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)

By presenting this case report describing Parinaud's oculoglandular syndrome, we review the medical literature on its most frequent etiology: catscratch disease, a self-limited, systemic illness caused by a Gram-negative bacillus, Bartonella henselae, principally affecting children under 15 years of age. Typical symptoms include regional lymphadenopathy, fever, malaise, and fatigue, possibly with more severe complications such as splenomegaly, granulomatous hepatitis, and encephalopathy. Ocular manifestations may include follicular conjunctivitis, Parinaud's oculoglandular syndrome, neuroretinitis, optic neuritis, and chorioretinitis. Diagnosis is based on serologic tests, and when necessary, antimicrobial treatment can be considered.
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PMID:[Cat's cratch disease and Parinaud's oculoglandular syndrome]. 1502 49

The clinical hallmark of myasthenia gravis (MG) is fluctuating, painless weakness of muscles that most often affect extraocular, lower bulbar, or limb musculature. Predicting the probability of successful treatment for the patient assumes that the physician has made an accurate diagnosis. In this review, the practical differential diagnosis of MG is reviewed from the perspective of conditions (at presentation of symptoms and signs) that may mimic the disorder. The differential diagnosis includes disorders that limit eye movements (with or without associated diplopia), cause false-positive laboratory studies, and mimic MG but have normal eye movements. The differential diagnosis includes disorders that affect the upper brainstem, cranial nerves, neuromuscular junction, muscles, or local orbit anatomy. Nonneurological systemic diseases (i.e., encephalopathy, sepsis) can produce fluctuating ptosis or eye movements that can occasionally be confused with MG. Although MG is considered often in the differential diagnosis of weakness or fatigue symptoms that lack a correlate on neurological examination (subjective fatigue, breakaway weakness, chronic fatigue syndrome), MG is almost never found.
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PMID:Myasthenia gravis: diagnostic mimics. 1525 10

October 2004. A 49-year-old right-handed man developed progressive cognitive difficulties over a 4-month period. There was impairment in recent memory, calculations and language. He also developed fatigue, weight loss, gait imbalance and urinary incontinence. Past history included transfusion-associated Hepatitis C. Neurologic exam showed mild dysarthria, dysnomia, left sided neglect, bilateral Babinski signs, and a prominent grasp reflex. Laboratory testing provided no positive etiologic data. An EEG showed generalized intermittent slowing suggestive of a diffuse encephalopathy and decreased background in the right hemisphere, suggestive of a structural lesion. MRI showed multiple areas of high signal on FLAIR imaging and patchy enhancement. FDG-PET showed multi-focal areas of increased uptake, correlating with the abnormal areas on MRI, on a background of decreased uptake. A 4-vessel cerebral angiogram showed no abnormalities. A brain biopsy showed diffuse infiltrates of large malignant cells that were immunoreactive with antibodies to CD20, diagnostic of diffuse large B cell lymphoma. In summary, the clinical presentation suggested bilateral hemispheric involvement, which was supported by physical examination, EEG, MRI, and PET scans. The differential diagnosis for this presentation is limited to demyelinating disease such as multiple sclerosis, vascular dementia, and infiltrating neoplasm such as glioblastoma multiforme or lymphoma. Diagnosis was made by morphologic and immunohistochemical analysis of brain tissue.
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PMID:October 2004: a 49-year-old man with progressive dementia. 1591 74

We present here a patient with muscle fatigue and poor growth since the age of 6 y. The diagnosis of a mitochondrial disease was based on the presence of ragged red fibers in the muscle biopsy and on a combined defect of mitochondrial DNA-encoded respiratory enzymes. Epilepsia partialis continua with stroke-like episodes appeared 2 mo before death at the age of 18 and prompted a search for mitochondrial DNA mutations associated with mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes. Minisequencing of the patient's DNA samples revealed a heteroplasmic T3271C mutation with a 78-94% mutation load in her fibroblasts or autopsy-derived tissue samples. This is the ninth reported non-Japanese patient with T3271C mutation. Our patient shows that despite very high proportion of mutant mtDNA, the T3271C mutation can give rise to mild symptoms in childhood and to a rapid terminal phase that simulates encephalitis.
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PMID:A juvenile case of MELAS with T3271C mitochondrial DNA mutation. 1600 33

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

In chronic hepatitis type C fatigue, depression and neuropsychiatric complications of interferon treatment are more frequently reported than in the other parenchymal liver diseases. It contributes to a significant reduction of health related quality of life (HRQL) in those patients. It is believed that psychiatric disorders are the result of brain dysfunction caused by the virus. The hypothesis of neurotropic character of HCV infection is supported by the detection of HCV-RNA in brain tissue, identification of brain-specific quasispecies variants of hepatitis C virus, specific detection of negative-strand viral RNA in the astroglia of patients with acquired-immunodeficiency syndrome and demonstration of metabolic changes resembling HIV-1 encephalopathy in the basal ganglia of patients with chronic hepatitis C. On the other hand there is good evidence that decreased HRQL is directly related to the consciousness of infection and hence, is not of the organic nature. Some authors suggest that patient's worry and anxiety, aggravated by some mass-media and the lack of knowledge, may be a strong determinant of psychological status. Given the complex nature of symptoms in chronic hepatitis C therapy should include education on the natural history of HCV infection and results of treatment, psychotherapy and medical treatment of depression and anxiety. Moreover, antiviral therapy should be considered in highly motivated patients despite lack of clear clinical indications for treatment.
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PMID:[Chronic HCV infection--disease of body or disease of soul?]. 1619 May 74

