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Query: UMLS:C1762617 (weakness)
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Adult cotton top marmosets made niacin deficient by long-term dietary deprivation, developed a syndrome characterized by anorexia, weight loss, weakness, diarrhea, dermatitis, enterocolitis and stomatitis. The stomatitis was highlighted by a necrotizing gingivitis and periodontitis and by an ulcerative and atrophic glossitis.
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PMID:Studies on the biology of the periodontium of marmosets. XIII. Histopathology of niacin deficiency stomatitis in the marmoset. 40 31

Sixteen multiparous Holstein cows were allotted randomly to four groups of four cows each. Cows in 1 and 2 were uninfected. Those in 3 received 60,000 and those in 4 received 120,000 Sarcocystis bovicanis sporocysts per os approximately 30 days before the expected onset of lactation to produce nonclinical and clinical infections in 3 and 4, respectively. Combined stresses of infection, parturition, lactation, and high ambient temperatures caused all infected cows to develop clinical illness. Clinical signs included fever, anemia, glossitis, myositis, nasal discharge, hypersalivation, anorexia, and hind limb weakness; two cows died and two others were killed in extremis. Six cows in 3 and 4 developed high Sarcocystis-specific immunoglobulin G1 antibody. Uninfected control cows had no clinical signs and no rising concentrations of antibody against Sarcocystis antigen. When lactation began, cows were milked twice daily, and milk production was recorded for 70 consecutive days. All sarcocystis-infected cows (3 and 4) decreased feed intake and milk production compared with uninfected controls. The Wisconsin Mastitis Test on milk production compared with uninfected controls. The Wisconsin Mastitis Test on milk samples at 1, 2, 4, 8, and 12 wk of lactation did not differ among groups.
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PMID:Effects of sarcocystosis on milk production of dairy cows. 640 75

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 16-year old girl presented with rapid onset of muscular weakness and a history of severe dysphagia, dysphonia and significant wasting. On examination, she was dystrophic (BMI 15.7) and had signs of myopathy. Laboratory findings confirmed myopathy (CPK 106.4 microkat/L (6384 IU/L), AST 2.86 microkat/L (171.6 IU/L), myoglobin 1582 microg/L). There was profound hypokalaemia (S-K 1.8 mmol/L) suggesting hypokalaemic paralysis. Diagnosis of distal renal tubular acidosis (dRTA) was based on combination of hyperchloremic metabolic acidosis, severe hypokalaemia, high urinary pH and positive value of urinary anion gap. There was evidence of other signs of renal tubular impairment (urinary beta-2-microglobulin 213 mg/L, glomerulotubular proteinuria 1.01g/24h). Autoimmune tests (rheumatoid factor, antinuclear antibodies, autoantibodies to Ro/SSA and La/SSB) together with symptoms of xerostomia with swallowing difficulties and atrophic glossitis suggested primary Sjogren's syndrome (SS) as the underlying cause of dRTA. The renal biopsy confirmed chronic tubulo-interstitial nephritis compatible with this diagnosis. Full recovery of muscle weakness and hypokalaemia and acidosis followed after potassium and alkali replacement therapy. Corticosteroids were administered with subsequent addition of cyclosporine A because of disease activity. In conclusion, primary SS is a rare diagnosis in childhood and adolescence and should be considered in patients presenting with hypokalaemic paralysis, as this might be due to dRTA, even in the absence of apparent sicca syndrome.
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PMID:Hypokalaemic Paralysis Revealing Sjogren's Syndrome in a 16-Year Old Girl. 1927 13

Megaloblastic anemias are a subgroup of macrocytic anemias, in which distinctive morphologic abnormalities occur in red cell precursors in bone marrow, namely megaloblastic erythropoiesis. Of the many causes of megaloblastic anemia, the most common are disorders resulting from cobalamin or folate deficiency. The clinical symptoms are weakness, fatigue, shortness of breath and neurologic abnormalities. The presence of oral signs and symptoms, including glossitis, angular cheilitis, recurrent oral ulcer, oral candidiasis, diffuse erythematous mucositis and pale oral mucosa offer the dentist an opportunity to participate in the diagnosis of this condition. Early diagnosis is important to prevent neurologic signs, which could be irreversible. The aim of this paper is to describe the oral changes in a patient with megaloblastic anemia caused by a dietary deficiency of cobalamin.
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PMID:Oral manifestations of vitamin B12 deficiency: a case report. 1974 65

