Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old farmer developed aplastic anaemia after exposure to 2-methyl-4-chlorphenoxyactic acid while spraying weed killer. Muscular weakness, haemorrhagic gastritis and slight signs of liver damage occurred at the same time. All these symptoms, including blood dyscrasia , are consistent with those described as toxic effects of chlorphenoxyacetic acids in animal experiments. A causal relationship between aplastic anaemia and the 2-methyl-4-chlorphenoxyacetic acid thus seems probable. The anaemia was reversible, but the case serves as a warning that careful safety measures are required during the use of chlorphenoxyacetic acids and related compounds.
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PMID:Aplastic anaemia after exposure to a weed killer, 2-methyl-4-chlorphenoxyacetic acid. 80 93

Fusarium, a fungus, produces a potent mycotoxin that, when ingested with contaminated cereal grains, produces a serious illness in man called alimentary toxic aleukia (USSR) and Akakabi-byo (Japan). The illness includes gastrointestinal symptoms and weakness and if ingestion of Fusarium contaminated grain persists, culminates in aplastic anemia. A 66-year-old woman had Eaton-Lambert syndrome and a clinical course similar to alimentary toxic aleukia. Several months before her death, pancytopenia, initially thought guanidine-induced, developed and progressed to aplastic anemia despite discontinuation of guanidine 2 1/2 months before death. Autopsy showed numerous granuloma in the liver, spleen, esophagus, and cecum from which Fusarium oxysporum was isolated. Although the unique finding of systemic fusariosis may relate to altered host resistance terminally, a causal relationship with her defect of neuromuscular transmission and/or aplastic anemia is a distinct possibility.
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PMID:Fusariosis, myasthenic syndrome, and aplastic anemia. 123 2

BMT has become an important therapy for many hematologic disorders. Following BMT, the recipient may develop GVHD when it appears that immunocompetent donor lymphocytes react to host antigens. Acute and chronic GVHD represent two distinct syndromes. Acute GVHD has not been associated with primary neurologic involvement. Polymyositis has been reported in 12 patients with chronic GVHD, with the most common underlying illness being aplastic anemia. The clinical, serologic, and muscle biopsy features of the myositis in GVHD have been similar to those observed in idiopathic polymyositis. Weakness was moderate to severe and responded to prednisone, sometimes with the addition of azathioprine. Prognosis depended upon the underlying disease and not on the severity of the myositis. MG occurs rarely in chronic GVHD. Most patients with MG and GVHD have had aplastic anemia; those with aplastic anemia are more likely to have anti-AchR prior to BMT. The clinical manifestations of GVHD MG have not differed from classic autoimmune MG; each patient had elevated antiacetylcholine receptor antibodies titers. All patients have responded well to cholinesterase inhibitors but have received other immunosuppressants. These observations suggest that aplastic anemia is an important host factor in the development of the autoimmune disorders seen with chronic GVHD, certainly of myositis and MG. Herpes zoster peripheral nerve infections have occurred in patients with chronic GVHD. One patient had mononeuritis multiplex. In both acute and chronic GVHD, CNS impairment is usually caused by metabolic encephalopathy or infection. Primary CNS involvement has not been recognized.
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PMID:Neurologic complications of graft-versus-host disease. 304 48

A 4-year-old Airedale Terrier that had developed estrogen-induced aplastic anemia had a complete recovery after supportive treatment and weekly administrations of nandrolone decanoate. The anemia was induced iatrogenically by administration of estradiol cypionate (2 mg, IM each time) at 48- to 72-hour intervals. Clinical signs included lethargy, anorexia, and weakness; hemoglobin was 6.8 g/dl, PCV was 21%, and WBC was 1,500/dl. Supportive treatment included blood transfusions and administration of antibiotics, corticosteroids, and vitamins. Hematologic values returned to normal by day 81, and the dog has remained healthy for one year after treatment.
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PMID:Responsive estrogen-induced aplastic anemia in a dog. 361 Jul 89

The patient was a 59-year-old man who had been in hospital suffering from aplastic anemia with transfusion hemosiderosis. Sudden onset of weakness, shaking chills and headache was observed after his staying out overnight on July 25, 1981. His temperature was 39.3 degrees C and he complained of abdominal pain and abdominal distension. His blood pressure dropped to a dangerous level and tonic convulsions that had begun in the upper body gradually extended to the whole body and he died 23 hours after his return. V. vulnificus was isolated by the blood culture performed before death. During his stay away from the hospital, he had eaten raw cuttlefish, which was considered to be the source of infection. V. vulnificus is one of the halophilic marine vibrios and is isolated frequently in summertime from the sea foods and sea water near Japan. It has been disclosed that the presence of underlying diseases such as liver cirrhosis, hemochromatosis can predispose a person to fatal sepsis by V. vulnificus. In this case, besides leukocytopenia, the presence of hemosiderosis induced by many transfusions was considered to be a major cause leading to the fulminating course of the disease.
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PMID:[Fatal Vibrio vulnificus infection in a patient with aplastic anemia]. 667 24

A 53-year-old woman with polymyositis associated with thymoma subsequently developed pure red cell aplasia (PRCA). She was hospitalized because of fever and muscle weakness, and diagnosed as having polymyositis by muscle biopsy. Remarkable clinical improvement followed administration of prednisolone. Progressive anemia became evident, however, while prednisolone was being tapered. Erythroid aplasia and the presence of thymoma confirmed the diagnosis of PRCA. Further examinations revealed that cytotoxic T cells may play an important role in the pathogenesis of this case.
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PMID:Polymyositis associated with thymoma and the subsequent development of pure red cell aplasia. 754 45

