Protein-losing Gastroenteropathy Research Articles

著明な蛋白漏出をきたした薬剤起因性急性胃粘膜病変の1例

著明な蛋白漏出をきたした薬剤起因性急性胃粘膜病変の1例

Interaction of Ostertagia and Nematodirus species in sheep and the potential of serum fructosamine determination in monitoring gastrointestinal parasitism

Serum fructosamine concentration falls with an increase in plasma protein turnover. Since this increase is a feature of gastrointestinal parasite infection at all sites, a falling serum fructosamine level may be of general application in the interpretation of parasite-related events. The circulating fructosamine level was investigated in the lamb as an indicator of protein-losing gastroenteropathy associated with two parasites at different sites, Ostertagia circumcincta (abomasum) and Nematodirus spathiger (small intestine). Infection with 10,000 N spathiger infective larvae daily for seven weeks produced only slight clinical signs, and only a small change in serum fructosamine levels. 2500 O circumcincta L3 daily gave no clinical signs in most animals, but serum fructosamine was more strongly affected in this group. Concurrent infection with both organisms caused some degree of diarrhoea in all lambs, and a sustained fall in serum fructosamine, more accentuated than that observed in either of the single infection groups, supporting the value of serum fructosamine determination in monitoring gastrointestinal parasitism.

Diagnosis of protein-losing gastroenteropathy by 111In-transferrin scanning and fecal excretion test

Diagnosis of protein-losing gastroenteropathy by ¹¹¹In-transferrin scanning and fecal excretion test

A Rubella Epidemic in Sasebo, Japan in 1957, with Various Complications

Though the rubella vaccination programme for adolescent girls was introduced in Japan in 1977, rubella epidemics have occurred repeatedly. Also in Sasebo, Japan in 1987, we experienced various complications as follows: encephalitis (five cases), meningitis (three), thrombocytopenic purpura (four), vascular purpura (four), hemolytic anemia (two), pneumonia (eight), protein-losing gastroenteropathy (one), multiple organ disorder with encephalitis, purpura, myocarditis, hepatic and renal dysfunction (one), and congenital rubella syndrome (CRS: three). Disorders ranging over multiple organs seem to occur in acquired as well as congenital rubella infection. The incidence of encephalitis was estimated to be 1:1600 cases of rubella and two of five cases were apparently serious. Though the strategy for preventing rubella has been directed only against CRS, we should note the various and severe complications with acquired rubella infection, and should adopt two-stepped protection: vaccination of young children of both sexes and of adolescent girls.

A case of pyloric atresia associated with junctional epidermolysis bullosa

We describe an infant with congenital pyloric atresia associated with junctional epidermolysis bullosa, which is now recognized as an autosomal recessive syndrome. Laparotomy revealed a membrane in the pyloric antrum. Clinical manifestations included intractable diarrhoea and malnutrition due to protein-losing gastroenteropathy. A satisfactory nutritional state could not be obtained during the clinical course and the child died.

Late sequelae of gastric acid injury

The late sequelae of gastric acid injury follow a predictable pattern and often require operative correction. Pyloric and antral stenoses are the most commonly cited late complications of acid ingestion. Other late sequelae include intractable pain, achlorhydria, protein-losing gastroenteropathy, duodenal atonicity, radiographic abnormalities, mucosal metaplasia, and gastric carcinoma. Resection of the injured gastric segment appears to provide the most favorable long-term result. Diligent patient follow-up is required to ensure adequate restoration of gastrointestinal function and to correct late-appearing complications. The distinction between the expected sites of gastrointestinal injury in acid versus alkali ingestion has become less clear with the recent introduction of readily available concentrated liquid household alkaline products, and the incidence of late gastric sequelae of caustic injuries has increased accordingly.

Protein-Losing Gastroenteropathy and the Intestinal Clearance of Serum α1-Antitrypsin

Protein-losing gastroenteropathy, sometimes called exudative enteropathy, is a group of conditions in which hypoproteinemia results from excessive loss of plasma proteins via the gastrointestinal tract without proteinuria or decreased synthesis of plasma proteins. All plasma proteins can thus appear in the gastrointestinal tract, but hypoalbuminemia is the rule because of the long half-life of albumin.

