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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increase in the number of blood platelets to over 1,000,000/mm3 in elderly patients is generally considered secondary to a myeloproliferative or neoplastic disease. To report the case of an elderly woman hospitalized for extreme thrombocytosis associated with severe anaemia, who was found to be suffering from coeliac disease. The patient, aged 83 years, was hospitalized presenting with fatigue. Laboratory tests showed microcytic hypochromic anaemia (haemoglobin 4 g/dl) and extreme thrombocytosis (platelet count 1,400,000/mm3). Physical examination was normal, with the exception of marked thinness. There was no evidence of macroscopic bleeding from the gastrointestinal or genitourinary tracts. She had never suffered from gastrointestinal problems and had no family history of gastroenterological diseases. Oesophagogastroduodenoscopy and histology of the gastric and duodenal mucosa evidenced atrophic gastritis and an adenomatous polyp. The duodenal mucosa showed total villous atrophy, suggesting the diagnosis of coeliac disease. Antiendomysial IgA and anti-transglutaminase IgA antibodies were also positive. Colonoscopy was negative. An ultrasound examination of the abdomen was normal, and the spleen was within the normal range. A peripheral blood smear showed no alterations in erythrocyte morphology typical of hyposplenism due to coeliac disease. The platelet count decreased rapidly after blood transfusions, when both serum iron and ferritin levels were still below normal limits. Furthermore, we observed a significant inverse correlation between the platelet count and haemoglobin concentration (r = -0.94, P < 0.003). Platelet count and red blood cell count normalized after 2 months of a gluten-free diet; the haemoglobin concentration was also normal at this time. After 1 year of following a gluten-free diet, the patient remained well and had no complaints. There were no gastrointestinal disturbances. All haematological parameters were within normal limits. Intestinal biopsies showed normal villi and crypts without inflammatory infiltration of the lamina propria. This case shows that the association of haematological signs--extreme thrombocytosis and severe anaemia--considered in an elderly patient to be typical of myeloproliferative disorders or neoplastic conditions can be due to coeliac disease; thus, coeliac disease must also be considered among the possible diagnoses.
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PMID:Extreme thrombocytosis as a sign of coeliac disease in the elderly: case report. 1217 15

Type I gastric carcinoid tumors result from hypergastrinemia in 1%-7% of patients with pernicious anemia. We diagnosed pernicious anemia in a 48-year-old female patient with complaint of fatigue for three months. She had no gastrointestinal symptoms. Endoscopic examination ot the upper gastrointestinal tract revealed atrophic gastritis and a polypoid lesion in the corpus of 3-4 mm in size. Endoscopic polypectomy was performed. Histopathological examination of the specimen revealed positive chromogranin A and synaptophysin stainings compatible with the diagnosis of a carcinoid tumor. Serum gastrin level was increased, urinary 5-hydroxyindoleacetic acid was within the normal range. There was no other symptom, sign, or laboratory finding of a carcinoid syndrome in the patient. No metastasis was found with indium-111 octreotide scan, computed tomographies of abdomen and thorax. Type I gastric carcinoid tumors are only rarely solitary and patients with tumors < 1 cm in size may benefit from endoscopic polypectomy.
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PMID:Treatment of solitary gastric carcinoid tumor by endoscopic polypectomy in a patient with pernicious anemia. 1683 Mar 92

We report about a 27-year-old female with type I diabetes who was admitted with progressive fatigue and a sudden onset of icterus. As the underlying cause, we found pernicious anemia with hemolytic activity as part of polyglandular autoimmune syndrome (PAS) type II. Under vitamin B(12) substitution we saw a quick rise in hemoglobin and improvement of complaints. Type I diabetes is the most frequent component of PAS II, whereas pernicious anemia is a rather rare component; however, a latent form is seen in about 12% of patients with type I diabetes. Therapy for pernicious anemia consists of parenteral vitamin B(12) substitution. Because of an increased incidence of gastric cancer in chronic atrophic gastritis, endoscopic follow-ups of the chronic atrophic autoimmune gastritis seem to be recommended. Due to the diverse characteristic of PAS II, with development of additional components after years of latency, regular follow-up clinical examinations and lab work are mandatory to detect further need of hormone and vitamin replacement that may sometimes be substantial for survival.
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PMID:[Fatigue and icterus in a 27-year-old patient with diabetes mellitus type I]. 1696 70

