Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year-old female was well until few years ago when she was diagnosed as having Graves' disease. Methimazole (MMI) and Lugol's solution were prescribed. But 7 months later, she stopped taking them arbitrarily. Three months later, thirst and general fatigue appeared. Therefore insulin (60u/day) and MMI (30 mg/day) were administered and continued for 40 days. However no remarkable effect was brought about. She was then transferred to the radioisotope ward of Kumamoto Univ. Hospital and was treated with regular insulin only. Ten days later, she fell into thyroid storm associated with diabetic ketoacidosis and was transferred to our ward. We began to administer large volumes of transfusion, regular insulin, MMI, Lugol's solution, propranolol, hydrocortisone and digitalis. In 24 hours, ketoacidosis disappeared and she became alert. For hyperthyroidism, the dosage of MMI was increased to 60 approximately 45 mg/day and was continued for a month; however, her thyroid function did not normalize and agranulocytosis developed. MMI was discontinued, and she was treated with 131I. About a year later, she became euthyroid. Her diabetes mellitus was difficult to control during the hyperthyroid state but it was under good control with monocomponent lente insulin (36u/day) when the euthyroid state was resumed.
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PMID:[A case of thyroid storm associated with diabetic ketoacidosis (author's transl)]. 677 5

The aim of this study was to describe the clinical presentation and severity of the disease at onset in childhood during 1994. Based on the prospective national incidence registry, data were collected (using a modified version of the EURODIAB ACE questionnaire) from all diabetic children diagnosed during a full calendar year (1994). The ascertainment was 91%. Polyuria, polydipsia and weight loss were the most frequent clinical symptoms, but fatigue, abdominal pain and personality changes were also often reported. Almost one quarter of the children presented with diabetic ketoacidosis. There was no correlation between age, duration of symptoms, blood glucose levels and the severity of disease. The unacceptably high incidence of presentation ketoacidosis called for an urgent improvement of the diagnostic acumen of the physicians dealing with children.
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PMID:[Clinical diagnosis of childhood insulin dependent diabetes mellitus. Hungarian Epidemiological Group for Childhood Diabetes]. 902 72

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

We report a 43-year-old man who presented diabetic ketoacidosis 1 year after receiving kidney transplantation. He was a recipient of renal transplantation treated with metyl-prednisolone and tacrolimus regimen. The serum level of tacrolimus was 12.4 ng/ml, and he showed hyperphagia before a month of admission. A week before admission, he was aware of polydipsia, polyuria, and general fatigue. He visited our hospital and was found to have severe hyperglycemia (925 mg/dl), significant ketosis and mild metabolic acidosis (pH 7.341), although he had not been diagnosed as diabetes mellitus. He administrated in our hospital, and was treated with insulin for 5 weeks. He was not obese (BMI = 18.2 kg/m(2)) and had no family history of type 2 diabetes. He was finally treated with diet therapy alone. The 24 h urine C-peptide secretion on the third hospital day was low (8.4 microg per day). However, no autoantibodies against pancreatic islets were positive, and his insulin secretion was recovered at discharge suggesting that he was not type 1 diabetes. Although, tacrolimus has been reported to cause or worsen diabetes mellitus, the present case suggests that it could cause severe decrease in insulin secretion which leading to diabetic ketoacidosis in lean subject without previous history of diabetes mellitus.
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PMID:Sudden onset of diabetes with ketoacidosis in a patient treated with FK506/tacrolimus. 1187 16

Diabetic ketoacidosis is the most serious complication at the onset of type 1 diabetes mellitus (DM). In Germany, population-based data on its occurrence at DM onset are not yet available. In a population-based study in a North Rhine-Westphalian region, Germany, during 1993-95, data on the clinical presentation at type 1 DM onset were obtained from hospital records for 262 patients under 15 years of age (81% of eligible patients). Information on social status was obtained from 148 families by a standardized questionnaire. The most frequently reported symptoms were polyuria (93.9%), fatigue (64.2%) and weight loss (59.4%). Mean duration of symptoms was 3.5 weeks. At diagnosis 18.3% of the children presented impaired consciousness and 3.5% coma. Mean glucose level was 25.1 mmol/l. Severe ketoacidosis (pH < or = 7.2) was present in 16.0% of the children. Metabolic derangement was more severe in children under 5 years. Low social status was significantly associated with increased risk of severe ketoacidosis (OR = 3.54, 95% CI: 1.10-11.35). Frequency of ketoacidosis at DM onset needs to be reduced through increased public and medical awareness of the presenting characteristics of childhood DM.
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PMID:Clinical characteristics and predictors of severe ketoacidosis at onset of type 1 diabetes mellitus in children in a North Rhine-Westphalian region, Germany. 1238 11

