Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 32-yr-old man presented with acute renal failure preceded by a viral-like disease with high fever, bilateral loin pain, nausea, headache and slight thrombocytopenia. Renal biopsy revealed only minor tubulointerstitial abnormalities. Renal function completely normalised within 10 days after hospitalisation. The diagnosis of acute Hantavirus nephropathy was proved by serological examinations.
 ...
PMID:A sporadic case of acute Hantavirus nephropathy in The Netherlands. 257 28

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
 ...
PMID:Hemorrhagic fever with renal syndrome. 257 14

A 32-year-old black man from rural southeastern Texas had headache, fever, chills, bronchopneumonia, and an atypical rash, complicated by hypotension, lethargy, confusion, liver dysfunction, thrombocytopenia, and acute renal failure. The diagnosis of Rocky Mountain spotted fever (RMSF) was not suspected until eight days after the onset of symptoms. He was subsequently treated with chloramphenicol, followed by hemodialysis and aggressive supportive therapy. He recovered uneventfully with complete return of renal function. This case emphasizes that RMSF should be considered in the differential diagnosis of any obscure febrile illness even in nonendemic areas.
 ...
PMID:Viscerotropic Rocky Mountain spotted fever in southeastern Texas: report of a survivor with atypical manifestations and multiple organ failure. 271 89

Thirteen cases of hemorrhagic fever with renal syndrome (HFRS) have been observed in the Nancy area. Ten occurred during the summer of 1983 and three in April and May 1985. The clinical characteristics were in each case very typical: abrupt onset with high fever, myalgia, intense lumbar and abdominal pain, pulsatile headache, inflammatory syndrome, WBC count increase and thrombocytopenia. Acute renal failure occurred a few days later with oliguria (9 cases out of 13), massive proteinuria (9/13) and hematuria (6/13). All patients recovered without sequelae within 8-10 days. Renal biopsy performed in 8 patients showed slight tubular lesions with interstitial mononuclear cell infiltrate, congestion and diffuse interstitial edema, and in 2 cases hemorrhagic extravasation. No glomerular lesions were observed. Clinical, histological and epidemiological characteristics of these 13 French cases are highly similar to those of the Scandinavian Nephropathia Epidemica reports. The epidemiology of HFRS remains unclear as do its pathophysiological mechanisms.
 ...
PMID:[Hemorrhagic fever with renal syndrome. Apropos of 13 cases observed in Lorraine]. 287 52

A 34-year-old quadripara was hospitalized in the 33rd gestational week due to an acute hypertensive crisis, headache, upper abdominal pain, icterus, and proteinuria. Laboratory testing revealed hemolysis, hepatic dysfunction, and thrombopenia. The values returned toward normal after delivery by cesarean section. Diffuse bleeding in the surgical wound and acute renal failure necessitated two relaparotomies, intensive hemotherapy, and hemodialysis. Mother and child were released in good condition. Anesthesiological and obstetrical aspects of the HELLP syndrome are discussed.
 ...
PMID:[The HELLP syndrome--a rare form of preeclampsia. Anesthesiologic and obstetric aspects]. 291 50

A patient with a 12 hour history of headache, breathlessness and hypotension developed acute renal failure necessitating haemodialysis for 12 days. During recovery she developed hypertension, tachycardia and facial flushing. Investigations revealed a right adrenal phaeochromocytoma. Whilst postural hypotension is common in phaeochromocytoma, profound shock with acute renal failure is rare. This may have been precipitated by concomitant drug therapy, myocardial necrosis or by necrosis within the tumour.
 ...
PMID:Phaeochromocytoma presenting with cardiogenic shock and acute renal failure. 333 32

