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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertensive emergencies of 10 children with renal hypertension were analysed. Cause of renal disease are chronic renal failure in three, acute renal failure in three, hemolytic uremic syndrome in two, acute post streptococcal glomerulonephritis in one, and renal arterial stenosis in a further patient. Therapy should be started early in the course of the hypertensive emergency, first symptoms are headache and vomiting. Drug of first choice is diazoxide (3-5-(8)mg/kg i.v.). Three patients developed transitory hyperglycemia after repeated injections of diazoxide.
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PMID:[Hypertensive emergencies in children with renal hypertension (author's transl)]. 76 42

Oppenheimer and Fischberg's vasoconstriction-hypothesis on the pathogenesis of hypertensive encephalopathy was subsequently supported by animal experiments. Later on the role of decompensation of the autoregulatory mechanism of the cerebral blood flow was revealed. The transient symptomatology comprises headache, seizures, focal cerebral symptoms (hemiplegia etc.), visual disturbances, mental disorders, papiledema etc. The age-dependency of the influence of edema is probably expressed by the predominance of seizures in childhood and the long duration of the symptoms in our third and fourth patient. The differentiation between hypertensive encephalopathy and a local complication of hypertension (hemorrhage) can be difficult, not at least because the first disturbance may be followed by the second (patient 3). Hypertension is not always present as initial symptom (patient 1 and 2). Hence a series of blood pressure readings is required in acute cerebral incidents in childhood. Steroid-treatment may lead, especially in patients suffering from a hypocomplementemic form of membranoproliferative glomerulonephritis, to a sudden rise of the blood pressure and subsequently to hypertensive encephalopathy (patients 2 and 3). Hypertensive encephalopathy is a neuropediatric emergency. The urgent treatment with dioxaside, fursemide and sodium nitroprusside is shortly reviewed.
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PMID:Hypertensive encephalopathy in childhood. Diagnostic problems. 98 19

An analysis of 4 cases of the thrombotic thrombocytopenia in children of 4 to 10 years of age is performed. The disease was characterized by fever, purpura, headache and abdominal pains, arterial hypertension, microangiopathic haemolytic anemia, thrombocytopenia, increase of blood urea and serum creatinine, micro-haematuria and proteinuria. The duration of the disease was from 4 days to 7 months. Anuria, gangrene of the ears, scrotum, penis and soft tissues of legs and feet were registered in a 5-year-old patient with a fulminant disease. The cause of death of other patients was heart failure with acute lung oedema, brain haemorrhages and haemorrhagic pancreonecrosis. The diagnosis of the thrombotic thrombocytopenia was confirmed by the finding in the autopsy material of thrombotic microangiopathy of small arteries, veins, arterioles, venules and capillaries in kidneys and other organs and tissues. Kidney damage in fulminant disease is complicated by segmentary cortical necrosis, in a more prolonged disease--by glomerulosclerosis or mesangio-capillary glomerulonephritis.
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PMID:[Thrombotic thrombocytopenic purpura in children]. 180 69

We present two patients with Hantaan virus infection, admitted to the Department of Nephrology, Skopje, at the same time, with the same clinical presentation (chills, fever, abdominal pain, hemorrhages, nausea, headache, proteinuria, hematuria, oliguria, acute renal failure) but with different pathohistological findings and different disease courses. In the first case diffuse proliferative glomerulonephritis was found, with a complete recovery of renal function after a month, with a mild proteinuria and erythruria during the second and the third month. In the second case, glomeruli were normal in general, with slight mesangial proliferation found in two out of twenty, but interstitial edema, lymphocyte infiltrations and tubular changes were noted. Complete recovery was not noted after 3 months of follow-up. The patient is now without hemodialysis treatment, with polyuria, in the stable phase of chronic renal failure which is not improving.
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PMID:Different pathohistological presentations of acute renal involvement in Hantaan virus infection: report of two cases. 198 98

A 28 year old woman with systemic lupus erythematosus who developed chronic lupus peritonitis and ascites is described. Lupus peritonitis appeared with abdominal fullness, postprandial abdominal discomfort, and painless ascites. Four months later the patient developed vertigo, headaches, visual disturbances, serositis, and glomerulonephritis. Lupus peritonitis and the other disease manifestations responded to treatment with intravenous pulse methylprednisolone (four 1 g/m2 injections at one week intervals), oral azathioprine (200 mg daily), and diuretics.
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PMID:Chronic lupus peritonitis with ascites. 201 11

