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Shih-Hua Lin

Publications and source records attributed to Shih-Hua Lin.

At least 55 records · Page 3Linked to original sources
PubMed2004

Role of circulating cytokines and chemokines in exertional heatstroke.

OBJECTIVE: The interplay between inflammatory and anti-inflammatory cytokines, as well as chemokines, has not been well explored in exertional heatstroke. DESIGN: Prospective, observational study. PATIENTS: Seventeen military recruits who developed exertional heatstroke and 17 exertional controls who did not develop exertional heatstroke during the same training exercises. SETTING: University teaching hospital. MEASUREMENTS AND MAIN RESULTS: The severity of exertional heatstroke was evaluated using a Simplified Acute Physiology Score. Plasma cytokines and chemokines were determined using enzyme-linked immunosorbent assay kits. Body temperatures were 41.2 +/- 1.2 degrees C and 37.6 +/- 0.8 degrees C in exertional heatstroke and exertional controls, respectively. Significantly, plasma cytokines including interleukin (IL)-1beta (3.1 +/- 1.6 vs. 1.2 +/- 0.8 pg/mL; p <.05), tumor necrosis factor alpha (4.9 +/- 4.1 vs. 1.2 +/- 2.4 pg/mL; p <.05), IL-6 (15.8 +/- 3.2 vs. 1.2 +/- 1.2 pg/mL; p <.01), interferon gamma (7.3 +/- 4.9 vs. 2.4 +/- 4.1 pg/mL; p <.01), IL-2 receptor (1568 +/- 643 vs. 610 +/- 214 pg/mL; p <.01), IL-4 (2.5 +/- 1.2 vs. 1.2 +/- 0.8 pg/mL; p <.05), and IL-10 (12.9 +/- 9.4 vs. 2.5 +/- 4.9 pg/mL; p <.01) and serum chemokines IL-8 (84.2 +/- 79.9 vs. 10.4 +/- 3.2 pg/mL; p <.01), monocyte chemoattractant protein 1 (959 +/- 589 vs. 158 +/- 217 pg/mL; p <.01), and RANTES (12464 +/- 10505 vs. 5570 +/- 2894 pg/mL; p <.01) were elevated in exertional heatstroke compared with exertional controls. Among cytokines, IL-6, interferon gamma, and IL-2 receptor were positively correlated with Simplified Acute Physiology Score (r =.573, p <.01; r =.625, p <.01; and r =.56, p <.05, respectively). Among chemokines, only serum monocyte chemoattractant protein 1 was positively correlated with Simplified Acute Physiology Score (r =.78, p <.001). There was no correlation between either cytokines or chemokines and body temperature. CONCLUSIONS: Proinflammatory cytokines IL-1beta, tumor necrosis factor alpha, IL-6; T helper 1 cytokines INF-gamma and IL-2 receptor; and chemokines IL-8, monocyte chemoattractant protein 1, and RANTES are increased in patients with exertional heatstroke. T helper 2 cytokines may play a role as anti-inflammatory cytokines. IL-6, interferon gamma, IL-2 receptor, and monocyte chemoattractant protein 1 may serve as prognostic indicators of disease severity in exertional heatstroke.

Adult↗
PubMed2004

Protective effect of U74500A on phorbol myristate acetate-induced acute lung injury.

1. The present study was designed to determine whether U74500A could ameliorate acute lung injury (ALI) induced by phorbol myristate acetate (PMA) in our rat isolated lung model compared with any amelioration induced by dimethylthiourea (DMTU), superoxide dismutase (SOD) and catalase. 2. Acute lung injury was induced successfully by PMA during 60 min of observation. At 2 microg/kg, PMA elicited a significant increase in microvascular permeability (measured using the capillary filtration coefficient Kfc), lung weight gain, the lung weight/bodyweight ratio, pulmonary arterial pressure and protein concentration of the bronchoalveolar lavage fluid. 3. Pretreatment with 1.5 mg/kg U74500A significantly attenuated ALI; there was no significant increase in any parameters measured, except for pulmonary arterial pressure. The protective effect of U74500A was approximately the same as that of 600 mg/kg DMTU. However, 6000 U/kg SOD, 50,000 U/kg catalase and 6000 U/kg SOD + 50,000 U/kg catalase had no protective effect. 4. These experimental data suggest that U74500A significantly ameliorates ALI induced by PMA in rats.

