Gene/Protein Disease Symptom Drug Enzyme Compound
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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As in adults, desmopressin (DDAVP) can be used in children for prophylaxis of bleeding and to stop bleeding in many hereditary and acquired bleeding disorders. DDAVP is the treatment of choice in children with mild hemophilia and type 1 von Willebrand's disease (vWD). It is effective in some variants of vWD and in many patients with platelet function defects. It reduces the bleeding diathesis of children with uremia and drug-induced bleeding complications. In any case, a test dose of DDAVP has to be given to the patient to predict the hemostatic effect before relying on this drug for treatment. The response can be measured by shortening of the bleeding time (BT) and of partial thromboplastin time (PTT), indicating a rise of Factor (F) VIII or von Willebrand factor (vWF). Side effects such as facial flushing, transient headache, increased pulse rate, and drop in systolic blood pressure are mild and transient. They can be minimized when the dose is not exceeding 0.3 microg/kg body weight, and the infusion lasts at least 20 to 30 minutes. The strong antidiuretic action of DDAVP has some potential problems that are negligible in adults and older children when water intake is restricted. In infants and small children under the age of 18 months, however, DDAVP should be used with caution and with close surveillance in order to prevent water intoxication and electrolyte imbalance. The danger is increased when the patients receive parenteral fluid substitution. The advantages of DDAVP include the reduction in the use of plasma factor concentrates, thereby minimizing the danger of immunological or infectious complications, as well as the considerable reduction of costs realized by treatment with this form of medication. Fortunately, it can be applied successfully in the most frequent hereditary bleeding disorder, namely vWD type 1.
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PMID:Desmopressin (DDAVP) in bleeding disorders of childhood. 1006 51

A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 degrees C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm x 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm x 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa (Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20, 800/microL with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/microL. The prothrombin time/activated partial tissue thromboplastin was 10. 4/28.0 s (normal PT, 9.3-12.3 s; normal PTT, 21.3-33.7 s) and fibrinogen was 558 mg/dL (normal, 192-379 mg/dL). Urinalysis showed 1+ protein, 8-10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative Staphylococcus epidermidis. The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. Cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83-177 mg/dL). His urine lightened to yellow-brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal.
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PMID:A child with spider bite and glomerulonephritis: a diagnostic challenge. 1080 79

Crimean-Congo hemorrhagic fever was for the first time recognized in Yugoslavia in 1971. In this paper were presented clinical and laboratory findings of a patient infected with Crimean-Congo hemorrhagic fever in Kosovo in 1999. The disease was manifested with fever, headache, vomiting, myalgia, abdominal pain, pharyngitis, conjuctival injection, diarrhoea, hypotension, gingival bleeding, skin hemorrhages, hematuria, hepatomegaly, splenomegaly, jaundice, thrombocytopenia, prolonged prothrombin and partial thromboplastin time, high serum fibrinogen degradation product, leukocytosis, mild anemia, elevated levels of bilirubin and serum aminotransferases. Diagnosis was set clinically, epidemiologically and supported by serological tests. Supportive management of hypotension, multi-organ failure, coagulation disturbances the patient was of the utmost in the treatment together with the isolation and prophylactic measures.
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PMID:[Crimean-Congo hemorrhagic fever]. 1152 72

A 21-year-old male soldier was admitted due to a sore throat, headache, generalized lymphadenopathy and persistent fever for 12 days. Despite empirical antibiotic treatment for four days at a clinic prior to admission, he continued to have persistent abdominal pain over his right upper quadrant region and progressive jaundice was followed by shock. After admission, he developed an episode of clonic seizures and became delirious and agitated. An electrocardiogram showed first degree atrioventricular (AV) block and non-specific ST-T wave changes. Hematological studies revealed thrombocytopenia, hypofibrinogenemia, abnormal partial thromboplastin time (PTT) and a positive test for D-dimer. The cerebrospinal fluid analysis showed pleocytosis with white cells of 84/mm3 with a lymphocyte predominance, protein of 97 mg/dL and glucose of 79 mg/dL. Indirect immunofluorescence assay showed a fourfold rise in antibodies to Orientia tsutsugamushi in paired serum with IgM antibody titer of 1:640. The patient had a favorable response after parenteral chloramphenicol in addition to oral tetracycline. Early ricognition of scrub typhus and early prescription of anti-rickettsial agents prevent complications of central nervous system involvement and further deterioration of cardiac and hematological function.
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PMID:Meningoencephalitis, myocarditis and disseminated intravascular coagulation in a patient with scrub typhus. 1156 71

