[Treatment of acute gastrointestinal pain.]. / Die Behandlung akuter gastrointestinaler Schmerzen.

Abdominal pain is an important and the most frequent symptom of acute gastrointestinal diseases; crucial hints on the diagnosis can be gleaned from its location and from associated symptoms and signs. As symptomatic therapy the treatment of pain plays a major role in acute gastrointestinal diseases, e.g. the acute abdomen, acute pancreatitis, biliary colic, peptic ulcer disease and diverticulitis. Acute pain arising from peptic ulcer disease is effectively treated with the H(+)-, K(+)-ATPase inhibitor omeprazole or one of the H(2)-receptor antagonists. While moderate to severe pain caused by these conditions can be effectively treated by intravenous administration of nonopioid analgesic drugs, supplemented by butylscopolamine in a biliary colic, more severe pain or inadequate responsiveness to nonopioid analgesic drugs requires the intravenous administration of a highly potent opioid. Acute severe pain arising from biliary colic and acute pancreatitis should be treated with an opioid that does not influence the sphincter of Oddi or the pressure in the common bile duct, e.g. buprenorphine, nalbuphine or tramadol. An effective but not widely known therapy for colic pain is parenteral administration of a nonsteroidal anti-inflammatory drug, e.g. indomethacin or diclofenac.

[Spontaneous intramural hematoma of the intestinal wall--an unusual hemorrhagic manifestation of hemophilia A]. / Spontane Einblutung in die Darmwand--eine seltene Blutungsmanifestation der Hämophilie A.

Gastrointestinal bleeding is a well known event in patients suffering from blood dyscrasias. In contrast spontaneous nontraumatic hematoma of the bowel is a rare complication, requiring a different therapeutic management, which depends on localization and extent of the hematoma. We report about two hemophiliac patients presenting with acute abdominal pain caused by spontaneous intramural hematomas.

Hypokalemic rhabdomyolysis associated with Bartter's syndrome.

Severe potassium deficiency is an uncommon cause of rhabdomyolysis. We recently treated a 45-year-old patient with myalgia, serious generalized weakness, increased serum creatine kinase and myoglobin level as well as excessive hypokalemia. Histological examination of deltoid muscle biopsy showed rhabdomyolysis. After complete recovery of muscle damage by potassium substitution Bartter's syndrome proved to be the cause of initial and persistent hypokalemia.

Triacylglycerol biosynthesis in human small intestinal mucosa. Acyl-CoA: monoglyceride acyltransferase.

Acyl-CoA: monoglyceride acyltransferase (MGAT; EC 2.3.1.22) has been studied in human small intestinal mucosa by means of a spectrophotometric method based on the detection of liberated CoA employing 5,5'-dithiobis-(2-nitrobenzoic acid). With optimal assay conditions available the pH optimum was spread between 7.0 and 7.7 with a maximum at a pH of 7.4. Dependent on its concentration one of the substrates, palmitoyl-CoA, caused severe inhibition which was largely prevented by the addition of albumin. Using palmitoyl-CoA and 1-monooleoylglycerol as substrates specific activities were 23.0 +/- 8.4 in total homogenates compared with 92.9 +/- 28.3 nmol CoA released/min/mg protein in microsomal fractions from jejunal mucosa. Concerning the substrate specificity, a broad acyl-donor pattern exists with maximal activities for C10:0 to C16:0, the highest for C16:0. A preferential esterification of acyl-acceptors was shown for 2-monoacylglycerols as compared with the 1-isomers, and for monoacylglycerols with unsaturated versus saturated fatty acids. MGAT was mainly localized in the microsomal fraction. The properties of MGAT from human small intestine are discussed with respect to the intestinal enzyme from other species.

[Unexpected metabolic acidosis in severe lye poisoning (author's transl)]. / Unerwartete metabolische Azidose bei schwerer Lauge-Intoxikation.

A woman 38 years of age suffering from severe peroral lye intoxication, without shock, developed prolonged metabolic acidosis lasting for 8 days despite substitution therapy. Metabolic acidosis was caused by lactic acid. The increased lactic acid production in the marginal regions of the corroded upper digestive tract as well as the impaired lactate removal by the injured liver were most probably responsible for this lactic acidosis.

Unexpected metabolic acidosis in severe lye poisoning.

Prolonged metabolic acidosis developed in a 38-year-old patient suffering from severe peroral liquid lye poisoning without shock syndrome. Metabolic acidosis was caused by lactic acid. The combination of increased lactic acid production in the marginal regions of the necrotic intestinal areas and impaired lactate removal by the liver were most probably responsible for this lactic acidosis.

Studies on long chain fatty acid:CoA ligase from human small intestine.

Long chain fatty acid:CoA ligase (EC 6.2.1.3.) was examined in human small intestinal mucosa using the hydroxamate-trapping method. With optimal assay requirements using palmitate as substrate a significant difference of specific activities could be detected in the total homogenate from duodenum, 40.9 +/- 11.6 nmol/min per mg protein versus upper jejunum, 51.9 +/- 13.7 (P less than 0.05). The enzyme activity of the microsomal fraction of upper jejunum was 101.8 +/- 44 nmol/min per mg protein. ATP, CoA, and Mg2+ were essential constituents of the reaction. A broad pH-optimum was observed between 6.75 and 7.75 with a maximum at a pH of 7.25. Whereas palmitate in the presence of albumin revealed a wide range of optimal concentration in supporting maximal enzyme activity, oleate was found to strongly inhibit the reaction. Where substrate specificity with both the total homogenate and the microsomal fraction was concerned, maximal reaction rates were obtained with palmitate for the long chain saturated fatty acids C12:0' C14:0' C16:0' and C18:0' and with oleate for the long chain unsaturated fatty acids C18:1 C18:2' and C18:3' respectively. The highest specific activity of the enzyme was localised in the microsomal fraction. The kinetic data and properties of the long chain fatty acid: CoA ligase from human intestine are discussed with respect to the intestinal enzyme from other species.

