Cases reported "Liver Cirrhosis"

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1/15. Markedly elevated CA125 in hepatic cirrhosis: two case illustrations and review of the literature.

    CA125 is the most widely used tumor marker presently available for use in patients with epithelial ovarian cancer. Although elevated in a high percentage of patients with ovarian cancer, serum CA125 levels have also been detected in patients with numerous benign and malignant nongynecologic disorders, including various diseases of the liver. Despite this well-publicized fact, it has become apparent that the association between CA125 elevation, particularly the degree of elevation, and liver disease may not be as widely recognized as one would suspect. When marked CA125 elevations occur, diagnostic confusion is common. We describe two cases illustrative of this point. Both cases involve middle-aged women who presented with massive ascites and due to markedly elevated serum CA125 levels underwent exploratory laparotomy with hysterectomy and/or bilateral salpingo-oopherectomy before their referral to our center. Because preservation of a woman's reproductive organs is a significant concern, it is imperative that both primary care physicians and specialists are aware of such associations and the proper use of tumor markers.
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2/15. Bell's palsy during interferon therapy for chronic hepatitis c infection in patients with haemorrhagic disorders.

    Two adult patients with life-long severe haemorrhagic disorders commenced on interferon-alpha2b therapy for chronic hepatitis c infection. Both developed Bell's palsy several weeks after commencing therapy, They were started on steroids and, in addition, the first patient discontinued interferon-alpha2b therapy while the second patient elected to continue with therapy. In both cases facial paralysis improved over the ensuing weeks. Bell's palsy is often idiopathic but has been reported. in association with herpesviruses. It is not a recognised complication of chronic hepatitis B or C infection, or interferon-alpha2b therapy. However, the interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of nerve palsies, including optic tract neuropathy, occurring during interferon therapy, and immune-based mechanisms are thought to play a role in the aetiopathogenesis. No reports of Bell's palsy in association with interferon therapy were identified in our literature search, although one possible case has been reported to the Committee of safety in medicine. Although Bell's palsy in our patients may have occurred by chance, a neuropathic effect of interferon-alpha2b on the facial nerve cannot be excluded and we urge physicians using interferons to be aware of this potential side-effect.
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3/15. Multiple macroregenerative nodules in liver cirrhosis due to budd-chiari syndrome. case reports and review of the literature.

    Clinical, radiological, histological and immunohistochemical methods were used to define the nature of multiple rapidly growing hepatic nodules in 2 young patients with budd-chiari syndrome due to myeloproliferative diseases. In one patient, the arterial hyperperfusion of large nodules was demonstrated by dynamic computed tomography and angiography. The explanted livers of these patients showed multiple well-demarcated nodules up to 3 cm in diameter on the background of liver cirrhosis resulting from chronic hepatic congestion. Histologically, these nodules covered a spectrum ranging from adenoma-like lesions to nodules resembling focal nodular hyperplasia. They consisted of essentially normal hepatocytes, and variably contained fibrous septa including neoductules and large, mostly dysmorphic arteries. Sometimes, they were located close to still patent or recanalized veins. These rapidly growing hepatic nodules are best defined as macroregenerative nodules. The knowledge of this entity may help the physician to avoid misinterpretation of such nodules as carcinomas.
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4/15. EDTA-dependent pseudothrombocytopenia in a case of liver cirrhosis.

    Pseudothrombocytopenia (PTCP) is the consequence of an EDTA-activated platelet agglutination, resulting in a spuriously low platelet count. We report the case of a 54-year-old man with EDTA-dependent PTCP associated with liver cirrhosis. He couldn't undergo endoscopic examination and dental care for two years because of a previous diagnosis of severe thrombocytopenia secondary to liver cirrhosis. Lack of PTCP recognition may lead the physician to misdiagnosis and mismanagement of the patient.
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5/15. Resolution of refractory hepatic hydrothorax after chemical pleurodesis with minocycline.

    Management of refractory hepatic hydrothorax is a challenge to physicians in clinical practice. We reported two patients with hepatic hydrothorax, non-alcoholic cirrhosis and rapidly recurring pleural effusion. They failed to improve with diuretics and repeated thoracentesis. Refractory hepatic hydrothorax was successfully treated by minocycline-induced pleural symphysis. After pleurodesis, ventilatory function returned to normal in both patients. No recurrence of pleural effusion was noted. We suggest that minocycline pleurodesis is an alternative treatment for refractory hepatic hydrothorax because it is simple, safe and effective.
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6/15. Fulminant pneumonia due to aeromonas hydrophila in a man with chronic renal failure and liver cirrhosis.