A 27-year-old male, who had developed diabetes mellitus type 1 (DMT1) since the age of eighteen and alopecia areata universalis nine months later, attended the outpatient clinics complaining of general fatigue and shortness of breath. A Schilling test was indicative of pernicious anemia. Antigastric parietal cell (AGPA) and anti-intrinsic factor antibodies were positive, confirming diagnosis of pernicious anemia. Thyroid and Addison's disease were excluded. Gastroscopy revealed atrophic gastritis without any evidence of carcinoid tumors. The aim of this case, which, to our knowledge, is the first one to describe a correlation between diabetes mellitus Type 1 (DMT1), pernicious anaemia, and alopecia areata universalis, is to remind the clinician of the increased risk of pernicious anaemia and gastric carcinoids in DMT1 patients. Screening for AGPA followed by serum gastrin and vitamin B(12) levels constitute the most evidence-based diagnostic approach.
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PMID:Pernicious anemia in a patient with Type 1 diabetes mellitus and alopecia areata universalis. 1861 80

Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing beta cells and is characterised by the presence of insulitis and &and beta-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimoto's or Graves' disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA), 4 to 9% present with coeliac disease (CD), 0.5% have Addison's disease (AD), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimoto's thyroiditis), TSH receptor (for Graves' disease), parietal cell or intrinsic factor (for AIG /PA), tissue transglutaminase (for CD), and 21-hydroxylase (for AD). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimoto's hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves' hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.
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PMID:Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. 2000 14

Twenty cases of Dyphillobothrium pacificum (fish tapeworm) infections were prospectively studied to determine whether this tapeworm is associated with megaloblastic anemia, as commonly reported for D. latum infections. The most frequent symptoms were fatigue and mild abdominal pain, which were identified in approximately 66.6% of the 18 patients interviewed. Fourteen patients received treatment with niclosamide and all were cured. The other six patients spontaneously eliminated the tapeworms. One patient, who also had chronic diabetes and gastric atrophy, had low vitamin B12 levels and megaloblastic anemia. In all other patients, including three other patients with anemia, baseline vitamin B12 levels were in the reference range and did not significantly change when re-assessed three months later. Unlike D. latum, infection with D. pacificum is seldom associated with megaloblastic anemia or vitamin B12 deficit.
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PMID:Diphyllobothrium pacificum infection is seldom associated with megaloblastic anemia. 2298 55

We wish to highlight the unusual occurrence of gastric neuroendocrine cell hyperplasia and type I neuroendocrine tumours within three hyperplastic polyps. In all cases, the neuroendocrine component was present within and between the hyperplastic foveolar glands of the polyps and overall formed the minor part of the polyps. Two of the patients presented with epigastric pain and the other with fatigue from anaemia, and on endoscopy, all three were found to have superficially ulcerated gastric polyps in the body (cases 1 and 2) and fundus (case 3). Two of the cases had serologically proven autoimmune atrophic gastritis, while the third case had histological evidence of an atrophic gastritis, most likely also autoimmune in aetiology. Cases 1 and 3 had single hyperplastic polyps, while case 2 had three polyps. All polyps showed linear neuroendocrine cell hyperplasia within hyperplastic foveolar epithelium both at the surface and within deeper-situated glands. Neuroendocrine immunohistochemistry highlighted the neuroendocrine cell hyperplasia. The bulk of the neuroendocrine component was restricted to hyperplastic mucosa forming the polyps. Non-hyperplastic adjacent mucosa showed less prominent neuroendocrine cell hyperplasia. It is unclear whether the two pathologies occurred simultaneously or independently. The common feature and causal link is atrophic gastritis, which predisposed the gastric mucosa to the development of both neuroendocrine cell hyperplasia and tumours, and hyperplastic polyps.
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PMID:Gastric neuroendocrine cell hyperplasia and type 1 tumours occurring within gastric hyperplastic polyps. 2301 44

