Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The benefits of parenteral feeding need no longer be emphasised. However, qualitative and quantitative food supplements raise a certain number of difficulties which should be better known. Infection is the most frequent complication. It may be avoided by strict aseptic precautions throughout parenteral feeding. Hypoglycemia is a major risk owing to the possible consequence. Hyperglycemia and its consequence of osmotic polyuria is more frequent and should be controlled to avoid loss of water and salt. Complications due to the use of lipid emulsions are exceptional when soya oil is used. Hypophosphoremia should be corrected by increasing phosphate intake. Hypocalcemia is common; it is often associated with hypoproteinemia and sometime a low calcium intake, vitamin D deficiency or a sudden increase in phosphate intake. Vitamin deficiencies, hypomagnesemia, and oligo-element deficiencies should be correcty by appropriate supplements.
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PMID:[Parenteral feeding. Prevention of complications in adults during exclusive mid-term parenteral feeding]. 19 99

Infection with Mycobacterium intracellulare serotype 10 was diagnosed in 2 rhesus monkeys (Macaca mulatta) in a closed colony of 90 animals. The clinicopathologic presentation in 1 animal with advanced disease was characterized by a precipitous weight loss, therapeutically unresponsive diarrhea, anemia, weakness, prostration, refractory tuberculin tests (using mammalian old tuberculin and M bovis purified protein derivative tuberculin), and disseminated granulomas in the lungs, spleen, liver, kidneys, lymph nodes, salivary glands, and intestines. The lamina propria throughout the large and small intestines was infiltrated with mycobacteria-laden macrophages. Severe hypoproteinemia, hypoalbuminemia, hypoglobulinemia, mild hypocalcemia, and edema were compatible with a malabsorption-like syndrome. The 2nd animal was clinically normal, but a weak positive tuberculin reaction to M bovis purified protein derivative at 72 hours necessitated euthanasia. This animal's disease was characterized by microgranulomas in the lungs, bronchial lymph nodes, liver, and pancreas, without involvement of the gastrointestinal tract. There was no evidence of M intracellulare infection in the remaining 88 animals in the colony, as determined by mycobacterial cultures of tracheobronchial washings, additional tuberculin testing, thoracic radiography, and mycobacterial culture of the drinking water. Tuberculin testing and thoracic radiographs of personnel working with the nonhuman primates were also negative. These cases were considered to be important because both animals were infected with the same serotype and because there has been an increasing number of isolations of this organism in human infections throughout Massachusetts. Drug-sensitivity testing revealed the organism to be sensitive to cycloserine and resistant to isoniazid, rifampin, ethambutol, streptomycin, kanamycin, and pyrazinamide.
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PMID:Nontuberculous mycobacterial infection attributable to Mycobacterium intracellulare serotype 10 in two rhesus monkeys. 717 60

Theileria lawrencei tick-derived stabilate infection of 8 cattle resulted in the development of panleukopenia and hypoproteinemia. In addition to these changes, T. parva infection caused mild normocytic, normochromic, non-responsive anemia at either of two dose rates. Disseminated intravascular coagulation, as indicate by positive protamine paracoagulation tests, prolonged prothrombin and partial thromboplastin times, and thrombocytopenia, developed in cattle infected with either of the Theileria spp., and was probably an important intermediary mechanism leading to death. Infection of calves with a high dose of T. parva stabilate resulted in more rapid onset of clinico-pathologic changes than did the low dose infection. Theileria lawrencei infection produced a severe, acute syndrome, the clinico-pathologic alterations of which varied in time of onset and severity between those of the T. parva high dose and low dose groups.
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PMID:A comparative study of the disease in cattle caused by Theileria parva or T. lawrencei: II. Hematology, clinical chemistry, coagulation studies and complement. 720 9

Infection of naive North American horses with 10(4) cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV), designated AHSV/4SP, AHSV/9PI, and AHSV/4PI, reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively. Distinct clinicopathologic and hemostatic abnormalities were associated with each form of disease. Hemostatic abnormalities included increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times. Hemostatic findings indicated activation of the coagulation and fibrinolytic systems with clotting factor consumption in acute and subacute cases of African horsesickness. Hematologic abnormalities in acute and subacute cases of African horsesickness included leukopenia, decreased platelet counts, elevated hematocrit, and increased erythrocyte counts and hemoglobin concentration. Leukopenia was characterized by lymphopenia, neutropenia, and a left shift. Increased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase, hypocalcemia, hypoalbuminemia, hypoproteinemia, and elevated creatinine, phosphorus, and total bilirubin levels were present in some but not all horses. Metabolic acidosis, indicated by decreased total bicarbonate and increased lactate and anion gap, was present in horses with the acute form of disease. Mild thrombocytopenia and leukopenia were occasionally associated with the febrile form of disease. These results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness.
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PMID:Clinical pathology and hemostatic abnormalities in experimental African horsesickness. 777 Oct 50

