A role of neuropsychological test in the patients with chronic liver disease / 대한내과학회지

BACKGROUND: Minimal (subclinical) hepatic encephalopathy (mHE) currently diagnosed by psychometric tests or neurophysiological test adversely affects daily functioning. In view of its sociomedical relevance, simple and reproducible tests for routine diagnosis are required. The aims of this study are to evaluate cognitive function of patients with chronic liver disease by computerized neuropsychological test (STIM), and the difference of cognitive function according to Child classification. METHODS: Between June, 2002 and February, 2003 We enrolled 61 randomized consecutive patients diagnosed with chronic liver disease by biochemical tests, ultrasonographic finding or histology. This study used finger tapping, visual CPT, spatial memory test, Wisconsin card sorting test chosen from Neuscan and STIM system (Neurosoft company, U.S.A) and global-local processing test. RESULTS: In the present study, significant correlation was found between neurologic abnormalities and the degree of liver disease. The result of neuropsychological test showed that cognitive function was decreased according to the severity of chronic liver disease, especially liver cirrhosis. Cirrhotic patients, especially Child C group, exhibited selective deficits in complex attentional and fine motor skills, visuospatial perception, with preservation of memory. CONCLUSION: The STIM in this study is simple, objective and reproducible method because it can subdivide evaluation of cognitive function and computerize the measurement of response. We assume that STIM may be used early detection method of mHE if the study will be in a large scale. Because psychomotor deficits found in mHE could have a disadvanting influence on daily functioning of patients, e.g., driving abilty of a car or performance at work, we concluded early detection of mHE and aggressive treatment of mHE in clinically asymptomatic cirrhotic patients is necessary for improvement of their quality of life.

The Significance of Urine Sodium Measurement after Furosemide Administration in Diuretics-unresponsive Patients with Liver Cirrhosis / 대한간학회지

BACKGROUND/AIMS: The diagnosis of refractory ascites means a poor prognosis for patients with liver cirrhosis. The definition of refractory ascites has already been established, but using the dosage of diuretics that correlates with the definition of refractory ascites in an out-patient department will lower the compliance of the patient, as well as causing serious complications, such as hepatic encephalopathy and hyponatremia, as the dosage of diuretics is increased. Due to this fact, it is very difficult to apply this definition of refractory ascites to patients in a domestic out-patient department. In this study, in situations where there are difficulties in applying the diuretics dosage according to definition of refractory ascites, we tried to find out whether measuring the value of urine sodium after the administration of intravenous furosemide can be the standard in early differentiation of the response to diuretics treatment. METHODS: We reviewed 16 cases of liver cirrhosis with ascites and classified them into two groups by the response to diuretics. The diuretics-responsive ascites group was 8 cases and the diuretics-unresponsive ascites group consisted of 8 cases. After admission, we examined the patients' CBC, biochemical liver function test, spot urine sodium, and 24 hour creatinine clearance. After the beginning of the experiment, all diuretic therapy was stopped for 3 days. Daily we examined the patients' CBC, biochemical liver function test, and in the 3rd experiment day, we measured 24-hour urine volume and sodium. In the 4th experiment day, after sampling for ADH, plasma renin activity and plasma aldosterone level, we administrated the furosemide 80 mg I.V, and measured the amount of 8 hour urine volume and sodium. RESULTS: The plasma aldosterone level was significantly higher in the diuretics- unresponsive ascites group than in the diuretics-responsive ascites group. In the 4th experiment day, the amount of urine volume and sodium was very significantly lower in the diuretics-unresponsive ascites group than in the diuretics-responsive ascites group (1297.5 +/- 80.9 vs 2003.7 +/- 114.6 ml, p<0.005, 77.3 +/- 8.2 vs 211.8 +/- 12.6 mEq, p<0.001). CONCLUSIONS: In out-patient departments, the measurement of urine sodium 8 hours after administrating 80 mg of intravenous furosemide, will help in differentiating ascites patients with lower treatment response to diuretics.

Relationship of Propranolol Pharmacokinetic Parameters with Portosystemic Shunt in CCl4-induced cirrhotic Rats / 대한간학회지

