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 10-year-old boy was admitted with complaints of fever, pallor, fatigue and skin bleeds of 10 days duration and diagnosed as very severe aplastic anemia. He was given intensive immunosuppressive therapy but showed no response to therapy. He later evolved into acute myeloid leukemia. The occurrence of AML is reviewed and possible pathogenesis is discussed.
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PMID:Acute myeloid leukemia after intensive immunosuppressive therapy in aplastic anemia. 1620 56

A 29-year-old woman presented to the emergency department with exhaustion, fatigue, and abdominal pain. She reported having received a diagnosis of bulimia nervosa 10 years before. On examination, she had a marked pallor and was severely malnourished. Laboratory analysis revealed a dramatically low hemoglobin level of 1.7 g/dL (ref: 11.5-15.8 g/dL). Serum iron was quantified as 1.4 micromol/L (ref: 7-26 micromol/L), ferritin as 5 ng/mL (ref: 10-120 ng/mL), and the level of serum transferrin as 212 mg/dL (ref: 200-360 mg/dL). A duodenal biopsy revealed villous atrophy in the mucosal layer indicative for celiac disease. This diagnosis was confirmed by serum levels of endomysial antibodies, tissue transglutaminase antibody, and antigliadin antibodies. The newly diagnosed gluten-sensitive enteropathy is likely to be in part responsible for the severe symptoms reported. The extent of hemoglobin decline in combination with an astonishing lack of critical symptoms seen in this patient is a rarity. We conclude that anorectic patients with severe anemia and malnutrition should be evaluated for the presence of additional somatic conditions.
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PMID:Very severe iron-deficiency anemia in a patient with celiac disease and bulimia nervosa: a case report. 1629 20

Space motion sickness is experienced by 60% to 80% of space travelers during their first 2 to 3 days in microgravity and by a similar proportion during their first few days after return to Earth. Space motion sickness symptoms are similar to those in other forms of motion sickness; they include: pallor, increased body warmth, cold sweating, malaise, loss of appetite, nausea, fatigue, vomiting, and anorexia. These are important because they may affect the operational performance of astronauts. Two hypotheses have been proposed to explain space motion sickness: the fluid shift hypothesis and the sensory conflict hypothesis. The fluid shift hypothesis suggests that space motion sickness results from the cranial shifting of body fluids resulting from the loss of hydrostatic pressure gradients in the lower body when entering microgravity. The cranial fluid shifts lead to visible puffiness in the face, and are thought to increase the intracranial pressure, the cerebrospinal-fluid pressure or the inner ear fluid pressures, altering the response properties of the vestibular receptors and inducing space motion sickness. The sensory conflict hypothesis suggests that loss of tilt-related otolith signals upon entry into microgravity causes a conflict between actual and anticipated signals from sense organs subserving spatial orientation. Such sensory conflicts are thought to induce motion sickness in other environments. Space motion sickness is usually treated using pharmaceuticals, most of which have undesirable side effects. Further studies elucidating the underlying mechanism for space motion sickness may be required for developing new treatments.
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PMID:Space motion sickness: incidence, etiology, and countermeasures. 1693 70

Plummer-Vinson or Paterson-Kelly syndrome presents as a classical triad of dysphagia, iron-deficiency anemia and esophageal webs. Exact data about epidemiology of the syndrome are not available; the syndrome is extremely rare. Most of the patients are white middle-aged women, in the fourth to seventh decade of life but the syndrome has also been described in children and adolescents. The dysphagia is usually painless and intermittent or progressive over years, limited to solids and sometimes associated with weight loss. Symptoms resulting from anemia (weakness, pallor, fatigue, tachycardia) may dominate the clinical picture. Additional features are glossitis, angular cheilitis and koilonychia. Enlargement of the spleen and thyroid may also be observed. One of the most important clinical aspects of Plummer-Vinson syndrome is the association with upper alimentary tract cancers. Etiopathogenesis of Plummer-Vinson syndrome is unknown. The most important possible etiological factor is iron deficiency. Other possible factors include malnutrition, genetic predisposition or autoimmune processes. Plummer-Vinson syndrome can be treated effectively with iron supplementation and mechanical dilation. In case of significant obstruction of the esophageal lumen by esophageal web and persistent dysphagia despite iron supplementation, rupture and dilation of the web are necessary. Since Plummer-Vinson syndrome is associated with an increased risk of squamous cell carcinoma of the pharynx and the esophagus, the patients should be followed closely.
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PMID:Plummer-Vinson syndrome. 1697 5

