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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aetiology, pathogenesis, diagnosis and therapy of sepsis are dealt with in this paper. These problems are discussed on the basis of 151 patients treated for sepsis. The cases with monoinfection are 73.6% and those with polyinfection are 24.4%. Monoinfection is caused mainly by Staphylococci -65,3%, followed by E. coli - 15.2%, Proteus - 13% and Klebsiella - 3.3%. For the cases of polyinfection the gram-negative bacteria are 3:1 in respect to the gram-positive bacteria. The bacteriological finding from the haemoculture (92.8% mono- and 7.2% polyinfection) is not equal to this from the input source. Here also the cases of monoinfection are mainly caused by Staphylococci - 70.9%, followed by Proteus - 7.7%, E. coli - 6%, Klebsiella aerogenes - 5.1% and Streptococcus 2.6%. The gram-negative bacteria prevail in the cases of polyinfection. The virulent aggressive infection, bacteria resistant to antibiotics, the aggressive local infection, hypoproteinemia, anaemia, diabetes, a prolonged corticosteroid treatment and unsuitable antibiotic treatment are discussed as main factors predisposing to sepsis. All the 151 patients were treated with the complex therapy, recommended in this paper. It includes a surgical cleaning-up of the initial nidus, intensive reasonable antibiotic treatment against the gram-positive and gram-negative aerobes and anaerobes. Additionally, substitution of infusion therapy, parenteral nutrition, regulation of the pathophysiological deviations and stimulating therapy are carried out. 74.2% from the patients were cured, 25.8% died. 16.6% of the patients who died had sepsis caused by gram-positive bacteria, and 46.1% had sepsis caused by gram-negative bacteria. 17% of the patients who died had septicaemia and 22% had septicopyaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical problems of surgical infection. The Pirogov Institute for Emergency Medicine, Sofia]. 615 Jun 8

In order to investigate the influence of diabetes mellitus on immune complex-mediated nephritis , we produced Heymann nephritis in streptozotocin-induced diabetic rats (DM-HN group) in which the clinical course for 24 weeks and histological changes were examined. Nondiabetic rats with Heymann nephritis (HN group) and diabetic rats (DM group) were also examined as controls. The degree of proteinuria, hypoproteinemia, hyperlipidemia and anemia were more pronounced and the mortality rate was higher in the DM-HN group than in the HN group or in the DM group. Histologically, larger and more subepithelial or intramembranous electron-dense deposits as well as a more markedly thickened glomerular basement membrane (GBM) were observed in the DM-HN group than in the HN group. In conclusion, the nephrotic manifestations and histological changes in the GBM in Heymann nephritis were augmented by the association with diabetes mellitus.
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PMID:Autologous immune complex nephritis in streptozotocin-induced diabetic rats. 623 73

Review of the 55 reported cases of glucagon-producing tumors reveals that a distinctive clinical syndrome consisting of diabetes, a peculiar dermatitis termed necrolytic migratory erythema, weight loss and an increased tendency for thrombosis is associated with these neoplasms. Normochromic normocytic anemia, hypocholesterolemia, hypoproteinemia and generalized hypoaminoacidemia are frequent laboratory findings. Definitive diagnosis of a glucagonoma requires elevation of the fasting serum glucagon level. Selective arteriography of the pancreas has been the best method for localizing these neoplasms preoperatively, but the noninvasive technics of ultrasound and CAT scanning can also be helpful. When the tumor is benign, complete surgical excision can completely reverse all the clinical manifestations of the glucagonoma syndrome and result in lasting cure. Since, however, approximately three-fourths of these tumors are malignant, palliative therapy is frequently required. Cytoreductive surgery can decrease the amount of hormone-producing tissue and can improve or even temporarily reverse the clinical symptomatology. For disseminated disease, chemotherapy is necessary. The best results have been obtained with DTIC although streptozotocin has also been used.
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PMID:Clinical aspects of glucagon-producing islet cell tumors. 627 69

The undisturbed circulation of amniotic fluid is the result of an intact cooperation between three compartments: maternal organism, fetus and amniotic cavity. Impairment of one of these compartments can produce a pathological increase of amniotic fluid. This is possible by animal experiment through the way of producing a hypoproteinemia in the maternal organism, comparable with the situation of maternal EPH-gestosis. By increasing the intraamnial osmotic pressure after injection of hyperosmotic solution it is also possible to produce polyhydramnios in the animal experiment. This is corresponding to the clinical situation in maternal diabetes mellitus. In studies of pregnant rabbits, the analysis of ultrastructure of the amniotic epithelium showed some alterations which are compatible with secretory activity of the yolk-sac. The epithelium of the yolk-sac is comparable with the human chorion. The amniotic epithelium has only a function as a semipermeable membrane for the diffusion of amniotic fluid. Morphological examinations of the human placenta and the amniotic sac showed an increase of placental weight in cases of polyhydramnios. There was no increase, however, of the placental surface. Disturbances of circulation in the placental villi were not seen more frequently than in a control group. In cases of polyhydramnios there were more disturbances of villous maturation. The analysis of ultrastructure of the amniotic epithelium and the surface of the umbilical cord showed some possible ways for the increase of amniotic fluid volume.
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PMID:[Amniotic fluid circulation with special reference to hydramnios]. 635 36

