Heart failure is common in the elderly population. Approximately 6 to 10 percent of the population 65 years or older have heart failure. Heart failure is the most common reason for hospitalization in elderly patients. Etiology of heart failure is often multifactorial in the elderly. The common causes of heart failure include ischemic heart disease, valvular heart disease, hypertensive heart disease, and cardiomyopathy. Exacerbation of heart failure in the elderly is often accompanied by precipitating factors which include arrhythmia, renal failure, anemia, infection, adverse effect of drugs and noncompliance with medication and/or diet. Diagnosis of heart failure may be difficult in the elderly because symptoms of heart failure are often atypical or even absent. Heart failure with preserved systolic function is common in the elderly because aging has a greater impact on diastolic function. It is important to recognize that very old patients with heart failure are underrepresented in clinical trials.
(Internal Medicine 42: 383-388, 2003)

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Objective To clarify risk factors for hepatocellular carcinoma (HCC) other than hepatitis B surface antigen (HBsAg).
Patients and Methods We investigated serum HBV-DNA and other factors in 146 patients with liver cirrhosis (LC) or HCC who were HBsAg negative. We analyzed the clinical background of the patients, status of hepatitis B (HBV) viral markers and platelet count as well as the presence of an HBV-DNA fragment by PCR and elucidated risk factors for HCC generation using a logistic regression model.
Results Among ten factors, we determined that four represented a significant risk for HBsAg negative HCC: male gender, total alcohol consumption, total cigarettes smoked, and the presence of an HBV-DNA fragment. Multivariate analysis showed that among the four factors, the HBV-DNA fragment was an independent factor associated with HCC.
Conclusion The presence of an HBV-DNA fragment irrespective of the status of antibodies to either HBsAg (anti-HBs) or hepatitis B core antigen (anti-HBc) is a pivotal factor associated with the development of HCC.
(Internal Medicine 42: 389-393, 2003)

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Objective The aim of this study was to report a series of Japanese patients with neuropathic symptoms following HCV infection.
Patients and Methods Fifteen patients with neuropathic symptoms and HCV infection were studied retrospectively (neuropathy group). We evaluated clinical and electrophysiologic findings. As a control group, we investigated prospectively 11 patients with chronic HCV hepatitis without neuropathic symptoms.
Results In the neuropathy group, the peripheral neuropathy was a multiple mononeuropathy (MM) in 8 patients, a polyneuropathy in 4 patients, a single cranial neuropathy in 2 patients, and a cervical radiculopathy in one patient. Five patients with MM had relapsing symptoms. Two patients showed a progression of neurologic symptoms following varicella zoster virus infection. Mixed cryoglobulinemia was noted in 4 of 13 tested patients. Circulating immunocomplexes were detected in 3 of 10 tested patients, and low complement (C3, C4, or CH50) levels were noted in 10 of 13 tested patients. Nerve conduction study (NCS) showed abnormal findings in 10 of 13 investigated patients. In the control group, only the frequency of low CH50 was significantly lower than that in the neuropathy group. Abnormal findings of NCS were found in 3 of 11 patients.
Conclusion We showed the presence of various types of neuropathies in patients with HCV infection. Our results suggest that relapsing MM is common in HCV positive neuropathy with or without cryoglobulinemia, and that the virus may modulate neurologic manifestations of other viral infections. Subclinical neuropathy may be present in some patients with HCV infection without neurologic symptoms.
(Internal Medicine 42: 394-399, 2003)

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Objective Systemic reactive AA amyloidosis is an intractable complication in patients with a long history of rheumatoid arthritis (RA). To help to more easily and reliably detect the presence of this form of amyloidosis in patients with RA and start intensive treatment as early as possible, we examined the sensitivity and usefulness of abdominal fat aspiration biopsy with phenol Congo red staining in the diagnosis of AA amyloidosis.
Patients and Methods Ten patients were diagnosed with systemic reactive AA amyloidosis secondary to RA (all women; mean age, 70.2±6.4 years; mean disease duration of RA, 20.3±11.2 years) based on histopathological examinations of biopsied specimens mainly from the gastroduodenal mucosa. Abdominal fat aspiration biopsy was performed in these patients, and the specimens were treated with both classical alkaline and phenol Congo red staining.
Results Phenol Congo red staining revealed amyloid deposits in all 10 patients, while conventional alkaline Congo red staining showed a positive result in 7 patients. In the patients with a positive result with alkaline Congo red staining, reactivity of one grade or two higher was demonstrated by the phenol Congo red method.
Conclusion Phenol Congo red staining is superior to the classical alkaline Congo red staining with respect to the detection of AA-amyloid deposits in biopsied abdominal fat tissue specimens. In addition to easy access and procedural safety, abdominal fat aspiration biopsy might contribute reliably to the diagnosis of systemic reactive AA amyloidosis secondary to RA when phenol Congo red staining is employed.
(Internal Medicine 42: 400-405, 2003)

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The development of hepatocellular carcinoma (HCC) requires persistent hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. The other origins are extremely rare. A 63-year-old woman was admitted to our hospital for work-up of hepatic mass. She took Cyclophosphamide for Wegener granulomatosis for 21 years. Serum HBV and HCV markers were negative. A diagnosis of HCC was made by the imaging findings, and an extended left lobectomy of the liver was performed. Histologically, the tumor was diagnosed as moderately differentiated HCC. We thus considered the HCC in this case as a complication of the long-term Cyclophosphamide by the absence of known causes of HCC.
(Internal Medicine 42: 406-409, 2003)