A 6-year-old boy was hospitalized because of dark feces and facial pallor of 1 weeks duration. Other gastrointestinal symptoms, including vomiting and abdominal pain, were absent, but he felt dizziness when standing and fatigue on effort. Hematologic studies revealed iron-deficiency anemia, and endoscopy showed gastric erosions and a duodenal ulcer. All test results for Helicobacter pylori infection, including H. pylori antigen in stool, anti-H. pylori IgG immunoassay in serum, and the (13)C-urea breath test, were positive. Because an H. pylori-associated gastric ulcer had been diagnosed with endoscopy in the patients father 3 years earlier, father-son transmission was suspected. The patient was treated with triple-agent eradication therapy (proton pump inhibitor [lansoprazol], amoxicillin, and clarithromycin) for 2 weeks. One month after therapy was completed, eradication of H. pylori was confirmed by negative results on the stool antigen test. Peptic ulcer disease can occur in young children, as in this case. The stool antigen test kit is a useful and reliable method that can be used even in preschool children to diagnose H. pylori infection.
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PMID:Helicobacter pylori infection with a duodenal ulcer in a 6-year-old boy. 1710 82

The iron deficiency is the first cause of anaemia. In healthy young adult, anemia is well tolerated because of its progressive installation. The most common symptoms of anemia are pallor, fatigue and dyspnea. In biological exams, anemia is classically associated with microcytosis and hypochromia. The origins of microcytic anemia are iron deficiency, inflammatory aetiologies, thalassemia and sideroblastic anaemia. The iron-deficiency diagnosis includes two explorations: biological and clinical. The biological exploration is based on interpretation of serum biologics tests as blood iron, ferritin, transferrin with saturation, total iron-binding capacity and its soluble receptors. This interpretation is simple if it is not associated with clinical disorders influencing the internal iron cycle. The clinical exploration must always be followed by a careful assessment of the underlying cause as blood loss. The most common causes in women of reproductive age are gynaecologic. In men and menopausal women, the gastrointestinal tract bleeding is source of anemia. Therapeutic management of anemia is oral iron therapy. Etiological diagnostic of microcytosis is essential before iron therapy. If not, the treatment could be inefficient or it could mask or delay the etiological diagnostic.
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PMID:[Iron deficiency anaemia: clinical presentation, biological diagnosis and management]. 1749 37

If an abscess is not able to establish drainage through the skin surface or into the oral cavity, it may spread diffusely through fascial planes of the neck's soft tissue. Once the infection descends into the submandibular space, it may extend to the lateral pharyngeal space, and then to the retro-pharyngeal space. From here, it may reach the thyroid gland. The authors here describe a case of submandibular phlegmon derived from a periapical abscess of inferior premolar, which has reached the thyroid gland. The damage caused to the gland resulted in the release of a conspicuous quantity of thyroid hormones, thus causing a thyrotoxic pattern: temperature, cutaneous pallor, excessive perspiration, tremor, tiredness, weight loss, increased appetite, and tachycardia. Additionally, the gland's edema caused dysphagia and dysphonia commonly seen with thyroid gland enlargement. After dental drainage and appropriate anti-inflammatory and antibiotic therapy, administration of oral beta-blockers and corticosteroid therapy were performed to counteract thyrotoxicosis in order to prevent recurrences. Finally, a root canal was performed once the thyrotoxicosis had been resolved.
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PMID:Acute thyroiditis of odontogenic origin. 1793 25

