Perplexing hyperkalaemia.
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Biomedical subjects
Publications and source records attributed to Shih-Hua Lin.
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We previously demonstrated that hyperbaric oxygen (HBO) treatment alleviated lipopolysaccharide (LPS)-induced acute lung injury in rats. However, the mechanisms responsible for the protective effect are still not fully understood. To obtain further information on the protective effect of HBO, in this study we investigated the role of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in intratracheal spraying LPS-induced acute lung injury in rats after HBO or hyperoxia treatment. The results showed that HBO but not hyperoxia attenuated the TNF-alpha level in plasma and bronchoalveolar lavage (BAL) fluid, NO concentration in BAL and plasma, and inducible NO synthase protein expression in lung tissue based on the Western blotting and immunohistochemical staining.
The application of artificial neural network (ANN) to predict outcome and explore potential relationships among clinical data is increasing being used in many clinical scenarios. The aim of this study was to validate whether an ANN is a useful tool for predicting the target range of plasma intact parathyroid hormone (iPTH) concentration in hemodialysis patients. An ANN was constructed with input variables collected retrospectively from an internal validation group (n = 129) of hemodialysis patients. Plasma iPTH was the dichotomous outcome variable, either target group (150 ng/L 300 ng/L). After internal validation, the ANN was prospectively tested in an external validation group (n = 32) of hemodialysis patients. The final ANN was a multilayer perceptron network with six predictors including age, diabetes, hypertension, and blood biochemistries (hemoglobin, albumin, calcium). The externally validated ANN provided excellent discrimination as appraised by area under the receiver operating characteristic curve (0.83 +/- 0.11, p = 0.003). The Hosmer-Lemeshow statistic was 5.02 (p= 0.08 > 0.05) which represented a good-fit calibration. These results suggest that an ANN, which is based on limited clinical data, is able to accurately forecast the target range of plasma iPTH concentration in hemodialysis patients.
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Control mechanisms for potassium (K(+)) excretion in humans developed in Palaeolithic times when diets were sodium poor and episodically K(+) rich. Nevertheless, our understanding of the regulation of K(+) excretion comes from experiments in rats with large sodium and K(+) intakes. Our objective was to identify how K(+) excretion was regulated when rats consumed a low NaCl diet to reflect Palaeolithic conditions. Rats that were given mineralocorticoids plus either NaCl, mannitol, or NaHCO(3) had a small kaliuresis. In contrast, KCl load induced a large kaliuresis and a near-maximal luminal [K(+)] in the terminal cortical collecting duct ([K(+)](CCD)). The time course of events was important. The rise in the [K(+)](CCD) was prompt, but the initial kaliuresis was only modest. Over the next 4 h, kaliuresis increased markedly due solely to a higher calculated distal flow rate, which appeared to be due to diminished reabsorption of NaCl in the loop of Henle; of note, the measured papillary [K(+)] rose. In summary, the increase in the [K(+)](CCD) in rats given KCl is likely to be due to an increase in the number of luminal K(+) channels rather than to mechanisms that are known to induce a lumen-negative voltage in cortical distal nephron segments. The higher distal flow rate might be due to a higher interstitial [K(+)], which inhibited NaCl reabsorption in the loop of Henle. Thus, to understand which of the potential control mechanisms are operating, one must look very closely at the conditions imposed by the experimental setting.
BACKGROUND: Because of the continuing rise in pneumococcal vaccine costs and limits on funding of such costs, vaccination priorities in Taiwan were assessed. METHODS: Data of a randomly selected sample of 200,448 people were analyzed to identify the highest risk groups. Patients were subgrouped on the basis of age and gender, and estimates were made of cumulative admissions, pneumonia recurrence rate, and associated costs of hospital care and medical treatment over the period 1997-2002 for each subgroup. RESULTS: The per capita costs of medical treatment for pneumonia in those aged 65 years or above were found to be highest in those with chronic lung disease (19,906,086 US dollars), heart disease (19,692,769 US dollars), and diabetes mellitus (8,613,973 US dollars). CONCLUSION: Elderly adults over age 65 years with these chronic diseases should be considered high-priority candidates for pneumococcal vaccination.