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

A case of malignant lymphoma in the skull after head injury associated with whole bone metastasis is reported. The patient was a 66-year-old man who was admitted to Almeida Memorial Hospital because of headache and general fatigue 2 months after head injury. After admission tumors appear in the frontal and occipital region and grew rapidly. Plain craniogram revealed large map-like bone destructions and multiple punched out lesions. Bone scintigram with 99mTc-MDP revealed multiple accumulations of RI in the skull, vertebrae, ribs and pelvis. CT scan revealed destructive, markedly enhancing bone tumor which was compressing the brain as an extradural mass in the left frontal and occipital regions. Pathological examination of the tumor revealed malignant lymphoma of non-Hodgkin type and diffuse pleomorphic type. Though combination chemotherapy with ACNU, FT 207, PSK, CHOP (Cyclophosphamide, Adriamycin, Vincristine and Predonisone) and Acracinomycin A was performed after operation, and brought forth regression of tumor size and improvement of clinical symptoms transiently, he died 6 months after the onset because of recurrence in many bones with pathological fracture and complications such as pneumonia, DIC and acute renal failure. At autopsy the tumors were found to be localized only in the bones, but in none of lymphnode or visceral organs. Malignant lymphoma appearing initially as a skull tumor is rare, and its diagnosis and treatment were discussed.
 ...
PMID:[A case of malignant lymphoma in the skull after head injury associated with multiple bone tumors]. 408 41

Hantavirus-induced acute renal failure is a worldwide occurring disease and rarely known and diagnosed in Germany and in Western Europe. Its various clinical features are embraced by the term Hemorrhagic Fever With Renal Syndrome (HFRS). Cardinal symptoms of the mild European form called Nephropathia epidemica (NE) leading to diagnosis are: abrupt onset, fever, pain (abdominal, loin-, or headache), acute renal failure, proteinuria and/or hematuria, polyuria, and thrombocytopenia. Etiologic agent of NE is the vole transmitted Puumula-serotype of Hantaviruses. Severe courses of HFRS characterized by hemorrhagic complications occur in Asia and Southeast Europe and are caused by the serotypes Hantaan (Korean Hemorrhagic Fever), Seoul (rat associated) and Belgrade (both Epidemic Hemorrhagic Fever). Serological evidence of IgG and/or IgM-antibodies by indirect immunofluorescent antibody assay (IFA), enzyme linked immunosorbent assay (ELISA) or mu-capture-ELISA proves the diagnosis and allows distinction of the infecting virus type. Transmission occurs primarily through inhalation of virus contaminated aerosols or dust. Transmission between humans has never been observed. The incubation period ranges between four days to four weeks. All persons who have much outdoor activities in forests, open fields, farms, and nearby waters are at risk to be infected. Practical exposure prophylaxis seems rarely possible. Therapy of NE is only symptomatic, confined to the treatment of pain, diuretic therapy in oliguric patients, and volume and electrolyte substitution in volume depleted or polyuric patients. Sometimes temporary hemodialysis is needed. Renal history reveals commonly the pattern of acute interstitial nephritis with typical focal interstitial microhemorrhages.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Acute kidney failure caused by Hantaviruses]. 778 96

During an outbreak of haemorrhagic fever with renal syndrome (HFRS) in 1989, five children (3 girls, 2 boys, aged 6.8-16 years) with a severe form of the disease were treated; four of these were followed for 22-28 months. The main clinical features in all five patients were: fever, headache, myalgia, abdominal and back pain and vomiting; haemorrhagic syndrome was present in four children. Renal syndrome presented with severe acute renal failure in all five patients. All patients recovered. Serological confirmation by an indirect immunofluorescence assay, by enzyme immunoassay for IgM antibodies and by plaque reduction neutralization test showed infection by Belgrade virus in three and by Hantaan virus in two patients. It was not possible to differentiate these two serogroups on the basis of clinical features. This study provides further information on the circulation of different hantaviruses causing severe HFRS in Serbia.
 ...
PMID:Belgrade and Hantaan hantaviruses--the causative agents of severe haemorrhagic fever with renal syndrome in children in Serbia. 791 55


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>