Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This case was a 51-year-old woman, who had been diagnosed as having rheumatoid arthritis at some clinic and had been treated with both non-steroidal anti-inflammatory drugs and steroid 3 years before visiting our clinic. When she noticed a decrease in visual acuity and general fatigue in June 1985, she was referred to an ophthalmologist of our hospital, and found to have blood pressure of 240/150 mmHg and KW grade IV retinal findings. She was admitted in our department to examine and treat malignant hypertension. On admission, remarkable hypergammaglobulinemia (29.3%), arthralgia, arthral deformity and pericardial effusion were present thus, she was suspected to be suffering from malignant rheumatoid arthritis. Anti-nuclear antibody (64X), anti-nuclear ribonucleoprotein antibody (64X) and anti-RNase sensitive antibody of anti-extractable nuclear antigens (ENA) antibody (81920X) were positive, while anti-RNase resistant antibody of anti-ENA antibody was negative. Immunologically, her condition was consistent with mixed connective tissue disease (MCTD). Since urinary protein was positive and creatinine clearance was 46.0 ml/min, renal function was thought to be diminished. Her chest roentgenogram revealed cardiomegaly (CTR 67.5%) and an increase in pulmonary vascular shadow. An echocardiogram demonstrated the presence of pericardial effusion. Plasma renin activity was 3.3 ng/ml/h and it was suspected that an intrarenal ischemic change resulted in increased renin release from the juxta-glomerular apparatus, leading to the marked hypertension. Treatment was started with prednisolone 60 mg/day during 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of mixed connective tissue disease complicated with malignant hypertension]. 219 30

The introduction, more than twenty years ago, of beta-blockers in the treatment of arterial hypertension, represented a significant advance. With these medications, many hypertensive patients are effectively under control and malignant hypertension is practically inexistent. Today, the treatment of hypertension is markedly improved with the development of new, active medications, while the beta-blockers family has markedly evolved. The role of beta-blockers in the treatment of hypertension, must therefore be re-evaluated according to their properties as compared to those of other classes of antihypertensive medications. Indeed, there are standard contraindications to he use of beta-blockers, sometimes resulting in adverse reactions, either clinical (fatigue, sexual disorders, vasomotor syndromes)--much less frequent with the new molecules--or biological (especially serum lipid levels), the consequences of which remains ill-defined--some beta-blockers appear practically without any harmful effect. Actually, despite these drawbacks, usually minimal, there are numerous and strong arguments in favor of the use of beta-blockers in the treatment of hypertension: 1) their significant follow-up in the treatment of hypertension; this is a well-known argument; 2) their effectiveness in hypertension, as a single drug and single daily dose; 3) their cost, which is lower than that of new anti-hypertensive medications; 4) their cardio-protective role, demonstrated by experimental data (myocardial protection and anti-arrhythmic effect in experimental ischemia), and clinical data (improvement of left ventricular hypertrophy, control of blood pressure increase during exertion and stress, secondary prevention after myocardial infarction).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of beta-blockers in the treatment of arterial hypertension]. 256

Of 58 patients treated with captopril, 3 have now received the drug for more than 2 years and 22 for more than one year. This study concerns 38 patients treated for 6 months, captopril having been given alone during the first 2 months. They all had severe hypertension (diastolic BP Greater Than 110 mmHg) which had resisted previous treatments in normally effective doses, including at least one beta-blocker, dihydralazine and a diuretic. After 6 months blood pressure levels were normal in 53% of the patients, reduced in 31% and unchanged in 16%. Clinical improvement was habitual with, in particular, disappearance or decrease of tiredness and dyspnoea. Since some side-effects of the drug, such as granulopenia, proteinuria and ageusia, are mainly observed with high dosage, captopril is usually administered in doses lower or equal to 400 mg/day. In resistant or malignant hypertension it must be used in combination with salt-free diet, a beta-blocker and/or prazosin. Clinical, haematological and renal surveillance is necessary during treatment. When these precautions are observed, captopril constitutes a very useful drug for the treatment of patients with severe resistant hypertension.
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PMID:[Treatment of severe resistant arterial hypertension with captopril. 58 patients, including 38 treated for more than 6 months (author's transl)]. 702 47

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55

Although an association between oral contraceptives (OCs) and arterial hypertension has been well-documented, most studies have found only mild or moderate hypertension with reversal to normal levels 3 months after OC discontinuation. This paper presents two cases in which young women developed severe left ventricular hypertrophy and renal failure due to OC-induced malignization of hypertension. The first patient, a 23-year-old, was admitted to the hospital with a 3-day history of headache, mental confusion, and aggressiveness. 6 months before presentation, severe arterial hypertension had been diagnosed. At that time, she was advised to discontinue OCs (30 mcg of ethinyl estradiol and 150 mcg of levonorgestrel), which she had been taking for a year; she did not comply with this directive. The second patient, 21 years old, was admitted with accelerating hypertension. She had initiated OC use (30 mg of ethinyl estradiol and 150 mcg of levonorgestrel) 6 months earlier. 3 months after starting OC use, she developed headache and fatigue. Both women had a hemorrhagic cerebral accident as a complication of malignant hypertension. All neurologic, renal, and cardiovascular complications were reversible after OC discontinuation. OC-related malignant hypertension can be averted through effective control of blood pressure in OC users.
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PMID:Cardiac and neurologic complications in malignant hypertension due to oral contraceptive use. 786 96