Findings are reported from a study conducted to determine the clinical features and outcome of shigellosis in young infants. The authors reviewed the hospital records of 159 infants of no greater than age 3 months and those of 159 children aged 1-10 years with shigellosis who were admitted to the Diarrhea Treatment Center in Dacca, Bangladesh. 82.8% of infants had a history of nonbloody diarrhea, 59.9% moderate or severe dehydration, 12% bacteremia, 32.7% fever, 1.9% abdominal tenderness, and 0% rectal prolapse. 42.7% of children had a history of nonbloody diarrhea, 32.1% moderate or severe dehydration, 5.0% bacteremia, 58.6% fever, 12.6% abdominal tenderness, and 8.3% rectal prolapse. Infections caused by Shigella boydii and Shigella sonnei were more common in infants, while Shigella dysenteriae type 1 infections were less common in infants than in older children. There was an equivalent proportion of Shigella flexneri infections in the two groups. Infants were twice as likely to die as older children. Only 17 infants were being exclusively breastfed at the onset of their illness. Multiple logistic regression analysis identified the independent predictors of death among infants to be gram-negative bacteremia, ileus, decreased bowel sound, hyponatremia, hypoproteinemia, and a lower number of erythrocytes detected on the microscopic examination of stool specimens. Diarrhea management algorithms which rely exclusively upon clinical findings of dysentery to diagnose and treat shigellosis are likely to be unreliable in this high-risk age group.
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PMID:Shigellosis in neonates and young infants. 802 64

A 2-year-old female Quarter Horse was evaluated for hind limb lameness, fever (40 degrees C [104 degrees F]), and lethargy of 2 weeks' duration. Hypoproteinemia characterized by hypoalbuminemia and hyperfibrinogenemia was detected. Abdominal ultrasonography revealed thickening of the right dorsal colon wall. Treatment was instituted for putative right dorsal coliis. Lameness evaluation localized signs of pain to the lumbar vertebrae or pelvis. Radiography performed with the horse standing and nuclear scintigraphy revealed no abnormalities. Ventrodorsal pelvic radiography revealed a focal area of bony lysis and proliferation involving the cranial portion of the pubic symphysis. Aspiration yielded purulent exudate containing Rhodococcus equi, which was susceptible to erythromycin. Treatment included surgical debridement of the abscess and oral administration of erythromycin and rifampin. The horse's hind limb lameness completely resolved within 20 days. Infections of the pubic symphysis should be considered when lameness localized to the pelvis is associated with fever and an inflammatory leukogram.
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PMID:Osteomyelitis of the pelvis caused by Rhodococcus equi in a two-year-old horse. 1268 88

When blood plasma proteins are depleted by bleeding, with return of washed red cells (plasmapheresis), it is possible to bring the dog to a steady state of low plasma protein in the circulation and a uniform plasma protein production on a basal diet. These dogs become test subjects by which the potency of various diet factors for plasma protein regeneration can be measured. Plant and grain proteins are quite well utilized to form new plasma protein in these test dogs but soy bean meal probably should be rated at the head of this list. It is utilized with unexpected promptness and favors the production of albumin in contrast to other plant proteins which distinctly favor globulin production. Long plasmapheresis periods on basal rations rich in grain proteins lower the resistance of these animals to infection. Spleen, brain, and stomach when fed with the basal diet in these test dogs show less favorable potency ratios-10.2, 11.8, and 13.6 respectively. This means the grams of tissue protein which must be fed to produce 1 gm. of new plasma protein. Fasting periods indicate that the dog can contribute only 4 to 6 gm. of plasma protein each week-an insignificant contribution presumably derived from the host's tissue proteins. Infection and intoxication disturb the plasma protein production of these standardized dogs and may reduce the output of plasma proteins to very low levels in spite of considerable food intake. There may be a very sharp drop in the plasma protein level during the first day of intoxication (Dog 33-324). Some of these observations may be of value in a study of clinical conditions associated with hypoproteinemia.
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PMID:BLOOD PLASMA PROTEIN REGENERATION CONTROLLED BY DIET : EFFECTS OF PLANT PROTEINS COMPARED WITH ANIMAL PROTEINS THE INFLUENCE OF FASTING AND INFECTION. 1987 Apr 72

Human liver tissue has been assayed to determine the amount of hemoglobin production factors in normal and abnormal states. Standardized dogs made anemic by blood removal have been used in this biological assay. Normal animal liver as control is rated as 100 per cent. Normal human liver tissue as compared with the normal animal control contains more of these hemoglobin production factors-a biological assay ratio of 120 to 160 per cent. Infections, acute and chronic, do not appear to modify these values, the concentration of hemoglobin-producing factors falling within the normal range. Pernicious anemia and aplastic anemia both show large liver stores of hemoglobin-producing factors-a biological assay ratio of 200 to 240 per cent. Therapy in pernicious anemia reduces these liver stores as new red cells are formed. Secondary anemia presents a low normal or subnormal liver store of hemoglobin-producing factors-an assay of 60 to 130 per cent. Hemochromatosis, erythroblastic anemia, and hemolytic icterus in spite of large iron deposits in the liver usually show a biological assay which is normal or close to normal. Polycythemia shows low reserve stores of hemoglobin-producing factors. Leukemias present a wide range of values discussed above. Hypoproteinemia almost always is associated with low reserve stores of hemoglobin-producing factors in the liver-biological assays of 60 to 80 per cent. Hypoproteinemia means a depletion of body protein reserve stores including the labile protein liver reserves-a strong indication that the prehemoglobin material (or globin) is related to these liver stores. Pregnancy, eclampsia, and lactation all may present subnormal liver stores of hemoglobin-producing factors. Exhaustion of protein stores lowers the barrier to infection and renders the liver very susceptible to many toxic substances. It should not be difficult to correct hypoproteinemia under these conditions and thus relieve the patient of a real hazard.
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PMID:HEMOGLOBIN PRODUCTION FACTORS IN THE HUMAN LIVER : ANEMIAS, HYPOPROTEINEMIA, CIRRHOSIS, PIGMENT ABNORMALITIES, AND PREGANCY. 1987 Dec 36