BACKGROUND: This study was designed to determine the relationship of propranolol pharmacokinetic parameters with portosystemic shunt in CCl4-induced cirrhotic rats. METHODS: Cirrhotic rats(n=6) were induced by intramuscular injection of CCl4 in olive oil(two time per weeks) for 12 weeks. Controls (n=6) were injected intramuscularly with the same dose of olive oil for 12 weeks. We evaluated the amount of portosystemic shunt by thallium-201 per rectal scintigraphy. After intravenous bolus injection of propranolol (2mg/kg) to rats, the serum propranolol concentrations were analyzed by a HPLC-fluorimetric detector system. Pharmacokinetic parameters such as C0, AUC, t(1/2(beta)), and CLp were determined in each group. Then, a small amount of heptic tissue was obtained and subjected to determination of the hepatic collagen content by quantitating 4-hydroxyproline and were inspected by microscope after hematoxylin and eosin stain. RESULTS: In liver biopsy, liver fibrosis progressed in CCl4-induced cirrhotic rats. The serum concentrations of propranolol were significantly (p < 0.01) elevated in CCl4-induced cirrhotic rats. Mean amount of 4-hydroxyproline, mean H/L ratio, and mean AUC in CCl4-induced cirrhotic rats was significantly (p < 0.01) higher than that in control rats. There was a relationship between AUC, H/L ratio, and amount of 4-hydroxyproline. CONCLUSION: H/L ratio may help in the selection of drug dosage (especially blood flow dependent drug) in pre-clinical studies for chronic liver disease during the drug development process.

Endoscopic transmural cyst drainage of pancreatic pseudocyst / 대한내과학회지

No abstract available.

Five-year Follow-up of Clinical and Laboratory Data of Early Liver Cirrhosis Patients Confirmed by Liver Biopsy / 대한간학회지

BACKGROUND/AIMS: It is important to evaluate the general status of the liver including the structural and inflammatory aspects, as well as the functional aspects, in order to determine a patient's treatment modality and prognosis. METHODS: 55 Child-Pugh class A liver cirrhosis patients confirmed by liver biopsy have been categorized into 4 groups based on the shunt index and p-value(Y= 3.3431 - 0.8160 ALT/AST ratio-0.0343 X prothrombin time+2.6963 X shunt index, p = e(y)/(e(y)+1)), which was obtained by Thallium- 201 scan ; group I - shunt index less than 0.3 and p-value less than 0.7; group II - shunt index less than 0.3 and p-value more than 0.7; group III - shunt index more than 0.3 and p-value less than 0.7; and group IV - shunt index more than 0.3 and p-value more than 0.7. Statistical analyses used were ANOVA, paired t-test, and Chi-square test. RESULTS: 1. The laboratory data after a 5-year follow-up also showed a significant difference between four groups. 2. In group IV, the Child-Pugh class after 5 years worsened, and complications of liver cirrhosis such as esophageal varix, ascites, and hepatic encephalopathy occurred more frequently. 3. In group II, the laboratory data after a 5-year follow-up indicated some improvement. CONCLUSION: It can be seen that even early in patients with initially the same cirrhosis, the course of the illness can progress to a variety of different situations. The measurement of shunt index and the p-value of cirrhosis will be more helpful in the follow-up evaluation and predicting its prognostic index in liver cirrhosis patients.

Assessment of malnutrition in patients with liver cirrhosis / 대한내과학회지

BACKGROUND: Malnutrition frequently occurs in patients with liver cirrhosis independently for its etiology and can modify prognosis of the disease. Since malnutrition was observed at all clinical stages, but more frequently seen at advanced stages, early and detailed nutritional assessment in all patients with liver cirrhosis is important. The aims of this study are to define the nutritional status and the difference of nutritional index according to etiology and Child classification in patients with liver cirrhosis in Korea. METHODS: A total 138 cirrhotic patients (41 alcoholic cirrhosis, 97 virus-related cirrhosis) were studied. The diagnosis of cirrhosis was based on clinical, laboratory and ultrasonographic criteria and liver biopsy. The patients were divided into three groups according to the severity of their liver disease as assessed by the Child-Pugh classification. Nutritional parameter of protein (serum albumin, serum transferrin, total lymphocyte count) were measured. RESULTS: The patients with protein malnutrition are as follows: albumin 55, transferrin 68, total lymphocyte count 8. The frequency of moderate to severe protein malnutrition was high in alcoholic cirrhosis.: albumin (<2.9 g/dL) (26.8% vs 17.5%), transferrin (<180 mg/dL) (48.5% vs 24.8%), total lymphocyte count (<1200 number/L) (2.4% vs 2.0%). The mean value of nutritional index correlated with the degree of liver function impairment. (Child C showed the lowest value). CONCLUSION: In spite of limitation of nutritional index in this study, our study showed that severe protein-energy malnutrition was rare in Korea, and protein-energy malnutrition was not only more common in alcoholic cirrhosis but related to the severity of liver disease. Therefore, our data suggests that clinician should understand the importance of not imposing unnecessary restrictions and supplementation on protein intake for fear of imbalance of nutrition.

