Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptoms and signs of the urogenital estrogen deficiency syndrome occur relatively late in a women's life when endogenous estrogen levels are well below those required to stimulate endometrial growth. At age 60 and above symptoms are common and progress with advancing age. The first and most common complaint is vaginal dryness, but symptoms of lost control of micturition as well as urge incontinence are also frequent. Recurrent infections of the lower urinary tract are common, as well as dyspareunia and a sensation of burning and itching. One third of women above age 60 suffer from urogenital estrogen deficiency syndromes, a figure that rises to two thirds at the age of 75. With a rapid growth of the elderly female population, these symptoms are an increasing burden to the individual as well as to any given health care system. Several clinical trials have repeatedly demonstrated the efficacy in alleviating these symptoms of low daily estrogen doses as exemplified by 8 micrograms/day of vaginally administered estradiol. For reasons not completely understood, the urogenital tissues respond to this low estrogen level but the endometrium does not. Hence, estrogen therapy aiming at mitigating urogenital deficiency symptoms could be given without a progestogen. No side effects have been described for vaginal preparations, and neither absolute nor relative contraindications exist. No protection is offered against cardiovascular disease or osteoporosis, though. In 1991, vaginal low-dose estrogens were declared OTC preparations in Sweden. The costs for the society for this program can be limited to the costs of medication only, for medical monitoring is not compulsory. The clinical efficiency is remarkable, and urogenital symptoms are almost abolished in elderly women receiving this type of treatment, which is practically devoid of side effects.
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PMID:Medical and surgical strategies for treating urogynecological disorders. 882 92

Primary biliary cirrhosis (PBC) is a slowly progressive chronic cholestatic disease of the liver thought to be caused by immune destruction of the interlobular bile ducts. One-third of patients are asymptomatic and one-third of these develop symptoms within 5 years. Therapeutic regimens should be directed at the control of symptoms, prevention of complications and specific therapy aimed at controlling progression of the disease. Symptoms may be secondary to cholestasis or due to other associated diseases. The cause of pruritus secondary to cholestasis remains unknown; the anion exchange resin cholestyramine generally brings relief. In patients resistant or intolerant to this therapy, rifampin may be helpful, as well as ultraviolet light without sunblock. Liver transplantation may rarely be the only option for uncontrollable pruritus. Clinical manifestations of keratoconjunctivitis-sicca and xerostomia need constant attention to prevent corneal ulcers and dental caries. Preventative therapy includes regular screening for thyroid dysfunction and replacement therapy when necessary and the administration of the fat soluble vitamins A, D and K once hyperbilirubinaemia is present. Osteoporosis is a complication of all cholestatic liver disease. There is no satisfactory preventative therapy. It may be appropriate to give hormone replacement therapy to all post-menopausal women with PBC to reduce osteoporosis. Liver transplantation is the best option for those with fractures. Oesophageal varices may develop early in the course of PBC, non-selective beta-blocker therapy should be used as prophylaxis against variceal haemorrhage. The only specific therapy shown to cause both a biochemical and survival benefit in patients with PBC is ursodeoxycholic acid (UDCA). Treatment with UDCA delays progression, but does not result in a cure of this disease. Currently, liver transplantation is the only definitive treatment available for end-stage disease.
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PMID:Treatment of primary biliary cirrhosis. 884 Feb 32

To evaluate the efficacy and long-term course of topical steroids treatment in oral lichen planus (OLP), an open trial has been carried out in 30 patients with atrophic-erosive or symptomatic varieties of OLP confirmed histologically with relative contraindications for systemic steroid treatment (namely, liver disease, peptic ulcer, diabetes, blood hypertension or osteoporosis). The treatment was the following: Fluocinonide (Topsyn) 0.025% in 4% idrossiethylcellulose gel applied 3 times/daily for two months, 2 times/daily for the next 2 months and 1 times/daily for other 2 months. Moreover, chlorhexidine (Plakout) 0.12%, 3 mouthwashes/daily and miconazole gel (Micotef) applied 1 times/daily were used for the entire period of the steroid therapy as antimycotics. The clinical evaluation of signs and symptoms was assessed on a scale of 0 to 5 and of 0 to 3, respectively. Twenty patients concluded the entire therapeutical scheme, whereas 5 (17%) interrupted the treatment for the appearance of side-effects (namely, gastroesophageal disturbances, mucosal bleeding and pruritus), 1 interrupted voluntarily the treatment and 4 cases did not present at the controls. No cases of oral candidiasis were seen. Eighteen patients (90%) had improvements of oral lesions with significant statically reductions in the scores of signs (p < 0.002) and of symptoms (p < 0.02) (Wilcoxon test). We emphasize also that in 61% of the responders the oral conditions were stable after 6 months of follow-up. In conclusion our results suggest the following: a) fluocinonide is an effective and safe drug for the treatment of OLP, especially in addition with chlorehixidine and miconazole; b) the stability of our results demonstrates that probably an adequate steroid therapeutical scheme is more useful than continuous steroid administration in the treatment of OLP.
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PMID:[The topical treatment of atrophic-erosive oral lichen planus with fluocinonide in a bioadhesive gel, chlorhexidine and miconazole gel. A totally open trial]. 892 75