Blood has a number of rheological properties which partially determine flow, especially at capillary level, and its capacity to deliver oxygen. It is non-Newtonian, pseudoplastic, thixotropic and viscoelastic. Viscosity can be studied with different types of viscosimeters (coaxial cylinder or capillary viscosimeters). It can be defined by the ratio of stress of deformation to rate of deformation. Viscosity depends on macrorheological parameters: hematocrit, serum proteins, especially fibrinogen and globulins, and also on microrheological parameters: degree of aggregation and red blood cell deformability. Viscosity rises when the temperature falls and decreases with the radius of the tube through which the blood flows (Fahraeus-Linqvist effects). Blood viscosity is studied clinically at different temperatures, and, above all, at different rates of deformation by carefully recording the hematocrit. Plasma viscosity, fibrinogen, albumia and immunoglobulin levels, the viscosity of blood cell suspensions in normal saline must also be taken into consideration. Special investigations (rheoscopy, filtrability) provide information about red cell aggregation and deformability. Hyperviscosity syndromes are observed with: --raised hematocrit (polycythemia and pseudopolycythemia), --conditions with raised serum proteins or changes in their composition (especially hyperfibrinogenemia, raised immunoglobulins, low albumin levels); inflammatory syndromes, dysglobulinemias (Fahey's syndrome of plasma hyperviscosity), --low temperature (hypothermia), --increased red cell aggregability (shock, fat embolism), --reduced red cell deformability due to various congenital and acquired conditions (sickle cell anemia, renal failure, hyperlipoproteinemia, thrombosis, diabetes). Conversely, hypoviscosity may occur with a low hematocrit, hypoproteinemia, hypofibrinogenemia, and hyperthermia. Increased viscosity results in a slowing of blood flow, stagnation of its constituents and in ischemia. Therapeutic interventions may be considered on the different components of the hyperviscosity syndrome: hemodilation, plasmapheresis, dispersion of aggregants, agents acting on red cell deformability.
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PMID:[Blood hyperviscosity syndromes. Classification and physiopathological understanding. Therapeutic deductions]. 636 7

The features of 41 proven or suspected cases of pancreatic glucagonoma and one possible case of renal glucagonoma have been reviewed. Glucagonoma is one form of islet cell neoplasm and involves pancreatic alpha cells. It may occur more frequently in women and is more likely to be malignant than insulinoma. Patients may present with glucose intolerance, an erythematous, eczematous dermatitis, glossitis, stomatitis, vaginitis and unexplained weight loss. Anemia, hypoproteinemia, hypoaminoacidemia and hypolipidemia may also be present. Malignant glucagonoma metastasizes frequently to liver. An evaluation for possible glucagonoma may be considered in a patient with the characteristic eczematous dermatitis, glossitis or stomatitis and glucose intolerance, an unusual or atypical history of diabetes mellitus, or hepatomegaly with other characteristics of glucagonoma. Initial evaluation may include measurement of fasting plasma glucagon concentration, and an oral glucose tolerance test with measurements of plasma glucose and glucagon levels. Extreme fasting hyperglucagonemia, and a paradoxical rise in plasma glucagon concentrations after glucose ingestion should strongly suggest the presence of glucagonoma. Radiographic demonstration of pancreatic glucagonoma is best carried out by celiac arteriography. Surgical excision of the tumor is the treatment of choice. Nonresectable lesions may respond to chemotherapy with streptozotocin. Treatment for the various dermatologic or metabolic complications of glucagonoma which include glucose intolerance, hypoproteinemia, hypocholesterolemia and anemia may not be satisfactory. Glucose intolerance is usually mild and may be adequately treated with dietary or insulin therapy. Rarely, glucagonoma with massive destruction of the pancreas or other factors may induce severe glucose intolerance. In contrast, the anemia, skin rash, and hypoproteinemia do not respond to conservative therapies tested thus far. Glucagonoma is a model for studying the importance of glucagon in causing the hyperglycemia of diabetes mellitus. Study of patients with glucagonoma does suggest that glucagon has some role in the etiology of hyperglycemia in diabetic states; however, as in studies on diabetes, investigations on glucagonoma do not demonstrate that glucagon has a primary role in producing severe glucose intolerance.
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PMID:Clinical and metabolic aspects of glucagonoma. 698 81

