Acute suppression of albumin synthesis in systemic inflammatory disease: an individually graded response of rat hepatocytes.

The effects of an inflammatory insult on albumin of the rat liver were investigated at the cellular level and were correlated with serum albumin concentration. After SC injection of turpentine, the livers were perfused and fixed in vivo; serial liver sections were stained using a streptavidin-ABC-immunoperoxidase technique with an antibody to rat albumin. Albumin and total protein were measured at intervals after turpentine injection in whole livers and in serum. Fibrinogen was determined in plasma only. Twenty-four hours after turpentine injection serum albumin had dropped by 25% and was at 50% of its initial value at Day 3. Serum fibrinogen increased 2.4-fold within 24 hr and decreased thereafter. Liver homogenates showed no significant changes in albumin concentration. Immunohistochemically, all hepatocytes stained positive for albumin in normal animals. During inflammation, the immunostainable albumin content vanished entirely in a majority of all hepatocytes while remaining unchanged in other cells, thus producing a strikingly patchy staining pattern. No signs of resumption of albumin accumulation in depleted hepatocytes were seen after 8 days, despite a clear trend towards normalization of serum albumin concentration. These results suggest that individual hepatocytes differ widely in their response to agents that suppress albumin synthesis in an acute-phase reaction.

[High incidence of unexplained hypoalbuminemia in an internal medicine practice]. / Hohe Inzidenz ungeklärter Hypalbuminämien in einem internistischen Krankengut.

The frequent observation of hypoalbuminemia in patients without hepatic disease or renal protein loss led us to compare different methods of direct and indirect serum albumin measurement. One hundred patients were randomly selected and analysed retrospectively and the serum albumin was related to clinical, hematological and biochemical parameters. 51Cr labeled albumin was injected intravenously in 6 healthy volunteers and 8 patients with hypoalbuminemia to obtain further information on the pathogenesis of hypoalbuminemia. The results obtained by the method using bromcresol purple were almost identical with those obtained by immunological methods. On the other hand, serum electrophoresis gave results that were a mean 14% higher than those with the method using bromcresol purple. Nearly half of the patients selected randomly, generally without signs of liver disease or renal protein loss, were hypoalbuminemic. There was no correlation with the age, sex, blood sedimentation rate, serum orosomucoid, hemoglobin, aminotransferase or the prothrombin time. 51Cr labeled albumin showed normal disappearance in four patients and an accelerated disappearance in another four patients. Hypoalbuminemia is a common finding in internal medicine which is underestimated in incidence and extent when serum electrophoresis is used. There is no correlation with the age and the hematological or chemical parameters measured. Both reduced synthesis and/or increased loss or catabolism are important factors in the pathogenesis of hypoalbuminemia.

Acute ischaemic colitis in a female long distance runner.

A 34 year old female long distance runner is reported with bloody diarrhoea. Colonoscopy revealed patchy haemorrhagic mucosal lesions throughout the colon. The most extensive lesions were found in the sigmoid colon. Histologic examination disclosed mucosal haemorrhage, dilated capillaries, patchy fibrosis and superficial erosions. Additional findings in this patient were haemorrhagic gastritis, microscopic haematuria and rhabdomyolysis. The only medication taken by the patient was oral contraceptives. We conclude that ischaemic colitis is one of the possible mechanisms leading to gastrointestinal blood loss in competitive runners.