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A 52-year-old man with Chilaiditi syndrome and mental retardation was admitted to Kanagawa Rehabilitation Hospital for severe hypoglycemic coma with malnutrition. This patient was first diagnosed as partial isolated adrenocorticotropin deficiency according to his symptoms and clinical course, but he was finally diagnosed as preclinical Cushing's syndrome. Manifestations of this case seemed unusual in spite of autonomic cortisol secretion and the detailed mechanisms of symptoms were unclear. The present case indicates that preclinical Cushing's syndrome may present with various manifestations, and careful diagnosis is necessary.
(Internal Medicine 42: 410-415, 2003)

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A 39-year-old man was diagnosed with hepatitis B virus-related cirrhosis, and because of hepatic exacerbations with icterus and ascites, he had been repeatedly hospitalized. He was treated with lamivudine. Several months later, his ascites disappeared and his liver function was improved from class C to A according to the Child-Pugh classification. Two years later, one small hepatocellular carcinoma was detected, and he underwent a successful hepatectomy. From this case, we consider lamivudine to be useful for improving hepatic function in decompensated liver cirrhosis type B and lamivudine might enable surgical resection of hepatocellular carcinoma.
(Internal Medicine 42: 416-420, 2003)

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Hypoglycemia is fatal if associated with sepsis in endstage renal disease (ESRD) patients. We report a hemodialysis patient of Streptococcal toxic shock syndrome presenting with hypoglycemia. She was found to be severely hypoglycemic with a plasma glucose level of 16 mg/dl. Immunoreactive insulin levels were undetectable throughout the clinical course. Several factors including reduced renal gluconeogenesis, reduced hepatic glucose output and excessive peripheral glucose utilization may account for the hypoglycemia in this patient. In conclusion, we would like to draw attention to the fact that septic ESRD patients without diabetes are prone to develop profound hypoglycemia with serious consequences.
(Internal Medicine 42: 421-423, 2003)

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We report a case of spontaneous remission of a massive CNS lesion with eosinophilic infiltrate. This 69-yearold man had eosinophilia without any systemic disorder or laboratory evidence of the most common causes of hypereosinophilia. MRI of the brain suggested an infiltrating neoplasm, but histological examination of a needle biopsy specimen failed to show evidence of a neoplasm. Instead, the tissue demonstrated rarefaction and gliosis with striking perivascular and parenchymal infiltrates of eosinophils. The MRI abnormality and eosinophilia disappeared spontaneously. We speculate that eosinophil-derived neurotoxins might have been the cause of the transient CNS disorder observed in this patient.
(Internal Medicine 42: 424-427, 2003)

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A 71-year-old man presented with gradually progressing cognitive decline following acute febrile exanthematous disorder. The MRI showed an abnormality in the bilateral limbic systems. An elevation of cerebrospinal fluid (CSF) protein with lymphocyte pleocytosis was noted. Immunoblot of the CSF revealed the presence of anti-white matter antibodies that mainly recognized astrocytes. Intravenous steroid followed by oral steroid reduced the symptoms to a remarkable degree. The patient has now been successfully sustained with steroid for more than two years. We considered that this case is classified as non-paraneoplastic limbic encephalitis, and acquired autoimmunity played a major role in the pathogenesis of this case.
(Internal Medicine 42: 428-432, 2003)

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Intracranial dissecting aneurysms cause ischemia, but anticoagulation or antiplatelet agents are administered to most ischemic patients without angiographical investigation. A 55-year-old woman succumbed to a Subarachnoid hemorrhage (SAH) during antiplatelet therapy for ischemia caused by a dissecting aneurysm at the anterior cerebral artery, which was identified by conventional angiography on day 11 after admission. The authors emphasize that all dissecting aneurysms manifesting ischemic attack can cause hemorrhage. Therefore, emergency angiography is recommended for patients with ischemia complaining of a headache. If dissection is identified, it may be better to regulate the blood pressure of the patient strictly without anticoagulation or antiplatelet therapy.
(Internal Medicine 42: 433-435, 2003)

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We treated a case of adult-onset severe-form anaphylactoid purpura. This case had been diagnosed as anaphylactoid purpura pathologically by skin biopsy. However, his clinical manifestations were atypical in view of complicated massive gastrointestinal hemorrhage. Intensive therapy including corticosteroid and cyclophosphamide transiently improved his condition. Nevertheless, the beta-D-glucan value in peripheral blood was gradually elevated. Prophylactic use of fluconazole failed to prevent contraction of invasive mycosis. Finally, he suddenly suffered from diffuse cerebral hemorrhage. Postmortem examination revealed systemic invasive aspergillosis as the cause of death.
(Internal Medicine 42: 436-442, 2003)

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A 40-year-old woman with a history of fever and arthralgia since age 17 had received long-term prednisolone (PSL) therapy. She was diagnosed with Takayasu's arteritis in 1980 and given PSL. The symptoms were well controlled until she developed itching in 1998. Laboratory tests showed elevated levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyltranspeptidase, total cholesterol, and immunoglobulin M (IgM). She tested positive for anti-mitochondria antibody and for both IgG and IgM anti-pyruvate dehydrogenases. Liver biopsy findings were typical of primary biliary cirrhosis (PBC). Our pa tient's clinical course suggested that an adequate amount of PSL to control Takayasu's arteritis does not necessarily prevent the development of PBC.
(Internal Medicine 42: 443-445, 2003)

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