Systemic lymphomas may involve the liver but rarely cause fulminant hepatic failure (FHF). Acute liver failure from primary hepatic lymphoma (PHL) is even less common with most patients succumbing to the sequelae of FHF before the correct diagnosis is made. We report a patient who underwent successful orthotopic liver transplant (OLT) and chemotherapy for FHF secondary to PHL. This previously-well male developed profound coagulopathy and encephalopathy 6 weeks after the onset of jaundice and fatigue. Workup failed to reveal the underlying cause of his liver failure and the patient soon required urgent OLT. Pathologic evaluation of his explanted liver revealed a malignant T-cell rich, large B-cell non-Hodgkin's lymphoma with widespread hepatocellular necrosis. The patient made an excellent clinical recovery and is undergoing CHOP-Rituxan chemotherapy. This scenario demonstrates that lymphoma should be considered in the differential diagnosis of FHF without clear etiology because of the potential for intervention with transplant and chemotherapy.
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PMID:Fulminant hepatic failure from primary hepatic lymphoma: successful treatment with orthotopic liver transplantation and chemotherapy. 1624 51

Spinal tuberculosis is usually secondary to lung or abdominal involvement and may also be the first manifestation of tuberculosis. Spinal tuberculosis (often called Pott's disease) is by definition, an advanced disease, requiring meticulous assessment and aggressive systemic therapy. Physicians should keep the diagnosis in mind, especially in a patient from a group with a high rate of tuberculosis infection. This review aims on updating the knowledge on spinal tuberculosis and its management. Skeletal involvement has been reported to occur in approximately 10% of all patents with extrapulmonary tuberculosis, and half of these patients develop infection within the spinal column. Symptoms of spinal tuberculosis are back pain, weakness, weight loss, fever, fatigue, and malaise. It is much more prone to develop neurological manifestation, paraplegia of varying degree. The palpation of spinous process in routine clinical examination is the most rewarding clinical method and is an invaluable measure for early recognition. Diagnosis of spinal tuberculosis is made on the basis of typical clinical presentation along with systemic constitutional manifestation and the evidence of past exposure to tuberculosis or concomitant visceral tuberculosis. Magnetic resonance imaging can define the extent of abscess formation and spinal cord compression. The diagnosis is confirmed through percutaneous or open biopsy of the spinal lesion. Surgery is necessary as an adjunct to antibiotic therapy if the vertebral infection produces an abscess, vertebral collapse, or neurologic compression. Some patents need aggressive supportive care owing to tuberculous meningitis or encephalopathy. Moreover, the importance of immediate commencement of appropriate treatment and its continuation for adequate duration along with the proper counseling of the patient and family members should not be underestimated for successful and desired outcome.
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PMID:Pott's spine and paraplegia. 1657 Mar 78

Chronic liver disease results in more than 1 million physician visits and more than 300,000 hospitalizations per year in the United States. More than 27,000 patients annually progress to end-stage liver disease (ESLD), liver failure, or death. Patients with ESLD experience such complications as encephalopathy, malnutrition, muscle wasting, ascites, esophagogastric variceal hemorrhage, spontaneous bacterial peritonitis, fatigue, and depression. Despite significant improvements in palliation, patients' quality of life diminishes and their disease will often inexorably progress. Liver transplantation, a valid treatment option, increases life and reduces many symptoms. With the current shortage of organs, up to 10% to 15% of these patients die without receiving an organ. Many patients also are not candidates for transplantation due to comorbid illness. In addition, some patients receive a transplant but succumb to complications of the transplant itself. Such patients and families face the conundrum of a potentially treatable yet often fatal illness. Through the case of a 55-year-old woman with a life-long history of hepatitis B virus infection who is awaiting transplant, we discuss the transplant eligibility process and the struggle with maintaining hope for a cure in the face a life-threatening illness. In all of these circumstances, the health care team must combine elements of palliative care with life-sustaining therapy to maximize the patient's quality and quantity of life.
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PMID:Integrating palliative care for liver transplant candidates: "too well for transplant, too sick for life". 1677 29

At the beginning of the AIDS pandemic, affective disorders (such as depressed mood) were seen in a considerable number of HIV-1-infected individuals. These disorders were a result of the poor physical condition of the patients, brain involvement by the virus (e.g. encephalopathy) or a reaction to disadvantageous living conditions (losing friends, jobs, etc.). In the era of highly active antiretroviral therapy (HAART), mental illness related to physical weakness is declining, as is the incidence of HIV-1-associated encephalopathy. However, depressed mood and fatigue caused by efavirenz (a standard component of HAART) is becoming increasingly important, particularly in individuals who are infected long-term with HIV-1. Whatever the cause of affective disorders, their presence has been shown to negatively influence adherence to HAART and HIV-1 disease progression. Specialist knowledge of HIV-1 infection, and HAART and its psychiatric complications (particularly in subgroups of patients such as drug abusers and older people), is needed to care adequately for patients. Furthermore, prospective studies are needed to more fully differentiate between the various aetiologies of affective disorders seen in individuals living with HIV/AIDS and to determine their incidence and prevalence. Such information is important to ensure that affective disorders are recognised and adequately treated, which will in turn improve the efficacy of HAART.
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PMID:Affective disorders in patients with HIV infection: impact of antiretroviral therapy. 1673


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