[Indications for ERCP in acute pancreatitis].
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Biomedical subjects
Publications and source records attributed to R Nitsche.
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Forty radiolucent gallbladder stones from eight patients were fragmented in vitro by extracorporeal shockwave lithotripsy, using the electromagnetic lithotripter Lithostar Plus (Siemens) at five different energy levels. The stones were characterized by size, computed tomography (CT) density, and cholesterol content. The largest residual fragment was measured after every 20 to 100 shock waves. As expected, fewer shock waves were required to achieve fragmentation at higher energy levels. When stones of the same size were compared, there were remarkable differences in the number of shock waves required for fragmentation. These differences must originate in other properties of the stones than size and number. Two different modes of fragmentation were observed: in one group of stones small, flat fragments were chipped off at the beginning of fragmentation ('chipping mode'). These stones initially lost about 25% of their weight as small fragments (< 1 mm) before breaking centrally into some large fragments. In the other group stones initially lost only about 10% of their weight as small fragments (< 1 mm) at the beginning of fragmentation and early broke centrally into some large fragments ('breaking mode'). Stones showing the chipping mode were almost pure cholesterol stones (> 97%) and required significantly less shock waves than stones of the same size showing the breaking mode (cholesterol content, 64-94%). This mode of fragmentation could not be predicted by CT density.
A 39 year old man had been suffering from chronic bowel symptoms of changing intensity. At the age of 37 the diagnosis of nontropical sprue was made. After institution of a gluten free diet the patient improved, but soon diarrhea started again. In the examination of peripheral blood smear, bone marrow and small intestinal mucosal biopsies a dominant eosinophilia was found. Since several attacks of abdominal colics and finally an acute abdomen occurred, a laparotomy was indicated. This operative intervention showed a perforation of the intestine and tumors in the bowel wall as well as numerous lymphomas spread over the whole mesentery. The histological examination of both the small intestine resect and the lymphomas proved the diagnosis of a highly malignant Non Hodgkin lymphoma (middle and large cell pleomorphic T-cell lymphoma with transition into a large cell anaplastic lymphoma [ki-1 lymphoma]). The patient received a chemotherapy with COEP but died 4 weeks after the surgery.
During examination before surgical correction of pes valgus a 20-year-old man reported having 3-5 pasty, foul smelling diarrhoeic motions per day for the past 3 years. He was noted to have rather thick lips and Marfan-like body build. Erythrocyte sedimentation rate was 18/34 mm, serum activity of GOT 22.5 U/l, GPT 35.7 U/l. Faecal weight was increased to 640 g/d, fat content to 12 g/d. Serum levels of the carcinoembryonic antigen (2494 ng/ml; normal: < 2.5) and of calcitonin (1,619,760 pg/ml; normal < 100) were elevated. Gastroscopy, partial coloscopy, colon-contrast imaging, ultrasonography and computed tomography of the neck and abdomen, as well as magnetic nuclear imaging of the neck were all normal. But laparoscopy revealed the liver to be infiltrated by small whitish nodules which immunohistologically proved to be metastases of a C-cell carcinoma. Total thyroidectomy was performed and the diagnosis of a C-cell carcinoma of the thyroid confirmed intra-operatively. After the operation the diarrhoea was stopped with codeine (9 mg/d). In case of tumour progression, therapy with octreotide, a somatostatin analogue, will be carried out. The concomitant occurrence of C-cell carcinoma, Marfan-like body build, thick lips and skeletal changes is typical of multiple endocrine neoplasia type 2B, which is caused by a chromosomal defect.
An 18-year-old female patient was admitted with ascites, right upper abdominal tenderness and peripheral edema. Angiography showed complete occlusion of the vena cava inferior up to the level of the right atrium. By open heart surgery, masses of thrombotic material were pulled out of the v. cava inferior/vv. iliacae which histologically contained tumor cell populations consistent with a hepatocellular carcinoma. Celiacography showed a highly vascularized tumor in the right hepatic lobe. Histologically, it proved to be fibrolamellar subtype hepatocellular carcinoma.
