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 17-year-old girl previously in good health presented with a 2-month history of recurrent, high-grade fever; general fatigue; anorexia; a 10-kg weight loss; and multiple, painful, reddish skin lesions on the lower abdomen. Some lesions were ulcerated, with an oily yellowish brown discharge. A systemic review was unremarkable other than bleeding from the nose. Her medical and family histories were unremarkable. On examination, the patient was pale, jaundiced, and febrile (temperature of 39 degrees C). She had enlarged lymph nodes in the axillary and inguinal areas. There was moderate hepatosplenomegaly. Local skin examination revealed multiple erythematous, tender, and firm subcutaneous nodules of variable size (1-2 cm) on the lower abdomen. Some nodules were ulcerated, with oily yellowish brown discharge and overlying ecchymosis (Figures 1 and 2). Mucous membranes were free of lesions. Laboratory investigations showed pancytopenia, an elevated erythrocyte sedimentation rate (>80 mm/h), normal renal function tests, abnormal hepatic function tests (alanine aminotransferase 172 U/L, aspartate aminotransferase 229 U/L, alkaline phosphatase 725 U/L, and total bilirubin 100 mmol/L [normal range 0-18 mmol/L]), conjugated bilirubin 45 mmol/L (normal range 0-5 mmol/L), and high triglycerides 855 mg/dL (normal range 20-200 mg/dL). Prolonged prothrombin time, 26 seconds (normal range 13-16 seconds); prolonged activated partial thromboplastin time, 61 seconds (normal range 26-38 seconds); positive disseminated intravascular coagulation studies evidenced by low fibrinogen, 74 mg/dL (normal range 160-350 mg/dL); and positive fibrinogen degradation products were also noted. Throat, midstream urine, and blood culture results were negative. Serologic tests for syphilis, HIV, and hepatitis B and C viruses were negative. Epstein-Barr virus and cytomegalovirus serologic values revealed evidence of past infection. Tuberculin and Coombs tests were negative. The alpha1-antitrypsin level was normal. Antinuclear and anti-smith antibodies, rheumatoid factor, and cryoglobulins were negative. CT showed enlarged lymph nodes in the axillary and inguinal areas, bilateral small pleural effusion, moderate hepatosplenomegaly, severe fatty infiltration of the liver, and thickening of lower abdominal subcutaneous tissue. A liver biopsy showed steatohepatitis. Bone marrow aspirate and trephine were normal. A deep punch biopsy of a nodule from the right lower abdomen revealed lobular panniculitis with atypical lymphocytes and large macrophages with cytophagocytosis ("beanbag" cells) (Figures 3 and 4). Immunohistochemistry showed that these atypical cells were positive for CD3, CD8, granzyme B, and perforin, and negative for CD56. T-cell gene rearrangement studies on skin lesions revealed a monoclonal T-cell receptor (gamma-chain) gene rearrangement, supporting the diagnosis of subcutaneous panniculitis-like T-cell lymphoma. On presentation, the initial treatment included 6 U of fresh frozen plasma, 2 U of packed red blood cells, and 2 g IV fibrinogen for 3 consecutive days. The patient was started on prednisolone 60 mg orally once daily and cyclosporine A 5 mg/kg/d orally in two divided doses. The fever and other systemic symptoms and skin lesions resolved within 2 weeks after the treatment. The prednisolone dose was tapered gradually, and a maintenance dose of cyclosporine A was continued. The patient's condition remained in remission at 12-month follow-up; there was no evidence of clinical relapse.
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PMID:Subcutaneous panniculitis-like T-cell lymphoma with hemophagocytic syndrome successfully treated with cyclosporin A. 1685 14

Patients with infectious mononucleosis caused by the Epstein-Barr virus frequently present to the accident and emergency department. The most common presenting symptoms are fever, fatigue, odynophagia and malaise. Although significant airway compromise is rare and occurs in an estimated 1-3.5% of cases, it may present as a potentially life-threatening situation demanding immediate intervention. We present two such cases and discuss their management.
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PMID:Upper airway obstruction in infectious mononucleosis. 1719 26

The aim of this audit was to assess the yield of a selection of laboratory tests as part of the clinical assessment of the fatigued athlete. Clinical charts and blood test results of fifty consecutive athletes who presented with the primary complaint of fatigue were retrospectively reviewed. Blood tests results reviewed were: haematology (haemoglobin, red cell count, mean cell volume, mean cell haemoglobin content, platelets, white cell count, differential white cell count); erythrocyte sedimentation rate; serum biochemistry (urea, creatinine, electrolytes, urate, glucose, liver function tests, albumin, globulin); blood iron status (serum iron, total iron binding capacity, percent transferring saturation, and ferritin concentration); thyroid stimulating hormone; and immune measures (Epstein-Barr virus serology, cytomegalovirus serology). We identified only 3 abnormal results that contributed to the diagnosis of medical disease as a cause for fatigue. Laboratory testing identified 2 fatigued female athletes with serum ferritin concentration between 15 microg L(-1) and 20 microg L(-1) plus two of the other criteria of iron concentration (serum iron <10 micromol L(-1), iron binding capacity > 68 micromol L(-1), or transferrin saturation <15%). We concluded that the yield from a selection of blood tests investigating fatigued athletes was low. Future study is needed to further define the role of laboratory testing and to study whether low iron stores in the absence of anaemia is related to symptoms in fatigued athletes.
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PMID:An audit of clinically relevant abnormal laboratory parameters investigating athletes with persistent symptoms of fatigue. 1733 43

