Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
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Transferrin structure, metabolism and physiological functions (iron transport, activation of cellular growth, bacteriostatic effect) are described with reference to the last informations available from the literature. This analysis results in a better understanding of the mechanisms involved in its physiopathological variations. Decreased serum transferrin levels are the result of a reduction of the biosynthesis (hepatic deficiencies, malnutrition), or an increase of catabolism (acute, chronic and malignant infections), or an increase of intestinal or renal losses, or very infrequently genetic disorders. Increased serum transferrin levels are the result of either hyposiderosis or an oestrogenic impregnation. Alcoholism and diabetes are responsible of qualitative modifications of this protein.
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PMID:[Transferrin]. 265 5

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

Marked weight loss is the major nutritional defect in chronic pancreatitis. Inadequate food intake owing to recurrent or near continuous pain usually accounts for the initial 10 to 20 per cent of loss of body weight, which decreases again with the onset of diabetes and is often precipitous with the development of steatorrhea. Treatment of pain, control of diabetes, and intensive pancreatic replacement therapy for steatorrhea usually causes weight gain, but seldom to ideal weight. It appears that the patient's body weight gets set at a new "weight-stat." Although isolated abnormalities of small bowel function tests can be elicited and deficiencies of fat-soluble vitamins, calcium, zinc, selenium, and so forth may be demonstrated, these rarely lead to clinical syndromes, as with demonstrable low B12 uptake in some 10 to 15 per cent of patients. In the late stage of the disease and particularly in NATP, extreme protein-calorie malnutrition may occur, which may not be correctable even by hyperalimentation. Although the mortality of the disease was reportedly higher in areas of socioeconomic deprivation, it appears from recent studies in Switzerland and other developed countries that mortality during a 12-year period may be in the region of 50 per cent worldwide.
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PMID:Nutritional deficiencies in chronic pancreatitis. 268 Sep 66

We have discussed the relationship between systemic illness, infection, and lung disease. As we have seen, patients with a wide variety of disease states, including advanced age, diabetes mellitus, alcoholism, collagen vascular disease, cancer, heart failure, and organ transplantation are potentially at increased risk for pneumonia because of disease-related impairments in host defenses. In addition, two virtually ubiquitous conditions in hospitalized patients, malnutrition and therapeutic interventions (especially with common medications), frequently add to the risk of airway invasion by bacterial pathogens. Systemic illness not only makes lung infection more common, but may adversely affect outcome and resolution, as well as determine the clinical presentation of pneumonia. In one particular population, the intubated and mechanically ventilated patient, the risk of infection is particularly high, and nosocomial pneumonia is a major cause of mortality. To the extent that the host response itself leads to the symptoms and signs of infection, systemically ill individuals may have subtle clinical features when serious bacterial invasion is present. Many components of the host defense system can become abnormal with serious illness, but a common mechanism that ties many systemic diseases to pneumonia is an alteration in airway epithelial cell receptivity for bacteria, namely, bacterial adherence, a process that mediates airway colonization, the first pathogenetic step on the road to pneumonia. The impetus for understanding how serious illness promotes lung infection is that once these mechanisms are identified, potential preventative strategies to minimize infection risk in the individual with systemic disease may be developed. The relationship among systemic illness, the lung, and infection also exists in a different direction: infection of a systemic nature (the septic syndrome) can lead to disease in the lung (ARDS). We have described the features of the septic syndrome and identified how it may lead to lung injury, usually by indirect means, through activation of inflammatory mediators that are carried to the lung via the vasculature. Although it is frequently impossible to predict which specific patient with systemic sepsis will develop acute lung injury, the current state of knowledge does permit us to identify high-risk individuals. Surprisingly, clinical assessment rather than biochemical testing is the best predictor of the development of acute lung injury. Patients with severe injury, profound shock and multiple systemic insults are most prone to acute lung injury in the presence of systemic sepsis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Respiratory infections and acute lung injury in systemic illness. 268 63

Urinary and serum zinc levels were determined in 51 patients with chronic pancreatitis. Urinary zinc excretion in patients with chronic calcified pancreatitis (832 +/- 111 micrograms/day) (mean +/- SE) but not in noncalcified pancreatitis (684 +/- 65 micrograms/day) was significantly higher than in normal controls (418 +/- 46 micrograms/day). The urinary zinc excretion increased with deterioration of exocrine pancreatic function. Serum zinc levels in advanced pancreatitis (105.9 +/- 4.5 micrograms/100 ml) were significantly higher when compared to the pancreatitis with normal exocrine pancreatic function (91.6 +/- 3.0 micrograms/100 ml), but the difference was less pronounced than for urinary zinc excretion. This may be due to complicating diabetes, which usually lowers serum zinc. Serum zinc and urinary zinc excretion were low in a patient with chronic calcified pancreatitis complicated with a pulmonary abscess and hypoalbuminemia. In conclusion, urinary and serum zinc levels in chronic pancreatitis were increased as a result of exocrine pancreatic dysfunction. Association of diabetes may lower serum zinc, and associated malnutrition depresses both urinary and serum zinc levels.
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PMID:Urinary and serum zinc levels in chronic pancreatitis. 271 4

