Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroendocrine tumors, particularly those of gastrointestinal tract origin, have a predisposition for metastasizing to the liver, causing parenchymal substitution and paraneoplastic syndrome. Lipiodol embolization combined with anticancer drugs is a recent tool in regional therapy. It has been proven that chemoembolization reduces tumor bulk and hormone levels, and that it palliates the symptoms of many patients with liver-dominant neuroendocrine metastases. Beginning in December 1988, ten patients with unresectable and chemotherapy-refractory liver metastatic neuroendocrine tumors were treated with chemoembolization based on a mixture of lipiodol, mitomycin, cisplatin, epirubicin, followed by gelfoam powder and contrast media. Toxicity encountered included: upper right quadrant pain requiring narcotics, elevation of lactate dehydrogenase, alkaline phosphatase, and transaminases. One patient had liver abscess and persistent fever for 2 weeks. We obtained two complete remissions lasting 12 and 34 months and 5 partial remissions. The median survival was 22 months. Four patients had urinary elevation of 5-hydroxyindolacetic acid (5-HIAA). They showed more than a 75% decrease in urinary secretion after treatment. In a patient with transplanted liver we noticed a partial response lasting 7 months. We conclude that chemoembolization will improve the clinical condition of a significant percentage of patients with liver metastases, that future therapy of carcinoid tumors will be based on specific tumor biology and that treatment will be customized for each individual patient combining the use of cytoreductive procedures including radiofrequency ablation, laser treatment and chemoembolization.
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PMID:Intra-arterial hepatic chemoembolization in liver metastases from neuroendocrine tumors: a phase II study. 1533 Mar 28

In this study, histopathological and biochemical changes due to chronic usage of morphine or tramadol in liver and kidney were assessed in rats. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4, 8, 10 mg/kg/day in the first, second and the third ten days of the study, respectively. Tramadol group (n = 10), received the drug intraperitoneally at doses of 20, 40 and 80 mg/kg/day in the first, second and the third ten days of the study, respectively. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinin, blood urea nitrogen (BUN) and malondialdehyde (MDA) levels were measured in the serum. Liver and kidney specimens were evaluated by light microscopy. Serum ALT, AST, LDH, BUN and creatinin levels were significantly higher in morphine group compared to the control group. Serum LDH, BUN and creatinin levels were significantly increased in the morphine group compared to the tramadol group. The mean MDA level was significantly higher in morphine group compared to the tramadol and control groups (P < 0.05). Light microscopy revealed severe centrolobular congestion and focal necrosis in the liver of morphine and tramadol groups, but perivenular necrosis was present only in the morphine group. The main histopathologic finding was vacuolization in tubular cells in morphine and tramadol groups. Our findings pointed out the risk of increased lipid peroxidation, hepatic and renal damage due to long term use of opioids, especially morphine. Although opioids are reported to be effective in pain management, their toxic effects should be kept in mind during chronic usage.
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PMID:Liver and kidney toxicity in chronic use of opioids: an experimental long term treatment model. 1588 61

A 74-year-old woman was admitted to our hospital because of vomiting and abdominal pain. She had been well until 24 hours before admission, when she had had her last meal. She had not eaten anything unusual. She developed pain in the left lower abdominal quadrant, and difficulties with her bowel movements. An enema was given unsuccessfully. There was progressive distension of the abdomen. The patient started to vomit gastric and later bilious contents. No history of abdominal symptoms or weight loss was reported. She currently takes oral antidiabetic agents and an angiotensin II blocker because of hypertension. On physical examination she was not in distress and was afebrile, blood pressure 130/100 mmHg, pulse rate 88 beats/min. On auscultation increased bowel sounds with rushes of high-pitched sounds were heard. Her abdomen was distended and a large tender mass filling the whole left lower quadrant without signs of peritoneal irritation was found. There were no faeces on rectal examination. The leucocyte count was 10.2 mmol/L, haemoglobin 7.2 mmol/L, C-reactive protein 36 mg/l and lactate dehydrogenase 535 U/l. Under suspicion of a mechanical bowel obstruction without signs of peritonitis, the patient was treated with a nasogastric tube, fasting and enemas on which she improved. An abdominal X-ray in bed taken on day two showed no bowel distension (figure 1). After removing the nasogastric tube on day two the nausea returned. Abdominal examination was unchanged. An abdominal computed tomography (CT) scan after drinking oral contrast and intravenous contrast was performed (figure 2).
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PMID:A patient with abdominal distension. 1595 87

