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

We have reported two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease. Case 1: a 45-year-old woman noticed a diffuse goiter, palpitation and emaciation in 1977. Laboratory studies confirmed that she had Graves' disease, and she was treated with antithyroid drug. In 1986, when the hyperthyroidism was subsided, she showed progressive symmetrical weakness and numbness in her limbs, and she was almost in tetraplegia at 1987. Markedly slowed motor and sensory nerve conductions and elevated CSF proteins as well as clinical manifestations confirmed the diagnosis of CIDP. Following corticosteroid-pulse therapy and plasmapheresis resulted in good recovery in both motor and sensory impairment, though two-times of relapses were observed. Case 2: a 33-year-old man first noticed weakness in his legs in 1977, motor and sensory disturbances progressed for 12 years. Slowed nerve conduction, high CSF proteins and two-times of relapses in early phase indicated that the CIDP was the diagnosis. In 1989 he complained general fatigue, hyperhidrosis and body-weight loss. The serum thyroid hormone levels were high, and other laboratory studies confirmed the presence of Graves' disease. The cases with both CIDP and Graves' disease has rarely been reported. The background mechanism of this association is not well understood, but the susceptibility to CIDP and Graves' disease may be related to the HLA antigens and immunoglobulin Gm allotypes of which are the genes linked to the major histocompatibility complex and controlling immune responses. The present two cases commonly shared several HLA-DR antigens, but their significance should be confirmed by examining many cases.
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PMID:[Two cases of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with Graves' disease]. 178 65

Ten patients with adrenal cortical carcinoma were treated from 1966 to 1986. There were 7 males and 3 females. The typical clinical manifestations, marked increase of 17-ketosteroid, 17-hydroxycorticoids and DHA, and negative dexamethasone suppression test were essential for the diagnosis. Of the ten patients, eight had secretive function and their 17-ketosteroid and 17-hydroxycorticoids varied from 36.8-93 mg% and 32.5-150 mg%, respectively. DHA was measured in 5 cases with the result of 6.95-44mg%. Those without secretive functions or obvious endocrine disturbances were usually misdiagnosed as kidney tumor, splenomagaly, liver tumor or pancreatic mass. Wood had summarized that nonsecretive ACC patients commonly had fever, pain, exhaustion syndrome (emaciation, fatigue, perspiration, anorexia), mass and distant metastasis. Adrenal scan, IVU, abdominal aortic arteriography, retroperitoneal pneumography and CT were helpful in localization. The differential diagnosis between ACC and adenoma by pathology was difficult. It is generally agreed that if the mass is larger than 100 grams, capsulated, having blood or lymphatic vessel invasion, hemorrhage, necrosis and calcification or even distant metastasis, malignant tumor should be considered. Surgical removal of the tumor is the only effective treatment. For advanced or recurrent lesions, selective adrenal artery thrombosis could be used. One of the ten patients was thus treated by this facilitated subsequent surgery. Postoperative chemotherapy, such as O.P-DDD, might be used in some cases.
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PMID:[Adrenal cortical carcinoma (ACC)--report of 10 cases]. 297 73

An intestinal carcinoid with multiple metastases was identified in a 5-year-old male Shih Tzu with a clinical history of anemia, fatigue, anorexia, vomiting, intermittent diarrhea, intestinal bleeding, and progressive emaciation. There was a yellowish-white mass 15 mm in diameter in the anterior jejunum and white nodules consistent with metastases in many organs. Histopathologically, the mass consisted of neoplastic cells arranged in lobules, trabeculae, or closely interdigitating islands of cells. Neoplastic cells were generally polygonal with round hyperchromatic nuclei, modest amounts of eosinophilic cytoplasm, and eosinophilic cytoplasmic granules. Mitoses were common. Rosette formations of tumor cells were apparent in metastatic tumors. Immunohistochemically, tumor cells stained positive for cytokeratin 13, synaptophysin, protein gene product 9.5, neuron-specific enolase, chromogranin A, calcitonin gene-related peptide, serotonin (5-HT), and Leu-7. Serum 5-HT concentrations for this dog were increased 10-fold compared with those of normal dogs. All findings were consistent with a diagnosis of a malignant intestinal carcinoid.
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PMID:Immunohistochemical evaluation of a malignant intestinal carcinoid in a dog. 1263 63

Patients with anorexia nervosa (AN) often show normal to elevated physical activity levels despite severe weight loss and emaciation. This is seemingly in contrast to the loss of energy and fatigue characteristic of other starvation states associated with weight loss. Despite the fact that historical accounts and clinical case studies of AN have regularly commented on the elevated activity levels, the behavior has become only recently the subject of systematic study. Because rodents and other species increase their activity upon food restriction leading to weight loss when given access to an activity wheel--a phenomenon referred to as activity-based anorexia or semi-starvation-induced hyperactivity (SIH)-it has been proposed that the hyperactivity in AN patients may reflect the mobilization of phylogenetically old pathways in individuals predisposed to AN. Exogeneous application of leptin in this animal model of AN has recently been shown to suppress completely the development of SIH. Hypoleptinemia, as a result of the food restriction, may represent the initial trigger for the increased activity levels in AN patients and in food-restricted rats. In the first and second parts of our review, we will summarize the relevant findings pertaining to hyperactivity in AN patients and in the rat model, respectively. We conclude with a synopsis and implications for future research.
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PMID:Hyperactivity in patients with anorexia nervosa and in semistarved rats: evidence for a pivotal role of hypoleptinemia. 1281 7