Cholestatic liver disease is primarily caused by impaired bile production on the level of hepatocytes and cholangiocytes. Clinically cholestasis can be divided into intrahepatic and extrahepatic forms based on the presence or absence of dilated bile ducts (sonography). Intrahepatic cholestasis is most frequently caused by end stage liver cirrhosis followed by primary cholangiopathies and canalicular transport defects in hepatocytes. The causes of the most important cholangiopathies, such as Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC) are so far not known. Therefore, drug therapy of cholestatic liver disease focuses on the improvement of symptoms such as fatigue, pruritus, abdominal discomfort, jaundice, xanthoma, hypercholesterolemia, portal hypertension, blood count abnormalities, osteoporosis/osteomalacia, and the prevention of complications such as bile-duct strictures in PSC and development of cholangiocarcinoma. The first choice drug in the treatment of cholestatic liver disease of various causes is urosodeoxycholic acid (UDCA), that has been shown to decrease bile acid toxicity in general and prolong the transplant free survival of patients with PBC. If cholestasis persists cirrhosis of the liver is the major complication and liver transplantation may be the definitive treatment in advanced cases of cholestatic liver disease.
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PMID:[Cholestatic liver diseases]. 945 66

The diagnosis of primary biliary cirrhosis (PBC) is most often made in the asymptomatic phase, sometimes before the development of abnormal liver biochemistry. The antimitochondrial antibody remains the predominant hallmark, although not all patients test positive, even when the most sensitive techniques are used. The etiology of PBC remains elusive; studies suggest that the interlobular bile duct destruction is immune based, and associated autoimmune diseases are common. There are no surrogate markers that predict outcome in asymptomatic patients, whose chance of survival is less than that of age- and sex-matched populations but much better than the median survival of eight years in patients with symptomatic PBC. Symptoms common in this disease are fatigue, pruritus and xanthelasma, as well as complications of portal hypertension and osteoporosis. Treatment includes symptomatic and preventive measures, as well as specific therapeutic measures. Immunosuppressive therapy has yielded disappointing results in the long term management of PBC, and the only therapy shown to improve survival is the hydrophobic dihydroxy bile acid ursodeoxycholic acid. Treatment at a dose of 13 to 15 mg/kg/day is optimal, given in separate doses or as a single dose at least 4 h from giving the oral anion exchange resin cholestyramine, which may be used to control pruritus. However, liver transplantation remains the only cure for this disease, and the best postoperative survival is seen in patients whose serum bilirubin does not exceed 180 micromol/L at the time of liver transplantation. Recurrence takes place but is rarely symptomatic and does not deter from the benefits of transplantation.
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PMID:Update on primary biliary cirrhosis. 1065 26

Primary biliary cirrhosis (PBC) is a presumed autoimmune disease of the liver, which predominantly affects women once over the age of 20 years. Most cases are diagnosed when asymptomatic (60%). The antimitochondrial antibody is present in serum in most, but not in all, patients with PBC. The disease generally progresses slowly but survival is less than an age- and gender-matched general population. The symptomatic patient may have fatigue, generalized pruritus, portal hypertension, osteoporosis, skin xanthomata, fat soluble vitamin deficiencies, and/or recurrent asymptomatic urinary tract infections. Many nonhepatic autoimmune diseases are found in association with PBC and may prompt initial presentation. To date, immunosuppressive therapy has not been shown to prolong survival in PBC. The hydrophilic bile acid, ursodeoxycholic acid (UDCA), has been shown when given in a dose of 13 to 15 mg/kg daily for up to 4 years to delay the time to liver transplantation or death. This therapy also causes a significant improvement of all the biochemical markers of cholestasis but has no beneficial effects on any of the symptoms or associated disorders. Treatment with UDCA does not obviate the need for liver transplantation. Therapies to prevent complications arising from malabsorption, portal hypertension, and/or osteoporosis are required as well. Good control of pruritus can be achieved in most patients. PBC is diagnosed with increasing frequency, but the agent(s) responsible for this slowly progressive destruction of the interlobular bile ducts remains elusive and hence a specific therapy remains unavailable.
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PMID:Management of primary biliary cirrhosis. The American Association for the Study of Liver Diseases practice guidelines. 1073 59

