Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old woman with traumatic rupture of the thoracic descending aorta had a history of previous blood transfusion 23 years ago. This time, she received 4,600 ml of blood transfusion during the replacement procedure of thoracic aorta. On the 12th postoperative day, she had acutely progressive severe jaundice, anemia and hepatosplenomegaly. All transfused blood was compatible by bromelin method before operation. Serological studies revealed a secondary response of hemolytic transfusion reaction due to anti E and anti c antibodies. She fell into severe bilirubinemia (66 mg/dl) and anuria, and died on 19th day after operation. A positive Coombs test in a patient who has been transfused recently must be interpreted with great caution. The "coated" cells may be incompatible donor cells in a patient who has antibodies from a prior transfusion. The incompatibility occasionally leads to delayed transfusion reaction that may stimulate "autoimmune" hemolytic anemia.
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PMID:[Fatal delayed hemolytic transfusion reaction in a postoperative case of traumatic aortic rupture]. 211 89

A 50 year old man with chronic lymphocytic leukemia (CLL) and extreme hyperleukocytosis (600 x 10(9)/liter) presented with a respiratory distress syndrome, congestive heart failure with cardiomegaly, endotoxic shock and anuria. Examination revealed nodes in all areas and hepatosplenomegaly; laboratory studies showed hypoxemia and a chest X-ray diffuse bilateral alveolar infiltrates. He was treated twice by leukapheresis using a cell separator. This procedure removed 10.1 x 10(10) white blood cells with marked clinical improvement and resolution of air-space diseases over the subsequent 48 hours. Despite this unusual indication for leukapheresis in CLL, this procedure may be of value in treating the leukemic phase of CLL with pulmonary leukostasis.
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PMID:[Therapeutic leukapheresis in a leukostasis syndrome complicating chronic lymphoid leukemia]. 324 94

Of 4651 admissions between February 1995 and February 1996, 1043 had a presumed diagnosis of malaria. Six hundred and twenty-seven cases were confirmed by thick blood film examinations. The highest prevalence was in October (124/480 admissions) and the lowest in March (12/303). Sixty-five children died while 562 survived, 12 with defects. The first treatment in 422 children was chloroquine, in 143 quinine, in 59 halofantrin, and in three pyrimethamine with sulfadoxine (Fansidar). 23/422 patients started on chloroquine were switched to halofantrine, two to quinine. A higher mortality was associated with coma, convulsions, hepatosplenomegaly, pulmonary congestion, jaundice, haemoglobinuria, bladder paralysis, anuria. Anaemia and fever were more severe and hypoglycaemia more frequent in children who died than in children who survived (packed cell volume 18.5 +/- 7.1 per cent vs. 25.6 +/- 7.6 per cent, p < 0.001; temperature 39 +/- 1.1 degrees C vs. 38.7 +/- 0.9 degrees C, p < 0.05; random blood sugar < 40 mg/100 ml; 76 vs. 22 per cent, p < 0.01). There was no difference in the median age, pretreatment duration, and prevalence of diarrhoea and sickle cell disease. The male to female ratio was 1.5:1 in the surviving children vs. 1:1.03 in the dead.
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PMID:Malaria prevalence and outcome in the in-patients of the Paediatric Department of the State Specialists Hospital (SSH), Maiduguri, Nigeria. 960 1

We report a case of a 22 years old type 1 diabetic man with a history of weight loss, weakness, anorexia, fever and recurrent urinary tract infection since February 2001. In April 2001, he presented anuria due to obstructive acute renal failure. Hepatosplenomegaly and lymphadenopathy were absent at physical examination. Laboratory tests revealed a high level of gamma globulin (53.4 g/l) and anaemia (haemoglobin 7.7 g/100 ml) without leukopenia and thrombocytopenia. CT scan showed multiple retroperitoneal lymphadenopathies causing compression of the two ureters, hydro-ureter associated with hydronephrosis, hepatosplenomegaly and multiple pulmonary nodes. Lymphadenopathies, anaemia, high level of gamma globulin, high titres of anti-leishmanial antibodies and the excellent outcome after treatment with meglumine antimoniate (Glucantime) confirmed visceral leishmaniasis. This report documented an unusual clinical presentation of Visceral leishmaniasis in a diabetic patient.
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PMID:[Obstructive acute renal failure revealing visceral leishmaniasis in a diabetic patient]. 1272 15

Allopurinol is a xanthine oxidase inhibitor used in management of chronic gout. It acts by reducing the amount of uric acid by inhibiting purine metabolism. A middle-aged hypertensive female who was on allopurinol for 7 months presented with generalized weakness and exertional dyspnea. Investigations revealed pancytopenia: normocytic normochromic anemia (Hb-3.2g/dL, TLC-3400/mm3) and severe thrombocytopenia (Platelets-1000/mm3) with mild hepatosplenomegaly and grade 2 medico renal disease with normal cardiac status. Nutritional, hemolytic and infective causes were ruled out. She was transfused with fresh whole blood, platelets, administered empirical antibiotics and started on steroids. Initially, she responded to treatment but later developed an episode of convulsions with anuria and succumbed to leukopenic sepsis secondary to hypo/aplastic anemia probably due to allopurinol. Allopurinol is used extensively in the management of chronic gout and is well tolerated due to its safety profile. But we here report a case of allopurinol induced aplastic anemia leading to the demise of a patient. Allopurinol though safe needs careful monitoring.
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PMID:Allopurinol: Sorrow to the marrow. 3275 32