Cage layer fatigue was first noticed after laying hens began to be housed in cages in the mid-20th century. Hens producing eggs at a high rate were most susceptible to the disease. Early research revealed that cage layer fatigue was associated with osteoporosis and bone brittleness. Severe osteoporosis leads to spontaneous bone fractures commonly in the costochondral junctions of the ribs, the keel, and the thoracic vertebrae. Vertebral fracture may damage the spinal cord and cause paralysis. Osteoporosis appears to be inevitable in highly productive caged laying hens. The condition can be made worse by metabolic deficiency of calcium, phosphorus, or vitamin D. Hens in housing systems that promote physical activity tend to have less osteoporosis and rarely manifest cage layer fatigue. Genetic selection may produce laying hens that are less prone to bone weakness. The welfare implications of osteoporosis stem from pain, debility, and mortality associated with bone fracture. The chicken has well-developed neural and psychological systems specialized to respond to pain associated with trauma and inflammation. Although studies on the chicken have not focused on pain due to bone fracture, physiological and behavioral similarities to other species allow inference that a hen experiences both acute and chronic pain from bone fracture. There is little information on osteoporosis in commercial caged layer flocks, however, evidence suggests that it may be widespread and severe. If true, most caged laying hens suffer osteoporosis-related bone fracture during the first laying cycle. Osteoporosis also makes bone breakage a serious problem during catching and transport of hens prior to slaughter. Estimates of mortality due to osteoporosis in commercial caged layer flocks are few, but range up to a third of total mortality. Many of these deaths would be lingering and attended by emaciation and possibly pain. Osteoporosis-related bone breakage during processing has reduced the marketability of spent caged laying hens, contributing to the need to develop humane on-farm killing methods to support alternative means of spent hen disposition. Overall, the evidence indicates that cage layer osteoporosis is a serious animal welfare problem. A determined effort must be made to make the laying hen no longer susceptible to the harmful effects of excessive bone loss.
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PMID:Welfare implications of avian osteoporosis. 1497 68

Chronic fatigue and immune dysfunction syndrome (CFIDS) is a recognized human illness with zoonotic implications that is rarely described in animals. Eight birds of prey examined between 1992 and 1995 and sharing common symptoms (asthenia, inability to fly, poor appetite and emaciation) underwent laboratory tests revealing immunodeficiency, anaemia, high creatine kinase levels and low serum magnesium levels. Diagnosis of CFIDS was based upon these features. The effectiveness of an arsenic-based medication, thiacetarsamide sodium, administered intravenously for 2-3 days at low dosages (0.1 ml/kg/day) has been demonstrated by checks carried out 10, 20 and 30 days after therapy. The symptoms and the immune and haematological dysfunctions disappeared within 2-4 weeks of treatment. In all patients, micrococcus-like organisms found adhering to the outer surface of many red blood cells, had disappeared at post-treatment controls. Two of five blood cultures were positive for Staphylococcus spp. (S. intermedius and S. xilosus). Consideration is given to the pharmacological activity of an arsenic-based drug in animal illnesses resembling CFIDS.
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PMID:Chronic fatigue and immune dysfunction syndrome associated with Staphylococcus spp. bacteraemia responsive to thiacetarsamide sodium in eight birds of prey. 1512 82

We report herein the case of a 28-year-old man presenting with hyperglycemic chorea-ballism (HCB) in addition to mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). He was admitted to a local hospital due to weight loss, general fatigue and thirst. The patient had diabetes mellitus, with a blood glucose level of 738 mg/dl and HbA1c of 19.8%. Although insulin therapy improved hyperglycemia, he noticed involuntary movements in the right upper and lower limbs, which subsequently extended to the left side. The patient was thus transferred to our hospital. He displayed short stature (154 cm) and emaciation, and a maternal family history of diabetes mellitus was elicited. He had no history of stroke-like episode, headache, vomiting and seizure. Neurological examination revealed low intelligence (IQ 57), mild sensorineural deafness, and chorea-ballism in the extremities and head without ptosis or eye movement disturbance. Brain computed tomography (CT) demonstrated areas of high density, while T1-weighted magnetic resonance imaging (MRI) revealed extreme hyperintensity and T2-weighted MRI showed hyperintensity in bilateral caudate nuclei, putamina and globi pallidus. HCB was diagnosed. In, CSF, lactate level was increased to 43.9 mg/dl (n, 4-16), pyruvate level was 1.65 mg/dl (n, 0.3-0.9) and total protein concentration was 59 mg/dl. Histological examination of a biopsy sample from the biceps brachii muscle demonstrated ragged-red fibers. An A3243G point mutation in the tRNA(Leu(UUR)) gene was detected, indicating the presence of MELAS. Involuntary movements improved on treatment with haloperidol up to 4.5 mg/day. HCB usually appears in elderly individuals, and cases less than 40-years-old are very rare. The mitochondrial dysfunction in MELAS may accelerate development of HCB.
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PMID:[A case of MELAS presenting juvenile-onset hyperglycemic chorea-ballism]. 1611 32