[Local myocardial necrosis and cardiac tamponade due to a central venous catheter (author's transl)]. / Herzwandnekrose und Herzbeuteltamponade als Folge eines zentralen Venenkatheters.

A case of a paraventricular brain abscess, which favourably responded to conservative intensive therapy, is reported. A central venous catheter was the cause of myocardial necrosis leading to cardiac tamponade. In an attempt to tap the effusion, the partly necrotic cardiac wall was perforated. Only by recognition of the danger, by intensive clinical observation of a patient and by regular checkup of the catheter tip were the fatal complications following central venous catheterization avoided.

[Zinc deficiency syndrome during long-term parenteral nutrition in a patient with Crohn's disease and cirrhosis of the liver. Casuistry and zinc-pharmacokinetic (author's transl)]. / Zinkmangelsyndrom während kompletter parenteraler Langzeiternährung bei Morbus Crohn und Lebercirrhose Kasuistik und Zink-Pharmakokinetik.

A 29 year old patient with Crohn's disease and posthepatitic HBsAg-positive cirrhosis developed zinc deficiency in the course of complete parenteral nutrition. Zinc deficiency was proven by a low plasma zinc level of 12 microgram/dl. The daily input of zinc was 0.5 mg as calculated from the zinc concentration of infusion solutions used in parenteral nutrition during 3 1/2 months of treatment. The clinical picutre was that of acrodermatitis enteropathica. Cirrhosis of the liver and Crohn's disease were contributory causes of zinc deficiency. 6 bolus injections of 12-36 mg of zinc (total amount 144 mg) were given during 13 days. The plasma zinc level increased to 60-80 microgram/dl. 52% of the total amount of zinc injected were excreted by urine. The plasma half-life times of zinc were independent from basic zinc concentrations and averaged 1.55 +/- 0.22 h. It is concluded that severe signs of zinc deficiency will develop during parenteral nutrition in the presence of conditions leading to a negative zinc balance. In the case of long-term complete parenteral nutrition zinc should be substituted from the beginning of the treatment on.

[Acute leukemia in multiple myeloma: case histories, a review of the literature and assessment of the incidence]. / Akute Leukämie bei multiplem Myelom: Kasuistik, Literaturübersicht, Inzidenzschätzung.

The results of a follow-up study of 112 patients with multiple myeloma are presented. Three of these patients developed acute leukaemia during the respective period of clinical observation (maximum: 11 years)--one case of acute myeloblastic leukaemia, myelomonocytic leukaemia and erythroleukaemia, respectively. For estimating the incidence of acute leukaemia in the presence of multiple myeloma an extended life table method was applied. On the basis of our data this method gave a probability of 5.9% for a patient to develop acute leukaemia at any time after the diagnosis of multiple myeloma. In a statistical discussion this result is considered to confirm the assumption of a highly increased AL-risk in patients with multiple myeloma. In a survey of the literature some important data of 100 cases with the association acute leukaemia--multiple myeloma are reported.

Uptake and metabolism of long chain fatty acids in isolated chicken intestinal epithelial cells.

The uptake and metabolism of long chain fatty acids in isolated mucosal cells from chicken small intestine are studied. The viability of the isolated enterocytes is proven by linear oxygen consumption, CO2 and lactate formation form glucose and the active transport of glucose. The transport of palmitic and oleic acid is mediated by passive diffusion. This is demonstrated by the following results: (1) no saturation kinetics in the concentration range of 0.1--10.0 mM; (2) no competitive inhibition of the uptake by structurally related compounds; (3) no influence of 2,4-DNP and cyanide of the uptake; (4) the uptake is independent of sodium ions. Uptake rates of palmitic and oleic acid from suspensions are significantly higher than from the corresponding fatty acid-bovine serum albumin complexes. In both cases the uptake of palmitic acid proceeds faster than the uptake of oleic acid. Palmitic acid is oxidized to CO2 and incorporated into glycerides by enterocytes. Glucose serves as a glyceride-glycerol precursor. Its addition decreases the oxidation of the fatty acids and enhances glyceride synthesis markedly. Free glycerol is phosphorylated by enterocytes and can also serve as a glyceride-glycerol precursor.

[Angiokeratoma corporis diffusum (Fabry's disease). Biochemical diagnosis in plasma]. / Angiokeratoma corporis diffusum (Morbus Fabry) Biochemische Diagnostik im Blutphasma

In a 35-year-old man with the full picture of Fabry's disease there was an almost fourfold increase of trihexosylceramide concentration in plasma and a decrease in the alpha-galactosidase activity to 13 percent as compared with the values from a control group. Using the same biochemical methods it could be shown that two nephews of the patient are hemizygote carriers and that two sisters and the mother of the patient are heterozygote carriers. Causative treatment of the disease is unknown. In this patient the attacks of pain could be permanently improved with phenytoin and carbamazepin.