To evaluate the effects of rosiglitazone (ROS) on serum adiponectin and C-reactive protein (CRP) in nonobese subjects with impaired glucose tolerance (IGT), we enrolled 21 patients with body mass index < or =24 kg/m(2) to receive ROS 4 mg daily for 12 weeks. Fifteen age-, sex-, and body mass index-matched healthy subjects were recruited as controls. A 75-g oral glucose tolerance test (OGTT), hemoglobin A(1c), fasting glucose, insulin, C-peptide, lipid profiles, adiponectin, and CRP levels were determined before initiation and at the end of the 12-week ROS treatment. Insulin resistance and beta-cell function were calculated using the homeostasis model assessment method (HOMA-IR and HOMA-beta, respectively). Compared with healthy controls, the ROS-treated subjects had significantly higher glycemic indices, HOMA-IR, CRP, and glucose and insulin concentrations in response to OGTT, and lower HOMA-beta level. After 12 weeks of ROS therapy, the results showed statistically significant changes from baseline in 2-hour plasma glucose during OGTT (9.4 +/- 0.3 vs 8.3 +/- 0.4 mmol/L, P < .05), HOMA-IR (2.6 +/- 0.2 vs 1.9 +/- 0.3, P < .05), HOMA-beta (63.4 +/- 12.5 vs 90.1 +/- 13.0, P < .05), and glucose and insulin concentrations during OGTT in nonobese subjects with IGT. In addition, elevation of serum adiponectin and decrease in CRP levels were significantly found after ROS treatment. Of 21 patients treated with ROS, 5 subjects were converted to normal (converter), 1 progressed to diabetes, and 15 remained in IGT status (nonconverter). There was a significant amelioration in HOMA-IR (-2.10 +/- 1.03 vs -0.07 +/- 0.33, P < .05) without significant changes in adiponectin and CRP levels in converter compared with nonconverter. We conclude that ROS effectively enhanced insulin sensitivity and beta-cell function to improve adiponectin and CRP levels in nonobese patients with IGT. The amelioration of insulin resistance may be a major determinant to predict the conversion of IGT independent of the changes in adiponectin and CRP.
We report a 59-year-old man with cryptococcal meningoencephalitis who presented with typical features of syndrome of inappropriate antidiuretic hormone secretion (SIADH). There was no evidence of lung disease or drugs causing SIADH. Studies for endocrine functions and tumor markers were normal. The patient's hyponatremia was refractory to treatment (Na 120-125 mmol/L) after resolution of the cryptococcal infection. Three months after completion of antifungal treatment, a radiograph of the chest disclosed widening of the mediastinum. Computed tomography revealed a mediastinal mass. A tentative diagnosis of extrapulmonary cryptococcoma or a tumor was made. Positron emission tomography using F-fluorodeoxy glucose demonstrated an intense uptake mass in the mediastinum without lesions elsewhere in the body. A biopsy of the mass clearly showed small cell carcinoma (SCC) with positive immunoreactivity for arginine vasopressin and atrial natriuretic peptide. The hyponatremia completely resolved and tumor size dramatically decreased after chemotherapy. To the best of our knowledge, this is the first case of mediastinal SCC associated with SIADH. Patients with otherwise unexplained SIADH should be meticulously scrutinized for a possible malignancy.
Pylephlebitis, also called septic thrombophlebitis of the portal vein, is a life-threatening complication of intra-abdominal infection. Although rare, it remains a less recognized entity with a high rate of mortality. We present a 66-year-old man with acute infected choledocholithiasis complicated with Bacteroides fragilis bacteremia. The contrast-enhanced computed tomography scan of the abdomen showed nearly total thrombotic occlusion of the left portal vein. The comprehensive studies for hypercoagulation disorders all yielded negative results. After endoscopic extraction of bile duct stones and broad-spectrum antibiotic therapy, the patient recuperated with complete recanalization of the occluded portal vein. To our knowledge, pylephlebitis associated with acute infected choledocholithiasis has never been reported. This report details the clinical features, radiographic findings, pathogenesis, and treatment of this distinctly unusual manifestation. Early identification of pylephlebitis and underlying intra-abdominal infection can be achieved by exquisite imaging studies with raised awareness in the clinical setting. Eradication of infectious foci and judicious administration of antimicrobials are essential to reduce the catastrophic morbidity and mortality of pylephlebitis.
