Biochemie Thrombophlebitis

Bromelain: Biochemie, Pharmakologie und medizinische Anwendung (zur Enzym-Therapie)

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Biochemie Thrombophlebitis CUPRIMINE® (PENICILLAMINE) Capsules

Biochemie Thrombophlebitis planning to use penicillamine should thoroughly familiarize themselves with its toxicity, special dosage considerations, and therapeutic benefits. Penicillamine should never be used casually, Biochemie Thrombophlebitis. Each patient should remain constantly under the close supervision of the physician.

Patients should be warned to report Biochemie Thrombophlebitis any symptoms suggesting toxicity. Penicillamine is a chelating agent used in the treatment of Wilson's disease. It is a white or practically white, crystalline powder, freely soluble in water, slightly soluble in alcohol, and insoluble in ether, acetone, benzene, Biochemie Thrombophlebitis, and carbon tetrachloride.

Although its configuration is D, it is levorotatory as usually measured:. The structural formula is:. It reacts readily with formaldehyde or acetone to form a thiazolidine-carboxylic acid. Each capsule contains the following inactive ingredients: Penicillamine is a chelating agent recommended for the removal of excess copper in patients with Wilson's disease.

From in vitro studies which indicate that one atom of copper combines with two molecules of penicillamine, Biochemie Thrombophlebitis would appear that one gram of penicillamine Biochemie Thrombophlebitis be followed by the excretion of about milligrams of copper; however, the actual amount excreted is about one percent of this, Biochemie Thrombophlebitis.

Penicillamine also reduces excess cystine excretion in cystinuria. This is done, at least in part, by disulfide interchange between penicillamine and cystine, resulting in formation of penicillamine-cysteine disulfide, a substance that is much more soluble than cystine Biochemie Thrombophlebitis is excreted readily, Biochemie Thrombophlebitis.

Penicillamine interferes with the formation of cross-links between tropocollagen molecules and cleaves them when newly formed. The mechanism of action of penicillamine in rheumatoid arthritis is unknown although it appears to suppress Biochemie Thrombophlebitis activity.

Unlike cytotoxic immunosuppressants, penicillamine markedly lowers IgM rheumatoid factor but produces no significant depression in absolute levels of serum immunoglobulins. Also unlike cytotoxic immunosuppressants which act on Biochemie Thrombophlebitis, penicillamine in vitro depresses T-cell activity but not B-cell activity.

In vitroBiochemie Thrombophlebitis, penicillamine dissociates macroglobulins rheumatoid factor although the relationship of the activity to its effect in rheumatoid arthritis is not known. In those patients who respond, however, the first evidence of suppression of symptoms such as pain, tenderness, and swelling is generally apparent within three months.

The optimum duration of therapy has not been determined. In all patients receiving penicillamine, it is important that CUPRIMINE be given on an empty stomach, at least one hour before meals or two hours after meals, Biochemie Thrombophlebitis, and at least one hour apart from any other drug, food, milk, antacid, zinc or iron-containing preparation, Biochemie Thrombophlebitis. This permits maximum absorption and reduces the likelihood of inactivation by metal binding in the gastrointestinal tract.

Food, antacids, Biochemie Thrombophlebitis, and iron reduce Liz Burbo Varizen ist of the drug. The drug appears in the plasma as free penicillamine, penicillamine disulfide, and cysteine-penicillamine disulfide.

When prolonged treatment is stopped, Biochemie Thrombophlebitis, there is a slow elimination phase lasting days, Biochemie Thrombophlebitis. The drug also binds to erythrocytes and macrophages.

A small fraction of the dose is metabolized in the liver to S-methyl-D-penicillamine. Excretion is mainly renal, mainly as disulfides. CUPRIMINE is indicated in the treatment of Wilson's disease, cystinuria, Biochemie Thrombophlebitis, and in patients with severe, active rheumatoid arthritis who have failed to respond to an adequate trial of conventional therapy. Wilson's disease hepatolenticular degeneration occurs in individuals who have inherited an autosomal Biochemie Thrombophlebitis defect that leads wie man Krampfadern zu Hause mit Milch behandeln an accumulation of copper far in excess of metabolic requirements.

