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)

Early pathological abnormalities in human immunodeficiency virus (HIV-1)-related dementia have not been well documented. We report a homosexual man with fatigue and intermittent diarrhea in whom early HIV-1-related dementia was demonstrated during neurological screening in the Multicenter AIDS Cohort Study. Within 4 months he died of massive epistaxis, and the brain revealed astrocytosis of white matter and mild pallor of myelin staining in the absence of inflammation, multinucleated giant cells, and brain atrophy.
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PMID:Neuropathological changes in early HIV-1 dementia. 281 44

An intense vaso-vagal reaction characterizes all the reflex induced cardiovascular syncopes. In these syndromes the vagal cardio-inhibitor effect on heart rate is more evident than the vasodilatation and fall in blood pressure. The vasodepressor mechanism is uncommon even in carotid sinus syndrome. We have studied 6 male patients, age range 56-73 years (mean age: 64) with recurrent vasodepressor syncopes. The following were always present during such episodes: generalized malaise, profound fatigue, pallor, cyanosis, copious sweating, lack of peripheral pulses, severe fall in blood pressure (BP) (systolic BP less than or equal to 50-60 mmHg or unrecordable), mental disorientation and/or syncope. The first diagnosis in our patients was carotid sinus syndrome, but, the clinical picture was quite different from classic carotid sinus syndrome: triggering factors were not present, the vasovagal episodes were longer, the syncopes more frequent and severe, and the VVI pacing uneffective. Further investigations, including computerized axial tomography, showed--in all these patients--a malignant tumour originally localized in or near the parapharyngeal space. We think that the symptoms of our patients can be attributed to parapharyngeal tumour and that the parapharyngeal space lesions are able to cause severe vasovagal attacks and syncope. The pathogenetic mechanism in this syndrome, due to neural irritation of the glossopharyngeal afferent fibres, is similar to the glossopharyngeal neuralgia-asystole syndrome, but it obviously doesn't involve pain-pathways since none of our patients had pain. Therefore, this syndrome differs from glossopharyngeal neuralgia- asystole syndrome in the presence of tumours and in the absence of neuralgia and initiating factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A new reflex cardiovascular syndrome: recurrent vasodepressive syncope caused by lesions or tumors of the parapharyngeal space. Etiopathogenesis, clinical picture, differential diagnosis with carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Therapy by intracranial resection of the 9th cranial nerve]. 319 43

Hypoglycaemia (blood glucose 1.3-2.5 mmol/l) was induced in twenty-eight diabetic children by reduction of their morning meal. Fatigue and pallor were the most common signs of hypoglycaemia. Compared to findings during normoglycaemia, plasma concentrations of adrenalin, noradrenalin and cortisol were significantly higher at glucose nadir. Plasma glucagon concentration at glucose nadir was correlated to the fasting C-peptide concentration and inversely to the duration of diabetes. Children who lacked C-peptide also lacked glucagon response to hypoglycaemia. The parents' opinion of the need to give carbohydrates corresponded to the blood glucose level. The presence of adrenergic signs correlated to the plasma adrenalin and the neuroglucopenic signs to blood glucose. The lowest glucose level correlated inversely to the concentration of free insulin. When facilities for glucose infusion are lacking, a rational step in treating the unconscious hypoglycaemic child seems to be the injection of glucagon, considering the blunted or absent glucagon secretion.
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PMID:Hypoglycaemia in childhood diabetes. I. Clinical signs and hormonal counterregulation. 329 49

Data for 26 patients with membranoproliferative glomerulonephritis, type I (MPGN I) and 22 with membranoproliferative glomerulonephritis, type III (MPGN III), as distinguished by glomerular ultrastructure, were analyzed to determine differences in presentation, complement perturbation, and glomerular morphology by light microscopy. MPGN III was detected with greater frequency by the chance discovery of hematuria and proteinuria in the otherwise healthy individual (MPGN III, 63%; MPGN I, 30%; P = .01) and never, in the absence of renal failure, presented with systemic symptoms such as ease of fatigue, weight loss, and pallor, as may patients with MPGN I. The more frequent detection of MPGN III by chance is evidence that its onset is insidious and that for long periods it produces no symptoms or signs. Glomerular proliferation is also less than in MPGN I. Further, in MPGN III, the complement perturbation and glomerular immunofluorescence give no evidence of classical pathway activation, for which there is abundant evidence in MPGN I. Even with severe hypocomplementemia in MPGN III, C3 nephritic factor, another cause of hypocomplementemia, is rarely detectable and then in very low concentration. The cause of the complement perturbation in MPGN III has so far escaped identification. Although these observations give evidence that MPGN III is distinct from MPGN I, there is compelling evidence from other studies that a predisposition to both types is inherited and that similar genetic factors are operative in the two types. Because their genetic basis appears to be the same, it must be concluded that despite their differences, types I and III are variants of the same disease.
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PMID:Differences between membranoproliferative glomerulonephritis types I and III in clinical presentation, glomerular morphology, and complement perturbation. 382 60