OBJECTIVES: To identify a clinically reliable index of thyrotoxic periodic paralysis (TPP), a life-threatening emergency with unique and effective therapies. DESIGN: Diagnostic study. SETTING: University teaching hospital. PATIENTS: Fifty-three consecutive patients with hypokalemic paralysis during a 3-yr period and 30 thyrotoxic patients without paralysis as the thyrotoxic control group. INTERVENTIONS: For patients with hypokalemic paralysis, blood and second-void spot urine samples were obtained and measured by routine laboratory prior to therapy. For the thyrotoxic control group, blood and spot urine were collected when they visited outpatient clinics. MEASUREMENTS AND MAIN RESULTS: Twenty-nine patients fulfilled the criteria for TPP. Compared with the thyrotoxic control group, the TPP group had significant decreases in plasma potassium (K) and phosphate concentrations associated with very low urine K and phosphate excretion. Compared with the non-TPP group, the TPP group had significantly lower plasma creatinine and phosphate levels, a significantly higher urine calcium to creatinine ratio (0.25 +/- 0.12 vs. 0.08 +/- 0.07 mg/mg, p < .001), and a significantly lower urine phosphate to creatinine ratio (0.08 +/- 0.05 vs. 0.31 +/- 0.23 mg/mg, p < .001). The urine calcium to phosphate ratio had greater discriminatory power between TPP and non-TPP hypokalemic paralysis (4.1 +/- 2.3 vs. 0.5 +/- 0.6 mg/mg, p < .001). Using a urine calcium to phosphate ratio cutoff value of 1.7 mg/mg, sensitivity and specificity for TPP were 100% and 96%, respectively. CONCLUSIONS: Hypercalciuria and hypophosphaturia are characteristic features of TPP.
PURPOSE OF REVIEW: Regulation of potassium (K) excretion was examined in an experimental setting that reflects the dietary conditions for humans in Paleolithic times (high, episodic intake of K with organic anions; low intake of NaCl), because this is when major control mechanisms were likely to have developed. RECENT FINDINGS: The major control of K secretion in this setting is to regulate the number of luminal K channels in the cortical collecting duct. Following a KCl load, the K concentration in the medullary interstitial compartment rose; the likely source of this medullary K was its absorption by the H/K-ATPase in the inner medullary collecting duct. As a result of the higher medullary K concentration, the absorption of Na and Cl was inhibited in the loop of Henle, and this led to an increased distal delivery of a sufficient quantity of Na to raise K excretion markedly, while avoiding a large natriuresis. In addition, because K in the diet was accompanied by 'future' bicarbonate, a role for bicarbonate in the control of K secretion via 'selecting' whether aldosterone would be a NaCl-conserving or a kaliuretic hormone is discussed. SUMMARY: This way of examining the control of K excretion provides new insights into clinical disorders with an abnormal plasma K concentration secondary to altered K excretion, and also into the pathophysiology of calcium-containing kidney stones.
We report a 66-year-old Chinese man with chronic renal insufficiency (creatinine 1.7 mg/dL) and gout suffering from slurred speech and right hemiplegia for 3 days. Acute cerebral infarction was confirmed by computed tomography. Conscious disturbance occurred on the tenth hospital day without significant changes on imaging study when compared with a previous scan. Hypercalcemia (total calcium 14.1 mg/dL) and acute exacerbation of chronic renal failure (serum creatinine 2.5 mg/dL) were noticed. Hypercalciuria (FECa 3.2%), and low serum levels of intact parathyroid hormone and 1,25(OH)2D3 suggested nonparathyroidal hypercalcemia. An extensive workup failed to identify any etiology of hypercalcemia. Hypercalcemia and renal failure were temporarily ameliorated after aggressive volume expansion and loop diuretic treatment but recurred 2 weeks later. Immobilization hypercalcemia was considered after the exclusion of other discernible causes and was successfully treated with rehabilitative exercises and bisphosphonates without further recurrence during a 2-year follow-up. Clinical alertness to immobilization as a possible cause of hypercalcemia may avoid unnecessary and invasive examinations, life-threatening complications and annoying recurrences.
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BACKGROUND: There is increased oxidative stress in patients undergoing haemodialysis (HD); however, little is known of how different dialysis membranes contribute to the oxidative stress induced by the dialysis procedure per se. We therefore studied the influence of two different dialysis membranes on oxidative stress during HD. METHODS: Eight patients undergoing HD three times per week were enrolled in this cross-controlled study. Patients sequentially received HD using polysulphone (PS) and regenerated cellulose (RC) dialysis membranes for 1 week each. Blood samples were collected in the last section of each hollow fibre 0, 15, 120 and 240 min after starting HD. We determined superoxide anion production derived from neutrophils, superoxide dismutase (SOD) and glutathione peroxidase (GPx) derived from washed red cells, plasma myeloperoxidase (MPO), plasma thiobarbituric acid-reactive substances (TBARS), plasma advanced oxidation protein products (AOPP) and serum 8-hydroxy-2'-deoxyguanosine (8-OHdG). RESULTS: Leukocyte numbers, including neutrophils, lymphocytes and monocytes, decreased significantly after 15 min of dialysis, more so with RC than with PS membrane. For both membranes, superoxide anion production transiently increased during the first 15 min whereas the post-dialysis production was decreased. Plasma MPO levels persistently increased during dialysis with the two membranes. Moreover, the increase was more marked with RC than with PS membrane. AOPP and 8-OHdG levels increased progressively when using RC membranes. There were no significant differences in SOD, GPx, TBARS, AOPP and 8-OHdG levels between the two membranes. CONCLUSIONS: The biocompatibility of the dialyser affects oxidative stress production during a single dialysis session. The measurement of MPO may serve as a reliable marker of the degree of oxidative stress induced using dialysis membranes of different biocompatibilities.