Clinical vignette: A 38-year-old man consults you in the GI clinic because of frequent episodes of epigastric pain, nausea, and tiredness. His blood count shows signs of mild iron deficiency anemia. Upper GI endoscopy was normal, but antral and corpus biopsy specimens show evidence of gastric atrophy and Helicobacter pylori infection. Colonoscopy and capsule endoscopy showed no evidence of lesions in the large or small bowel. He receives a standard one-week course eradication therapy consisting of a proton pump inhibitor (PPI), amoxicillin, and clarithromycin. His symptoms improve, but his infection persists and he remains mildly anemic. He asks you whether the infection must be eradicated, as he read on the Internet that it can cause stomach cancer. He is also concerned about the anemia.
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PMID:Iron deficiency and Helicobacter pylori-induced gastric cancer: too little, too bad. 2325 61

We present a case of a 50-year-old female patient with a history of depressive disorder and anaemia (attributed to menorrhagias). She was admitted to the cardiology department with symptoms of fatigue on moderate exertion for several months, with worsening in the month before hospitalisation. Echocardiography revealed a severe mitral stenosis of rheumatic aetiology. Laboratory tests showed microcytic and hypochromic anaemia, reduced iron stores and vitamin B12 levels, and positive serum antiparietal cells autoantibodies. Endoscopy showed focal areas of erythema in the stomach, corresponding histologically to chronic atrophic gastritis. In this context, two distinct clinical entities were diagnosed in the same patient: severe rheumatic mitral stenosis and autoimmune gastritis. The patient was started on vitamin B12 and iron supplementation and underwent surgical correction of the valvular disease. There was symptomatic improvement in her signs of fatigue.
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PMID:A case of rheumatic valvular heart disease and autoimmune gastritis. 2553 34

A case of autoimmune polyglandular syndrome (APS) is presented. A 45-year-old man was admitted due to fatigue, malaise and inappetence. He had a history of primary hypothyroidism and was on levothyroxine substitution therapy. One year before, he was diagnosed with normocytic anemia and vitamin B12 deficiency, which was treated with vitamin B12 substitution therapy. Physical examination revealed hypotension and marked hyperpigmentation. Laboratory testing showed hyponatremia, hyperkaliemia and severe normocytic anemia. Endocrinological evaluation disclosed low morning cortisol and increased adrenocorticotropic hormone levels. Hence, the diagnosis of Addison's disease was established. Additional laboratory workup showed positive parietal cell antibodies. However, his vitamin B12 levels were increased due to vitamin B12 supplementation therapy, which was initiated earlier. Gastroscopy and histopathology of gastric mucosa confirmed atrophic gastritis. Based on prior low serum vitamin B12 levels, positive parietal cell antibodies and atrophic gastritis, the patient was diagnosed with pernicious anemia. Hydrocortisone supplementation therapy was administered and titrated according to urinary-free cortisol levels. Electrolyte disbalance and red blood cell count were normalized. This case report demonstrates rather unique features of pernicious anemia in a patient with Addison's disease. It also highlights the link between type II and type III APS. Not only do they share the same etiological factors, but also overlap in pathophysiological and clinical characteristics. This case report favors older classification of APS, which consolidates all endocrine and other organ-specific autoimmune diseases into one category. This is important since it might help avoid pitfalls in the diagnosis and treatment of patients with APS.
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PMID:COEXISTENCE OF ADDISON'S DISEASE AND PERNICIOUS ANEMIA: IS THE NEW CLASSIFICATION OF AUTOIMMUNE POLYGLANDULAR SYNDROME APPROPRIATE? 2641 23


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