In 190 patients, we studied changes in intellectual status during perioperative period using Hasegawa's Dementia Scale (HDS-R), and analyzed preoperative, intraoperative, and postoperative risk factors. HDS-R is one of the most popular scoring tests for evaluating dementia or delirium. Risk factors impairing preoperative score were aging, and preoperative complications including cerebral vascular disease, old myocardial infarction, arrythmia, and diabetes mellitus. Risk factors impairing postoperative score were, in addition to above-mentioned factors, hypoproteinemia and postoperative stressful conditions such as prolonged fever, pain, bed rest, and naso-gastric tube. In the patients who showed postoperative score deterioration, the incidence of old myocardial infarction, hypertension, and postoperative stressful conditions was significantly greater. In the patients who showed postoperative score improvement, local anesthesia including epidural and spinal anesthesia was used more often. In conclusion, aging or preoperative complications such as cerebral vascular disease, old myocardial infarction, arrythmia, and diabetes mellitus are high risks for the development of postoperative dementia and delirium under general surgical procedures and general anesthesia. Intraoperative management with patients awake using local anesthesia and postoperative stress-less conditions are important to avoid postoperative dementia.
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PMID:[Changes in intellectual function during perioperative period evaluated by Hasegawa's Dementia Scale]. 769 25

A nine-year old girl with T cell acute lymphoblastic leukemia (ALL) had acute severe neurologic complications at the end of the remission-induction chemotherapy course. Thirty-six hours following triple intrathecal (IT) therapy and intravenous (IV) administration of L-asparaginase (L-asp), tetraplegia developed and she became unconscious. She had bouts of hypertension and persistent tachycardia unresponsive to digitalis therapy. Magnetic resonance imaging (MRI) showed multiple brain white matter hyperintensities and filling defects in the saggital sinus, suggesting thrombosis. Over the 40 days, in addition to her neurologic compromise she also had transient diabetes mellitus, severe hyperlipidemia, hypoproteinemia and edema, liver and heart failure and staphylococcus aureus sepsis with prolonged bone marrow depression. Despite, coexistence of all these chemotherapy related complications, her neurologic functions and multiple organ failure improved gradually. After a 70 days' period of interruption, chemotherapy was resumed and continued without any further complications. Although, the etiology of her extensive sensitivity to some drugs remains unclear, we believe that it is important to document these unusual events in this child.
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PMID:Coexistence of life threatening chemotherapy related leukoencephalopathy, saggital sinus thrombosis and multiple organ failure in a child with acute lymphoblastic leukemia: an unusual case with clinical recovery. 932 1

The therapeutic effect of probucol on hypercholesterolemia in cyclosporine A (CyA)-treated renal transplant patients was prospectively studied. Twelve posttransplantation patients aged 34.2+/-2.5 years with serum total cholesterol (t-CHL) of 250 mg/dL or greater, whose serum creatinine was 2.9 mg/dL or less, and who had no diabetes mellitus or hypoproteinemia, were treated with probucol, 250 mg twice daily for 3 months. Seventeen age-matched (36.8+/-1.6 years) normal volunteers served as control. Blood was drawn after at least a 12-hour fast to measure lipids in serum and lipoprotein fractions, apoproteins (apo), lipoprotein fractions, lethicin cholesterol acyl transferase (LCAT), free fatty acids (FFA), and CHL-ester. Serum t-CHL, triglycerides (TG), and phospholipids (PL) in posttransplantation patients before treatment were significantly higher compared with normal control subjects. Very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions in these patients were significantly expanded. The pretreatment levels of serum apo AII, B, CII, and CIII were significantly increased compared with those of normal controls. After treatment with probucol, serum t-CHL, LDL-CHL, high-density lipoprotein (HDL)-CHL, PL, LDL-PL, and apo AI were significantly decreased, and CHL-ester significantly increased compared with the pretreatment levels. These data suggest that although probucol causes a decrease in HDL-CHL, it may act anti-atherogenically by modulating HDL metabolism and stimulating reverse transfer of CHL from peripheral tissue.
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PMID:Effect of probucol on serum lipoprotein and apoprotein profiles in renal transplant patients. 946 11

We report herein the case of a 70-year-old woman with enteropathy accompanied by protein loss, the cause of which was found to be thrombophlebitis of the mesenteric vein. The patient was admitted to our hospital for investigations to determine the cause of hypoproteinemia. She had suffered an episode of left abdominal pain with high fever and vomiting lasting 10 days, 8 months prior to her admission. She also had a 6-year history of uncontrolled diabetes. The alpha1-antitrypsin clearance was 85.7 ml/day, suggesting protein-losing enteropathy. A scintigraphy with 99m-technetium-human serum albumin disclosed protein leakage into the intestine. X-Rays and computed tomography showed a stenotic and thickened area of small intestine 50 cm in length. Thus, a laparotomy was performed to resect this part of the intestine which was found to have undergone past thrombophlebitic changes. Following the operation, the alpha1-antitrypsin clearance decreased to within the normal range and the patient gained 5 kg in weight.
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PMID:Protein-losing enteropathy due to thrombophlebitis of the mesenteric vein: report of a case. 974 3


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