Animals↗
PubMed2003

Primary Sjögren's syndrome associated with Gitelman's syndrome presenting with muscular paralysis.

A 38-year-old woman presented with muscle cramping of 4 extremities and paralysis for months. Laboratory results showed an elevated antinuclear antibody titer; antibodies to the ribonucleoprotein antigen Ro; hypokalemia; hypomagnesemia with hyperreninemia, but abnormally high urine potassium and magnesium levels and low urine calcium levels; and a blunted diuretic effect to thiazide, but not furosemide, which met the criteria for Gitelman's syndrome (GS) and led to the diagnosis of primary Sjögren's syndrome (pSS). She received medical treatment, including a potassium supplement and aldosterone antagonist. GS as a presentation of pSS has never been reported in the literature. The features of renal diseases related to SS are reviewed. SS is the underlying cause of GS, which may precede the onset of the well-known sicca complex.

Adult↗
PubMed2003

Rosiglitazone improves glucose metabolism in nondiabetic uremic patients on CAPD.

BACKGROUND: Insulin resistance, a strong risk factor for atherosclerotic vascular disease, is present in uremic patients without diabetes on continuous ambulatory peritoneal dialysis (CAPD) therapy. Amelioration of insulin resistance may reduce associated long-term cardiovascular complications. The aim of the study is to investigate the effects of rosiglitazone (ROS), an insulin sensitizer, on glucose metabolism in CAPD patients without diabetes. METHODS: Fifteen uremic patients without diabetes on CAPD therapy were enrolled. All were administered ROS, 4 mg/d, for 12 weeks. A control group consisted of 15 age- and sex-matched healthy subjects. Oral glucose tolerance test (OGTT) results, fasting glucose and insulin levels, related blood biochemistry results, and C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) levels were determined before initiation and at 4 and 12 weeks of therapy. Insulin resistance was evaluated using the homeostasis model assessment method (HOMA-IR). A whole-body insulin sensitivity index (ISI) and insulinogenic index for insulin production were calculated from OGTT results. RESULTS: CAPD patients showed significantly greater HOMA-IR and glucose intolerance compared with healthy controls. After 4 and 12 weeks of ROS therapy, there were no significant changes in body weight, blood pressure, dialysis adequacy, hemoglobin level, hemoglobin A(1c) level, liver function, lipid profile, or intact parathyroid hormone, CRP, IL-6, or TNF-alpha levels. There was a significant decrease in HOMA-IR (3.2 +/- 0.6, 2.2 +/- 0.4, and 2.1 +/- 0.4; P < 0.05). During the OGTT, there was a significant decrease in the area under the glucose curve and a significant increase in ISI (3.5 +/- 0.4, 5.0 +/- 0.7, and 5.3 +/- 0.7; P < 0.05), but no significant change in insulinogenic index. CONCLUSION: ROS improved insulin resistance in CAPD patients without diabetes. Whether long-term use of ROS reduces cardiovascular risk needs further study.

Adult↗
PubMed2003

Diagnosing thyrotoxic periodic paralysis in the ED.

Thyrotoxic periodic paralysis (TPP) and sporadic periodic paralysis (SPP) are the most common causes of hypokalemic periodic paralysis (HPP) in EDs in Asia. Their neuromuscular presentations are almost indistinguishable. We conducted this study to identify clinical clues that can help EPs distinguish between TPP and SPP. Thirty-four patients presenting to the ED with HPP were enrolled during a 3-year period. They did not have known hyperthyroidism before the attack and no family history of paralysis. They all had low K(+) excretion rates. Vital signs and blood biochemistry, including acid-base and electrolytes, were measured. TPP was subsequently established by thyroid function tests. Twenty patients had TPP and 14 patients had SPP. There was no significant difference in age and sex distribution between them. Systolic (SBP) but not diastolic blood pressure (SBP 145 +/- 4 vs 128 +/- 4 mm Hg, P < 0.001) and heart rate (106 +/- 3 vs 73 +/- 3 beats/min, P < 0.001) were significantly higher in those experiencing TPP than SPP. Among the biochemical factors, only plasma phosphate concentration (2.2 +/- 0.2 vs 3.2 +/- 0.2 mg/dL, P < 0.001) was significantly lower in those experiencing TPP than SPP. Systolic hypertension, tachycardia, and hypophosphatemia are clinical clues favoring the diagnosis of TPP.

