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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Haemorrhagic fever with renal syndrome (HFRS) is an acute disease caused by Hantavirus and clinically characterised by abrupt onset of fever, various haemorrhagic manifestations and transient renal and hepatic dysfunction. We retrospectively reviewed 63 cases of HFRS in children from 13 different hospitals in Korea who presented over a 15-year period. The age of the patients ranged from 7 to 15 years, with a male to female ratio of 8 to 1. Fifty-four (86%) patients were 10 years or older. On admission, 24 (38%) were in the febrile phase and 35 (56%) were in the oliguric phase. Fever (100%) abdominal pain (91%), headache (76%) and vomiting (73%) were the most common symptoms. Backache, subconjunctival haemorrhage and hypertension were also noted in about one-third of patients. Hypotension was documented in only 7 (11%) patients. Leucocytosis (> 10,000/mm3) and thrombocytopenia (< 150,000/mm3) were noted in more than two-thirds of patients. Elevated blood urea nitrogen and serum creatinine was observed in 94% by the 7th (median) day of illness. Elevated aspartate aminotransferase and/or alanine aminotransferase were found in more than two-thirds of patients. Renal biopsy was performed in 12 patients and revealed various stages of acute tubular necrosis with occasional interstitial cell infiltration and oedema. Only 2 showed evidence of interstitial haemorrhage. Eleven patients required 1-3 days of dialysis and the remaining patients required only conservative management. Three (5%) patients died of shock, respiratory failure and pulmonary haemorrhage. All other patients recovered without sequelae. Although childhood cases were much less common than adults, clinical and laboratory findings were in general similar between children and adults.
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PMID:Haemorrhagic fever with renal syndrome in Korean children. Korean Society of Pediatric Nephrology. 781 97

The clinical characteristics of serologically verified nephropathia epidemica, the Scandinavian form of hemorrhagic fever with renal syndrome, were studied in Swedish children who were < 15 years of age. In 1990 to 1992, 14 cases were prospectively followed. A retrospective survey during 1984 to 1990 disclosed another 18 cases. Among the 32 cases (20 boys, 12 girls, 3 to 15 years of age; median age, 11 years), the most common symptoms were fever (100%), headache (100%), abdominal pain (93%), vomiting (91%) and back pain (76%). Laboratory findings included elevated serum creatinine concentration (19 of 28) and thrombocytopenia (7 of 22). Urinalysis showed proteinuria (31 of 31 patients) and hematuria (24 of 30). Six children had mild hemorrhagic manifestations (epistaxis, metrorrhagia, and petechiae). No severe complications occurred. The clinical symptoms of children with nephropathia epidemica seem to be similar to those found among adult nephropathia epidemica cases.
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PMID:Nephropathia epidemica (hemorrhagic fever with renal syndrome) in children: clinical characteristics. 790 97

Quinine-induced immune thrombocytopenia with hemolytic uremic syndrome (HUS) is a recently defined clinical entity. In this paper we have attempted to characterize the natural history and laboratory abnormalities typical of quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome in nine patients experiencing ten episodes of the disease. In addition, review of other reported cases of probable quinine-induced HUS is presented. The disease was characterized by the onset of chills, diapheresis, nausea and vomiting, abdominal pain, decreased urine output, and petechiae following quinine exposure. All patients experience significant anemia, severe thrombocytopenia, increased lactate dehydrogenase, elevated serum creatinine, and oliguria. Quinine-dependent platelet-reactive antibodies were identified in eight of nine using flow cytometry. Unexpectedly, drug-dependent antibodies reactive with red cells and granulocytes were identified in four and eight patients, respectively. All patients were treated with plasma exchange (range 1-12 procedures), and seven required hemodialysis. All survive without residual abnormality. Our experience with nine patients with quinine-induced HUS and the nine additional cases reported by others and reviewed in this paper establishes this condition as a distinct clinical entity. Adult patients presenting with HUS should routinely be asked about exposure to quinine in the form of medication or beverages. The mechanism by which quinine-dependent antibodies produce renal failure is uncertain, but preliminary studies (described elsewhere) suggest that drug-induced antibodies reactive with endothelial cells and possibly margination of granulocytes in renal glomeruli may be responsible for this complication. The prognosis in quinine-induced HUS is better than in other forms of adult HUS.
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PMID:Quinine-induced immune thrombocytopenia with hemolytic uremic syndrome: clinical and serological findings in nine patients and review of literature. 797

