Lege Artis Medicinae

[Compounds – Plants...]

GRÉTSY Zsombor

JULY 20, 2006

Lege Artis Medicinae - 2006;16(07)

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[In the focus: periferal vascular diseases - Readers’ questions answered by dr. Éva Meskó]

MESKÓ Éva

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[Sustained oral anticoagulant therapy]

LENGYEL Mária, BODA Zoltán, PETHÔ Imre Iván

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[DIARRHOEA AND PSEUDOMEMBRANOUS COLITIS ASSOCIATED WITH ANTIBIOTIC TREATMENT]

LAKATOS László, LAKATOS Péter László

[Antibiotic treatment is complicated by diarrhea in 5 to 25% of the cases. Its prevalence depends on the antibiotic used, the patient’s age, the concomittant diseases and the immune response. The severity of the diarrhoea is variable ranging from a mild self-limiting disease lasting for 1 or 2 days to a severe condition with high mortality. The diarrhea may result from a direct effect on the gut, but more commonly it is the consequence of changes in resident gut flora. Clostridium difficile is responsible for 10 to 20% of all antibiotic-associated diarrhea cases. The clinical presentation varies from asymptomatic carriage to fulminant pseudomembranous colitis. This latter typically develops as a nosocomial infection, mainly in patients treated with cephalosporins, amoxicillin-clavulanic acid combination or clindamycin. Risk factors are advanced age, severe underlying disease, treatment in an intensive care unit, long hospitalization and invasive medical procedures. The clinical picture is characterized by frequent, watery (occasionally bloody) diarrhea, abdominal pain, tenesmus, fever, weakness. Fulminant colitis develops in 3-5% of cases. The diagnosis is based on testing for C. difficile toxins, but in selected cases rapid diagnosis can be made by flexible sigmoidoscopy. The treatment consists of the withdrawal of the implicated antibiotic along with administration of oral metronidazole or vancomycin which target C. difficile itself. Most patients respond to this treatment; however, the mortality of fulminant cases or those with severe underlying disease is high. Fifteen to 20% of the patients relapse and management of the recurrent cases is difficult. Combination treatment, probiotics and/or passive immunization may be used. Preventive measures include judicious use of antibiotics and aggressive control of the spread of C. difficile infection.]

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[WEGENER’S GRANULOMATOSIS PRESENTING AS MASTOIDITIS: A DIAGNOSTIC CHALLENGE]

NAGY Pál, SZABÓ László, DOMJÁN Gyula, GADÓ Klára, BALOGH Károly

[INTRODUCTION - Wegener's granulomatosis has an uncertain pathomechanism, but is probably autoimmune in origin. In typical cases the mucosa of the nose, paranasal sinuses and of the lower respiratory tract, as well as the lungs and the kidneys are affected. Patients present with sinusitis, recurrent pneumonia or renal disease associated with microhaematuria, pyuria or azotaemia. Fever, polyarthralgia or polyarthritis may also occur. The underlying pathologic changes are necrotizing vasculitis, granulomas and parenchymal necrosis. The diagnosis is based on a combination of the clinical picture, microscopic findings and immunofluorescent demonstration of cANCA. CASE REPORT - A 27-year-old woman presented with symptoms of unilateral mastoiditis. In the following 7 months she underwent 7 operations in 4 hospitals for a locally progressive, destructive process of uncertain etiology showing a septic course. The clinical picture was not specific, the cANCA test was not definitive, and the histologic findings were initially interpreted as nonspecific inflammation. Repeated biopsies, multiple reviews of the microscopic specimens, consultations, differential diagnostic considerations, and, finally, the success of the treatment with corticosteroids and cyclophosphamide led to the diagnosis of Wegener’s granulomatosis. Currently the patient has been in remission for 32 months. CONCLUSION - The definitive diagnosis of Wegener’s granulomatosis, particularly of its localized or limited form, may be problematic despite well-defined diagnostic criteria. Setting up the correct diagnosis may take months or years. In case of unusual respiratory or otological symptoms, and in view of ineffective medical or surgical treatment, Wegener’s granulomatosis has to be considered. An atypical clinical picture, inconclusive histologic, radiologic and laboratory findings warrant the need for close collaboration of various specialists. This is particularly important since state-of-the-art therapy of Wegener’s granulomatosis promises a favourable prognosis.]

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[POST-CHOLECYSTECTOMY SYNDROME AND SPHINCTER OF ODDI DYSFUNCTION]

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[After cholecystectomy, recurrent biliary-like pain, alone or in association with a transient increase in liver enzymes may be the clinical manifestation of the sphincter of Oddi dysfunction (SOD). Most of the clinical information concerning SOD refers to postcholecystectomy patients who have been classified according to clinical presentation, laboratory results and endoscopic retrograde cholangio-pancreatography (ERCP) findings as: biliary type I, biliary type II, and biliary type III. The prevalence of SOD has been reported to vary from 9 to 11% in unselected patients having postcholecystectomy syndrome up to 68% in a selected group of patients without organic disorder and complaining of postcholecystectomy pain. Diagnostic work-up of postcholecystectomy patients for suspected SOD includes liver biochemistry and pancreatic enzyme levels plus negative findings of structural abnormalities. Usually this would include transabdominal ultrasound, gastroscopy and ERCP. Depending on the available resources, endoscopic ultrasound and magnetic resonance cholangiography may precede endoscopic retrograde cholangiopancreatography in specific clinical conditions. In SOD patients, the endoscopic sphincter of Oddi manometry is the gold-standard diagnostic method to evaluate the abnormal motor function of the sphincter of Oddi. Quantitative evaluation of bile transit with cholescintigraphy is valuable in the decision whether to perform sphincter of Oddi manometry or to treat. The standard treatment for SOD is sphincterotomy. In biliary type I patients, the indication for endoscopic sphincterotomy is straightforward without the need of additional investigations. Slow bile transit on cholescintigraphy in biliary type II patients is an indication to perform endoscopic sphincterotomy without sphincter of Oddi manometry. Positive Nardi or Debray evocative test in biliary type III patients is an indication to perform sphincter of Oddi manometry. Medical therapy with nitrosovasodilatators, Ca-channel blockers, theophyllin compounds, β2 receptor agonists and anticholinerg drugs can be useful in biliary type II and type III patients preceding endoscopic sphincterotomy. If medical therapy fails, one might proceed to perform ERCP and endoscopic sphincterotomy but only in patients with abnormal SO manometry results.]

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