The excess copper is deposited in several organs and tissues, and eventually produces pathological effects primarily in the liver, Biochemie Thrombophlebitis damage progresses to postnecrotic cirrhosis, and in the brain, Biochemie Thrombophlebitis, where degeneration is widespread. Copper is also deposited as characteristic, asymptomatic, golden-brown Kayser-Fleischer rings in the corneas of all patients with cerebral symptomatology and some patients who are either asymptomatic Biochemie Thrombophlebitis manifest only hepatic symptomatology.

Two types of patients require treatment for Wilson's disease: The first objective is attained by a daily diet that contains no more than one or two milligrams of copper.

Such a diet should exclude, most importantly, chocolate, nuts, shellfish, mushrooms, liver, molasses, broccoli, and cereals and dietary supplements enriched with copper, and be composed to as great an extent as possible of foods with a low copper content. Distilled or demineralized water should be used if the patient's drinking water contains more than 0.

In symptomatic patients this treatment usually produces marked neurologic improvement, fading of Kayser-Fleischer rings, and gradual amelioration of hepatic dysfunction and psychic disturbances. Noticeable improvement may not occur for one to three months, Biochemie Thrombophlebitis. Despite this, Biochemie Thrombophlebitis, the drug should not be withdrawn. Temporary interruption carries an increased risk of developing a sensitivity reaction upon resumption of therapy, although it may result in clinical improvement of neurological symptoms see WARNINGS.

Treatment of asymptomatic patients has been carried out for over thirty years. Cystinuria is characterized by excessive urinary excretion of the dibasic amino acids, Biochemie Thrombophlebitis, arginine, lysine, ornithine, and cystine, and the mixed disulfide Biochemie Thrombophlebitis cysteine and homocysteine.

The metabolic defect that leads to cystinuria is inherited as an autosomal, recessive trait. Metabolism of the affected amino acids is influenced by at least two abnormal factors: Arginine, lysine, ornithine, and cysteine are soluble Biochemie Thrombophlebitis, readily excreted. There is no apparent pathology connected with their excretion in excessive quantities. Cystine, however, is so Biochemie Thrombophlebitis soluble at the usual range Biochemie Thrombophlebitis urinary pH that it is not excreted readily, and so crystallizes and forms stones in the urinary tract.

Stone formation is the only known pathology in cystinuria. Normal daily output of cystine is 40 to 80 mg. Conventional treatment is directed at keeping urinary cystine diluted enough to prevent stone formation, keeping the urine alkaline enough to dissolve as much cystine as possible, and minimizing cystine production by a diet low in methionine the major dietary precursor of cystine.

Patients must drink enough fluid to keep urine specific gravity below 1. It is capable of keeping cystine excretion to near normal values, thereby hindering stone formation and the serious consequences of pyelonephritis and impaired renal function that develop in some patients. Bartter and colleagues depict the process by which penicillamine interacts with cystine to form penicillamine-cysteine mixed disulfide as:.

In this process, it is assumed that the deprotonated form of penicillamine, PS', is the active factor in bringing about the disulfide interchange. Because CUPRIMINE can cause severe adverse reactions, its use in rheumatoid arthritis should be restricted to patients who have severe, Biochemie Thrombophlebitis, active disease and who have failed to respond to an adequate trial of conventional therapy.

Even then, benefit-to-risk ratio should be carefully considered. Although breast milk studies have not been reported in animals or humans, mothers on therapy with penicillamine should not nurse their infants.

Because of its potential for causing renal damage, penicillamine should not be administered to rheumatoid arthritis patients with a history or other evidence of renal insufficiency. The use of penicillamine has been associated with fatalities due to certain diseases such as aplastic anemia, agranulocytosis, thrombocytopenia, Goodpasture's syndrome, and myasthenia gravis. Because of the potential for serious hematological and renal adverse reactions to occur at any time, routine urinalysis, white and differential blood cell count, Biochemie Thrombophlebitis determination, and direct platelet count must be done twice weekly, together with monitoring of the patient's skin, lymph nodes and body temperature, during the first month of therapy, every two weeks for the next five months, and monthly thereafter.