A 37-year-old Japanese man with chronic myeloid leukemia (CML) developed myasthenia gravis 29 months after bone marrow transplantation (BMT) from an HLA one locus-mismatched brother. Proximal muscle weakness and bilateral ptosis occurred along with the exacerbation of chronic GVHD shortly after sudden cessation of cyclosporine (CYA) and prednisolone. The diagnosis of myasthenia gravis was made based on clinical symptoms and elevation of an anti-acetylcholine receptor antibody titer and all symptoms related to myasthenia gravis promptly diminished with the start of treatment for chronic GVHD. In most previously reported cases, the underlying disease was aplastic anemia (6 of 7 cases) and donors were of the opposite sex (6 of 7 cases). The haplotypes HLA B7 (3 of 5 cases), B35 (3 of 5 cases), and DR2 (3 of 3 cases) were common. All cases suffered from chronic GVHD. The present case had only chronic GVHD and HLA B7 as a background for myasthenia gravis after BMT. The abrupt cessation of immunosuppressive therapy may also be related to the development of myasthenia gravis after BMT.
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PMID:Myasthenia gravis after allogeneic bone marrow transplantation. 795 Nov 5

Systemic Lupus Erythematosus (SLE) may be associated with inhibition of hematopoiesis mediated by antibodies, T-cells or both. A 41-year-old woman with a five-year history of SLE treated with prednisone was admitted to Cabrini Medical Center in New York. The patient complained of fever, chills, arthralgias, general malaise, weakness and dyspnea on exertion, and showed malar rash, pallor, and a systolic ejection murmur along the left sternal border. Admission work up included a CBC with evidence of moderate pancytopenia, a normal EKG, and a normal chest X-ray. The patient's anemia was symptomatic and required a transfusion of packed red blood cells (PRBC's). Bone marrow biopsy and aspiration revealed an aplastic marrow with few hypoplastic islands of hematopoietic elements. The patient was treated with plasmapheresis, achieving immediate progress towards recovery. Bone marrow culture studies (erythroid BFU-E, and myeloid CFU-GM) were done by incubating various titers of the patient's acute phase plasma with normal bone marrow cells. This was done to determine if the patient's plasma contained any hematopoietic inhibitory activity, as has been reported in other cases. Our experiments demonstrated marked inhibition of erymathropoiesis and myelopoiesis in vitro, when various titers of the patient's plasma were included in the culture media. Control plasma produced no inhibition. These studies support the hypothesis that a circulating antibody which inhibits hematopoiesis may be produced in SLE patients with aplastic anemia, and be responsible for it.
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PMID:Inhibition of hematopoiesis by a plasma factor in a case of aplastic anemia associated with systemic lupus erythematosus. 863 71

A 20-year-old man with aplastic anemia developed myasthenia gravis (MG) 7 months after bone marrow transplantation (BMT) from an HLA one locus-mismatched sister. Proximal muscle weakness (predominant in the lower limbs) and dysphagia occurred without any other sign of graft-versus-host disease (GVHD), 1 month after cessation of immunosuppression with cyclosporine. The diagnosis of MG was based on clinical symptoms and on neurophysiologic investigations showing a significant increase of the Jitter in single-fiber electromyography and a significant decremental response during repetitive stimulation at slow rates, but antibodies against the acetylcholine receptor (AchRab) were negative. All clinical and neurophysiological signs normalized within 1 month of treatment with low-dose prednisolone and pyridostigmine, and the patient is perfectly well 1 year after cessation of all therapy. All cases of BMT-associated MG previously published are reviewed in comparison with ours. The originality of this new observation is that this case is the only one not associated with chronic GVHD and negative for AchRab. Alternatively, MG may have been the sole manifestation of chronic GVHD in this patient.
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PMID:Myasthenia gravis without chronic GVHD after allogeneic bone marrow transplantation. 970 30

Though aplastic anaemia in children is an important haematological disorder, not many studies have been undertaken in India and especially in the northern districts of West Bengal. The present study was carried out at North Bengal Medical College and Hospital to find the occurrence, clinical and hematological profile of children with aplastic anaemia. All the children (less than 15 years) having relevant history and clinical features underwent a complete blood count and bone marrow aspiration study (smear and histological sections) and trephine biopsy. Total number of children diagnosed were 21 (M = 17, F = 4), having an age range of 6-14.5 years (mean 11.36). Relevant aetiological factors were noted in 10 cases (47.61%), including history of exposure to insecticides, fungicides and fertilisers in 5 cases (23.81%). The common symptoms were due to anaemia (weakness, pallor in all cases), leucopoenia [fever in 16 cases (76.19%)] and thrombocytopenia [bleeding in 10 cases (47.61%)]. Severe and moderate aplastic anaemia were noted in 7 (33.33%) and 12 (57.14%) cases respectively. The calculated occurrence of aplastic anaemia is 1.96/million population of children/year in the four northern districts of West Bengal. The bone marrow aspiration was satisfactory in all cases. Histological sections of aspirated marrow particle produced better architectural relationship among different components. Aplastic anaemia is a major hematological problem among the children of northern districts of West Bengal. Simultaneous examination of smear and histological sections of marrow particles is a satisfactory method for detection of aplastic anaemia.
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PMID:Clinicohaematological analysis of aplastic anaemia among children of northern districts of West Bengal. 1958 82


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