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)

Two 6-month-old male infants with diarrhea, malabsorption, and hypoproteinemia, who were initially diagnosed as having combined immunodeficiency syndrome, recovered with intensive plasma therapy. Prior to the onset of diarrhea, they had normal serum protein and lymphocyte values. Immunologic features of combined immunodeficiency included lymphopenia, diminished B and T cells, cutaneous anergy, low immunoglobulin levels, and poor lymphocyte proliferative responses in vitro. Prior to therapy, both children had rectal ulcerations by proctosigmoidoscopy, colitis by rectal biopsy, and moderate to severe intestinal villus abnormalities by small bowel biopsy; plasma cells were absent Both had generalized malabsorption of all nutrients. Both infants were given irradiated fresh-frozen plasma for one to two months at 11 to 20 ml/kg/day to replace intestinal protein losses. During this time, diarrhea slowed, biopsy morphology improved, and immunoglobulin levels and T-cell function became normal. After discontinuance of plasma therapy, normal immune function and a normal stool pattern with reversal of malabsorption continued. Since intensive plasma therapy may have contributed to the reversal of the immunodeficiency state, a trial of such therapy is recommended in similar patients.
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PMID:Reversal of enterocolitis-associated combined immunodeficiency by plasma therapy. 698 21

An infant with allergic eosinophilic gastroenterocolitis is described. The patient presented with vomiting, diarrhea, gastrointestinal bleeding, and failure to thrive. Anemia, hypoproteinemia, and peripheral eosinophilia were also present. Gastrointestinal endoscopy revealed multiple mucosal ulcerations in the stomach, small intestine, and colon. Histological study of the affected areas showed infiltration of the mucosa by eosinophils, increased mucosal IgE plasma cells, and activated intraepithelial lymphocytes. Treatment with corticosteroids resulted in clinical and histological remission.
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PMID:Disseminated ulcerations in allergic eosinophilic gastroenterocolitis. 707 97

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

Juvenile polyps are generally considered to have no malignant potential. We report a 16-year old patients with juvenile polyposis coli who presented with diarrhea and hypoproteinemia. Some of her polyps had adenomatous histologic features and a large villoglandular polyp was present in the cecum. The usual nonoperative management of patients with juvenile polyposis may not be appropriate when the polyps show mixed histology. These patients are at risk to develop malignancy although the magnitude of risk is uncertain.
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PMID:Multiple adenomas in juvenile polyposis. 727 May 31

In 1956 we evaluated a patient who had a debilitating disease of a 2 yr duration, characterized by recurrent vomiting, diarrhea, cachexia, massive edema, hypoproteinemia, and dilated intestinal lymphatics. During our initial evaluation of this patient, we observed that 42% of her circulating protein pool was lost into her gastrointestinal tract daily, whereas normal gastrointesinal loss of protein does not exceed 1.6%. Her disease appeared to represent a classic example of intestinal lymphangiectasia. She was treated symptomatically for 13 yr with essentially no change. In 1969 the patient developed a stage IV diffuse, undifferentiated (non-Burkitt's) malignant lymphoma. Using immunoperoxidase staining, the neoplastic cells were found to contain cytoplasmic IgMKappa, suggesting that the lymphoma had a monoclonal B-cell origin. She was successfully treated with cyclophosphamide, vincristine, and prednisone. Shortly after the initiation of this systemic combination chemotherapy, her serum protein concentration returned to normal, her edema resolved, and she was cured of gastrointestinal symptoms. Moreover, repeat studies revealed that her protein loss had fallen to only 2%. The simultaneous cure of both the intestinal lymphangiectasia and lymphoma with combination chemotherapy suggests new relationships between these conditions as well as new possibilities for the treatment of acquired forms of intestinal lymphangiectasis associated with overwhelming gastrointestinal protein loss.
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PMID:Resolution of longstanding protein-losing enteropathy in a patient with intestinal lymphangiectasia after treatment for malignant lymphoma. 745 Apr 3

Following the Exxon Valdez oil spill, 347 oiled sea otters (Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.
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PMID:Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill. 748 8

Intestinal failure is a concept developed to define the situation wherein either severe primary gastrointestinal disease or a surgically induced short bowel syndrome exists and prevents an adequate oral intake of nutrients such that parenteral nutrition is required. Typically, because of disease associated problems, total parenteral nutrition is required in most cases of intestinal failure. The major cause of intestinal failure in both adults and children is surgical resection resulting in a short bowel syndrome. The clinical signs and symptoms of a short bowel syndrome include any combination of the following: intractable diarrhea, steatorrhea, failure to thrive, acidosis, dehydration, trace element deficiency syndromes, hypoproteinemia, hypovitaminosis, and anemia. It is often difficult to predict at the time of a bowel resection whether or not a short bowel syndrome will occur postoperatively. This is the case because any of a number of confounding problems such as (a) difficulty in precisely estimating the length of the remaining small bowel at the time of the operation, (b) the presence of disease in the residual small bowel that can produce further shortening or impair residual intestinal function, and (c) the presence or absence of the ileal cecal valve, which can be critical in determining the adaptability of the residual bowel.
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PMID:Intestinal failure and intestinal transplantation: new therapy for individuals sustaining large losses of bowel: a review. 759 82

Diarrhea is common in the acute care setting, particularly among critically ill patients. Factors that cause diarrhea are usually multifactorial; some of the most common include medications, hyperosmolar or rapidly delivered tube feedings, atrophy of intestinal epithelium or ischemic bowel, short bowel syndrome, pseudomembranous colitis, infection (Salmonella and Shigella species), opportunistic infections in patients with acquired immunodeficiency syndrome and severe hypoproteinemia. This article reviews different types and mechanisms of diarrhea commonly encountered in acute care. It includes current concepts of managing diarrhea, such as calculation of stool osmotic gap, identification of medications that cause diarrhea, modification of enteral therapy, and the use of antisecretory agents. Nursing responsibilities and contributions in the collaborative assessment and clinical management of diarrhea are also explored.
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PMID:Current concepts: management of diarrhea in acute care. 770 25

We describe a familial form of recurrent acute, life-threatening secretory diarrhea associated with distinctive jejunal histologic changes and IgG2 subclass deficiency. Symptoms begin abruptly with anorexia and vomiting, and progress within hours to massive secretory diarrhea and shock with profound neutropenia and hypoproteinemia, including hypoalbuminemia and hypogammaglobulinemia. Affected survivors recover quickly and thereafter grow and develop normally. Biopsy specimens obtained during remission from 3 adults and 11 children show club-shaped jejunal villi broadened by edema and histiocytes with imbibed fluid; the overlying intestinal epithelium and brush border appear normal, but the basement membrane is interrupted in some areas. No characteristic microorganisms have been identified in association with the syndrome. Clinical manifestations cease in the second decade, but the abnormal jejunal histologic pattern persists into adult life. Female and male patients are equally affected, although all fatal cases have been in female subjects. Inheritance appears dominant with variable penetrance: one family member without a history of diarrhea has characteristic biopsy findings and another appears to be an obligate carrier with normal biopsy findings. Affected individuals have a reduced serum concentration of IgG2. We believe that this familial enteropathy is a unique entity, not previously described.
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PMID:Familial enteropathy with villous edema and immunoglobulin G2 subclass deficiency. 862 57

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


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