Primary infection with Epstein-Barr virus (EBV) in childhood is usually asymptomatic, whereas infection in adolescence may result in infectious mononucleosis (IM) often followed by a fatigue syndrome. EBV latent membrane protein 1 (LMP1) is expressed in latency and in many EBV-associated tumours, including non-Hodgkin lymphoma (NHL). Given the regulatory nature of the CD4(+) T-cell response against LMP1 previously reported in healthy donors, we investigated whether patients with active EBV-driven disease can nevertheless mount effector [T-helper cell, type 1 (Th1)] anti-LMP1 responses. We therefore performed a longitudinal study of the nature of CD4(+) T-cell responses to LMP1 in four patients with IM, and five patients with NHL. In both groups, responses changed with time. During symptomatic infection or active tumour growth, responses were dominated by a Th1 effector phenotype, but switched to a regulatory interleukin-10 response upon recovery. In addition, the fine specificities of the T cells driving these responses evolved. This study showed the dynamic nature of CD4(+) T-cell responses to LMP1, and demonstrated that, although patients can mount Th1 effector responses, recovery from IM and NHL is associated with regulatory responses.
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PMID:CD4(+) T-cell responses to Epstein-Barr virus (EBV) latent membrane protein 1 in infectious mononucleosis and EBV-associated non-Hodgkin lymphoma: Th1 in active disease but Tr1 in remission. 1785 10

Primary infection with Epstein-Barr virus (EBV) often occurs subclinically during childhood, resulting in a latent infection of B lymphocytes. In this report, a chronic hepatitis B case who presented with a serologic profile mimicking acute hepatitis B virus (HBV) infection and exhibiting transient autoantibody positivities because of the polyclonal activation of B cells due to EBV reactivation has been presented. The test results of 56 years old male patient who suffered from fatigue and pain on the right upper quadrant, revealed high levels of liver enzymes (AST: 187 U/L, ALT: 569 U/L), positivity of HBsAg, anti-HBc IgG and anti-HBe, and negativity of anti-HBc IgM, HBeAg and anti-HBs. Since HBV-DNA level was found 405,974 copies/mL by quantitative real time polymerase chain reaction (PCR), the patient was taken into follow-up. At the 6th month AST and ALT levels further elevated (352 U/L and 609 U/L, respectively), and anti-HBc IgM and anti-HBs became positive in addition to the previous positive markers of HBV. With the suspicion of superinfection, further laboratory investigations yielded negative results in CMV-IgM and Paul Bunnel test, while positive results in EBV anti-VCA IgM and IgG, anti-EBNA IgM and IgG, anti-p22 IgM and IgG and anti-EA IgM. In the follow-up period high levels of autoantibody positivities [rheumatoid factor (42.200 U/ml), anti-nuclear antibody (1/100) and anti-Ro-52] together with increased levels of total IgG, IgM and IgA were detected. In the following months, the levels of transaminases, total immunoglobulins and HBV-DNA have distinctively decreased, and in the 20th month the previous HBV profile regained (HBsAg, anti-HBc IgG and anti-HBe positive, anti-HBc IgM and anti-HBs negative, HBV-DNA: 6984 copies/ml) and the other pathological test results returned to normal. As a result, ALT increases seen during the course of chronic hepatitis B should not always be considered as HBV manifestations and the unusual serologic patterns should be evaluated as a consequence of superinfection with various viral agents.
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PMID:[Polyclonal activation due to Epstein-Barr virus superinfection in a case with chronic hepatitis B]. 1817 82

Investigations into the underlying cause of chronic fatigue syndrome have advanced the field considerably in the past year. Gene microarray data have led to a better understanding of pathogenesis. Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments. Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue. Genomic studies showed that persistent cases express Epstein Barr virus-specific genes and demonstrate abnormalities of mitochondrial function. Studies of immune dysfunction extended observations of natural killer cytotoxic cell dysfunction of the cytotoxic T cell through quantitative evaluation of intracellular perforins and granzymes. Other research has focused on a subgroup of patients with reactivated viral infection. These advances should result in targeted therapies that impact immune function, hypothalamic-pituitary-adrenal axis regulation, and persistent viral reactivation.
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PMID:Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions. 1817 2