Adult↗
PubMed2003

A simple and rapid approach to hypokalemic paralysis.

Hypokalemia with paralysis (HP) is a potentially reversible medical emergency. It is primarily the result of either hypokalemic periodic paralysis (HPP) caused by an enhanced shift of potassium (K(+)) into cells or non-HPP resulting from excessive K(+) loss. Failure to make a distinction between HPP and non-HPP could lead to improper management. The use of spot urine for K(+) excretion rate and evaluation of blood acid-base status could be clinically beneficial in the diagnosis and management. A very low rate of K(+) excretion coupled with the absence of a metabolic acid-base disorder suggests HPP, whereas a high rate of K(+) excretion accompanied by either metabolic alkalosis or metabolic acidosis favors non-HPP. The therapy of HPP requires only small doses of potassium chloride (KCl) to avoid rebound hyperkalemia. In contrast, higher doses of KCl should be administered to replete the large K(+) deficiency in non-HPP.

Acid-Base Equilibrium↗
PubMed2003

An unrecognized cause of paralysis in ED: thyrotoxic normokalemic periodic paralysis.

Hypokalemic paralysis associated with hyperthyroidism (TPP) is a well-known acute electrolyte and muscle function disorder. Lesser known is normokalemic periodic paralysis associated with hyperthyroidism. We describe two cases of young men with acute muscular paralysis and bilateral impairment of sensation over the lower legs who had normal plasma potassium concentrations. They were initially misdiagnosed as having Guillain-Barré syndrome or hysterical paralysis. However, thyroid function tests showed elevated serum T(3) and T(4) and markedly depressed thyroid-stimulating hormone findings consistent with hyperthyroidism. Control of the hyperthyroidism completely abolished their periodic paralysis. Thyrotoxic normokalemic periodic paralysis (TNPP) should be kept in mind as a cause of acute muscle weakness to avoid missing a treatable and curable condition.

Adult↗
PubMed2003

Acute effect of pamidronate on PTH secretion in postmenopausal hemodialysis patients with secondary hyperparathyroidism.

BACKGROUND: The purpose of this study is to evaluate the acute effect of pamidronate on plasma ionized calcium (iCa) level reduction and dynamic parathyroid hormone (PTH) secretion in postmenopausal hemodialysis-dependent women with secondary hyperparathyroidism. METHODS: Twelve postmenopausal women undergoing regular hemodialysis with serum intact PTH levels greater than 200 pg/mL (200 ng/L) were included in this study. Pamidronate was administered intravenously as a single dose of 15 mg in the last hour of hemodialysis. PTH responses to hypocalcemia and hypercalcemia induced with 1 mEq/L (0.5 mmol/L) and 4 mEq/L (2 mmol/L) of dialysate calcium, respectively, were evaluated before and 1 week after pamidronate therapy. RESULTS: Pamidronate therapy resulted in a decrease in predialysis basal plasma iCa (iCa(base); P < 0.05) levels and an increase in maximal serum PTH (PTHmax; P < 0.001), basal PTH (PTHbase; P < 0.001), and minimal PTH levels (P < 0.001). The set point of serum calcium and the slope of the PTH-calcium curve were not altered by pamidronate therapy. An inverse correlation was present between iCa(base) and the PTHbase-PTHmax ratio before (r = -0.66; P < 0.05) and after (r = -0.84; P < 0.001) pamidronate therapy. CONCLUSION: Our study shows that pamidronate therapy is associated with reduced plasma iCa levels and increased PTH secretion, resulting in aggravated secondary hyperparathyroidism. These findings suggest that secondary hyperparathyroidism may worsen after the administration of pamidronate, at least in the short term, in postmenopausal hemodialysis patients.

Aged↗
PubMed2003

Thyrotropin-secreting pituitary adenoma presenting as hypokalemic periodic paralysis.