The presence of severe and mild neurotoxicity in our pediatric renal transplant recipients treated with tacrolimus was determined by chart review (severe neurotoxicity) and patient survey (mild neurotoxicity). 14 patients were studied (mean age 15 yr, 5 month, +/- 4.4 yr). 1 patient experienced seizures, felt to be related to malignant hypertension. No other episode of severe neurotoxicity was documented. Most patients (12/14) reported at least one mild neurologic symptom, and half stated their symptoms were present at least 'most of the time'. The most frequent complaints were myalgias (7/14, 50%) and tremors (7/14, 50%) followed by fatigue (5/14, 38%). Severe neurotoxicity may be relatively infrequent in pediatric renal transplant patients treated with tacrolimus. Milder neurologic complaints may be commonly seen in this population, but in general are not severe enough to cause discontinuation of tacrolimus.
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PMID:Evaluation of neurotoxicity in pediatric renal transplant recipients treated with tacrolimus (FK506). 936 32

A 47-year-old woman was admitted to our hospital for evaluation of general fatigue and dyspnea. She had been diagnosed with progressive systemic sclerosis (PSS) when she was 39 years of age, on the basis of Raynaud's phenomenon, proximal sclerosis, and pigmentation of the skin. On admission, her blood pressure was 206/128 mmHg. Funduscopy revealed grade III (Keith & Wagener) hypertensive retinopathy. Laboratory data showed positivity for anti-nuclear antibody and anticardiolipin beta 2 glycoprotein I antibody, and the plasma level of renin activity (PRA) was abnormally high. Chest X-ray and UCG revealed massive pericardial effusion. On the second hospital day, she was operated on for pericardiodiaphragmatic fenestration. The volume of pericardial effusion amounted to more than 2000 ml. Post operative malignant hypertension persisted. Laboratory data showed thrombocytopenia, hemolytic anemia, and acute renal failure. We diagnosed scleroderma renal crisis (SRC) associated with antiphospholipid syndrome. Following the initiation of angiotensin converting enzyme inhibitor (ACE-I) combined with calcium antagonist and alpha-one blocker, her blood pressure and PRA decreased. She also had been treated with aspirin 81 mg daily. These therapies were effective in recovering the platelet count and stopped the progression of anemia and renal failure. Although either the finding of large pericardial effusion or SRC is associated with poor prognosis in PSS, this case has had a good clinical course. In this case, the findings suggested that anti-phospholipid antibody may have contributed to the pericarditis and SRC.
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PMID:[A case of scleroderma renal crisis with massive pericardial effusion and positivity on antiphospholipid antibody test]. 965 14

A 49-year-old woman was admitted with fatigue, dyspnoea, pretibial oedema and decreased daily urination. Seven years ago she was treated with doxorubicin, bleomycin, vinblastine and dacarbazine, alternating with mechlorethamine, vincristine, procarbazine and prednisone and 80 Gy abdominal radiotherapy for Hodgkin's disease. Two years later, malignant hypertension was diagnosed. Angiotensin-2 antagonist and beta-blocker treatment was given. After increased serum creatinine levels were determined, renal angiography was performed and total obstruction in the left renal artery and near total obstruction in the right side was observed. She was admitted to our clinic with oliguria, and acute renal failure was diagnosed. Balloon angioplasty and stent implantation was performed to the right renal artery. After a polyuric period, serum creatinine reduced to near normal levels. Angiotensin-2 antagonist treatment worsened the course in this patient. Patients with resistant hypertension occurring years after abdominal radiotherapy should be evaluated for renal artery stenosis.
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PMID:Bilateral renal artery stenosis after abdominal radiotherapy for Hodgkin's disease. 1471 1

Relatively little is known about phenotypic variability in nonsyndromic nephropathy associated with the gene encoding the WT1 transcription factor. We report a 12-mo-old female who presented with vomiting, diarrhea, and fatigue in the setting of renal failure and malignant hypertension. Trio ultra-rapid whole-genome sequencing identified a novel, likely pathogenic, de novo missense variant (c.485T > A, p.Val162Asp) in WT1 in 46 h, consistent with a diagnosis of nephrotic syndrome type 4 (NPHS4; OMIM 256370). This disorder typically presents with nephrotic syndrome (gross proteinuria, hypoalbuminemia, and edema). Rapid diagnosis had an immediate impact on her clinical management in the pediatric intensive care unit. Diagnostic renal biopsy was avoided, and placement of permanent dialysis access, a gastrostomy tube, and bilateral nephrectomy were accelerated. This report expands the presenting phenotype of nonsyndromic nephrotic syndrome and/or renal failure due to heterozygous variants in WT1 (NPHS4). It also highlights the relationship between time to genomic diagnosis and clinical utility in critically ill infants.
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PMID:Clinical utility of ultra-rapid whole-genome sequencing in an infant with atypical presentation of WT1-associated nephrotic syndrome type 4. 3284 31