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)

Fifty-four elderly patients with thermoregulatory failure were evaluated retrospectively. The most commonly associated cause was underlying sepsis, which occurred in 78% of cases. Underlying conditions that increased the incidence of hypothermia were hypoproteinemia (50%), cachexia (30%), and neuroleptic medications (21%), most commonly thioridazine. Digoxin toxicity was a common finding (20% of all cases). One third of the patients developed hypothermia in warm months and half of them developed it while in the hospital. Patients who presented with hypothermia from out of the hospital had lower temperatures, were more bradycardic and hemoconcentrated, and died more rapidly than the in-hospital group. This could be explained by lower outside temperature or delay in diagnosis and treatment of the underlying disease. The overall mortality rate was extremely high (74%) in both groups. The mortality rate was not affected by age, sex, or degree of hypothermia. We conclude that thermo-regulatory failure in the elderly can occur in warm as well as cold environments or climates. The development of hypothermia in elderly patients should be promptly treated as sepsis unless proven otherwise, in light of the poor prognosis of this condition.
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PMID:Mortality in elderly patients with thermoregulatory failure. 274 25

Literature and original data are reported on a case of alpha-chain disease associated with small intestine lymphoma in a male patient aged 20. The disease manifested clinically with chronic diarrhea, malabsorption, hypoproteinemia, hypocalcemia, cachexia, discretely detected alpha-chain monomer. Morphologically, there was lymphoplasmacyte infiltration of the intestinal mucosal layer; capsule collagenization, clustering immunoblasts among microlymphocytes, a pronounced macrophagal reaction, intercellular crystalloid and lymph masses, follicular pattern disappearance, sites of cellular polymorphism revealed in an axillary lymph node. The latter finding evidenced for developing immunoblastic sarcoma.
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PMID:[Morphologic changes of the small intestine and lymph nodes in alpha-chain disease]. 314 43

A 6% incidence of nephrotic syndrome was noted in a colony of 400 Syrian hamsters (Mesocricetus auratus) over a period of 2 years. Clinical findings consisted of severe ascites and anasarca, anorexia, cachexia, and papular dermatitis. Serum and urine chemical analysis revealed proteinuria and hypoalbuminemia in all animals tested; hypoproteinemia and high concentrations of serum cholesterol, triglycerides, and creatinine were detected in some of the affected hamsters. Demodex aurati was detected in skin scrapings from 4 of 8 hamsters. Necropsy findings included subcutaneous edema, ascites, and hydrothorax, as well as atrophic kidneys and testes. Extensive deposits of type AA amyloid were detected histologically in kidney, liver, spleen, and adrenal gland; smaller deposits were found in thyroid gland and intestine. Other histologic findings included periodontitis and hyalinization of the small arteries of the testes.
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PMID:Nephrotic syndrome associated with renal amyloidosis in a colony of Syrian hamsters. 651 83

The toxicity of methotrexate and cyclophosphamide determined by LD50 was depressed in the early period of development of sarcoma Sa-180. In the late period of development of Sa-180 and in mice with leukemia L-1210 the toxicity was higher than in healthy mice. The growth of transplantable neoplasms leads to cachexia, hypoproteinemia and dysproteinemia.
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PMID:Acute toxicity of methotrexate and cyclophosphamide in mice inoculated with malignant neoplasms. 725 81

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

Simian immunodeficiency virus infection of macaques is a model for human immunodeficiency virus infection of humans. In vivo-titrated stocks of SIV are essential for the utilization of this model for vaccine development. The elicitation of anti-human cell antibodies by some vaccines prepared in human cells and the related protective effects of the vaccine produced in human cells suggest a need for new macaque-derived SIV stocks. Here we describe the titration and characterization of two stocks of SIVmac that were produced in primary rhesus macaque cells. The first virus is SIVmac251, isolated from tissues of macaque 251, and the second is a molecular clone designated as SIVmac239. A 50% rhesus monkey infectious dose (MID50) was titrated for each virus stock by intravenous inoculation. An additional five macaques were inoculated with 10 MID50 of the SIVmac251 stock and were followed for disease outcome. All five monkeys developed antigenemia by 14 days postchallenge. Two of the five monkeys developed strong anti-SIV humoral immunity, whereas three developed little or no humoral immunity. As has been observed previously, the rapidity of disease progression correlated with the lack of a strong antibody response. The three animals with low humoral immunity died within 7 months of challenge, with antigenemia, cachexia, hypoproteinemia, hypoalbuminemia, weight loss, and intractable diarrhea, while maintaining their circulating CD4 numbers. One animal died at 1.5 years of more typical simian AIDS.
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PMID:Titration and characterization of two rhesus-derived SIVmac challenge stocks. 819 74