Thyrotropin (TSH)-secreting pituitary adenoma presenting with hypokalemic periodic paralysis is extraordinarily rare and may be misdiagnosed. We describe a 44-year-old man who suffered from acute muscle weakness and inability to ambulate upon awakening in the morning. Physical examination showed hypertension, tachycardia, and symmetrical flaccid paralysis of all extremities. The major biochemical abnormality was hypokalemia (K+, 2.0 mmol/L) with low urine K+ excretion. A thyroid function study revealed elevated thyroid hormone levels and inappropriately high TSH concentrations (2.10 microU/mL). Brain magnetic resonance imaging delineated a pituitary tumor with suprasellar extension. After trans-sphenoidal removal of tumor, he became clinically and biochemically euthyroid without any further attack of paralysis. Pathological findings confirmed a TSH-secreting adenoma with exclusive TSH immunostaining. TSH-secreting pituitary adenoma must be kept in the differential diagnosis in any thyrotoxic periodic paralysis patients with detectable TSH levels to avoid delaying diagnosis and management.

Adenoma↗
PubMed2003

An unusual cause of hypokalemic paralysis: chronic licorice ingestion.

Long-term licorice ingestion is a well-known cause of secondary hypertension and hypokalemia. Nevertheless, its initial presentation with a very severe degree of hypokalemia and paralysis is exceedingly rare. We report an elderly Asian man who presented to the emergency department with marked muscle weakness that progressed to paralysis. His blood pressure was 160/96 mm Hg. The major biochemical abnormalities were hypokalemia (plasma K+ concentration, 1.8 mmol/L) and metabolic alkalosis (HCO - 3 , 36 mmol/L). His renal potassium excretion was higher (transtubular potassium gradient of 9). Plasma renin activity and aldosterone concentration were suppressed and cortisol concentration was normal. A detailed history revealed that he had ingested tea flavored with 100 g of natural licorice root containing 2.3% glycyrrhizic acid daily for 3 years. Note that renal potassium wasting and hypertension persisted for 2 weeks after discontinuing licorice consumption along with KCl supplement and spironolactone. Long-term licorice ingestion should be kept in mind as a cause of paralysis with an extreme degree of hypokalemia to avoid missing this recognizable and curable medical disorder.

Acid-Base Imbalance↗
PubMed2003

Midodrine improves chronic hypotension in hemodialysis patients.

BACKGROUND: The effects of midodrine on chronic hypotension in hemodialysis (HD) patients have not been well investigated. METHODS: We evaluated midodrine's effect on autonomic function and hemodynamics in 12 HD patients who had chronic systolic blood pressure less than 100 mm Hg. Midodrine (5.0 mg) twice a day was given for 4 weeks. Another 12 age- and sex-matched HD patients with normotension were selected as a control group. Autonomic function tests included the heart-rate responses to the Valsalva maneuver and 30:15 ratio as well as supine and standing blood pressure (BP) and sustained hand-grip test. Hemodynamic changes included 24-hour blood pressure, cardiac output, total peripheral resistance (TPR), and plasma renin and aldosterone concentrations. RESULTS: Compared with the control subjects, HD patients with chronic hypotension had more severe autonomic dysfunction and significantly lower TPR. After 4 weeks of midodrine therapy, sympathetic function (orthostatic and hand-grip tests) improved in conjunction with significant increases in mean arterial pressure (MAP) (79.5 +/- 4.9 to 85.0 +/- 5.1 mm Hg, P < 0.05) and TPR (768 +/- 37 versus 1097 +/- 72 dyne/sec/cm-5, P < 0.01) despite no significant change in Valsalva ratio, 30:15 ratio, and cardiac output. MAP changes were positively correlated with TPR changes (r = 0.82, P < 0.001). Supine plasma renin activity was significantly increased. In addition, MAP during HD was also significantly increased during midodrine therapy. CONCLUSIONS: Midodrine improves chronic hypotension in HD patients by modulating autonomic function and its direct effects on peripheral vessels.

