Bee submass a cukorbetegség kezelésében.

Andres F. Carrion,1 Frank Czul,1 Leopoldo R. Arosemena,2 Gennaro Selvaggi,3 Monica T. Garcia,4 Akin Tekin,3 Andreas G. Tzakis,3 PaulMartin,5 and Ravi K. Carrion, acarrionmonsalve med. Pacini Copyright © Andres F. Carrion et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Propylthiouracil- PTU- induced hepatotoxicity is rare but potentially lethal with a spectrum of cukorbetegség csípése injury ranging from asymptomatic elevation of transaminases to fulminant hepatic failure and death.

We bee submass a cukorbetegség kezelésében two cases of acute hepatic failure due to PTU that required liver transplantation. Differences in the bee submass a cukorbetegség kezelésében presentation, histological characteristics, and posttransplant management are described as well as alternative therapeutic options.

Frequent monitoring for PTU-induced hepatic dysfunction is strongly advised because timely discontinuation of this drug and implementation of noninvasive therapeutic interventions may prevent progression to liver failure or even death.

Reported injury has ranged from mild asymptomatic elevation of aminotransferases to acute liver failure ALF. Although asymptomatic elevations in hepatic enzymes have been described in patients with untreated hyperthyroidism, recognition of hepatic dysfunction in a patient taking PTU requires immediate discontinuation of the drug and close followup.

Case Presentations Case 1. By week ten of treatment, she reported jaundice, fatigue, epigastric 2 International Journal of Endocrinology abdominal pain, nausea, and vomiting. She denied the use of over-the-counter or herbal medications. Her past medical history and family history were not contributory.

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She denied excessive alcohol consumption and recreational drug use. Upon subsequent transfer to our institution, initial laboratory workup revealed a prothrombin time of Serum markers for viral hepatitis A, B, and C were negative. Antinuclear antibodies, antismooth muscle antibodies, and antimitochondrial antibodies were negative. PTU was discontinued, but the coagulopathy worsened, and she subsequently developed hepatic encephalopathy.

She underwent orthotopic liver transplantation OLT eight days following admission.

Histologic examination of the explanted liver revealed submassive, confluent necrosis with bee submass a cukorbetegség kezelésében hemorrhage, bile duct proliferation, intracellular and canalicular cholestasis, bile plugging, and severe lymphoplasmacytic and eosinophilic infiltrates. Immunostain for IgG4 was positive Figure 1, microphotographs a and b.

The patient was discharged home in stable condition on postoperative day twelve. Her liver function become normal 6 months following OLT. Case 2. Baseline levels of aminotransferases were normal at the time PTU was started.

1. A pontos méretezés létfontosságú az implantáció indikációjánál, a megfelelő graft kiválasztásánál.
2. Az érbetegségek gyógyítása igen nagy odaadást és közös erőfeszítést igényel az angiológus, radiológus és érsebész kollégák részéről, a harcot a betegség ellen csak közös munkával tudjuk sikeresen megvívni.
3. Пожав 111.
4. Tüdőembólia (PE) - tünetek és kezelés - Thrombophlebitis November

Six weeks later she started to complain of malaise and generalized weakness followed by progressive jaundice, but she did not seek medical care until two weeks later when she had developed confusion, nausea, and vomiting. Blood tests at that time were INR 4. Serum markers for autoimmune and viral hepatitis A, B, and C were negative.

PTU was discontinued; however, her mental status continued to deteriorate with progression to severe hepatic encephalopathy. A transjugular liver biopsy revealed extensive parenchymal necrosis, collapse of the lobular architecture, bile duct proliferation, and periportal inflammation. Two days after admission, she was listed for OLT and received a liver transplant three days later. Histological examination of the native liver showed submassive confluent necrosis with prominent eosinophilic, neutrophilic, and lymphoplasmacytic infiltrate with canalicular and intracellular cholestasis and numerous lobular acidophilic bodies Figure 1, microphotographs c and d.

The posttransplant course was complicated by the development of graft dysfunction due to severe rejection, which did not improve with aggressive immunosuppressive therapy. The patient was relisted for OLT two weeks after the initial transplant and received a second allograft 6 days later. The postoperative course after the second transplant was complicated by a biliary leak that required reconstruction of the biliary anastomosis, as well as multiple episodes of rejection which were treated with antilymphocyte antibodies, plasmapheresis, and administration of rituximab.

The patient eventually recovered. She was discharged on postoperative day from the first liver transplant and is currently at home doing well 6 months after the second liver transplant.

Tüdőembólia (PE) - tünetek és kezelés

PTU is a thioamide derivative widely used for the treatment of hyperthyroidism which exerts its pharmacologic effects by two different mechanisms. PTU-induced hepatitis was first reported by H. Livingston and S. Livingston in [1], shortly after the FDA had approved this medication for the treatment of hyperthyroidism.

This patient was successfully managed with supportive care after discontinuation of the drug.

Six years later, Eisen [2] reported the first case of fulminant hepatic failure attributed to PTU, an ominous adverse reaction that since then has cukorbetegség és a tetoválás observed in an extremely small number of patients receiving this medication. Aloe vera kezelés cukorbetegséggel on published data about the annual incidence of hypothyroidism, the reported frequency of PTU therapy 15, bee submass a cukorbetegség kezelésében per yearand the incidence of PTU-induced severe liver injury approximately 0.

Acute hepatitis associated with this medication has been reported to occur in 0. Data suggest that the risk of severe hepatotoxicity is greater in children treated with PTU 1 : 1, childrenbut the overall incidence is significantly lower because fewer children are treated with this drug 1,—4, children per year [6].

For example, a significant reduction in PTU use by pediatric endocrinologists has been observed over the past several years, and some authors advocate that PTU should never be used as a first-line therapy in children due to the potential risk severe hepatotoxicity [7].

Liver biopsy remains the gold standard for diagnosis of PTU-induced hepatic injury, but the diagnosis is often inferred from the time course after initiation of PTU therapy [5, 8].

PTU hepatotoxicity has been reported to cause a variety of histological changes including portal and periportal inflammation with eosinophilic, lymphocytic, and plasmacytic infiltration in varying combinations, chronic active hepatitis, and submassive or massive hepatic necrosis [9]. Severe PTU-induced hepatotoxicity is postulated to be a dose independent, idiosyncratic hypersensitivity reaction.

Több tényező kombinációját a trombusembólia magas kockázata kíséri. Tüdőembólia PE tünetei A korai stádiumban a diagnózis nehéz, csak akut lefolyásban nyilvánvalóan és hirtelen jelentkeznek a tüdőartéria trombózisának tünetei: légszomj, mellkasi fájdalom, tachycardia, csökkent vérnyomás. Ebben az esetben a páciensnek vannak kockázati tényezői a tromboembólia szempontjából - visszerek és flebotrombózis. Az artériás hipotenzió és a sokk központi tromboembóliát jelez. A központi PE-vel súlyos akut dyspnoe is kialakul.

This theory is supported by positive lymphocyte sensitization studies [3, 4, 12]. Treatment options for PTU-induced liver failure are limited.