Inactivation mutations of the luminal thiazide-sensitive NaCl cotransporter (NCC) in the distal convoluted tubules or the basolateral chloride channel (CLCNKB) in the distal nephron are the most common genetic mutations in Gitelman's syndrome (GS) or Bartter's syndrome (BS). We conducted clinical and molecular studies in Chinese patients with GS or BS. Twenty patients with chronic hypokalemia (15 males and five females, age 25 +/- 7 yr) from 15 unrelated Chinese families were investigated. All had renal K+ wasting, metabolic alkalosis, and normotension. The urinary calcium excretion rate was used to distinguish between BS or GS on clinical grounds. Clinical symptoms and biochemical studies were recorded. Molecular analysis included PCR single-strand confirmational polymorphism, direct sequencing of both the NCC and CLCNKB genes, and restriction fragment length polymorphism. Sixteen patients had a clinical diagnosis of GS with hypocalciuria and four BS without hypocalciuria. Four of these 20 patients did not have hypomagnesemia. The males had severe hypokalemia [1.9 +/- 0.4 mEq/liter (mmol/liter)] with paralytic episodes, whereas females had moderate hypokalemia [2.6 +/- 0.2 mEq/liter (mmol/liter)] and less severe symptoms. There were no mutations detected in CLCNKB. Twelve NCC mutations, including six novel mutations and nine recurrent ones, were identified. Allele frequency of the detected NCC mutations was 3% in 100 healthy subjects. Some GS patients with NCC mutations may have normocalciuria and/or normomagnesemia. Gender differences may account for phenotype variability. Screening of these identified NCC mutations remains the gold standard for the diagnosis of GS.
Hyponatremia can be classified as acute or chronic depending on its duration, and treatment options are tailored to this classification. However, it is sometimes difficult to differentiate acute from chronic hyponatremia in the Emergency Department (ED). The objective of this study was to identify characteristics to help diagnose and manage acute hyponatremia in the ED. Patients with acute hyponatremia in the ED were enrolled from a retrospective 2-year chart review. Eleven patients (0.8%) were identified with acute hyponatremia out of a total of 1321 hyponatremic patients. There were nine women and two men. The mean age was 48.9 years. The mean sodium (Na(+)) level was 115+/-4 mmol/L. Accompanying biochemical abnormalities included hypouricemia and hypouremia with increased fractional excretions of uric acid (UA) and urea. The estimated amount of water intake ranged from 2.5 to 10 liters (mean, 5.1+/-2.3 liters) during the day before ED presentation. All patients were treated with hypertonic saline and furosemide at a correction rate of 1.6+/-0.5 mmol/L/h. No patients had neurological sequelae after treatment. The causes of acute hyponatremia included induction of abortion with oxytocin (n=1), primary polydipsia on neuroleptic agents (n=2), polyethylene glycol (PEG) preparation for colonoscopy (n=1), diuretic therapy for hypertension (n=4), ecstasy use (n=1), and weight-reducing herbal teas (n=2). We conclude that in the right clinical setting, high free water intake and low serum urea and UA favor acute hyponatremia. A detailed drug history may be helpful in the differential diagnosis of acute hyponatremia.
Thyrotoxic periodic paralysis (TPP), a hyperthyroidism-related hypokalemia and muscle-weakening condition resulting from a sudden shift of potassium into cells, has been seen increasingly in Western countries. Failure to recognize TPP may lead to improper management. Many patients with TPP have no obvious symptoms related to hyperthyroidism. Therefore, several important clues may help in diagnosing and managing TPP: presentation in an adult male with no family history of periodic paralysis; presence of systolic hypertension, tachycardia, high QRS voltage, first-degree atrioventricular block on electrocardiography; presence of low-amplitude electrical compound muscle action potential on electromyography and no notable changes in amplitudes after low doses of epinephrinine; and typical acid-base and electrolyte findings such as normal blood acid-base state, hypokalemia with low urinary potassium excretion, hypophosphatemia associated with hypophosphaturia, and hypercalciuria. Immediate therapy with potassium chloride supplementation may foster a rapid recovery of muscle strength, but with a risk of rebound hyperkalemia. Nonselective beta-blockers may provide an alternative choice. Long-term therapy with definite control of hyperthyroidism completely abolishes attacks. Early diagnosis and prompt treatment of TPP prevent life-threatening complications of this treatable and curable disorder.