Gene/Protein Disease Symptom Drug Enzyme Compound
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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of protein S (PS) antigen, both total and free fractions, were measured together with C4b-binding protein (C4bp) and protein C (PC) antigen in 39 patients with disseminated intravascular coagulation (DIC), 34 with liver disease, 17 with collagen disease, 17 with diabetes mellitus, and 51 under stabilized warfarin treatment. In patients with DIC, mean concentrations of total PS and free PS were normal, while PC was reduced and C4bp were elevated. Total PS, free PS, C4bp and PC were all decreased in liver disease, elevated in diabetes mellitus, and normal in collagen disease. In warfarin-treated patients, total PS, free PS and PC were moderately decreased, but the decrease in C4bp was minimal. The concentration of PS correlated positively with PC in liver disease, diabetes mellitus, and during oral anticoagulation, but did not in DIC. These results indicate that PS and PC behave similarly when liver synthetic function is principally affected, but in contrast to PC, PS is hardly consumed during intravascular coagulation.
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PMID:Plasma protein S in disseminated intravascular coagulation, liver disease, collagen disease, diabetes mellitus, and under oral anticoagulant therapy. 252 31

Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2 subfraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides; omega-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLch levels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
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PMID:Nutritional management of plasma lipid disorders. 255 90

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

We retrospectively reviewed the long-term results in 46 patients who survived at least 1 year after liver transplantation. Only one death has occurred, and one patient has required retransplantation. Biochemical liver function tests showed median values in the normal range, except for mild elevation of serum gamma-glutamyltransferase. In patients with primary biliary cirrhosis, these test results were completely normal. A liver biopsy 1 year after transplantation disclosed normal histologic findings in 31 patients (67%). The other patients had either transient (acute rejection) or stable (chronic rejection) abnormalities, except for two patients with progressive graft dysfunction attributable to chronic rejection. A clinically significant vascular anastomotic abnormality was noted in one patient who had hepatic artery thrombosis. Late bile duct complications occurred in 15% of patients, all of whom had a satisfactory outcome after surgical or radiologic intervention. Cyclosporine-related nephrotoxicity and hypertension each occurred in 67% of patients; however, conversion to a low-dose cyclosporine-azathioprine regimen yielded stabilization of renal function after the first postoperative year, and hypertension has been easily controlled medically. Diabetes necessitating insulin treatment developed in three patients. The body weight of the study patients had increased by a median of 6.5 kg at 1 year but stabilized thereafter. Subjective well-being and satisfaction with life were reported by 91% of the patients. Of the 46 patients, 26 were employed, 16 were homemakers, and only 4 did not work, 2 because of transplant-related medical problems. Thus, we conclude that liver transplantation rehabilitates patients with end-stage liver disease and enhances their quality of life.
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PMID:Beyond 1 year after liver transplantation. 265 1

The authors evaluate five-year ultrasonographic material (13,672 examinations) focused on non-cystic liver disease. 8212 examinations (60.1%) were made as part of examinations of the gallbladder, 4919 (36%) as part of examination of the right sub-costal area or other organs and only 541 examinations (3.96%) were focused in the first place on the liver. The total number of examined patients included 7830 women (57.3%) and 5842 men (42.7%). Most frequently the ultrasonographic picture of steatosis was found--in 747 patients (5.46%), cirrhosis of the liver in 45 patients (0.33%), primary carcinoma of the liver was present in 7 patients (0.05%) and tumour metastases in 63 patients (0.46%). The group of women with steatosis comprised 42 diabetic women (32.06%), 78 overweight women (59.5%) and 18 with excessive alcohol intake for several years (13.7%). In the group of men with steatosis there were 48 diabetics (7.79%), 92 overweight (14.9%) and 479 with excessive alcohol intake extending over several years (77.7%). In the group of 34 men with cirrhosis excessive alcohol intake for years was found in 31 (91.2%), in the group of eight women with cirrhosis in five instances (62.5%). In abdominal ultrasonography liver disease must be actively searched for, in particular in patients with long-term alcohol intake, overweight, diabetes and long-term use of various hepatotropic drugs.
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PMID:[Non-cystic diseases of the liver in a 5-year ultrasonographic study]. 266 Apr

Primary or genetic haemochromatosis is an inherited disease characterized by an inappropriate degree of iron absorption with accumulation of excessive amounts of tissue iron. Parenchymal iron accumulation results in the typical clinical features of the disease including hepatic cirrhosis, diabetes, testicular atrophy and skin pigmentation. The disease is inherited in an autosomal recessive manner. The gene for the disease has not been identified but is tightly linked to the A locus of the histocompatibility complex on chromosome 6. The approximate homozygote frequency in Caucasians is 0.3% with an equal sex ratio. Excessive body iron stores have been described in a number of other conditions, particularly alcoholic liver disease. There is increasing evidence that many of these individuals are in fact also suffering from genetic haemochromatosis. Diagnostic tests including serum iron, transferrin saturation, serum ferritin and liver iron concentration make it possible to detect sufferers of the disease. Screening relatives of affected individuals with these tests allows a diagnosis to be made before permanent tissue damage has occurred. Removal of excess iron stores by repeated phlebotomy is the primary treatment. If iron is removed before significant tissue damage has occurred, the complications and natural course of the disease will be prevented provided reaccumulation of iron does not occur. Excessive iron accumulation with resultant organ damage also occurs in anaemias associated with ineffective erythropoiesis and after excessive parenteral iron administration or repeated blood transfusions. Similar clinical features may be seen. Chelation therapy is the mainstay of treatment in these cases where long-term venesection is not possible.
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PMID:The clinical manifestations of chronic iron overload. 266 Sep 35