A case of pancytopenia secondary to low-dose pulse methotrexate therapy in a patient with rheumatoid arthritis and renal insufficiency

Most reports on serious MTX toxicity have focused on hepatic abnormalities, while other effects, including hematologic reactions, have not been emphasized. We experienced a case of pancytopenia secondary to MTX therapy in a patient with RA and renal insufficiency. A 67-year-old woman with a 12-year history of active seropositive RA that was a response to non-steroidal anti-inflammatory drugs, hydroxychloroquinine and intra-articular steroid injections, had been followed up and was diagnosed as early chronic renal failure in October, 1993. Recently, because of significant morning stiffness and polyarthralgia, the decision was made to institute MTX treatment. This was begun as a single oral dose of 5mg/week. After 2 doses, the patient was admitted to the hospital with general weakness. Laboratory tests showed a hemoglobin level of 7.9 g/dl, WBC count 1800/mm3 and platelet count of 64000/mm3. The serum creatinine level was 6.1 mEq/dl and the BUN level was 82 mEq/dl. Liver function test results were normal, but the serum albumin level was 2.7 g/dl. The patient subsequently developed fever and blood transfusions, granulocyte colony stimulating factor (G-CSF) and intravenous prophylactic antibiotic therapy were required. Her condition was improved. In summary, Low-dose MTX-related adverse hematologic side effects, including fatal pancytopenia, are rare but are a cause of increasing concern in patients with RA and renal insufficiency. Close monitoring of associated risk factors, particularly impaired renal function, should be mandatory for all patients who are receiving MTX therapy.

Initial Transient Neurologic Recovery Followed by Delayed Deterioration of Osmotic Demyelination Syndrome: A Case Report / 대한신장학회잡지

In literatures, most of the studies of severe hyponatremia during or following its treatment has been concentrated with special references to the rate of correction and its neurologic outcomes. But, there is relatively few ones analyzing the diverse clinical manifestations of neurologic symptorns or complications during the course of treating severe hyponatremia. We experienced a catastrophic course related to hyponatremia in a 51 year woman with severe rheumatoid arthritis, who underwent knee joint replacement, and this case revealed the initial transient neurologic recovery for 3 days by the initial rapid correction of hyponatremia, then followed by delayed deterioration of osmotic demyelination syndrome leading to locked-in syndrome. Reported cases with similar clinical course (biphasic course) in the world lituratures were reviewed with special interests in the initial maximum rate of correction of hyponatremia and radiologic findings. This review suggests that clinicians treating the patients with severe symptomatic hyponatremia should be aware of the possibility of delayed neurologic sequelae despite the recovery of neurologic status as well as the degree of hyponatremia in the early treatment course of hyponatremia.

Clinical Analysis of Severe Hyponatremic Patients with Neurologic Symptoms / 대한신장학회잡지

OBJECTIVE: Severe hyponatremia is rare but constitute a true medical emergency since it has deleterious effects on the central nervous system. The etiology and clinical presentation of severe hyponatremia are diverse and nonspecific, furthermore, the optimal therapeutic approach is debatable at the present time. Therefore, the purpose of this study is to analyze the clinical manifestations of severe hyponatremic patients and to assess the outcomes with special reference to the rate of its correction. METHODS: This retrospective study analyzed the clinical course of 27 consecutive patients(pts) at a single medical center who presented with neurologic hyponatremic symptoms as well as a serum sodium (Na) concentration less than 125mEq/L. RESULTS: Of 27 hyponatremic patients, male to female ratio was almost equal, 13 to 14, and mean age was 67.1 years. The most common cause of hyponatremia was SIADH(11 pts, 40.7%), followed by hypovolemia(11 pts, 37.1%), and edema(4 pts, 14.8%). Hyponatremic neurologic symptoms included lethargy(33.3%), confusion with drowsy mentality (33.3%), dizziness(18.6%), and semicoma(7.4%), respectively. The rate of increase to a serum Na concentration to 125mEq/L during correction of hyponatremic averaged 0.56+/-0.49mEq/L/hr while the maximum increase in serum Na concentration during any period of the hospital course, mostly initial phase, averaged 0.69+/-0.63mEq/L/hr in all 27 pts, of whom 18 pts(66.7%) was less than 0.5mEq/L/hr, 3 pts from 0.5 to 1.0mEq/L/hr(11.1%), and 6 pts more than 1.0mEq/L/hr(22.2%). All 27 pts but one recovered from neurologic symptoms due to hyponatremia without neurologic sequale. Extrapontine myelinolysis with locked in condition was developed during the course of treating hyponatremia in a pts, of whom serum Na concentration before treatment was the lowest(92mEq/L) with the rate of correction to 125mEq/L by 1.26mEq/L/hr and the initial rate of correction within the first 6 hour by 3.17mEq/L/hr. No one died of hyponatremia itself during the course of its treatment but 3 deaths of 27 pts were attributed to the pts' severe underlying diseases. CONCLUSION: Surprisingly, these data revealed the relatively benign course of severe symptomatic hyponatremia. However, in assessing the outcome of severe symptomatic hyponatremia, the initial degree of hyponatremia as well as the rate of correction during its treatment, particularly the initial rate of correction within the first 6 hour, would be considered.