The above laboratory studies should then be promptly repeated. Leukopenia and thrombocytopenia have been reported to Biochemie Thrombophlebitis in up to five percent of patients during penicillamine therapy. Leukopenia is of the granulocytic series and may or may not be associated with an increase in eosinophils. Thrombocytopenia may be on Biochemie Thrombophlebitis idiosyncratic segmentale Varizen, with decreased or absent megakaryocytes in the marrow, when it is part of an aplastic anemia.

In other cases the thrombocytopenia is presumably on an immune basis since the number of megakaryocytes in the marrow has been Podmore Bienen aus Varizen to be normal or sometimes increased.

A progressive fall in either platelet count or WBC in three successive determinations, even though values Salbe aus Ödem mit Krampfadern still within the normal range, likewise requires at least temporary cessation.

Close observation of these patients is essential. In some patients the proteinuria disappears with continued therapy; in others, penicillamine must be discontinued. When a patient develops proteinuria or hematuria the physician must ascertain whether it is a sign of drug-induced glomerulopathy or is unrelated to penicillamine.

Rheumatoid arthritis patients who develop moderate degrees of proteinuria may be continued cautiously on penicillamine therapy, provided that quantitative hour urinary protein determinations are obtained at intervals of one to two weeks. Penicillamine dosage should not be increased Biochemie Thrombophlebitis these circumstances. In some patients, proteinuria has been reported to clear following reduction in dosage. In rheumatoid arthritis patients penicillamine should be discontinued if unexplained gross hematuria or persistent microscopic hematuria develops.

In patients with Wilson's disease or cystinuria the risks of continued penicillamine therapy in patients manifesting potentially serious urinary abnormalities must be weighed against the expected therapeutic benefits. When penicillamine is used in cystinuria, an annual x-ray for renal stones is advised. Cystine stones form rapidly, sometimes in six months. Up to one year or more may be required for any urinary abnormalities to disappear after penicillamine has been discontinued.

Because of rare reports of intrahepatic cholestasis and toxic hepatitis, liver function tests are recommended every six months for the duration of Biochemie Thrombophlebitis. In Wilson's disease, these are recommended every three months, at least during the first year of treatment. Goodpasture's syndrome has occurred rarely. The development of abnormal urinary findings associated with hemoptysis and pulmonary infiltrates on x-ray requires immediate cessation Biochemie Thrombophlebitis penicillamine.

Obliterative bronchiolitis has been reported rarely, Biochemie Thrombophlebitis. The patient should be cautioned to report immediately pulmonary symptoms such as exertional dyspnea, unexplained cough or wheezing.

Pulmonary function studies should be considered at that time. Myasthenic syndrome sometimes progressing to myasthenia gravis has been reported, Biochemie Thrombophlebitis. Ptosis and diplopia, with weakness of the extraocular muscles, are often early signs of myasthenia. In the majority of cases, symptoms of myasthenia have receded after withdrawal of penicillamine.

Most of the various forms of pemphigus have occurred during treatment with penicillamine, Biochemie Thrombophlebitis. Pemphigus vulgaris and pemphigus foliaceus are reported most Biochemie Thrombophlebitis, usually as a late complication of therapy. The seborrhea-like characteristics of pemphigus foliaceus may obscure an early diagnosis.

Treatment has consisted of high doses of corticosteroids alone or, in some cases, concomitantly with an immunosuppressant. Treatment may be required for only a few weeks or months, but may need to be continued for more than a year, Biochemie Thrombophlebitis.

Once instituted for Wilson's disease or cystinuria, treatment with penicillamine should, as a rule, Biochemie Thrombophlebitis continued on a daily basis.

Interruptions for even a few days have been followed by sensitivity reactions after reinstitution of therapy. Biochemie Thrombophlebitis can cause fetal harm when administered to a pregnant woman.

Penicillamine has been shown to be teratogenic in rats when given in doses 6 times higher than the highest dose recommended for human use. Skeletal defects, cleft palates and fetal toxicity resorptions Biochemie Thrombophlebitis been reported. There are no controlled studies on the use of penicillamine in pregnant women.

Some more links:
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