Eighty patients required surgical drainage of infections in the pleural space or lung during a four-year period (1984-1987). Thirty-nine patients had a history of heavy intravenous drug use and 28 of those not addicted to drugs were addicted to alcohol. Impaired immunity was believed to be present in 72 (90%) due to malnutrition (45 patients), acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (13), hepatic cirrhosis (1), diabetes (1), or multiple causes (12). Sixty-four patients had acute purulent empyema; 9, tuberculous empyema (often a mixed infection); 2, tuberculous pleural effusion with complications; 2, lung abscesses requiring open drainage; 2, chronic bronchopleural fistulae; and 1, empyema secondary to an esophageal perforation. Fifty-three (66%) were treated with tube thoracostomy only and 27 required additional procedures, including open drainage (19 patients), decortication (5), lung resection (2), chest wall resection (1), and parietal pericardiectomy (1). Overall mortality was high (30%); mortality had a strong correlation with malnutrition or immune deficiency. Very low serum albumin levels were common and were the most important single determinant of a fatal outcome: (table; see text) Other important determinants of mortality were: total lymphocytes less than 1000 (50% mortality); anergy to tests for delayed hypersensitivity (39% mortality); AIDS or AIDS-related complex (54% mortality). Analysis of the records of the 24 patients who died has led to the conclusion that despite the advanced disease present and the poor condition of most patients at least one third of the deaths could have been avoided if important errors in diagnosis and medical or surgical management could have been prevented.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malnutrition: an important determinant of fatal outcome in surgically treated pulmonary suppurative disease. 274 75

We studied community acquired pulmonary infections in general hospital. Forty-seven outpatients (group I) and 107 inpatients (group II) were analyzed respectively. The mean age of group I was 43.4 years old and that of group II was 57.4 years old. Significant underlying diseases were present in 45% of group I and 62% of group II. In group I, the underlying diseases were chronic respiratory diseases, and in group II, chronic respiratory diseases and other significant diseases such as diabetes mellitus, cardiovascular diseases, malnutrition or malignancy. All of group I and 81 cases of group II were pneumonia. Pleuritis with pneumonia (11), lung abscess or cavitary infection (11), and pyothorax (4) were included in group II. Etiologic organisms were determined in 48.6% of the cases in group I, and 44.0% in group II. Invasive methods such as transtracheal aspiration and percutaneous lung puncture aspiration were very useful for isolation of the pathogen. The pathogens isolated included H. influenzae (17), S. pneumoniae (10), M. pneumoniae (4), C. psittaci (4) in total cases. In group I, H. influenzae was mostly isolated and in group II, S. pneumoniae was mostly isolated and opportunistic pathogens were also isolated. The form of pneumococcal pneumonia was almost always focal pneumonia in this study. There were 8 fatalities (5.2%), all of which were very old or had other serious diseases.
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PMID:[Community acquired pulmonary infections in a general hospital]. 274 72

GH is secreted episodically. Its pattern is regulated by the interplay of a releasing and a release-inhibiting hormone of hypothalamic origin. Modulation occurs by metabolic factors (glucose, free fatty acids, ketone bodies, amino acids). Altered GH secretion has been observed in states of metabolic derangement such as diabetes mellitus, malnutrition and obesity. Further modulation occurs by extrahypothalamic CNS structures. In man--but not in animals, including subhuman primates--sleep has an important effect on GH secretion. A defective GH secretory pattern has been found to occur in several states of sleep disturbance, such as sleep deprivation, narcolepsy, severe psychosocial derangement, the apallic syndrome. Other CNS influences on GH secretion are related to stress, emotional changes and psychiatric disturbances. The exact mechanisms by which most of these influences are relayed to the GH secretory apparatus of the hypothalamus remain yet to be investigated.
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PMID:Hypothalamic control of GH secretion: pathophysiology and clinical implications. 285 44

The syndrome known as tropical diabetes seems to be distinct from the two main types common in developed countries. Major pancreatic exocrine disease may or may not be present, and within these two groups there are clinical and biochemical variants. For these conditions the term malnutrition-related diabetes has been proposed. Although malnutrition is a plausible unifying factor, there is a good case for retaining the term tropical diabetes until there is more information on clinical and biochemical features and on aetiology.
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PMID:Tropical or malnutrition-related diabetes: a real syndrome? 287 87

1028 (99%) of the 1038 inhabitants of the West African village of Agbave and a random sample of 353 (12.4%) of the population of 2850 in Kati, another West African village, were screened for diabetes. Also recorded were their anthropometric data, dietary habits, possession of antibodies to malaria, and serum IgG concentrations. About 85% of the study population consumed cassava root at least once a day. The mean (SD) capillary random blood glucose concentration was 5.1 (1.1) mmol/l in men and 5.1 (0.6) in women. The mean (SD) body mass index was 20.2 (1.8) in men and 20.7 (2.3) in women. The mean blood glucose was similar whether cassava was consumed once daily, more than once daily, or less than once daily. None of the 1381 subjects examined had diabetes. This finding suggests that a high carbohydrate/cassava intake (84% of a mean daily supply of 1916 calories) combined with a low protein consumption (8% of caloric supply) does not cause diabetes. This does not support the World Health Organisation hypothesis that malnutrition-related diabetes exists, at least not in this West African rural population.
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PMID:Absence of diabetes in a rural West African population with a high carbohydrate/cassava diet. 288 81


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