    A 40-year-old man on hemodialysis was admitted due to dyspnea and chest pain and was diagnosed with pneumonia and pericarditis. ampicillin was administered, but thereafter severe septic shock developed. The fulminant type of pneumonia progressed rapidly, and he died only 48 hours after the onset of symptoms. The autopsy and sputa culture revealed pneumonia due to aeromonas hydrophila. The source of this infection remained unkown. Interestingly, there were two types of A. hydrophila found during such a short period. The physician should suspect this disease by questioning the patient's history. Early treatment with adequate antibiotics is the only means of saving such a patient's life.
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7/15. Ovarian carcinoma in two patients with chronic liver disease.

    ascites is a common and debilitating complication of cirrhosis. However, patients with chronic liver disease are not spared from other causes of ascites and physicians should be careful not to miss an underlying malignancy. Ovarian cancer is an insidious disease, which is difficult to diagnose and it ranks first in mortality among all gynecological cancers. Here, we present two cases of patients with chronic liver disease that developed ascites not simply because of cirrhosis but as a manifestation of ovarian cancer. We would like to emphasize that the causes of ascites, other than the liver itself, should not be overlooked in patients with chronic liver disease.
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8/15. Fatal hepatic decompensation in a bone marrow transplant recipient with HBV-related cirrhosis following lamivudine withdrawal.

    lamivudine is a nucleoside analogue with a potent antiviral activity used as prophylaxis against hepatitis b virus reactivation in patients with chronic HBV infection receiving chemotherapy. No standard guidelines exist, however, for the duration of lamivudine treatment. We report a clinical case of a 56-year-old patient with HBeAg-negative cirrhosis who developed a multiple myeloma. He was treated with lamivudine for 1 year while receiving chemotherapy and a subsequent bone marrow transplant. Complete remission from multiple myeloma was achieved. Four months after lamivudine was withdrawn, he experienced HBV reactivation with jaundice, though no YMDD mutations were detected. The patient rapidly developed fatal decompensation with septicemia and renal failure. In conclusion, this case shows that physicians should avoid discontinuing nucleoside therapy in patients with HBV infection who undergo immunosuppression for concomitant neoplastic conditions.
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9/15. Integrating palliative care for liver transplant candidates: "too well for transplant, too sick for life".

    Chronic liver disease results in more than 1 million physician visits and more than 300,000 hospitalizations per year in the united states. More than 27,000 patients annually progress to end-stage liver disease (ESLD), liver failure, or death. patients with ESLD experience such complications as encephalopathy, malnutrition, muscle wasting, ascites, esophagogastric variceal hemorrhage, spontaneous bacterial peritonitis, fatigue, and depression. Despite significant improvements in palliation, patients' quality of life diminishes and their disease will often inexorably progress. liver transplantation, a valid treatment option, increases life and reduces many symptoms. With the current shortage of organs, up to 10% to 15% of these patients die without receiving an organ. Many patients also are not candidates for transplantation due to comorbid illness. In addition, some patients receive a transplant but succumb to complications of the transplant itself. Such patients and families face the conundrum of a potentially treatable yet often fatal illness. Through the case of a 55-year-old woman with a life-long history of hepatitis b virus infection who is awaiting transplant, we discuss the transplant eligibility process and the struggle with maintaining hope for a cure in the face a life-threatening illness. In all of these circumstances, the health care team must combine elements of palliative care with life-sustaining therapy to maximize the patient's quality and quantity of life.
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10/15. Anticoagulant-induced pseudothrombocytopenia occurring after transcatheter arterial embolization for hepatocellular carcinoma.

    Pseudothrombocytopenia (PTCP) is the in vitro phenomenon of anticoagulant-activated platelet agglutination that results in spuriously low platelet counts. We report the case of a 65-year-old man with EDTA- and sodium citrate-dependent PTCP occurring after transcatheter arterial embolization (TAE) for hepatocellular carcinoma (HCC) due to hepatitis c cirrhosis. Invasion of the portal and hepatic veins by HCC formed severe trans-tumoral arterio-venous shunts that were effectively treated by TAE. Two days after the therapy, PTCP was seen on blood count and continued for 4 months. The patient received unnecessary treatment for disseminated intravascular coagulation (DIC) until the diagnosis of PTCP was established. PTCP is a rare complication but should be considered after TAE for HCC; lack of recognition may lead the physician to misdiagnosis and patient mismanagement.
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