Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman was diagnosed as Crow-Fukase syndrome on July 1997, presenting with lymph node swelling, polyneuropathy, hepatomegaly, hypothyroidism, renal dysfunction, edema and skin change. Lymph node swelling and polyneuropathy improved in some degree after chemotherapy. She was admitted to our hospital on march 6, 1998 because of consciousness disturbance, right hemiparesis and non-fluent aphasia after fever and hypotension. The next day of admission, consciousness disturbance, right hemiparesis and non-fluent aphasia disappeared. MR images of the brain revealed low intensity on a T1-weighted image and high intensity on a T2-weighted image in the left parietal lobe. Furthermore, MR images also revealed diffuse hypertrophic dura matter with enhancement by Gd-DTPA, which made the diagnosis of chronic cranial pachymeningitis. The cerebral angiographies showed bilateral internal carotid artery occlusion. The cerebrospinal fluid showed normal cell count, total protein level of 82 mg/dl, and IgG level of 18 mg/dl. Since there has been very few case reports describing intimate relationship between Crow-Fukase syndrome and pachymeningitis, and between carotid occlusion and pachymeningitis, we speculated that the pachymeningitis might be associated with Crow-Fukase syndrome. Furthermore, pachymeningitis might be a cause of her bilateral carotid occlusion. The number of cases of Crow-Fukase syndrome associated with cerebrovascular disease was very rare. This is the first case which had bilateral internal carotid artery occlusion probably caused by chronic cranial pachymeningitis. Therefore, it is necessary to pay attention to cerebrovascular disease when the patient of Crow-Fukase syndrome is associated with pachymeningitis.
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PMID:[Crow-Fukase syndrome associated with Castleman disease showing hypertrophic cranial pachymeningitis and bilateral internal carotid artery occlusion]. 1039 73

A 68 year old Ecuadorian man was investigated for polyuria, polydipsia and weight loss of 3 kg during the previous two months. Insulin dependent diabetes mellitus was diagnosed 10 year before admission and treated with appropriate diet and insulin (35 U/d). 18 months before was diagnosed in El Ecuador of "multiple liver nodes non-suggestive of malignancy". Physical examination showed a large multinodular petrous hepatomegaly. There was no evidence of skin lesions. Results of laboratory studies included a basal plasma glucose level that ranged between 275-367 mg/dl (N=60-100), glycosylated haemoglobin of 8.9% (N<5) and a serum albumin of 2.8 gr./dl (N=3.4-4.8). At admission non-other laboratory alterations were detected. Computed tomography showed a mass on the head of the pancreas with loco-regional lymph nodes and liver metastases. Tumor markers were normal. Fine-needle aspiration cytology of the liver masses revealed the presence of liver metastases of a non-differentiated malignant tumor. A 111In-DTPAOC scintigraphy revealed the presence of somatostatin receptors in the liver metastases, also detecting the presence of multiple bone metastases in the axial and appendicular skeleton. Plasma glucagon level was 678 pg/ml (N<250). A diagnosis of metastatic glucagonoma was established and therapy with streptozocin, 5-FU, insulin and synthetic somatostatin analogs was initiated. Three months after the therapy initiation the patient was symptom free. Some weeks after the patient suffered from left hip pain, and a control 111In-DTPA scintigraphy showed progression of his bone metastases. In conclusion, glucagonoma must be suspected in all diabetic patients with metastatic liver, even in absence of necrotic migratory erythema. In these circumstances, plasmatic glucagon level and somatostatin receptors scintigraphy will be a useful tool for establishing the final diagnosis.
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PMID:[Diabetes mellitus and pancreatic tumor]. 1471 49