Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unlike other pituitary hormones, PRL is under tonic inhibition by the hypothalamus by way of the PRL inhibitory factor, dopamine. GAP and GABA may also be inhibitory. PRL-releasing factors include TRH and VIP and possibly others. Circulating PRL is predominantly monomeric, although some patients with hyperprolactinemia appear to have increased quantities of the less biologically active polymeric forms. PRL is secreted episodically, with an increase in the amplitude of the secretory pulses with sleep. A transitory increase also occurs in response to the protein component of meals. Basal PRL levels increase in response to the hormonal milieu of pregnancy, and suckling postpartum triggers PRL release. Pathologic increases of PRL owing to hypothalamic dysregulation occur with a variety of medications, including the neuroleptics, metoclopramide, antidepressants, methyldopa, reserpine and verapamil, abuse of opiates and cocaine, renal insufficiency, cirrhosis, hypothyroidism, adrenal insufficiency, neurogenic stimulation, and idiopathically. Hyperprolactinemia also may occur from structural lesions of the stalk and hypothalamus, which cause disinhibition with or without maintenance of PRF activity, ectopic neoplasm production, and, most commonly, from prolactinomas. Diagnostic testing consists of routine chemistry and thyroid testing and imaging with MRI or CT. Dopamine agonists are the treatment of choice of prolactinomas of all sizes. Transsphenoidal surgery is an alternative for the patient who does not respond to medical therapy or who wishes definitive tumor removal, realizing that long-term cure is achieved in only 50% to 60% of patients with microadenomas and a much lower number in those with macroadenomas. Radiotherapy is reserved for patients who do respond to either medical or surgical treatment. Patients wishing to become pregnant usually are treated with bromocriptine, although prepregnancy surgical debulking may be advisable for those with large macroadenomas to reduce problems with tumor enlargement.
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PMID:Pathologic hyperprolactinemia. 148 80

A 53-year-old woman developed symptoms of slow speech, mild dementia, increased deep tendon reflex, ataxic gait, flapping tremor, and dystonic posture during two years. She had liver cirrhosis and hyperammonemia, which suggested a diagnosis of portal-systemic encephalopathy. MR T1-weighted images showed increased signal intensity in globus pallidus, internal capsule, substantia innominata, and a part of hypothalamus. T2-weighted images revealed abnormal findings as follows: high intense area in middle cerebellar peduncle, and low signal intensity of corpus callosum and pontine base. This is the first report about MRI abnormalities in substantia innominata, corpus callosum, and pontine base in a patient with portal-systemic encephalopathy.
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PMID:[A case of portal-systemic encephalopathy presenting characteristic MR images in globus pallidus, hypothalamus, corpus callosum, pontine base, and middle cerebellar peduncle]. 161 82

A clinical study and follow-up of 77 patients (63 males and 14 females) with hepatocellular carcinoma with age range from 22 to 80 years were collected from the Institute of Post Graduate Medicine and Research and eight private hospitals from Dhaka City. Past history of transfusion was present in 16 (20.8%), Jaundice in 20 (26%) and 13 (16.9%) patients had associated cirrhosis. HBs Ag was positive in 17 (33.33%) out of 51 patients and liver ultrasound suggested hypoechogenic lesion in 44 (57.2%) patients. CT was performed in 7 (9.1%) and in one MRI was done. Eight (50%) out of 16 patients had alphafetoprotein ranging from 1000-12000 ng/ml. Space occupying lesion was detected in 25 (71.4%) out of 35 cases by isotope scan and needle biopsy was confirmatory in 25 (32.5%). Commonest presentations were abdominal lump (96.2%), weakness (79.3%), weight loss (74%), and loss of appetite (78%). Fifty six (72.2%) patients were followed weekly till death (2.9 +/- 2.4 months). The mean survival was higher under 30 years (5.9 +/- 3.7 months; P less than 0.05). Serum bilirubin above 5 mg/dl with HCC also had poor prognosis (1.6 +/- 0.8 months; P less than 0.01) Those who had prothrombin time higher than 16 seconds died earlier (1.6 +/- 0.7 months; P less than 0.01). Survival was poor in those who had the tumour size over 7 cm (2.5 +/- 0.9 months; P less than 0.01).
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PMID:Clinical profile: prognostic index in hepatocellular carcinoma. 166 11

What then are the lessons to be learned about prevention and treatment of hemochromatosis? Early diagnosis is essential. The best indicator would be testing of serum iron and total saturation followed by a serum ferritin if elevated. Once these indices are abnormally high, MRI and or a liver biopsy should confirm the stage of the iron over-loaded state. If indeed the patient is not iron-overloaded (normal liver biopsy in the face of high saturation and ferritin level) phlebotomies should be performed until these indices are normal and then maintained at a normal level. This should entail four to six phlebotomies a year. Family members should also be screened and managed in a like manner. HLA typing may be a partially helpful screening device. The abnormal gene is closely linked on chromosome 6 with HLA histocompatibility loci. Now, by means of HLA typing, we can identify heterozygote carriers and homozygous (abnormal) among first degree relatives of patients with hemochromatosis. Unfortunately, HLA typing can only be used within a given family and cannot be used to screen the general population. It is estimated that 70% of hemochromatoics have the antigen HLA-A3; however, so does 28% of the (well) general population. Patients with unexplained cirrhosis, arthritis, liver disease, diabetes, impotency, cardiomyopathy and neurological symptoms should be screened in a like manner. Routine health practice profile chemistries must include a serum iron and iron saturation, and if high followed by a serum ferritin. Once diagnosed, therapy must be maintained with phlebotomy for the life time of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemochromatosis: diagnosis and treatment. 179 61