We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.
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PMID:An adult with acute poststreptococcal glomerulonephritis complicated by hemolytic uremic syndrome and nephrotic syndrome. 1618 9

The mechanisms behind the development of work-related trapezius pain are suggested to involve both peripheral and central components, but the specific contribution of alterations in muscle nociceptive and other substances is not clear. Female patients with chronic trapezius myalgia (N=19; TM) and female controls (N=20; CON) were studied at rest, during 20 min repetitive low-force exercise and recovery, and had their interstitial concentrations of potassium (K(+)), lactate dehydrogenase (LDH), interleukin-6 (IL-6) and collagen turnover determined in the trapezius muscle by the microdialysis technique. K(+) levels were at all time points higher in TM than in CON (P<0.0001). Baseline levels of LDH and IL-6 were similar in both groups. In response to exercise pain intensity, rated perceived exertion, and the concentrations of K(+), LDH and IL-6 increased significantly in both groups. [K(+)] immediately decreased to baseline levels in CON but remained elevated during the first 20 min of recovery in TM (P<0.01) whereafter it returned to baseline level. In all subjects taken together mean [K(+)] correlated negatively with pressure pain threshold of trapezius (P<0.001), positively with mean pain intensity VAS (P<0.001) and mean perceived exertion (P<0.001). Rises in muscle LDH and IL-6 as well as the anabolic ratio for collagen type I was not significantly different between groups. In conclusion, patients with chronic pain in the trapezius muscle had increased levels of interstitial potassium. This finding could be causally related to myalgia or secondary to pain due to deconditioned muscle or altered muscle activity pattern.
Pain 2005 Dec 15
PMID:Increased levels of interstitial potassium but normal levels of muscle IL-6 and LDH in patients with trapezius myalgia. 1629 53

Local anesthetics (LAs) suppress sympathetic sprouting, which correlates with neuropathic pain. However, the precise mechanism of the suppression is unknown. Nerve growth factor (NGF) contributes to the sympathetic sprouting, and NGF signaling starts with NGF-stimulated autophosphorylation of TrkA, which is a high affinity receptor of NGF. We examined the effects of lidocaine, bupivacaine, and procaine on NGF signaling under suppression of NGF-stimulated neurite outgrowth in PC12 cells, which is a cellular model of sympathetic sprouting. To investigate the effect of these LAs on NGF-mediated neurite outgrowth of PC12 cells, cells were incubated with 40, 400, and 4000 microM of each LA. The effect of LAs on NGF-stimulated TrkA activity was examined to analyze autophosphorylation of TrkA using immunoprecipitation and immunoblotting. Cytotoxic effects of LAs on PC12 cells were also assessed by lactate dehydrogenase release and by propidium iodide staining. Lidocaine (400 microM), bupivacaine (40 and 400 microM), or procaine (4000 microM) suppressed either neurite outgrowth or autophosphorylation significantly without cytotoxicity. The inhibition of NGF-stimulated tyrosine kinase activity of TrkA might be involved in the mechanisms of suppression of neurite outgrowth induced by LAs.
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PMID:Local anesthetics suppress nerve growth factor-mediated neurite outgrowth by inhibition of tyrosine kinase activity of TrkA. 1642 43

Liver involvement in tuberculosis in absence of miliary tuberculosis is rare. This study was performed to analyse the spectrum and response to treatment of hepatic tuberculosis in the absence of miliary abdominal tuberculosis. Retrospective analysis of seven cases of hepatic tuberculosis without miliary abdominal tuberculosis who presented at the single tertiary referral center were analyzed. All patients presented with fever and hepatomegaly. Five of them had pain in upper abdomen and vomiting. HIV serology was positive in one patient. All patients had normocytic normochromic anaemia, raised erythrocyte sedimentation rate (Mean 65). Mild elevation of liver enzymes and low albumin (Mean 2.4 gm%) with reversal of albumin globulin ratio (Mean 0.6) were seen in all. Two had jaundice. Prothrombin time was normal in all and lactate dehydrogenase values were elevated in all (Mean 794 IU/L). On ultrasonography, 2 had multiple hypodense lesion, 1 had coarse echotexture of liver, 1 had hyperechoic pattern and 3 had just hepatomegaly. Complete resolution of liver lesions on treatment with 4-drug anti-tuberculosis drug chemotherapy was seen. In conclusion, liver tuberculosis has protean manifestations with nonspecific alteration of liver function tests and is best diagnosed on liver biopsy. Overall response to therapy is satisfactory.
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PMID:Hepatic tuberculosis in absence of disseminated abdominal tuberculosis. 1653 64