Adrenergic alpha-Agonists↗
PubMed2003

Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) commonly precedes the overt symptoms and signs of hyperthyroidism and may be misdiagnosed as other causes of paralysis (non-TPP). Because the cardiovascular system is very sensitive to elevation of thyroid hormone, we hypothesize that electrocardiographic manifestations may aid in early diagnosis of TPP. METHODS: We retrospectively identified 54 patients who presented to the emergency department (ED) with hypokalemic paralysis during a 3.5-year period. Thirty-one patients had TPP and 23 patients had non-TPP, including sporadic periodic paralysis, distal renal tubular acidosis, diuretic use, licorice intoxication, primary hyperaldosteronism, and Bartter-like syndrome. Electrocardiograms during attacks were analyzed for rate, rhythm, conduction, PR interval, QRS voltage, ST segment, QT interval, U waves, and T waves. RESULTS: There were no significant differences in age, sex distribution, and plasma K+ concentration between the TPP and non-TPP groups. Plasma phosphate was significantly lower in TPP than non-TPP. Heart rate, PR interval, and QRS voltage were significantly higher in TPP than non-TPP. Forty-five percent of TPP patients had first-degree atrioventricular block compared with 13% in the non-TPP group. There were no significant differences in QT shortening, ST depression, U wave appearance, or T wave flattening between the 2 groups. CONCLUSION: Relatively rapid heart rate, high QRS voltage, and first-degree AV block are important clues suggesting TPP in patients who present with hypokalemia and paralysis.

Acidosis, Renal Tubular↗
PubMed2002

Aristolochic acid-induced Fanconi's syndrome and nephropathy presenting as hypokalemic paralysis.

Hypokalemic paralysis rarely is seen as the presenting feature in patients with Fanconi's syndrome. We describe a 60-year-old man who presented with the inability to ambulate on awakening in the morning. The pertinent history revealed he had consumed Chinese herbs for leg edema for 5 months. Physical examination was unremarkable except for extracellular fluid volume depletion and total paralysis of both lower extremities. Laboratory investigation showed hypokalemia (1.8 mEq/L), hyperchloremic metabolic acidosis (Cl-, 111 mEq/L, and HCO3-, 14.0 mEq/L), hypophosphatemia (0.9 mg/dL) with hyperphosphaturia, hypouricemia (1.3 mg/dL) with hyperuricosuria, and glycosuria, consistent with Fanconi's syndrome. Mild renal insufficiency (serum creatinine, 1.7 mg/dL) also was noticed. Blood and urine screens for heavy metals, autoantibodies, and monoclonal gammopathy were negative. A renal biopsy specimen revealed typical findings of aristolochic acid-associated nephropathy. Aristolochic acids were detected in the consumed Chinese herbs. This case highlights that consumption of Chinese herbs containing aristolochic acids may cause Fanconi's syndrome and should be considered as a cause of hypokalemic paralysis.

Acute Kidney Injury↗
PubMed2002

Must metabolic acidosis be associated with malnutrition in haemodialysed patients?

BACKGROUND: Metabolic acidosis was evaluated in the past as an independent variable of catabolism in haemodialysis (HD) patients. Nevertheless, it could in theory reflect a higher acid production from protein oxidation. The aim of this study was to evaluate the incidence and basis of metabolic acidosis in conjunction with a nutritional assessment in a HD population (n=120). METHODS: Three groups were identified based on three consecutive monthly predialysis plasma bicarbonate concentrations (P(HCO3)) and pH values. The effect of correction of metabolic acidosis on nutritional parameters was also studied in acidotic patients. RESULTS: The mean P(HCO3) ranged from 19.2+/- 0.4 mmol/l in group A (n=21) to 24.4+/-0.3 mmol/l in group B (n=80) and 27.5+/-0.4 mmol/l in group C (n=19). The adequency of dialysis (Kt/V) and ultrafiltration rates was comparable in the three groups. When compared with group B, group A had significantly higher body mass index (BMI), triceps skin fold thickness (TSF), dietary protein intake (DPI), normalized protein catabolic rate (nPCR) as well as serum creatinine, K(+) and intact parathyroid hormone (I-PTH). In contrast, when compared with group B, group C had a significantly lower DPI, nPCR, plasma creatinine and albumin. There was no significant difference in plasma inflammatory markers such as C-reactive protein (CRP) and interleukin 6 (IL-6) among all three groups. There was a significant negative correlation between P(HCO3) and nPCR (P<0.001), DPI (P<0.001), creatinine (P<0.001). Over a period of 6 months, the correction of metabolic acidosis in the HD patients did not affect nutritional parameters. CONCLUSION: These findings suggest that metabolic acidosis as a result of a higher protein intake does not detrimentally affect nutritional status.

Acidosis↗