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In a prospective study of 42 high-grade lymphomas which were categorized according to the Kiel classification, the clinical significance of immune genotyping was studied. Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements were investigated. In 33 cases the immune genotype confirmed the phenotype. In one case with equivocal phenotype a TCR beta-chain rearrangement proved the T-cell origin of the lymphoma. None of the cases showed a bigenotype. There were eight lymphomas with immunoglobulin and TCR beta-chain and gamma-chain genes in germline configuration, which were divided into a group of immature lymphomas and a group of lymphomas with a more mature phenotype. The immature lymphomas had widespread disease, rapid progression, and favorable prognosis after intensive chemotherapy. The group of T-cell and Ki-1 lymphomas with null-cell genotype was clinically heterogeneous. Three of four cases were secondary lymphomas after lymphomatoid papulosis, lymphomatoid granulomatosis, or Hodgkin's disease. All cases presented with extranodal involvement. Only one of these patients is in continuous remission. In conclusion, the lack of immunoglobulin and TCR beta-chain and gamma-chain gene rearrangements does not exclude the diagnosis of high-grade malignant lymphoma, especially in cases with unusual extranodal involvement. However, the DNA analysis identifies a null-cell genotype subset of high-grade lymphomas which may have clinical significance.
A postoperative T tube cholangiogram after cholecystectomy in a 62 year old patient showed two retained calculi of 14 mm diameter each. Endoscopic sphincterotomy was not possible because of previous Billroth II gastrectomy. The stones were disintegrated by electromagnetically generated extracorporeal shock waves. The T tube was replaced by a balloon catheter and the papilla of Vater was dilatated allowing passage of stone fragments. We conclude that retained bile duct stones can be removed without sphincterotomy or percutaneous extraction by extracorporeal shock wave lithotripsy and papillary dilatation. This method should be considered especially in patients with Billroth II gastrectomy.
To evaluate the physiological role of cholecystokinin (CCK) in humans, we studied the influence of the specific CCK receptor antagonist loxiglumide (CR 1505) on gallbladder contraction, pancreatic enzyme output, plasma CCK concentrations, mouth-to-cecum transit time (MCTT), stool weight, and fecal fat excretion. Infusion of CCK-8, producing CCK plasma levels of 10-12 pmol/l, decreased gallbladder volume to 21% of the initial volume (P less than 0.01) and increased bilirubin output 8- to 10-fold and pancreatic enzyme secretion 2- to 4-fold. Infusion of loxiglumide (10 mg.kg-1.h-1 iv) abolished CCK-8-stimulated enzyme and bilirubin output. Basal gallbladder volume increased 68% during loxiglumide infusion (P less than 0.001) and 137% (P less than 0.001) after 7 days of oral loxiglumide treatment (3 x 1.6 g/day). Gallbladder contraction and bilirubin output in response to the intraduodenal instillation of a liquid meal (382 kcal) was completely inhibited by loxiglumide; gallbladder volume even increased 45% postprandially during loxiglumide infusion (P less than 0.02) and 145% after long-term loxiglumide treatment (P less than 0.001). Meal-stimulated pancreatic enzyme output was diminished 46-53% after acute and 25-29% after chronic administration of loxiglumide. Meal-stimulated integrated plasma CCK-immunoreactive (CCK-ir) concentrations, determined by RIA, were 3.2-fold higher during loxiglumide infusion (P less than 0.02); plateau CCK levels were markedly elevated (10.1 +/- 1.4 vs. 3.7 +/- 0.5 pM). Plasma CCK-like bioactivity, measured by a sensitive bioassay, was identical to CCK-ir levels in the absence of loxiglumide; in the presence of loxiglumide, no circulating CCK-like bioactivity was detectable, indicating complete inhibition of plasma CCK. MCTT was augmented 24% (P less than 0.05). Oral treatment with loxiglumide increased stool weight 72% (P less than 0.01) and fecal fat excretion 186% (P less than 0.001). In conclusion, 1) meal-induced gallbladder contraction and fasting tone are primarily controlled by CCK; 2) the contribution of CCK to the intestinal phase of postprandial pancreatic enzyme secretion is 40-50%; 3) GI motility and absorption are partially controlled by CCK; and 4) postprandial CCK secretion is substantially augmented by loxiglumide via an unknown mechanism.
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Owing to the presence of hyperlipoproteinemia IIa, twelve patients without gallstones were treated daily with 20 mg, 40 mg and 80 mg of Lovastatin, each dose being administered for 4 weeks. At the conclusion of each 4-week treatment phase, bile was obtained from the fasting patient following injection of 5 micrograms ceruletid i.v. with the aid of a duodenal tube. The long nucleation time of bile was not shortened by the therapy. The bile cholesterol saturation index showed a decline with Lovastatin, which was particularly obvious in patients with an initially oversaturated bile. In contrast to other lipid-reducing agents (e.g. fibrates), Lovastatin does not lead to increased lithogenesis of the bile, but may in certain circumstances have an prophylactic effect against the formation of gallstones.