The aim of this prospective cohort study was to determine whether serum uric acid level is useful as a predictor of survival in terminally ill cancer patients. One hundred eighteen terminally ill cancer patients, including 63 (53.4%) males, were categorized into four groups by serum uric acid levels and followed up until death or to the end of the study. Cox's proportional hazard model was adopted to evaluate the joint effect of some clinicobiological variables on survival. From an initial model containing 51 variables, a final parsimonious model was obtained by means of a stepwise method. Repetitive dispersion analysis was performed for serum uric acid level in 39 subjects for 3 weeks until death. During the study period, 113 (95.76%) subjects expired, and the median survival time was 14 days. In univariate analysis, survival time of the fourth highest group (> or =7.2mg/dL) was significantly shorter than that of the others (hazard ratio (HR)=2.784, P<0.001). After adjustment for low performance status, moderate to severe pain, prolonged prothrombin time, hypocholesterolemia, and high lactate dehydrogenase (LDH) level, high serum uric acid level (> or =7.2mg/dL) was significantly and independently associated with short survival time (HR=2.637, P=0.001). Serum uric acid levels were also significantly increased between the first and the second week before death. These findings suggest that serum uric acid level can be useful in predicting life expectancy in terminally ill cancer patients.
J Pain Symptom Manage 2006 Jun
PMID:Uric acid as a prognostic factor for survival time: a prospective cohort study of terminally ill cancer patients. 1679 89

Pulmonary hypertension is associated with sudden death and is a risk factor for mortality in adult patients with sickle cell disease. The high mortality despite only mild-to-moderate increases in pulmonary vascular resistance remains an unresolved paradox. Accordingly, little is known about the cardiovascular effects of stressors, such as vaso-occlusive pain crisis (VOC) and exercise, which may acutely increase pulmonary pressures and impair right heart function. We therefore evaluated pulmonary artery pressures by echocardiogram in 25 patients with sickle cell disease in steady-state and during VOC, and by right heart catheterisation with exercise in a second cohort of 21 patients to determine whether pulmonary hypertension worsens during acute cardiopulmonary stress. TRV increased during VOC (P < 0.001), and the increased pulmonary pressures during VOC were associated with decreases in haemoglobin levels (P < 0.001), and increases in lactate dehydrogenase (P < 0.001) and plasma haemoglobin levels (P = 0.03). During exercise stress performed during cardiac catheterisation, mean pulmonary artery pressures (P < 0.001) and pulmonary vascular resistance increased (P < 0.001) in all subjects. These data suggest that acute elevations in pulmonary pressures during VOC or exercise may contribute to morbidity and mortality in patients with sickle cell disease.
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PMID:Severity of pulmonary hypertension during vaso-occlusive pain crisis and exercise in patients with sickle cell disease. 1715 1

This study evaluated lactate dehydrogenase (LDH) as a prognostic factor for survival time in terminal cancer patients. We prospectively followed 93 consecutive inpatients with terminal cancer in one general hospital. Cox's proportional hazard model was used to adjust the influence of some clinical and laboratory variables on survival time. For 25 patients, LDH levels at 2 weeks and 1 week before death were compared by paired t test. In multivariate analysis, elevated LDH level (313 IU/L) was confirmed as an unfavourable indicator for survival time (hazard ratio=2.087, p=0.002). Serum LDH levels were significantly increased as the patients approached death. A combined index comprising LDH levels, C reactive protein levels, uric acid levels, presence of moderate to severe pain, fatigue, hypotension and performance status demonstrated a good stratification value for predicting survival time. Our results showed that serum LDH level can be a useful predictor of survival time of terminally ill cancer patients.
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PMID:Lactate dehydrogenase as a prognostic factor for survival time of terminally ill cancer patients: a preliminary study. 1734 86


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