Fifteen patients with liver cirrhosis and two control groups were examined. The first control group consisted of 7 healthy volunteers, and the second group of 17 patients with nonfocal liver diseases. The T1 and T2 relaxation times were calculated from signal intensities read out from a region of interest centrally located in the liver. T1 relaxation time was longer in the patients with liver cirrhosis than in the two reference groups. Ten patients had a liver biopsy taken prior to the MRI study. No correlation was found between histopathology and the measured relaxation times.
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PMID:Prolonged T1 in patients with liver cirrhosis: an in vivo MRI study. 208 30

Splenomegaly was evaluated by a 0.1 T MR system using multi-echo SE image. (TR = 1500 msec., TE = 40, 80 and 120 msec.) Calculated measurement of T2 relaxation time was obtained. Material consists of 32 cases including 14 liver cirrhosis, 3 chronic myelocytic leukemia, 1 malignant lymphoma and 14 normals. 1) T2 value of normal spleen measured 113.7 +/- 5.68 msec. 2) Splenomegaly due to congestion had the prolonged T2 value of 122.6 +/- 10.25 msec. 3) T2 value of splenomegaly with malignant cell infiltration such as leukemia and lymphoma were shorter than normal spleen. Good histological correlation was obtained in MRI findings of splenomegaly due to congestion and malignant cell infiltration.
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PMID:[MRI of splenomegaly]. 223 8

Five of six patients with angiographically proved Budd-Chiari syndrome (hepatic venous outflow obstruction) showed multiple specific MRI abnormalities: striking reduction in caliber or complete absence of the hepatic veins, "comma-shaped" intrahepatic collateral vessels, and/or marked constriction of the intrahepatic inferior vena cava. The sixth patient had angiographically proven sinusoidal hepatic venous obstruction and patent central hepatic veins; MRI showed ascites but revealed no specific features of the Budd-Chiari syndrome. Patients with end-stage cirrhosis also showed compressed, distorted hepatic veins; however, these cirrhotic livers were distinguished by their small size, nodular surface, and extrahepatic collateral varices. In patients without cirrhosis or the Budd-Chiari syndrome, normal hepatic, portal, and inferior caval veins were routinely seen when technically adequate MRI examinations were obtained (94 of 100 cases). Four of the six patients with Budd-Chiari syndrome had been treated surgically. In three, MRI identified patent portocaval shunts. In the fourth, angiographically confirmed shunt stenosis was demonstrated by MRI.
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PMID:MRI of the Budd-Chiari syndrome. 242 7

Three cases of hepatocellular carcinoma with remarkable fatty metamorphosis were reported. When we encounter lipomatous tumor with liver cirrhosis on CT and MRI, further examination is necessary because of its high possibility of hepatocellular carcinoma.
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PMID:[Three cases of hepatocellular carcinoma with remarkable fatty metamorphosis]. 255 96

Clinical studies using 31P and 1H MRS with a whole body 2.0 T MRI/MRS system are described. In most cases, techniques to quantitate absolute molar concentrations of metabolites in various organs were used. In the brain, AIDS, chronic stroke, and white matter lesions were associated with alterations of brain 31P metabolites. Epilepsy was associated with increased pH in the seizure focus. In the heart, dilated cardiomyopathy was associated with increased PDE/ATP while PCr/ATP was unchanged. In the liver, alcoholic hepatitis and cirrhosis were associated with diminished hepatic ATP while alcoholic hepatitis had increased pH and cirrhosis had decreased pH. This allowed differentiation of normal liver, alcoholic hepatitis, and alcoholic cirrhosis without biopsy. In the prostate, malignancy was associated with increased PME/ATP and decreased PCr/ATP. The PME/PCr was greatly increased in malignant prostate with no overlap in normals. Other cancers outside the brain had increased PME and effective treatment was often associated with diminished PME. 1H MRS of the brain was performed using ISIS and outer volume suppression pulses for volume localization. Excellent high resolution 1H water-suppressed spectra were obtained at echo times as short as 30 ms, showing well resolved peaks for lactate, N-acetylaspartate, glutamate, choline, creatinine, and inositol. 1H MRS demonstrated that the uptake of ethanol by the brain was slower than the rise of ethanol in blood. 31P spectroscopic imaging of the brain with resolution of 2.25 x 2.25 x 2.5 cm produced metabolic images and high resolution spectra from desired regions of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical magnetic resonance spectroscopy of brain, heart, liver, kidney, and cancer. A quantitative approach. 270 9

MRI was performed on formalin-fixed autopsied liver specimens of nine patients with liver cirrhosis. Tiny low-intensity nodules were demonstrated in four specimens, in which microscopic examination revealed hemosiderin deposits in pseudolobules. In one specimen with mild hemosiderin deposits, low-intensity nodule was not seen on MRI. This result suggests that there is a close relationship between MRI demonstration of low-intensity nodules and iron deposits in pseudolobules of liver cirrhosis.
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PMID:[MRI demonstration of pseudolobules of liver cirrhosis--particular reference to iron deposits on autopsy specimens]. 279 60


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