Antiphospholipid antibodies are a heterogeneous family of immunoglobulins that includes lupus anticoagulant and anticardiolipin antibodies. They are strongly associated with a clinical syndrome characterized by venous and arterial thrombosis and spontaneous fetal losses. This syndrome may be primary or else secondary to autoimmune or neoplastic diseases. The cardiovascular system is frequently involved with mitral or aortic insufficiency, juvenile myocardial infarction, and primitive pulmonary hypertension. However, the occurrence of intracardiac thrombi is rare. We describe a case of an intracardiac right atrial thrombus in a 19-year-old asymptomatic woman who was admitted in December 1998 to the Thrombosis Center owing to the finding, during routine work-up, of a prolonged activated partial thromboplastin time (71 s) and thrombocytopenia (71 x 1000/mm3), a positive antinuclear antibody test (1/320), positivity for lupus anticoagulant, and increased IgG (92 GPL-U/ml) and IgM (27 MPL-U/ml) anticardiolipin antibodies. Six months later, the patient presented with headache, edema and cyanosis of the face and jugular swelling. Transthoracic and transesophageal echocardiography revealed a right atrial mass which was clearly distinguishable from the tricuspid valve and extended to the superior vena cava. The patient was successfully submitted to surgical excision of the thrombus. Histology revealed that the mass was adherent to an abnormal septum consisting of mesenchymal tissue. Although the American Rheumatology Association criteria for the diagnosis of systemic lupus erythematosus were not fulfilled, the positivity of antinuclear antibody test is in favor of a lupus-like syndrome. The decision to opt for surgical excision of the thrombus was determined by the unclear nature of the atrial mass. It may be necessary that such patients be submitted to anticoagulant therapy for the rest of their lives or temporarily (6-12 months). This underscores the importance of the anatomical abnormality as a promoting factor. Transthoracic echocardiography (as well as transesophageal echocardiography in selected cases) must be considered as an essential component of the initial diagnostic work-up in patients presenting with antiphospholipid antibodies.
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PMID:[Left atrial thrombosis in patients with antiphospholipid antibody syndrome and mesenchymal abnormal septum]. 1172 15

Severe acute respiratory syndrome is a new disease that is highly contagious and is spreading in the local community and worldwide. This report is of a hospital medical officer with severe acute respiratory syndrome. He presented with sudden onset of fever, chills, myalgia, headache, and dizziness in early March 2003. He developed progressive respiratory symptoms and bilateral pulmonary infiltrates during the second week of his illness. Blood tests showed lymphopenia, mild thrombocytopenia, and prolonged activated partial thromboplastin time with normal d-dimer level. His chest condition gradually responded to ribavirin and corticosteroids, and serial chest X-ray showed resolving pulmonary infiltrates. The importance of early diagnosis lies in the potential for early treatment, leading to better response.
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PMID:Severe acute respiratory syndrome in a doctor working at the Prince of Wales Hospital. 1277 57

Inherited thrombophilia is a risk factor for dural sinus thrombosis (DST). To our knowledge, this is the first description with autopsy findings of a patient with DST associated with heterozygous factor V Leiden and a short activated partial thromboplastin time (aPTT). A 51-year-old woman presented with a 3-day history of headache, nausea, right-sided weakness, and focal motor seizure; she died 3 days after admission. At autopsy, a gross examination showed hemorrhage of bilateral parietal lobes and left primary motor cortex, uncal and tonsillar herniation, and pulmonary embolus of the right upper lobe. A microscopic examination of the brain showed an organizing thrombus in the superior sagittal sinus, diffuse cerebral edema, and extensive venous congestion. Laboratory studies showed heterozygous factor V Leiden by polymerase chain reaction and a very short aPTT of 17 seconds (reference range, 22-30 seconds). The combination of a heterozygous factor V Leiden mutation and a short aPTT may have contributed to the fatal DST in this patient.
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PMID:Fatal dural sinus thrombosis associated with heterozygous factor V Leiden and a short activated partial thromboplastin time. 1452 55