Vibration exercise (VE) is a new neuromuscular training method which is applied in athletes as well as in prevention and therapy of osteoporosis. The present study explored the physiological mechanisms of fatigue by VE in 37 young healthy subjects. Exercise and cardiovascular data were compared to progressive bicycle ergometry until exhaustion. VE was performed in two sessions, with a 26 Hz vibration on a ground plate, in combination with squatting plus additional load (40% of body weight). After VE, subjectively perceived exertion on Borg's scale was 18, and thus as high as after bicycle ergometry. Heart rate after VE increased to 128 min-1, blood pressure to 132/52 mmHg, and lactate to 3.5 mM. Oxygen uptake in VE was 48.8% of VO2max in bicycle ergometry. After VE, voluntary force in knee extension was reduced by 9.2%, jump height by 9.1%, and the decrease of EMG median frequency during maximal voluntary contraction was attenuated. The reproducibility in the two VE sessions was quite good: for heart rate, oxygen uptake and reduction in jump height, correlation coefficients of values from session 1 and from session 2 were between 0.67 and 0.7. Thus, VE can be well controlled in terms of these parameters. Surprisingly, an itching erythema was found in about half of the individuals, and an increase in cutaneous blood flow. It follows that exhaustive whole-body VE elicits a mild cardiovascular exertion, and that neural as well as muscular mechanisms of fatigue may play a role.
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PMID:Acute physiological effects of exhaustive whole-body vibration exercise in man. 1073 81

Primary biliary cirrhosis is a cholestatic autoimmune disease of the liver. Its prevalence has significantly increased over the last seven years, therefore it can no longer be considered to be a rare liver disease. It is seen in 94/100,000 women older than 40 years. The treatment consists of administration of ursodeoxycholic acid, better therapy results seem to be achieved by combining UDCA with immunosuppressants. While UDCA-monotherapy proved to extend the time until liver transplantation and thus leads to life prolongation, this could not yet be shown for the combination therapies. Therapy of the often agonizing pruritus and of osteoporosis remains problematic. Frequently this can only be managed by the combination of several treatment measures.
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PMID:[Cholestatic hepatopathy: primary biliary cirrhosis]. 1090 60

Primary biliary cirrhosis (PBC) is a chronic, cholestatic disease of unknown etiology commonly affecting women. It is characterized by progressive destruction of the small intrahepatic bile ducts and portal inflammation, leading to fibrosis and cirrhosis. The major signs and symptoms of PBC, which include pruritus, lethargy, the sicca syndrome, and osteoporosis, closely resemble the manifestations of hypervitaminosis A. Based on a review of the literature and other observations connecting PBC with retinoid metabolism (vitamin A and its derivatives), the hypothesis is proposed that exposure to excess endogenous retinoids contributes to the pathogenesis of PBC and may be to the cause of some of the signs and symptoms associated with the disease.
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PMID:Possible role of endogenous retinoid (Vitamin A) toxicity in the pathophysiology of primary biliary cirrhosis. 1096 36

Fifteen percent of premenopausal women, 10-40% of postmenopausal women, and 10-25% of women receiving systemic hormone therapy experience urogenital atrophy. The most common symptoms are dryness, burning, pruritus, irritation, and dyspareunia. Estrogen loss, drugs, and chemical sensitivities are causes. Estrogen or hormone replacement therapy (ERT-HRT) is the treatment of choice in postmenopausal women. Dosages prescribed for menopause symptoms or to prevent osteoporosis (and, potentially, other conditions) can restore the vagina to premenopausal physiology and relieve symptoms. Concomitant progestins are necessary for women with an intact uterus to minimize or eliminate estrogen-induced endometrial cancer. Low-dosage oral and vaginal ERT can relieve urogenital atrophy but might not produce systemic effects. Progestins are not necessary with vaginal rings and vaginal tablets. If ERT is given only to treat urogenital atrophy, estrogen creams 1 or 2 times/week may prevent recurrence after symptoms are resolved. Progestins are not required for occasional estrogen cream use. Vaginal moisturizers provide longer relief by changing the fluid content of endothelium and lowering vaginal pH. Vaginal lubricants provide short-term relief. Women with contraindications to ERT-HRT could use lubricants for intercourse-related dryness or moisturizers for more continuous relief. The lay press promotes agrimony, black cohosh, chaste tree, dong quai, witch hazel, and phytoestrogens for vaginal dryness and dyspareunia; however, no evidence exists to support these specific claims. Pharmacists should be actively involved in identifying, preventing, and treating urogenital atrophy.
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PMID:Urogenital atrophy: prevention and treatment. 1131 May 20


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