A Case of Recovery from Suspended Animation caused by Puffer fish Poisoning: a case report

Tetrodotoxin is a neurotoxin produced by about 90 species of puffer fish and causes paralysis of central nervous system and peripheral nerves by blocking the movement of all monovalent cations. Ingestion of tetrodotoxin produces clinical manifestations such as paresthesias(within 10-45 min), vomiting, lightheadedness, salivation, muscle twitching, dysphagia, difficulty in speaking, convulsion and death that expressed by cardiopulmonary arrest with loss of brain stem reflex sometimes. Tetrodotoxin prevents or delays ischemia induced neuronal death by way of following 3 mechanisms. Firstly, it reduces the energy demand of the brain tissues. Secondly, it delays or even prevents anoxic depolarization. Finally, it diminishes ischemia induced cell swelling and cerebral edema. We report a case of puffer fish poisoning which presented with cardiopulmonary arrest and loss of brain stem reflex, but completely recovered by aggressive cardiopulmonary resuscitation.

Pulmonary Diffusing Capacity in Patients with Liver Cirrhosis / 대한내과학회지

About a third of the patients with decompensated liver cirrhosis have reduced arterial oxygen saturation and are sometimes cyanosed in the absence of any apparent lung or heart disease; There is a reduction of diffusing capacity without a restrictive ventilatory defect. The aim of this study was to determine diffusing capacities in patients with chronic liver- diseases. The diffusing capacities and arterial oxygen saturations were measured in 25 patients with chronic active hepatitis(CAH), 9 early cirrhotics (early LC), 36 cirrhotics(Child's class A) and 11 cirrhotics(Child's class B). The anterior tibial area was observed for pitting edema, and Thallium-201 test per rectum(shunt index) was done. Hypoxemia was not observed in all subjects. The number of cases with decreased pulmonary diffusing capacity (DLco) is 3/25(12.0%) for CAH, 3/9(33.3%) for CAH with early liver cirrhosis(LC), 17/36(47.2%) for LC(Child's class A) and 6/11(54.5%) for LC(Child's class B). The mean+/-standard deviation of Dlco(% predicred) are 93.1+/-12.1 for CAH, 85.7+/-12.3 for CAH with early LC, 82.2+/-14.7 for LC(Child's class A) and 80.4+/-6.9 for LC(Child's class B), There is a significant difference between DLco in CAH and that in LC(Child's class A)(p0.3) had significantly lower DLco than these with lower shunt index(0.3) or pitting edema. This may be due to an increased systemic blood flow shunt and an increased generalized interstitial edema. Pulmonary function tests including diffusing capacity may be useful as prognostic parameters in patients with chronic liver disease, especially in those with CAH or early LC.

Thiazide-induced Electrolyte Disturbance with Altered Mental Status / 대한신장학회잡지

We report a severe case of hyponatremic encephalopathy in a 38 year old schizophrenic patient with polydipsia that was very likely precipitated by hydrochlorothiazide given for the accompanied hypertension in this patient. On admission via emergency room, this patient's electrolyte imbalances include not only hyponatremia but also hypokalemia, hypomagnesemia and metabolic alkalosis, which have been well known as the complications of thiazide diuretics. Fortunately, this patient recovered from comatose condition with the treatment of hyponatremia at the correction rate of about 0.5mEq/L/hr in addition to potassium and volume replacements. However, this case gives us the warning that the presence of hyponatremic condition such as polydipsia should be ruled out before thiazide diuretics prescribed for patients with schizophrenia, and other electrolytes imbalance in addition to hyponatremia as the complications of thiazide diuretics should be looked for the simultaneous treatment for them.

Renal potassium wasting and hypocalciuria ameliorated with magnesium repletion in Gitelman's syndrome

A woman aged 45 years was presented with hypokalemic metabolic alkalosis and hypomagnesemia associated with renal potassium and magnesium wasting. Her 24-hour urinary calcium excretion was strikingly low despite normocalcemia and normal creatinine clearance, which is one of characteristic findings of Gitelman's syndrome (GS). She was evaluated for the responses following Mg supplementation for 10 days, which showed marked increments in serum potassium and magnesium as well as improvements of the degree of renal potassium wasting and hypocalciuria. This amelioration of abnormal biochemical pictures in this patient after Mg supplementation proposes that the hypokalemia with renal potassium wasting and hypocalciuria may be caused by abnormal Mg metabolism.