Effect of non-steroidal anti-inflammatory agents on plasma protein concentration of ponies

The recent findings of oral phenylbutazone administration causing a protein-losing gastroenteropathy in ponies are described. Similar investigations in ponies using either meclofenamic acid or naproxen at the therapeutic dose for two weeks followed by a further week of treatment at twice this dose rate were carried out. Neither drug produced any adverse clinical signs. Although a decrease in total plasma protein occurred with meclofenamic acid, this was not associated with a protein-losing gastroenteropathy.

Erratum

The authors report a case of intestinal lymphangiectasia that was clearly demonstrated during abdominal lymphoscintigraphy using Tc-99m Sb colloid. Although lymphoscintigraphy has been used in many different clinical situations, this is, to our knowledge, the first scintigraphic description of this disease. Clinical and pathologic presentations of intestinal lymphangiectasia are briefly reviewed. Some possible approaches to the confirmation of the presence of a protein-losing gastroenteropathy are mentioned.

Cronkhite-Canada syndrome

A case study is presented of a 57-year-old male who showed typical clinical features of Cronkhite-Canada syndrome. Numerous polypoid lesions were found in the stomach, duodenum, ileum, colon and rectum accompanied with characteristic ectodermal changes. Tests indicated a protein-losing gastroenteropathy. Intestinal lactase deficiency was demonstrated by the lactose tolerance test. Scanning electronmicroscopy of the gastric and colonic mucosa revealed prominent secretion of mucoid substances and distortion in the gastric pits and colonic crypts. These abnormal findings were interpreted as having a direct relationship to the loss of protein into the gastrointestinal tract.

Intestinal lymphangiectasia complitated with protein-losing gastroenteropathy in a case of mitral regurgitation

Intestinal lymphangiectasia complitated with protein-losing gastroenteropathy in a case of mitral regurgitation

Lymphangiectasia of the small intestine: description and pathophysiology of the roentgenographic signs.

Waldmann in 1961 redefined primary protein-losing gastroenteropathy and renamed the condition "lymphangiectasia". This abnormality, usually seen in infancy, is characterized by enlargement of folds and signs of hypersecretion in the small bowel. Enlargement of folds occurs secondary to edema of the valvulvae conniventes and lymphatic dilatation. Hypersecretion may be the result of rupture of dilated lymphatics or transudation of protein across an intact capillary epithelium. The clinical, roentgenographic, and pathologic findings are described. The pathophysiology of this condition is discussed.

Experimental Protein-Losing Gastroenteropathy

The tissue fibrinolytic activity of intestinal mucosa was studied in rats with protein-losing gastroenteropathies experimentally produced by X-irradiation, 5-fluorouracil treatment, or ligation of the thoracic duct. The first two models showed an increase of fibrinolytic activity and of 131I-polyvinylpyrrolidone excretion and the third showed normal fibrinolysis. In addition, it was demonstrated that 131I-polyvinylpyrrolidone excretion in the first two groups was markedly reduced by injections of trans-4-aminomethyl cyclohexane carboxylic acid, a potent antiplasmin agent. This finding affords strong support to the authors' previous clinical observation that tissue fibrinolysis in the digestive mucosa plays an important role in the pathogenesis of protein-losing gastroenteropathy associated with diseases of the mucosa.

Ménétriers Disease

Serial morphological, secretory, and serological observations of a patient with Ménétrier's disease disclosed hypergastrinemia, antibodies to parietal cells and dietary substances, and an acute reduction of gastrointestinal protein loss after atropine administration. Transformation of the gastric mucosa from hypertrophy to atrophic gastritis was associated with disappearance of the protein-losing gastroenteropathy and serum antibodies and reduction of the serum gastrin concentration.

A new fiberintestinoscope type FIS-T1 patterned after intestinal biopsy tube.