The authors examined 133 patients with urolithiasis, treated with hydrochlorothiazide and 81 patients treated with allopurinol. In those treated with hydrochlorothiazide the calciuria and Ca/creat. index declined, and uricaemia rose. After treatment uricosuria increased significantly in 41% patients. The detection of diabetes did not exceed the prevalence in the population. In patients treated with allopurinol the uricaemia and uricosuria declined, a hepatic disorder with supraliminal rise of ALT was recorded in 23% of the patients and led to discontinuation of treatment in 15% of the patients.
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PMID:[Adverse effects of drug metaphylaxis of urolithiasis]. 272 Jul 29

We report the first case of primary pulmonary sporotrichosis in Japan. A 53-year-old man was admitted to our hospital for further examination of the abnormal shadows on chest X-ray film. Six months before admission, he was admitted to another hospital because of alcoholic liver disease and diabetes mellitus. Since the initial chest film showed cavities with infiltration in the left upper lung field, he was treated with antituberculous drugs despite negative sputum cultures for mycobacterium. In spite of the medication, his chest X-ray film revealed another cavitary lesion, so he was referred to our hospital. He had been asymptomatic during this period. Chest X-ray on admission disclosed multiple cavities in the left upper lobe and a cavity in the right lower lobe. Repeated sputum specimens, bronchial washings and brushings for cytology and cultures were all negative. In an attempt to clarify the pathogen, percutaneous lung aspiration (PLA) was performed. The PLA sample yielded a positive culture of Sporothrix shenckii. After the diagnosis, S. schenckii was also cultured from sputa. A sporothrix skin test and yeast agglutination test for S. schenckii were positive. In the absence of a history for skin lesion, the patient was diagnosed as a primary pulmonary sporotrichosis. As iodide therapy was ineffective, he was started on a regimen of intravenous amphotericin B. However his renal function progressively deteriorated, so amphotericin B was discontinued. Now he receives miconazole intravenously and is still under careful observation. As far as we know, this is the first report of primary pulmonary sporotrichosis in Japan. The possibility of sporotrichosis should be considered in any cases of undiagnosed cavitary lung diseases.
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PMID:[A case of primary pulmonary sporotrichosis]. 274 77

Glucose tolerance test was done in 61 patients with liver disease, 54 with porphyria cutanea tarda and 62 controls. The results showed that 45 patients (73.8%) from the liver disease group, 19 (35.2%) from the porphyria cutanea tarda (PCT) group and only 7 individuals (11.3%) from the control group had an abnormal glucose tolerance test. The differences were significant. Although nutritional state is known to influence the glucose tolerance test, we did not find any significant difference in the mean body mass index between those with an abnormal glucose tolerance test and those without in both groups of patients. Furthermore, the prevalence of an abnormal glucose tolerance test in those above and below 40 years in each group of patients was not significantly different, indicating that age probably played no significant role in this study. Therefore, glucose intolerance is common among Ethiopian patients with liver disease and PCT. As some patients with an abnormal glucose tolerance test may be expected to develop asymptomatic diabetes, we recommend that periodic blood glucose determinations should be part of the management.
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PMID:Glucose tolerance in adult Ethiopian patients with liver disease and porphyria cutanea tarda. 275 29

The significance of hepatic changes in methotrexate-treated RA patients is unclear at this time. In our group of RA patients, there was a slight increase in the incidence of triaditis and fat during methotrexate therapy. Disease duration greater than or equal to 10 years was associated with increased hepatic triaditis before treatment. Age greater than 50 years was associated with increased hepatic fat before and after treatment. It appears that patients' ages and duration of underlying RA account for some changes, independent of methotrexate therapy. Several of our patients changed from higher to lower histologic grade or had an apparent decrease in fibrosis, fat, or triaditis on the pathologists' reports and the blind readings of the repeat biopsies. This may be explained by sampling error. More importantly, some of these changes may not be of clinical significance. One report of methotrexate-induced cirrhosis in patients with psoriasis demonstrated that in all but one of 14 patients who continued receiving methotrexate the cirrhosis decrease or did not progress. This may also be true of the hepatic fibrosis seen in RA after methotrexate treatment. In this study, there did not appear to be changes seen on pretreatment liver biopsy that were predictive of subsequent fibrosis or cirrhosis. Our data indicate that pretreatment biopsy is unwarranted in a population similar to ours. However, our practice has been to try to avoid methotrexate in patients with diabetes, prior liver disease, alcoholism, or obesity because of previous reports suggesting that these patients are at increased risk for the development of cirrhosis. Only the above-mentioned patient, eventually diagnosed as having cirrhosis, might have been handled differently. Including the study, none of the approximately 700 RA patients in the literature having liver biopsies after methotrexate therapy have developed cirrhosis consequent to its use. Most of these had received a total dose of approximately 1,500 mg in small weekly doses, and alcohol was prohibited. Below this cumulative dose the risk of clinically significant liver damage in carefully selected patients is very low. In view of this experience, the recommendation that RA patients have liver biopsies after 1,500 mg of methotrexate (a holdover from the psoriasis literature) may be too conservative in low-risk RA patients, provided methotrexate is administered weekly and alcohol is prohibited. Recognizing that the absolute need for biopsy is unproven, a more realistic milestone for those choosing biopsy might be after each 2,000 to 2,500 mg.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prospective analysis of liver biopsies before and after methotrexate therapy in rheumatoid patients. 277 58


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