1. To assess the risk of end-stage renal disease (ESRD) associated with the regular use of three classes of non-narcotic analgesics, we performed a case-control study of 340 patients with ESRD on a haemodialysis maintenance program and 673 hospital controls. 2. The overall odds ratio estimate for non-narcotic analgesics taken at least every other day for 30 days or longer before the first symptom of renal disease was 2.89 (95% CI, 1.78 to 4.68). 3. The risk increased in relation to the use duration. 4. The previous regular consumption of combinations containing phenacetin was strongly associated with ESRD (odds ratio, 19.05; 95% CI, 2.31 to 157.4). The odds ratio for previous regular consumption of salicylates was 2.54 (95% CI, 1.24 to 5.20) and for pyrazolones 2.16 (95% CI, 0.87 to 5.32). 5. An analysis for possible confounding by a history of repeated headaches, arthritis, kidney stones, hypertension, and diabetes did not alter the results. 6. The odds ratio estimates for different pathological subgroups of ESRD patients in relation to previous use of any non-narcotic analgesic were glomerulonephritis. 10.57 (95% CI, 1.25 to 89.0), interstitial nephritis, 3.33 (95% CI, 1.21 to 9.17), cystic kidney disease, 0.71 (95% CI, 0.25 to 1.97), and unknown, 5.15 (95% CI, 2.29-11.57). 7. The results of this study suggest that the regular consumption of analgesics should be routinely considered as a risk factor for any non-congenital cause of chronic renal failure. They also suggest that the risk of ESRD associated with the regular consumption of phenacetin is much higher than the risk associated with other non-narcotic analgesics.
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PMID:End-stage renal disease and non-narcotic analgesics: a case-control study. 227 70

The clinical findings during a major epidemic of Q-fever which affected 415 people in the Val de Bagnes (Valais, Switzerland) in the autumn of 1983 are reported. Q-fever symptoms were evident in 191 cases but inconspicuous or absent in 224 cases. The symptoms most frequently reported were prolonged high fever, headaches, severe exhaustion, loss of appetite, cough and myalgia. Amongst disorders which accompany acute Q-fever, pneumonia and granulomatous hepatitis are very frequent, while myopericarditis and glomerulonephritis are less frequently observed. Endocarditis, a later complication of Q-fever, is a severe illness which more frequently affects patients with underlying valvular lesions. New serological techniques now permit more rapid and more accurate diagnosis of both acute and chronic Q-fever.
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PMID:[Clinical aspects observed during an epidemic of 415 cases of Q fever]. 389 64

A variety of prodromal symptoms of viral hepatitis (urticaria, fever, arthralgias, headache, polyradiculonevritis) are attributed to A, B, C, D or E hepatitis only when jaundice appears, and because they disappear with it. Spectacular extrahepatic symptoms (polyarteritis nodosa, cryoglobulinemia, glomerulonephritis, marrow aplasia...) may be associated with B or C hepatitis without any liver symptom. Some of the extrahepatic symptoms observed during chronic hepatitis C therapy with interferon (thyroid dysfunctions, cutaneo-mucous lichen) may be related to the immunomodulatory effects of interferon rather than to virus C itself.
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PMID:[Extra-hepatic manifestations of viral hepatitis]. 772 20

A 13-year-old girl with a severe headache, blurred vision, altered mental status, seizures, high blood pressure, edema and hematuria is presented. With a previous history of upper respiratory tract infection, acute onset of edema, gross hematuria, high ASO and low C3 levels, she was diagnosed with acute poststreptococcal glomerulonephritis (APSGN) and hypertensive encephalopathy. Computed tomography (CT) revealed symmetric hypodense areas representing edema in the parieto-occipital regions. As noted in previous reports, these CT findings are of value in establishing the diagnosis of hypertensive encephalopathy. In this particular case the CT appearance and the subsequent clinical improvement without any neurological deficit supported the diagnosis of hypertensive encephalopathy due to APSGN. We emphasize that awareness of the CT findings of hypertensive encephalopathy may facilitate in making the correct diagnosis in symptomatic hypertensive patients, especially in cases with an unusual presentation or clinical course.
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PMID:Cranial computed tomographic findings in a patient with hypertensive encephalopathy in acute poststreptococcal glomerulonephritis. 782 39

No commemoration of the bicentennial of Mozart's death would be complete without some consideration of that premature yet predictable demise. Mozart's premonitions of death are well known and apparently played a role in the composition of the K.626 Requiem and perhaps other works. His death has traditionally been ascribed to infectious causes, chiefly rheumatic fever or post-streptococcal glomerulonephritis, exacerbated by intemperance and chronic penury. Pathology has been difficult because of his supposed burial in a pauper's grave, the location and contents of which were later supposedly lost. Mozart's burial place in St. Mark's Cemetery in Vienna was known and, in the parlance of the day, "reorganized" a decade later, as the occupants of plots were disinterred to make room for the more recently decreased. A skull believed to the Mozart's was saved by the successor of the gravedigger who had supervised Mozart's burial, and then passed into the collections of the anatomist Josef Hyrtl, the municipality of Salzburg, and the Mozarteum museum (Salzburg). Forensic reconstruction of soft tissues related to this skull reveals substantial concordance with Mozart's portraits. The skull suggests premature closure of the metopic suture, which has been suggested on the basis of his physiognomy. A left temporal fracture and concomitant erosions raise the question of chronic subdural hematoma, which would be consistent with several falls in 1789 and 1790 and could have caused the weakness, headaches, and fainting he experienced in 1790 and 1791. Aggressive bloodletting to treat suspected rheumatic fever could have decompensated such a lesion to produce his death on December 5, 1791.
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PMID:Mozart's chronic subdural hematoma. 799 Nov 48


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