A 67-year-old woman with chronic alcoholism was referred to our hospital with a 3-month history of progressive weakness in all four extremities and a 5-day history of hoarseness. On admission, she presented with glossitis and laryngitis. Neurological examination revealed weakness in all extremities and nerve conduction studies showed polyneuropathy. She was diagnosed with thiamine deficiency and administered intravenous multivitamins, including thiamine, pyridoxine and mecobalamin. Although the weakness in her extremities was ameliorated after treatment, her glossitis and laryngitis did not improve and psychosis subsequently occurred. After administration of nicotinamide, her psychosis and laryngitis dramatically improved. She was diagnosed with pellagra after detection of decreased serum levels of niacin and thiamine. Weakness may have been due to thiamine-deficient neuropathy or multiple vitamin deficiencies, as it improved with thiamine, pyridoxine and mecobalamin therapy. Because of lack of response to thiamine therapy, we concluded that the psychosis and laryngitis were caused by pellagra. Although stomatitis and glossitis in pellagra has been well documented, laryngitis and hoarseness appear to be very uncommon conditions. Differences in the turnover rates or energy requirements between the gastrointestinal tract and larynges may be a reason for the rarity of laryngeal involvement in pellagra. We should be vigilant to hoarseness, caused by laryngitis, which can be the predominant symptom in pellagra.
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PMID:Hoarseness in pellagra. 2150 51

A 39-year-old woman was admitted to our hospital with an eight-month history of dyspnea on exertion, weakness and increasing fatigue. She reported repeated episodes of menometrorrhagia and underwent a myomectomy. She is not a vegetarian. Her menstrual bleeding: 3-5 days per month. Two months ago, she complained of burning sensation of the tongue upon swallowing food and noted brittle nails. She tolerated soft foods. On physical examination, she was pale; her nails were very thin, fragile and somewhat concave. Her oral examination showed angular stomatitis, depapillated tongue and glossitis. The clinical diagnosis was anemia and dysphagia. Laboratory tests were: Hb: 7.0g/dL, MCV: 57.42fL, MCH: 15.82 pg; leukocytes: 4,980; reticulocytes: 2.18%, reticulocyte index: 0.1%, serum iron: 21ug/dl, total iron binding capacity (TIBC): 286, transferrin saturation: 7% and serum ferritin: 27ng/ml. The peripheral blood smear showed anisocytosis and hypochromic microcytic cells. Thevenon test was negative. Abdominal ultrasound: uterine myoma. A barium swallow X-ray showed a 2-mm linear filling defect between the 4th and 5th cervical vertebrae in the anteroposterior and lateral view; it protruded from the anterior wall and reduced esophageal lumen by 60%. In the endoscopy, we found a fibrous web in the cricopharyngeal area. Serial dilatations were performed over a guidewire using Savary-Gilliard dilators with diameter up to 14 mm, improving dysphagia. She was treated with transfusional therapy and parenteral iron. She was discharged with ferrous sulfate and folic acid. The Plummer-Vinson syndrome, Paterson-Brown-Kelly or sideropenic dysphagia is characterized by dysphagia, irondeficiency anemia and upper esophageal web. The syndrome is described as very rare.
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PMID:[Plummer-Vinson syndrome: report of a case and review of literature]. 2302 85

In developed countries, vitamin B12 (cobalamin) deficiency usually occurs in children, exclusively breastfed ones whose mothers are vegetarian, causing low body stores of vitamin B12. The haematologic manifestation of vitamin B12 deficiency is pernicious anaemia. It is a megaloblastic anaemia with high mean corpuscular volume and typical morphological features, such as hyperlobulation of the nuclei of the granulocytes. In advanced cases, neutropaenia and thrombocytopaenia can occur, simulating aplastic anaemia or leukaemia. In addition to haematological symptoms, infants may experience weakness, fatigue, failure to thrive, and irritability. Other common findings include pallor, glossitis, vomiting, diarrhoea, and icterus. Neurological symptoms may affect the central nervous system and, in severe cases, rarely cause brain atrophy. Here, we report an interesting case, a 12-month old infant, who was admitted with neurological symptoms and diagnosed with vitamin B12 deficiency.
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PMID:Cerebral atrophy in a vitamin B12-deficient infant of a vegetarian mother. 2507 73

A European goldfinch (Carduelis carduelis), a canary (Serinus canaria), and a lovebird (Agapornis roseicollis) captive-bred at three different private aviaries in Spain were submitted for necropsy with a history of weakness and ruffled feathers, weight loss associated with glossitis, and respiratory disease, respectively. Microscopically, enterocytes in the jejunum and ileum contained colonies of gram- and Stamp-positive, oval to elliptical microorganisms within parasitophorous vacuoles in the apical cytoplasm. Nested PCR using MSP primers that target microsporidian RNA genes produced amplicons of expected size for Encephalitozoon species, and analysis of forward and reverse DNA sequences confirmed the presence of Encephalitozoon hellem in all cases. The main cause of death of all three birds consisted of concurrent infections. However, intestinal encephalitozoonosis may have contributed to exacerbated catabolism. Encephalitozoonosis (or microsporidiosis) has been rarely described in passerine birds.
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PMID:Encephalitozoon hellem infection in aviary passerine and psittacine birds in Spain. 2692 Oct 40