenting with acute Mycoplasma pneumoniae infection.

BACKGROUND: The diagnosis of drug-induced liver injury relies on comprehensive clinical assessments due to the absence of an established biomarker or pathognomonic features of liver histology. However, prompt recognition of a culprit drug as the cause of liver injury is the most important aspect in the management of hepatotoxicity. CASE SUMMARY: A 63-year-old white male (85 kg) was admitted because of community-acquired pneumonia with associated pericarditis and subclinical hepatitis, subsequently related to acute Mycoplasma pneumoniae infection (diagnostic positive immuno-globulin M enzyme immunoassay, on hospital days 5 and 20). The patient had received cisplatin and radiotherapy from March to May 2006, as treatment for pharyngolaryngeal squamous cell carcinoma T3N0M0 without subsequent evidence of localized or meta-static recurrent disease (last oncologic consultation, May 17, 2007). He reported alcohol ingestion until March 2006 but no known liver disease, blood transfusion, or exposure to mushrooms or industrial cleaning solvents. Results of serologic tests for viral and nonviral infectious hepatitis, iron and copper studies, and tests for autoantibodies were normal or negative. The patient became initially asymptomatic and fever disappeared following sequential treatment with levo-floxacin (500 mg BID), doxycycline (100 mg BID), and naproxen (500 mg TID). However, on hospital day 10 jaundice and a significant elevation (alanine aminotransferase, 1577 U/L; aspartate amino-transferase, 1754 U/L; alkaline phosphatase, 189 U/L) of serum transaminases appeared. Despite the discontinuation of all medication, the patient gradually deteriorated and died 27 days after admission due to acute fulminant hepatic failure. Autopsy revealed massive hepatic necrosis, inflammatory changes with presence of eosinophils, and cholestasis. An objective causality assessment scale (Council for International Organizations of Medical Sciences/Roussel Uclaf Causality Assessment Method scale) suggested that each of the 3 drugs could "probably" (score = 6) be related to the patient's fulminant hepatitis. The Naranjo Adverse Drug Reactions Probability Scale assessment for the same drugs indicated a "possible" causal relation (score = 2). CONCLUSION: We report a case of lethal hepatitis possibly/probably associated with levofloxacin, doxy-cycline, and naproxen in a patient with acute M pneumoniae infection.

Antiarrhythmic effects of JTV-519, a novel cardioprotective drug, on atrial fibrillation/flutter in a canine sterile pericarditis model.

UNLABELLED: Effect of JTV-519 on AF. INTRODUCTION: A new cardioprotective drug, JTV-519, blocks Na+ current and inwardly rectifying K+ current and inhibits Ca2+ current. However, its role in atrial electrophysiology is unknown. We investigated the antiarrhythmic effects of JTV-519 on atrial fibrillation/flutter in the canine sterile pericarditis model. METHODS AND RESULTS: In nine dogs with sterile pericarditis, 38 episodes of sustained (>30 sec) atrial fibrillation (8 dogs) and 24 episodes of sustained atrial flutter (7 dogs) were induced by rapid atrial pacing. When atrial fibrillation or atrial flutter was sustained >15 minutes, it was cardioverted and reinduced. The inducibility of atrial fibrillation/flutter, the atrial effective refractory period, and the intra-atrial conduction time were compared before and after the continuous infusion of JTV-519 (0.03 mg/kg/min). JTV-519 significantly decreased the mean number of sustained atrial fibrillation episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). In contrast, atrial flutter was still inducible in 4 dogs after JTV-519 (from 2.7 +/- 2.5 to 1.6 +/- 2.1, P = NS). JTV-519 significantly prolonged effective refractory period (from 123 +/- 18 to 143 +/- 14 msec, from 127 +/- 18 to 151 +/- 12 msec, and from 132 +/- 13 to 159 +/- 9 msec at basic cycle lengths of 200, 300, and 400 msec, respectively, P < 0.01), but it did not affect the intra-atrial conduction time (from 47 +/- 11 msec to 48 +/- 11 msec, P = NS). CONCLUSION: JTV-519 had significant protective effects on atrial fibrillation in the canine sterile pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for atrial fibrillation.

[A case of recurrent squamous cell carcinoma of cervix successfully treated with BOMP].

Combination chemotherapy consisting of bleomycin, vincristine, mitomycin C and cisplatin (BOMP) was applied to a case (57 years old) with recurrence of squamous cell carcinoma of the cervix. The patient with FIGO stage IIIb cervical carcinoma had been treated with radiotherapy seven years ago. She was affected by malignant pericardial effusion, and was treated with direct intrapericardial administration of cisplatin (20 mg). After instillation, ultrasonography and computed tomography showed the wall thickening of colon and marked ascites. Barium enema showed the circumferential narrowing and serrations of colon, and it was diagnosed to be carcinomatous peritonitis. She was treated with BOMP consisting of BLM (5 mg, i.m., days 1 - 5), VCR (1 mg, i.v., day 5'), MMC (8 mg, i.v., day 5), and CDDP (70 mg, d.i.v., day 5). After three courses of BOMP therapy, she achieved a complete response with few toxic effects and did not require special care. She has been free of disease for six months and her performance status is 0. This encouraging result warrants the use of this combination chemotherapy regimen in other patients with recurrent squamous cell carcinoma of the cervix.

Hemophilus influenzae purulent pericarditis in children: diagnostic and therapeutic considerations.

Purulent pericarditis is an unusual complication of infection in infancy and has been associated with an extremely high mortality rate. Early diagnosis followed by combined antibiotic therapy and surgical drainage of the pericardium has markedly improved survival. Between APril, 1975, and February, 1979, nine patients with purulent pericarditis secondary to Hemophilus influenzae type B were treated at the Oklahoma Children's Memorial Hospital. In every case signs and symptoms of congestive heart failure were present, and a pericardial effusion was demonstrated by echocardiography and confirmed by pericardiocentesis. The organism was identified with countercurrent immunoelectrophoresis and antibiotic sensitivity determined by rapid beta lactamase assay. All patients were treated with a combination of parenteral antibiotics and open surgical drainage of the pericardium. There were no deaths and all patients demonstrated marked improvement following operation. Follow-up echocardiography revealed no evidence of pericardial effusion or signs of constriction in any patient.

Primary meningococcal pericarditis presenting with tamponade.

An unusual case of a patient with primary meningococcal pericarditis presenting with tamponade is reported. tdespite repeated aspiration and appropriate antibiotic therapy with eradication of group C Neisseria meningitidis, pericardial effusion continued to reaccumulate. Institution of high-dosage corticosteroid therapy resulted in rapid resolution of the effusion. Only six other cases of primary meningococcal pericarditis have been reported in the English literature. Early manifestations of this disease are due to bacterial invasion of the pericardium. The later phase of intensive reaccumulation of sterile pericardial fluid may conceivably be related to meningococcal endotoxin and appears to be responsive to corticosteroid or salicylate therapy. Recognition of this phenomenon may obviate the necessity for a pericardiectomy.