[Code guideline for gastroenterology--a practical guide].
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Biomedical subjects
Publications and source records attributed to U Rosien.
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Prospective payment systems using the diagnosis related groups (DRG) payment mechanism have been introduced in many countries all over the world. In June 2000 the Australian Refined Diagnosis Related Groups System (AR-DRG) was chosen as the model which will be introduced in 2003 as the control instrument for the hospital dependent public health system in Germany. Background and possible implications for gastroenterologists and hepatologists are discussed.
UNLABELLED: Most cystic lesions of the pancreas are pseudocysts caused by acute or chronic pancreatitis. Congenital cysts are rare and may occur in congenital syndromes like von Hippel-Lindau syndrome. Cystic tumors of the pancreas may be difficult to distinguish clinically; however, because of their malignant potential, in particular in cases of mucinous types, diagnostic verification is crucial. Hence, in all cases of cystic lesions of the pancreas, which are not a sequela of an etiological confirmed acute or chronic pancreatitis, a cystic neoplasm must be ruled out. Differential diagnosis may be difficult even with ultrasonography, computertomography, endoscopic retrograde cholangiopancreatography and serum analyses; endoscopic ultrasound, magnetic resonance tomography and analysis of the cyst content may be of particular value. The therapeutic approach for pseudocysts is now well established and guided by symptoms and complications. If a cystic neoplasm is suspected, surgical resection of the complete lesion is warranted. CONCLUSION: The most important differential diagnosis in all cystic lesions of the pancreas with atypical presentation includes a cystic neoplasm. Therefore complete resection is indicated whenever the suspicion cannot be ruled out.
In most cases pain in the right upper abdominal quadrant is of biliary origin. Diseases of the biliary system are often visualized by ultrasonography; however, a negative test does not rule out a biliary cause. Moreover, a number of several non-biliary diseases have to be considered. Patient history, physical examination and laboratory findings determine the further diagnostic approach and include radiologic (i.e. CT/scintigraphy) and/or endoscopic (upper GI endoscopy, ERCP) examinations. In difficult diagnostic situations specialized diagnostic tools may be indicated (e.g. manometry in suspected dysfunction sphincter of the Oddi.
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HISTORY: A 75-year-old woman who had undergone a hysterectomy with adnexectomy followed by radiotherapy for endometrial carcinoma complained of postprandial nausea with vomiting after eating solid foods and of cramp-like abdominal pain, but her appetite was good. She had lost 25 kg in weight over 13 months. EXAMINATION: Physical examination, laboratory tests, radiology and gastroscopy were unremarkable. Gastric scintigraphy showed abnormally prolonged emptying. TREATMENT AND COURSE: Nausea and vomiting stopped at once after erythromycin (a motilin agonist) had been administered. It was at first given intravenously after meals (50 mg three times daily for 5 days), then orally for 10 weeks (250 mg three times daily before meals). Subsequent examination revealed normal gastric emptying. The symptoms did not recur after erythromycin had been discontinued. CONCLUSION: Erythromycin is an effective drug against gastroparesis caused by radiotherapy, because it acts even when the enteric nerves are damaged.
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Hereditary fructose intolerance is a recessively-transmitted disorder of metabolism caused by deficiency of aldolase B in the liver, intestine and kidney, that responds favourably to an exclusion diet. The occurrence of fatal hepatorenal failure in a 16-year-old girl, who had received infusions of fructose and sorbitol during minor surgery, led us to suspect that she had suffered from hereditary fructose intolerance. Molecular analysis of leucocyte DNA obtained from her brother who had had a long-standing aversion to fruit and sugar, showed two previously unknown mutations in the aldolase B gene. An initiation codon mutation, M-1T, was inherited from the father, whereas Y203X, inherited from the mother, is a nonsense mutation that replaces a tyrosine codon by the ochre termination signal. The only source of genomic DNA from the index case was a fixed fragment of necrotic liver that had been obtained by needle aspiration postmortem and was embedded in paraffin wax. Analysis of aldolase B genes in this sample by procedures based on the polymerase chain reaction (PCR) confirmed the presence of both mutations in the proposita, the diagnosis of hereditary fructose intolerance, and the cause of death.
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