The preleukemic syndrome occurs mainly after middle age. We report 11 patients, aged 62 to 92 years, who presented with weakness, fatigue, malaise and pallor. Eight patients died; survival from the time of diagnosis was between 2 and 21 months. Two of them developed acute myelomonocytic leukemia. A third patient developed Philadelphia chromosome-negative chronic myeloid leukemia within 9 months. Serum unsaturated B12 binding capacity and transcobalamin I were elevated in this patient, preceding the transformation to chronic myeloid leukemia. Five other patients died from sepsis or pneumonia. All patients were anemic, and 10 were leukopenic. Bone marrow was hypocellular in 1 and hypercellular in 10 cases. Chromosomal studies were performed in five patients, with three showing abnormal findings: 47xx, trisomy 8 and a tetraploid karyotype 92xxyy5q-. No cytotoxic treatment should be given during the preleukemic phase until transformation to acute leukemia occurs. Since preleukemic patients are very susceptible to infections, early diagnosis of the condition is important, as is supportive care in the case of surgery.
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PMID:Preleukemic syndrome in elderly patients--report of 11 cases. 385 73

Two groups of 15 women with moderately severe post-partum hypotension were assigned at random to receive treatment with either 200 mg dimetophrine or placebo, orally, over a period of 10 days. Systolic blood pressure increased steadily and significantly during the first 5 days of treatment, from 100.0 +/- 1.2 mmHg to 128.0 +/- 1.2 mmHg with dimetophrine; with placebo, the increase from 99.8 +/- 1.1 mmHg to 104.7 +/- 1.1 mmHg was significantly less. Similar results were observed in diastolic blood pressure measurements. Overall, all 15 patients responded to dimetophrine but only 4 spontaneously recovered on placebo. At the same time, heart rate moved towards normal with dimetophrine (from 82.4 +/- 2.0 to 75.5 +/- 1.1 beats/min); with placebo, significantly less recovery was observed (from 79.5 +/- 2.3 to 78.6 +/- 1.5 beats/min). Concomitant with the recovery of perfusion pressure, the associated symptoms (asthenia, paleness, fatigue, dizziness, sweating, headache, vertigo) significantly decreased in intensity, all except vertigo to a significantly greater extent with dimetophrine than with placebo. Subjective tolerance was good in both groups; clinically relevant variations in haematological or haematochemical parameters measured were absent, except for the expected normalization of leucocyte count.
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PMID:Effective treatment of post-partum hypotension with dimetophrine: a placebo-controlled, double-blind trial. 389 65

Thirty in-patients with chronically reduced arterial blood pressure and relevant subjective symptoms were treated over a 15-day period with oral doses of either 400 mg dimetophrine twice daily or placebo, according to a prospective, randomized, double-blind design. Systolic and diastolic blood pressures and heart rate were monitored at 5-day interval: subjective specific symptoms (scored 0 to 3 in order of increasing severity), haematology and haematochemistry were recorded before and after treatment. Both systolic and diastolic blood pressures increased significantly after dimetophrine all through the observation period. After 5 days, systolic blood pressure had already reached significantly higher values in comparison with the placebo-treated group, as did diastolic blood pressure by the 10th day. Overall, during the observation period, an increase from 82.7 +/- 1.0 to 112.3 +/- 2.1 mmHg was observed in systolic and from 54.3 +/- 1.3 to 62.7 +/- 1.4 mmHg in diastolic blood pressure with dimetophrine, whereas with placebo, systolic blood pressure increased from 80.4 +/- 1.5 to 93.7 +/- 2.9 mmHg and diastolic blood pressure remained unchanged (53.3 +/- 1.4 mmHg). Concomitantly, heart rate decreased significantly with dimetophrine from 88.1 +/- 2.5 to 77.2 +/- 1.4 beats/min, whereas it remained almost unchanged with placebo (from 83.9 +/- 2.5 to 80.0 +/- 1.9 beats/min). The associated symptoms (asthenia, paleness, drowsiness, fatigue, sweating, vertigo and headache) were largely relieved by dimetophrine (70.0% decrease) but not by placebo (37.4%). All symptoms except drowsiness and vertigo were reduced to a significantly larger extent with dimetophrine than with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind clinical evaluation of dimetophrine in chronically reduced arterial tension. 639 91