A 24-year-old woman hospitalized with fever, general fatigue, and upper abdominal pain was found to have liver dysfunction and an increase in atypical lymphocytes in peripheral blood. Serum immunological studies showed positive Epstein-Barr virus (EBV) VCA IgM antibody and human herpesvirus 6 (HHV-6) IgM and IgG antibodies, and negative EBV VCA IgG and EBNA antibodies on admission. Liver function was back within normal limits 8 weeks after onset, EBV VCA IgM and IgG antibodies were positive, EBNA and HHV-6 IgM antibodies were negative, and the HHV-6 IgG antibody titer was 8 times higher than that on admission. This case was diagnosed as infectious mononucleosis due to EBV with suspected reactivation of HHV-6.
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PMID:[A case of infectious mononucleosis due to Epstein-Barr virus with suspected reactivation of human herpesvirus 6]. 1830 80

We report a case of acute Epstein-Barr virus (EBV) infection in which the clinical syndrome and pattern of F-18-2-fluoro-2-deoxy-D-glucose (FDG) uptake mimicked malignant lymphoma. A 53-yr-old man presented with 2 wk of high fevers, night sweats, sinus congestion and severe fatigue. The patient was treated for 1 wk with broad-spectrum antibiotics for acute sinusitis without any improvement. Persistence of fevers and presence of abnormal lymphadenopathy seen on the abdominal computed tomography (CT) were concerning lymphoma with B symptoms. FDG positron emission tomography (PET) showed avid FDG uptake in numerous abdominal/pelvic nodes, liver, spleen and bone marrow. These findings were highly suspicious for lymphoma. Patient underwent a pelvic lymph node biopsy which showed large granular lymphocytes that were predominantly T cells. Bone marrow biopsy showed diffuse infiltration with plasmocytoid cells that were not kappa lambda restricted. Additional diagnostic workup became available showing positive EBV IgM titers and negative IgG levels indicating acute infectious mononucleosis. Lymph node biopsy stained positively with EBV-encoded RNA. We concluded that patient's abnormal FDG PET was most likely secondary to acute EBV infection. After 2 months, follow-up FDG PET/CT showed marked improvement in lymphadenopathy and decreased hypermetabolic activity in the liver and spleen. Other than EBV, there are many other FDG-avid non-malignant conditions that may lead to false-positive PET scans. FDG accumulates in inflamed and infected lesions with increased glucose metabolism. This case underscores the importance of maintaining a broad differential and restricting use of PET scans for staging.
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PMID:FDG PET/CT findings in acute adult mononucleosis mimicking malignant lymphoma. 1846 55

In Europe and the USA, the incidence of primary nasal natural killer (NK)/T-cell lymphoma is rare. The skin is one of the predilection sites for dissemination. Cutaneous dissemination is a poor prognostic sign and is consistently fatal. We describe the case of a 17-year-old white German girl with a primary nasal NK/T-cell lymphoma and cutaneous dissemination. She presented with multiple maculopapular patches involving the trunk and thighs, and a 4-week history of headache, fever and fatigue. Biopsies of the skin and the nasal mucosa were taken. Pathological examination of both specimens revealed a NK/T-cell lymphoma. Epstein-Barr virus RNA was detected in the lymphoma cells by in situ hybridization. Unfortunately, the patient died of disease within 1 week.
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PMID:Cutaneous dissemination of nasal NK/T-cell lymphoma in a young girl. 1861 30

This article posits that infection of the peripheral ganglia causes at least some cases of Chronic Fatigue Syndrome (CFS), with a neurotropic herpesvirus, particularly varicella-zoster virus (VZV), as the most likely cause of the infection. Virtually all CFS symptoms could be produced by an infection of the peripheral ganglia, with infection of the autonomic ganglia causing fatigue, postural hypotension, and sleep disturbances, and infection of the sensory ganglia causing sensory symptoms such as chronic pain. Furthermore, infections of the peripheral ganglia are known to cause long-term nerve dysfunction, which would help explain the chronic course of CFS. Herpesviruses have long been suspected as the cause of CFS; this theory has recently been supported by studies showing that administering antiherpes agents causes substantial improvement in some CFS patients. VZV is known to frequently reactivate in the peripheral ganglia of previously healthy adults and cause sudden, debilitating illness, making it a likely candidate as a cause of CFS. Moreover, many of the symptoms of CFS overlap with those of herpes zoster (shingles), with the exception that painful rash is not one of the symptoms of CFS. A model is therefore proposed in which CFS is one of the many manifestations of zoster sine herpete; that is, herpes zoster without rash. Furthermore, re-exposure to VZV in the form of chickenpox has become less common in the past few decades; without such re-exposure, immunity to VZV drops, which could explain the increased incidence of CFS. Co-infection with multiple herpesviruses is a possibility, as some CFS patients show signs of infection with other herpesviruses including Epstein-Barr, Cytomegalovirus, and HHV6. These three herpesviruses can attack immune cells, and may therefore promote neurotropic herpesvirus reactivation in the ganglia. The possibility of VZV as the causal agent in CFS has previously received almost no attention; the possibility that CFS involves infection of the peripheral ganglia has likewise been largely overlooked. This suggests that the search for a viral cause of CFS has been far from exhaustive. Several antiherpes drugs are available, as is a vaccine for VZV; more research into such agents as possible treatments for CFS is urgently needed.
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PMID:Does varicella-zoster virus infection of the peripheral ganglia cause Chronic Fatigue Syndrome? 1952 May 22


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