A 62-year-old man presented with fatigue, pallor and mild weight loss. Laboratory studies showed Hb 7.6 g/dl, Hct 21.8%, WBC 108x10(9)/1, PLT 143x10(9)/1. At morphological examination, circulating cells appeared as 60% blasts and 40% lymphocytes, with smudge cells. A bone marrow aspirate showed infiltration by blasts (50%) and lymphocytes (40%); alpha-naphtyl-acetate esterase was positive in 90% of blasts, while myeloperoxidase was positive in 10%. The immunologic phenotype of blasts was characterized by the co-expression of CD13, CD33, CD14, CD4, CD15, CD64, CD117, HLA-DR, CD11b. Lymphocytes were characterized by a B-CLL immunophenotype: CD19+, CD5+, CD23+, CD20+(dim), FMC7+(dim), K light chain+(dim). Karyotype was normal and PCR assays for AML-ETO, CBFbeta-MYH11, PML-RARalpha, BCR-ABL and bcl-1/JH translocation were negative. Coexistence of CLL and AML with monoblastic features was diagnosed. Simultaneous appearance of CLL and AML has rarely been described and represents a peculiar biological phenomenon.
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PMID:Association of B-chronic lymphocytic leukemia and acute myeloid leukemia. 1798 6

The aim of this study is to assess clinico-pathological parameters and find out the correlation between them and their possible prognostic value. We made a retrospective analysis of a group of 468 patients with gastric adenocarcinoma which were operated in the 3rd Surgical Clinic--Cluj Napoca--01.01.1998-31.12.2003. The median age was 62 years. Patients in pTNM 0 stage were significantly younger than the rest of patients, with an average of 7.5 years. The male/female ratio was 1.7:1, this ratio being significantly higher in cases with proximal gastric cancers. There was not found any significant correlation between the interval : onset of symptoms and surgery, and pTNM stage. The most frequent signs and symptoms were epigastric pain, weight loss, indigestion, fatigue, pallor and loss of appetite, each of them were found in more than 40% patients. Multivariate analysis of symptoms showed that weight loss (p=0.00638) was independently correlated to advanced pTNM stages. The number of signs and symptoms was significantly correlated to advanced pTNM stages (p=0.000026). This significant group of patients studied has maintained characteristics encountered in populations with higher incidence of gastric adenocarcinoma, men being more frequently affected, distal localization and intestinal histologic type being encountered more frequently.
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PMID:[Clinical aspects with prognostic value in gastric cancer--analysis of 468 cases with gastric adenocarcinoma]. 1845 96

Hypersensitivity to inulin (polyfructan) is a rare event; two cases of food allergy and some patients presenting with allergy and hypersensitivity after inulin infusion have been reported. An 11-year-old boy suffering from severe immunoglobulin (Ig)A nephropathy (IgAN) experienced both anaphylactic reaction and concomitant relapse of his nephropathy following inulin infusion, used for measuring glomerular filtration rate (GFR) 2 years after the appearance of his initial symptoms. Pruritus, wheezing and cough were observed during a first renal function test; results of prick and intradermal tests were negative for inulin. The patient presented with pallor, asthenia and oliguria when a second inulin infusion was performed under dexchlorpheniramine, leading to the immediate cessation of the infusion. He was readmitted 2 days later because of fatigue and nausea related to acute renal failure. A drug-induced acute interstitial nephritis was first suspected. However, due to the presence of macroscopic haematuria and proteinuria, a renal biopsy was performed and showed acute proliferative relapse of IgAN. The underlying mechanism of inulin hypersensitivity is not well known. We can hypothesize that inulin had activated the innate immune system. Inulin may, thus, have been the initiating event of the renal relapse, acting like an infection, in a patient with IgA-mediated immunological dysregulation.
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PMID:'Renal hypersensitivity' to inulin and IgA nephropathy. 1853 47


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