The thoracic-outlet-syndrome, a symptom complex consisting of arterial, venous and neural disorders of the upper extremity, is caused by compression of the neurovascular structures between the clavicle and the first rib. Other reasons are congenital abnormalities like a cervical rib, an abnormal first rib, acquired anatomic lesions like fractures and traumata or functional factors. The younger-and middle-age groups are most commonly involved. The symptoms are depending upon the point at which compression occurs and include pain, paresthesias, numbness, fatigue, pallor, coolness or swelling and enlargement of the arms. At physical examination a systolic murmur is heard in the supraclavicular region in 30 percent and the pulse of the upper extremity often is reduced. Diagnostic measurements include roentgenogram of the chest and the cervical spine, pulsed doppler-ultrasonography, nerve conduction-velocity testing and an arterio-venography. Treatment is nonoperative in patients with mild symptoms (shoulder-girdle-exercises) and operative in patients with severe or persistent symptoms. The operative treatment of choice is resection of the first rib by an axillary route. Risks are minimal, and the results are good to excellent in 90% of the cases. Because the thoracic outlet syndrome is very rare in childhood, we report a 13 year old girl which has undergone bilateral operation with excellent result.
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PMID:[Compression syndrome of the upper thoracic outlet (thoracic outlet syndrome)--report on a 13-year-old girl]. 649 88

The classical symptoms of malabsorption syndrome are diarrhea, steatorrhea, weight loss, and fatigue. Tetany, ecchymosis, anorexia, bone pain, pallor, muscle wasting, hyperpigmentation, apathy, digital clubbing, abdominal distention which contrasts in view of the reduced common statement are other signs of malabsorption. Long before the onset of these symptoms there may be a disinterest in regular daily activities often associated with the passage of three soft stools per day and with the remarkable sign of difficulties in flushing bulky stools. Anamnesia, clinical examination in connection with common laboratory findings, small intestinal x-rays and endoscopic investigations associated with biopsies of the small (and large) bowel as well as estimation of stool fat excretion, xylose- and Schilling-test allow the diagnosis in most of the cases.
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PMID:[Clinical aspects and differential diagnosis of malabsorption]. 684 29

A case of erythroleukemia coexistent with pulmonary emphysema is reported. A 67-year-old male was admitted to our hospital in May 1981, with a few year history of cough, sputum and fatigue. He had already been diagnosed as having pulmonary emphysema and moderate anemia. On physical examination, except for pallor, no other findings were remarkable. The initial hematological examination showed hemoglobin, 9.6 g/dl, red cell count, 251 x 10(4)/microliters, platelet count, 7.3 x 10(4)/microliters, white cell count, 2600/microliters with neither myeloblasts nor erythroblasts. A sternal marrow aspiration revealed 21% myeloblasts and 40% erythroblasts including 7.5% megaloblastoids. Periodic Acid Schiff staining was strongly positive for a part of erythroblasts. A chest X-P finding was typical for pulmonary emphysema. Pulmonary function was moderately damaged. He was started on chemotherapy with AAAP (ACNU 50 mg/d i.v. drip over 4 hr x 4d, adriamycin 20 mg/d i.v. push x 4d, Methotrexate 20 mg i.v. push x 4d). The first course of AAAP brought him a complete remission with both disappearance of myeloblasts and erythroid precursors with megaloblastoid nuclei in the marrow and the normalization of white cell count and platelet count in the blood. He was discharged in September 1981 after completion of a consolidation chemotherapy with AAAP. Since then, he received two courses of AAAP as an intensification chemotherapy and has been in complete remission for more than 13 months. His pulmonary function has not been affected and no myocardial damage has been seen throughout AAAP therapy. Thus, AAAP therapy seems to be an excellent chemotherapy even for an aged patient with erythroleukemia.
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PMID:[A case report of an aged patient with erythroleukemia coexistent with pulmonary emphysema, responding well to AAAP therapy]. 696 34


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