We reviewed the thirty cases of cytomegalovirus infections with occurred in previously healthy patients, hospitalised for fever from 1981 to 1992. Pregnant women, transplant recipients, HIV infected persons and all immunocompromised subjects were excluded. We observed 34 cases (18 women, 16 men) whose mean age was 34 years (17 to 79). Fever appeared progressively (73%), persisted more than 15 days (87%) and was well tolerated. The main functional symptoms were headaches, myalgia (53%), profuse sweat (50%), abdominal pain, diarrhea, recent loss of weight, dry cough (51%). Splenomegaly was present in 24% of the cases. Chest X ray was always normal. Differential blood count was always inverse and an authentic mononucleosis syndrome was present in 91%: it appeared mainly 13 days after onset of symptoms. Hepatic abnormalities were nearly constant, especially cytolytic (97%) (transaminases three or four times upper the normal limit) but also cholestatic (62%). Thrombopenia has been noticed once (48,000/mm3). Serological diagnosis was confirmed with Elisa test (anti CMV Ig M: 30 cases) or complement fixation test (seroconversion: one, significant increase of the titers: two). CMV viremia, studied in seven patients, was positive in three. Spontaneous or treated (NSAI in 30%) outcome was nearly always favourable (97%). Two patients presented severe complications: meningo encephalitis and spleen rupture. CMV infection in previously healthy patients has to be suspected, without waiting for the mononucleosis syndrome, in view of a prolonged, well tolerated febrile illness, without pharyngitis, associated with hyperlymphocytosis and mild cytolysis. A careful follow-up is needed to detect the rare but severe complications.
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PMID:[Clinical, biological and developmental aspects of cytomegalovirus infection in immunocompetent patients: apropos of 34 hospitalized patients]. 805 48

To diagnose possible cytomegalovirus (CMV) infection in a 64-year-old man after renal transplantation, polymerase chain reaction (PCR), pp65 antigenaemia assay (pAA) and virus isolation in cell culture were routinely performed on a weekly basis. The PCR obtained virus DNA in peripheral blood lymphocytes for the first time in the fifth week. Two weeks later the patient complained of feeling unwell with abdominal pain and vomiting on eating. Two days later he developed a fever up to 38 degrees C and nocturnal sweats. Gastroscopy revealed marked antral gastritis which histologically showed typical cytomegalic "owl-eye" cells. The pAA was clearly positive and the cell culture started in the fifth week now showed a cytopathogenic effect. CMV gastritic having been diagnosed treatment consisted of 175 mg ganciclovir intravenously twice daily for 10 days. He became symptom-free after two days. The only side effects were thrombocytopenia down to 67,000/microliters and a rise in transaminase activities, changes which regressed later. To ensure early diagnosis and treatment of any CMV infection, specific virus diagnostic tests should be routinely undertaken after transplantation of organs from CMV-positive persons into CMV-negative patients.
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PMID:[Acute cytomegalovirus gastritis after kidney transplantation. Its diagnosis by the polymerase chain reaction, antigenemia assay and immunohistochemistry]. 822 13

A 74-year-old man developed bilateral arterial thrombosis of the lower limbs related to heparin-associated thrombocytopenia syndrome (HATS). On day 4 after thrombectomy of both limbs, abdominal pain, fever, hypotension, abdominal tenderness appeared. Acute acalculous cholecystitis was suspected and cholecystectomy was carried out although the gallbladder was not imflamed. Later on, hyponatremia in addition to the aforesaid signs suggested the diagnosis of adrenal insufficiency. Diagnosis was confirmed by low cortisol and aldosterone plasma concentration and by CT scan, which showen two enlarged adrenal glands. HATS might explain two unexpected facts: occurrence of adrenal hemorrhage during heparin therapy with coagulation tests within the therapeutic range and paradoxical thrombosis in the central vein of adrenal gland. HATS must be regarded as one cause of adrenal hemorrhage necrosis.
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PMID:Heparin-associated thrombocytopenia syndrome: an underestimated etiology of adrenal hemorrhage. 829 32