Severe acute respiratory syndrome (SARS) is a highly infectious disease with a significant morbidity and case fatality. The major clinical features include persistent fever, chills/rigor, myalgia, malaise, dry cough, headache and dyspnoea. Less common symptoms include sputum production, sore throat, coryza, dizziness, nausea, vomiting and diarrhoea. Older subjects may present with decrease in general well-being, poor feeding, fall/fracture and delirium, without the typical febrile response. Common laboratory features include lymphopenia with depletion of CD4 and CD8 lymphocytes, thrombocytopenia, prolonged activated partial thromboplastin time, elevated D-Dimer, elevated alanine transminases, lactate dehydrogenase and creatinine kinase. The constellation of compatible clinical and laboratory findings, together with the rather characteristic radiological features especially on HRCT and the lack of clinical response to broad-spectrum antibiotics, should quickly arouse suspicion of SARS. The positivity rates of urine, nasophargyngeal aspirate and stool specimen have been reported to be 42%, 68% and 97%, respectively, on day 14 of illness, whereas serology for confirmation may take 28 days to reach a detection rate above 90%. Recently, quantitative measurement of blood SARS CoV RNA with real-time RT-PCR technique has been developed with a detection rate of 80% as early as day 1 of hospital admission but the detection rates drop to 75% and 42% on day 7 and day 14, respectively.
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PMID:SARS: clinical features and diagnosis. 1501 29

Children are susceptible to infection by SARS-associated coronavirus (SARS-CoV) but the clinical picture of SARS is milder than in adults. Teenagers resemble adults in presentation and disease progression and may develop severe illness requiring intensive care and assisted ventilation. Fever, malaise, cough, coryza, chills or rigor, sputum production, headache, myalgia, leucopaenia, lymphopaenia, thrombocytopaenia, mildly prolonged activated partial thromboplastin times and elevated lactate dehydrogenase levels are common presenting features. Radiographic findings are non-specific but high-resolution computed tomography of the thorax in clinically suspected cases may be an early diagnostic aid when initial chest radiographs appear normal. The improved reverse transcription-polymerase chain reaction (RT-PCR) assays are critical in the early diagnosis of SARS, with sensitivity approaching 80% in the first 3 days of illness when performed on nasopharyngeal aspirates, the preferred specimens. Absence of seroconversion to SARS-CoV beyond 28 days from disease onset generally excludes the diagnosis. The best treatment strategy for SARS among children remains to be determined. No case fatality has been reported in children and the short- to medium-term outcome appears to be good. The importance of continued monitoring for any long-term complications due to the disease or its empiric treatment, cannot be overemphasised.
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PMID:Clinical picture, diagnosis, treatment and outcome of severe acute respiratory syndrome (SARS) in children. 1553 Dec 51

The effect of pentosan polysulfate sodium on warfarin pharmacokinetics and pharmacodynamics was investigated in healthy subjects. Warfarin was titrated to an international normalized ratio between 1.4 and 1.8. Subjects continued their titrated dose of warfarin and received pentosan polysulfate sodium 100 mg or placebo every 8 hours for 7 days. The Cmax of R- and S-warfarin was approximately 840 to 890 ng/mL and 680 to 730 ng/mL, respectively, and was similar in the absence and presence of pentosan polysulfate sodium. The half-life for R- and S-warfarin was 52 to 56 hours and 36 to 40 hours, respectively. Prothrombin time, partial thromboplastin time, and the international normalized ratio for warfarin + placebo and warfarin + pentosan polysulfate sodium were comparable. The AUC(INR) indicated no treatment effect (P = .772); however, there was a period effect. Analysis of variance for the treatments by period indicated no treatment effect (P > .1). Adverse events were mild and included headache, epistaxis, and rash. Most adverse events were unrelated to treatment and were seen during warfarin titration. Pentosan polysulfate sodium did not affect warfarin pharmacokinetics or pharmacodynamics.
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PMID:Pharmacokinetics and pharmacodynamics of warfarin when coadministered with pentosan polysulfate sodium. 1602 2


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