Clinical and laboratory data of 165 newly diagnosed diabetic children at Chang Gung Children's Hospital in Taiwan from 1993 to 2003 were analyzed. The age distribution was categorized as 0-1 years: 19 (11.5%), 2-4 years: 39 (23.6%), 5-9 years: 61 (37%), and 10-16 years: 46 (27.9%); the incidence showed spring/winter peak and a mid-summer trough but not statistically significant (chi2= 1.86, p=0.61). The most common symptoms on presentation were polydipsia, weight loss, polyuria, and fatigue. Very young diabetic children had a higher incidence of having dyspnea at presentation (p=0.029) and had significantly lower levels of C-peptide (p=0.0086) and HbA1c (p=0.0025). The prevalences of GAD antibody and insulin autoantibodies were 67% and 49%, respectively. Children with severe diabetic ketoacidosis (DKA) were younger at diabetes onset (p=0.36, not to the statistical significance), had a higher incidence of preceding febrile illnesses (p=0.05), lower T4 and T3 levels (p=0.0008, 0.02), and higher white blood cell counts (p=0.03) than the mild group. In conclusion, diabetes in very young children is not rare and is more associated with more severe insulin deficiency. Young age at diabetes onset and preceding febrile illness may provoke severe DKA. High alertness is necessary for prompt diagnosis and management.
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PMID:Clinical features of type 1 diabetic children at initial diagnosis. 1562 64

This article, which is partly biographical and partly scientific, summarizes a life in academic medicine. It relates my progress from benchside to bedside and then to academic and research administration, and concludes with the teaching of human biology to college undergraduates. My experience as an intern (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the controls in human fuel metabolism. Circulating free fatty acids were then unknown, insulin could not be measured in biologic fluids, and beta-hydroxybutyric acid, which was difficult to measure, was considered by many a metabolic poison. The central role of insulin and the metabolism of free fatty acids, glycerol, glucose, lactate, and pyruvate, combined with indirect calorimetry, needed characterization in a near-steady state, namely prolonged starvation. This is the main topic of this chapter. Due to its use by brain, D-beta-hydroxybutyric acid not only has permitted man to survive prolonged starvation, but also may have therapeutic potential owing to its greater efficiency in providing cellular energy in ischemic states such as stroke, myocardial insufficiency, neonatal stress, genetic mitochondrial problems, and physical fatigue.
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PMID:Fuel metabolism in starvation. 1684 98

Lactate production under anaerobic conditions is indicative of human performance levels, fatigue, and hydration. Elevated lactate levels result from several medical conditions including congestive heart failure, hypoxia, and diabetic ketoacidosis. Real-time detection of lactate can therefore be useful for monitoring these medical conditions, posttrauma situations, and in evaluating the physical condition of a person engaged in strenuous activity. This paper represents a proof-of-concept demonstration of a lactate sensor based on surface-enhanced Raman spectroscopy (SERS). Furthermore, it points the direction toward a multianalyte sensing platform. A mixed decanethiol/mercaptohexanol partition layer is used herein to demonstrate SERS lactate sensing. The reversibility of the sensor surface is characterized by exposing it alternately to aqueous lactate solutions and buffer without lactate. The partitioning and departitioning time constants were both found to be approximately 30 s. In addition, physiological lactate levels (i.e., 6-240 mg/dL) were quantified in phosphate-buffered saline medium using multivariate analysis with a root-mean-square error of prediction of 39.6 mg/dL. Finally, reversibility was tested for sequential glucose and lactate exposures. Complete partitioning and departitioning of both analytes was demonstrated.
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PMID:Lactate and sequential lactate-glucose sensing using surface-enhanced Raman spectroscopy. 1768 22

Fulminant type 1 diabetes, classified as a subtype of nonautoimmune type 1 diabetes, may result in severe complications for both mother and fetus due to the sudden onset of diabetic ketoacidosis. Little is known about the clinical features of pregnancy with fulminant type 1 diabetes. We present a case of fulminant type 1 diabetes during pregnancy, along with a review of the published literature. A 31-year-old Japanese woman presented with sudden onset of nausea and vomiting at 36 weeks' gestation and was provisionally diagnosed with acute gastroenteritis. She was referred to us for investigation of exaggerated general fatigue and intrauterine fetal death. Based on blood and urinary examinations, she was diagnosed with diabetic ketoacidosis, caused by fulminant type 1 diabetes. Although her ketoacidosis was improved, insulin therapy was needed. Awareness of this disease can lead to prompt diagnosis and treatment and consequently, improved maternal and fetal prognosis.
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PMID:Fulminant type 1 diabetes during pregnancy: A case report and review of the literature. 1768 29

A 57-year-old man was admitted to our hospital complaining of general fatigue and appetite loss. The initial chest radiograph showed infiltration in the left upper lung field. Cefozopran was administered. Concomitant diabetic ketoacidosis was treated with hydration and rapid-acting insulin. However he was intubated and ventilated because of deteriorated respiratory condition and ketoacidosis on the 3rd hospital day. Urinary legionella antigen was detected the same day, therefore ciprofloxacin and imipenem were initiated. On the 4th hospital day, he developed acute renal failure and was treated with continuous hemodiafiltration. In addition, he developed adult respiratory distress syndrome on the 6th hospital day, therefore siveletat sodium was given. The patient gradually began to improve and was extubated on the 17th hospital day. After that he was transferred to the metabolic ward on the 24th hospital day for control of his diabetes mellitus. Despite the severe complications in his clinical course, including diabetic ketoacidosis, acute renal failure and ARDS, detection of Legionella pneumophila by a urinary antigen test, Gimenez stain and sputum culture made prompt and proper administration of antibiotics possible, finally yielding a desirable outcome.
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PMID:[A case of Legionella pneumonia with diabetic ketoacidosis rescued despite the development of acute renal failure and ARDS]. 1960 25


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