A 71-year-old man with an aortobifemoral bypass graft had experienced several episodes of severe pain in the thoracic and lumbar spine, followed by severe abdominal pain, during the preceding two weeks. Physical examination, chest X-ray, ultrasonography and computed tomography of the abdomen provided no specific pointers to a diagnosis. He was anaemic (haemoglobin 95 g/l), but had a normal WBC count with neutrophilia (up to 91%) and thrombocytopenia (up to 24,000/microliters). The transaminase and lactate dehydrogenase activities were raised, as were the bilirubin level and the retention values. There was a metabolic acidosis (pH 7.20). Because of suspected septicaemia ciprofloxacin (twice daily 200 mg) was administered intravenously. But the patient gradually lost consciousness, required mechanical ventilation and died 24 hours after admission in circulatory failure. Autopsy revealed a meningoencephalitis, carcinoma of unknown primary with bone marrow carcinomatosis as well as widespread carcinomatosis of blood and lymph vessels. The findings of blood, urine and sputum cultures, available only postmortally, revealed growth of tetracycline-resistant Salmonellae enteritidis.
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PMID:[Lethal Salmonella enteritidis meningoencephalitis in an adult with a carcinoma of an unknown primary site]. 778 29

Hepatic rupture and infarction associated with toxemia of pregnancy usually occur in multiparous women close to 30 years of age. The most important presenting symptom is right upper-quadrant abdominal pain. Sonography is the most expedient way of making the diagnosis of either rupture or hemorrhagic necrosis, but computed tomography is more sensitive. Elevated transaminase levels and thrombocytopenia or disseminated intravascular coagulation may occur acutely but resolve quickly. Termination of pregnancy is the cornerstone of any treatment plan. Many cases may not require operative treatment other than inspection. In others, surgical hemostasis will be lifesaving. We describe four preeclamptic women, two with ruptured subcapsular hematomas and two with hemorrhagic infarction. Radiological and laboratory evidence of liver damage and recovery are presented.
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PMID:Massive hepatic necrosis in toxemia of pregnancy. 845 48

Two males aged 12 and 38 years presented with widespread severely pruritic blackish spots for 15 days. Widespread slate-grey patches and erythematous hyperpigmented plaques were observed with a positive Darier's sign. There were associated neck swellings, abdominal pain, anorexia, weight loss and bleeding gums in both. Peripheral blood and bone marrow showed blast cells, anaemia and thrombocytopenia. Cell surface markers confirmed the presence of acute lymphoblastic leukaemia. Skin biopsy showed an infiltrate of lymphoblasts as well as mast cells. Partial response was noted with cytotoxic therapy in 1 patient. Thus lesions mimicking urticaria pigmentosa may be the presenting sign of acute lymphoblastic leukaemia.
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PMID:Urticaria-pigmentosa-like lesions in acute lymphoblastic leukaemia (2 cases). 845 53

Four cases of adrenal insufficiency due to bilateral adrenal haemorrhage in patients with antiphospholipid syndrome are reported. The 1st patient had repeated episodes of thrombosis on a background of altered general condition; he was examined by computed tomography (CT) which showed enlarged and presumably tumoral adrenal glands; adrenal insufficiency was present and improved under hormone replacement therapy; the thrombotic episodes were attributed to the antiphospholipid antibodies; after a 5-year follow-up the antiphospholipid syndrome remained alone, and further examinations showed progressive adrenal atrophy. The 2nd patient had systemic lupus erythematosus with thrombocytopenia; because of abdominal pain CT was performed, showing bilateral adrenal enlargement; treatment with intravenous pulses of cyclophosphamide and high-dose immunoglobulins combined with corticosteroids failed, and splenectomy was performed disclosing an old adrenal haematoma which was evacuated. The 3rd patient had bilateral and asymmetrical adrenal hypertrophy at CT; subsequently, systemic lupus erythematosus was diagnosed with anti-prothrombinase and anticardiolipin accounting for the initial findings; follow-up examinations showed the formation of pseudocysts in the adrenals; following myocardial infarction the patient died of cerebral haemorrhage, and autopsy confirmed the presence of old, bilateral adrenal haematomas. The 4th patient had recurrent vein thrombosis associated with distal ischaemia, which prompted CT in search of a neoplasia; this examination revealed 2 large adrenal haematomas while anticardiolipin antibodies were found. In patients with antiphospholipid syndrome any functional or morphological abnormality of the adrenals should prompt a search for bilateral adrenal haemorrhage. Conversely, in all cases of adrenal insufficiency a search for antiphospholipid antibodies should be part of all aetiological investigations, and this search should be carried out prior to withdrawing corticosteroids in cases of systemic lupus erythematosus with antiphospholipid antibodies.
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PMID:[Antiphospholipid syndrome. A new cause of bilateral hemorrhage of the adrenal glands. 4 cases]. 851 Nov 42


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