We characterized the effect of the specific cholecystokinin (CCK) receptor antagonist loxiglumide (CR 1505) on gallbladder contraction, pancreatic enzyme output and plasma CCK concentrations determined by radioimmunoassay and bioassay. Gallbladder emptying and bilirubin output in response to the intraduodenal administration of a mixed liquid meal were completely inhibited by an intravenous infusion of loxiglumide (10 mg/kg/h). In contrast, meal-stimulated pancreatic enzyme secretion was diminished by only 30-40%. CCK concentrations in response to the test meal were 3-fold higher during infusion of loxiglumide, as determined by radioimmunoassay. In the absence of the antagonist, the bioassay measured CCK plasma levels identical to those determined by radioimmunoassay. In the presence of loxiglumide, CCK-like bioactivity was not detectable, indicating that the plasma concentrations of the CCK receptor antagonist were sufficient to abolish all circulating CCK-like bioactivity. We conclude that fasting volume and meal-induced contraction of the gallbladder are controlled by CCK. Postprandial pancreatic enzyme secretion, however, is mainly mediated by non-CCK-dependent mechanisms. Plasma CCK-like immunoreactivity is increased by loxiglumide, whereas plasma CCK-like bioactivity is zero in the presence of an CCK-receptor antagonist.
Over the last seven years self-inflicted diarrhoea was diagnosed in seven patients with chronic diarrhoea which was deliberately induced by the secret intake of laxatives. Six of the patients were female, four of them in paramedical occupations. All also had loss of weight and hypokalaemia between 2.1 and 2.9 mmol/l. All had accepted extensive and interventional procedures during a mean of five hospital admissions, with minimal pathological findings and no aetiological diagnosis. They had undergone numerous therapeutic measures, in one instance even several operations and parenteral feedings. Making the correct diagnosis was decisively impeded and delayed by the patients' seeming cooperativeness. In four patients the diagnosis was finally made by demonstrating laxatives in the urine, in two others by finding hidden tablets in the room, in one by demonstrating melanosis of the colon. A factitious cause of chronic diarrhoea should be excluded if no other cause can be established.
A boy aged 15 years developed Ménétrier's disease with considerably elevated gastrointestinal protein loss. During treatment with ranitidine the gastric mucosa and the protein loss were normalized within 3 years. This therapy is being continued since 6 1/2 years meanwhile. A long-term treatment of Ménétrier's disease with ranitidine should, therefore, be tried in other cases.
Young and senescent rats (3 and 28-30 months old) were subjected to complete ischemia at 37 degrees C in order to study function and structure of mitochondria isolated from liver, heart muscle, and brain. The rates of energy-coupled respiration and ATP synthesis were found to decrease progressively in relation to time of ischemia. The respiratory rates in the absence of ADP (state 4 respiration) did not increase after exposure to ischemia, suggesting that ischemia primarily affects electron transport rather than the energy coupling system. Mitochondria of heart muscle were more affected by ischemia than mitochondria of brain and liver. Liver and heart muscle mitochondria obtained from young rats were found to be slightly more sensitive to short periods of ischemia than those isolated from senescent animals.
ST segment monitoring by Holter ECG was conducted in 80 consecutive patients 2-4 weeks before aortocoronary bypass surgery and three weeks and six months after surgery. Preoperatively, all patients were under maximal medical therapy. In 31 out of 80 patients medical therapy could be stopped and thus 24-h ST monitoring could also be conducted without medication. Preoperative and early postoperative (three weeks) examinations were performed under hospital conditions. At 6 months after surgery the patients were monitored at home during their everyday activities. Twenty-eight per cent of patients waiting for aortocoronary bypass surgery under full medication showed transient ischaemic episodes in 24-h Holter ECG. Seventy-eight per cent of these episodes were asymptomatic. Without medication, 55% of patients had transient ischaemia. The exercise ECG data partly predicted the Holter ECG data. Patients with ST segment depression greater than 0.1 mV during exercise ECG had on Holter monitoring more and longer lasting ischaemic episodes than those with ST segment depression less than or equal to 0.1 mV. In patients with asymptomatic ST segment depression during exercise ECG the relation of silent episodes to symptomatic episodes on Holter monitoring was 5.3:1 while in patients with symptomatic ST segment depression during exercise ECG this relation was 2.3:1. Three weeks after operation the informative value of the Holter ECG was very restricted due to changes in the resting ECG caused by the operation and because patients do not exert themselves much at this time. Six months after surgery, Holter ECG is more informative, especially when conducted at home.(ABSTRACT TRUNCATED AT 250 WORDS)
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