We describe a patient with paraneoplastic neurologic syndrome confirmed on postmortem examination. This 42-year-old man was admitted due to general fatigue, emaciation and acute-onset disorientation. Neurological examination revealed disorientation, moderate cognitive impairment, cerebellar ataxia, bilateral limitations and nystagmus in all directions during external ocular movement, swallowing disorder, bilateral Babinski sign, sensory disturbance in the distal parts of all extremities, and Romberg's sign. T-cell lymphoma was diagnosed following biopsy of the cervical lymph node. Neurological condition improved slightly after chemotherapy, but subsequently deteriorated. At about 6 years after the disease onset, brain magnetic resonance imaging (MRI) revealed atrophy of bilateral hippocampi and the upper vermis of the cerebellum. The patient died of pneumonia after a clinical course of about 6 years and 6 months. Pathologically, neuronal loss, reactive gliosis and perivascular lymphocytic infiltration were observed in the hippocampi, cerebellum, and inferior olivary nuclei. Lymphocytes around the vessels were positive for LCA and UCHL-1, but negative for CD8 and L26, and thus were considered to be T cells. No lymphoma cell was observed in the central nervous system or lymphatic organs. Based on the pathological findings, paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration and olivary pseudohypertrophy) associated with T-cell type malignant lymphoma was diagnosed. Only three other cases of paraneoplastic neurologic syndrome associated with T-cell lymphoma have been reported. In those cases, death occurred due to the deterioration of malignant lymphoma, whereas the present patient died about 6 years after the remission of malignant lymphoma. Prognosis may thus depend on the course of the malignant lymphoma. In the present patient, neurological symptoms deteriorated after remission of malignant lymphoma, and no pathological lesion were found in the lymphatic organs. Lesions in the central nervous system in paraneoplastic neurological syndromes may follow a course independent of the original malignant disease.
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PMID:[An autopsied case of paraneoplastic neurologic syndrome (limbic encephalitis, cerebellar degeneration, and pseudohypertrophy in the inferior olivary nuclei) associated with T cell lymphoma]. 1618 Jul 7

Cord blood, because of its rich mix of fetal and adult hemoglobin, high platelet and WBC counts, and a plasma filled with cytokine and growth factors, as well as its hypo antigenic nature and altered metabolic profile, has all the potential of a real and safe alternative to adult blood transfusion. Our team's experience (from 1st April 1999 to 1st July 2005) with 123 units of placental umbilical cord whole blood (62 ml-154 ml mean 85 ml +/- 8.4 ml SD, median 82 ml, mean packed cell volume 48.8 +/- 4.2 SD, mean percent hemoglobin concentration 16.3 g/dl +/- 1.6 g/dl SD; after collection the blood was immediately preserved in a refrigerator and transfused within 72 hours of collection) collected after lower uterine cesarean section (LUCS), and the transfusion to 16 consenting HIV-positive patients (12 cases had full blown AIDS) with anemia and emaciation is presented here. On the basis of our preliminary experience of cord blood transfusion, we are of the opinion that umbilical cord whole blood transfusion is safe in HIV-positive patients. This blood has the potential to carry more oxygen than adult blood and it does not trigger any clinical, immunological or non-immunological reaction after its transfusion to an adult host with a HIV-positive status. Apart from the correction of anemia, there was also definite improvement in the energy and fatigue levels in individuals with HIV, i.e., physical functioning, a sense of well-being and weight gain from two to five pounds, within three to ten months of the commencement of transfusion. There was also an immediate rise in CD34 levels of peripheral blood in the HLA-randomized host after transfusion, without any clinical graft vs host reaction.
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PMID:A preliminary report of 123 units of placental umbilical cord whole blood transfusion in HIV-positive patients with anemia and emaciation. 1690 52

A clinicopathological study was performed on 14 dogs with myelofibrosis (MF), in order to correlate clinical, laboratory, and histomorphological parameters and investigate factors of prognostic significance. The clinical signs included fatigue, weight loss, anorexia, and diarrhea. Physical findings included pale mucous membranes and wasting/emaciation. The major laboratory observations were moderate to severe, poorly-responsive anemia with various degrees of marrow cellularity and fibrosis. All dogs with severe, non-responsive anemia should have a bone marrow core biopsy, stained for connective tissue, in order to detect myelofibrosis. Myelofibrosis regressed in six dogs.
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PMID:Myelofibrosis: Review of clinical and pathological features in fourteen dogs. 1742 3


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