A new type of fiberintestinoscope (FIS-T1) patterned after an intestinal biopsy tube was developed for observing the small intestine beyond the ligament of Treitz. The flexible part of the new FIS has been made as pliable as the Cantor tube or the Miller-Abbott tube so that the tip of the new FIS is carried on into the small intestine by peristaltic activity along its natural configuration. A balloon attached near the tip of the new FIS acted as a bolus, enabling peristaltic activity to carry the fiberscope to the distal portion. In order to facilitate the passage of the fiberscope, it was also advisable to keep changing the posture and position of the body with a minimum of fluoroscopic exposure. Inflation of the balloon as well as air feeding through the air channel of the fiberscope made possible satisfactory observation. In a patient suffering from protein-losing gastroenteropathy, multiple white spots on the diffuse rough surface of the mucosa were visualized by using the new FIS. Histological finding of the biopsy specimen taken from near the ligament of Treitz by using the fiberduodenoscope showed dilated lymph vessels in the villi.

Letter: Treatment of protein-losing gastroenteropathy.

Letter: Treatment of protein-losing gastroenteropathy.

Constrictive pericarditis, intestinal lymphangiectasia, and reversible immunologic deficiency

A patient with constrictive pericarditis, secondary intestinal lymphangiectasia, and protein-losing enteropathy was demonstrated to have the characteristic immunologic deficiency associated with intestinal lymphangiectasia: hypogammaglobulinemia, lymphocytopenia, cutaneous anergy, impaired allograft rejection. and diminished in vitro lymphocyte proliferative responses. Following surgical correction of the cardiac abnormality, the intestinal lymphangiectasia and protein-losing gastroenteropathy resolved and was accompanied by a slow but progressive return of normal immune function. This documented reversal of the immunologic deficiency in intestinal lymphangiectasia supports the concept that the immune defect in this syndrome is due to the excessive loss of lymphocytes and immunoglobulins into the gastrointestinal tract.

蛋白漏出性胃腸症におけるPlasminogen Tissue Activator

蛋白漏出性胃腸症におけるPlasminogen Tissue Activator

Impaired lymphocyte transformation in intestinal lymphangiectasia: evidence for at least two functionally distinct lymphocyte populations in man.

Intestinal lymphangiectasia is a disease characterized by hypoproteinemia and edema resulting from protein-losing gastroenteropathy secondary to abnormal intestinal lymphatics. Immunologic abnormalities associated with this disease include hypogammaglobulinemia, lymphocytopenia, skin anergy, and impaired allograft rejection. In the present study, the in vitro blastogenic transformation of lymphocytes from 12 patients with intestinal lymphangiectasia was assessed in order to gain insight into the mechanism of the cellular immune defect in this disease. Peripheral blood lymphocytes from patients with intestinal lymphagiectasia showed impaired in vitro transformation to nonspecific mitogens, specific antigens, and allogeneic cells when compared to equal numbers of cells from normal individuals. Patients with the most deficient in vitro reactivity tended to have the lowest serum albumin concentration and the lowest absolute lymphocyte count. Lymphocytes obtained from chylous effusions in each of the four patients studied transformed more vigorously than peripheral blood cells from the same patients. These results may be explained by the loss of recirculating, long-lived lymphocytes into the gastrointestinal tract, resulting in a relative depletion of the population of lymphocytes necessary for in vitro blast transformation. This disease thus represents a clinical analogue of animals with experimental thoracic duct drainage, and provides evidence for the existence, in man, of two functionally distinct lymphocyte populations. In addition, these findings establish a new mechanism of impaired delayed hypersensitivity and defective in vitro lymphocyte transformation, i.e. the gastrointestinal loss and consequent depletion of the long-lived, recirculating population of lymphocytes from the peripheral lymphocyte pool.

Allergic protein-losing gastroenteropathy: Report of an unusual case: Huntley, C. C., Bowers, G. W., and Vann, R. L.: Southern Med. J. 63: 917, 1970

Allergic protein-losing gastroenteropathy: Report of an unusual case: Huntley, C. C., Bowers, G. W., and Vann, R. L.: Southern Med. J. 63: 917, 1970