Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our objective was to monitor serum and urine biochemical changes after oral sodium phosphate cleansing in a prospectively designed study. The study subjects were seven healthy, asymptomatic adults. Sodium phosphate 45 ml diluted in 45 ml water was given orally at baseline and 12 hr later. Calcium, ionized calcium, phosphorus, sodium, potassium, creatinine, and PTH were analyzed at 2, 4, 6, 9, 12, 14, 16, 18, 21 and 24 hr after the first challenge. Urinary calcium, phosphorus, sodium, potassium, and cyclic AMP were analyzed at baseline and every 2 hr after oral sodium phosphate. Blood pressure, pulse, and respiratory rate were recorded every 2 hr and symptom questionnaires using visual analog scales were completed. A marked rise in phosphorus (peak range 3.6-12.4 mg/dl, P < 0.001) and falls in calcium (P < 0.001) and ionized calcium (P < 0.001) were seen. Rises seen in PTH and urinary cAMP confirmed the physiologic significance of the biochemical effect. There were no significant changes in other serum and urine laboratory or clinical assessments. Reported significant symptoms included bloating, cramps, abdominal pain, and nausea. Significant hypocalcemia and hyperphosphatemia after oral sodium phosphate raises concern about its use in normal individuals. Oral sodium phosphate should not be administered in patients with cardiopulmonary, renal, or hepatic disease.
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PMID:Biochemical effects of oral sodium phosphate. 867 96

Amebic colitis is associated with serious complications and a high fatality rate if it progresses to its fulminant form. The purpose of this retrospective study was to determine the risk factors associated with fulminant amebic colitis. From February 1978 to February 1993, 60 adults were diagnosed with intestinal amebiasis at Chang Gung Memorial Hospital. Sixteen patients with massive bloody diarrhea, persistent systemic toxicity or signs of peritonitis were classified as having fulminant colitis, five of whom progressed to fulminant colitis after admission to the hospital. Forty-four patients with good responses to amebicides and without complications were classified as having moderate colitis. There was no amebiasis-related mortality among patients with moderate colitis. In contrast, five patients with fulminant colitis died. Early diagnosis and surgical treatment significantly decreased mortality when compared with conservative treatment. Significant factors associated with the development of fulminant intestinal amebiasis in univariate analyses were being male, age over 60 years, having an associated liver abscess, progressive abdominal pain, signs of peritonitis, leukocytosis, hyponatremia, hypokalemia and hypoalbuminemia. Only the factors of being over 60 years of age and hypokalemia were important in multivariate analyses. We conclude that early and extensive surgical treatment is mandatory for patients with typical presentations of fulminant amebic colitis on admission to the hospital, such as progression to peritonitis, persistent systemic toxemia and explosive bloody diarrhea. For other patients, especially the elderly and those with low serum potassium levels, close monitoring and observation for signs of fulminant colitis is important.
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PMID:Risk factors associated with fulminant amebic colitis. 877 50

For proper use of systemic GCS, a basic knowledge of the normal HPA axis, as well as knowledge of the pharmacology, clinical usage guidelines, and adverse reactions of these agents is imperative. Both short-term (acute) and long-term side effects should be well known by the physician. The pros and cons of oral and parenteral therapy for various disorders and in various situations should be recognized. For long-term therapy, an intermediate-acting agent such as prednisone in single, early morning doses is most commonly used to minimize suppression of the HPA axis. Alternate-morning doses produce even less suppression if the disease process will respond. A through patient history, including general medical history and medications the patient is taking, is important to anticipate any potential problems. Weight and blood pressure should be checked initially and every 1 to 3 months thereafter. Blood glucose, electrolytes, and lipid studies, including triglycerides, should be done approximately every 6 months. An ophthalmology examination should be performed every year, and stool examination for occult blood and chest radiography can be obtained as indicated. Bone density studies might be necessary in patients who are at high risk for osteoporosis. Specific acute situations may dictate other studies. The patient on long-term GCS should be kept as active as possible, as mild-to-moderate exercise helps prevent certain side effects, such as osteoporosis. The dose of oral GCS is best given with food to prevent gastrointestinal irritation, and agents to decrease gastric acidity might be needed in certain situations. Exposure to infections should be prevented, where possible, and treatment initiated at the first sign of systemic or cutaneous infection. Pain should be evaluated early, especially abdominal pain or bone pain; MRI is indicated if aseptic necrosis of bone is suspected. Both trauma and severe sun exposure should be avoided. Consultation with other specialists is strongly recommended when the situation dictates. Diet is one of the most important strategies to minimize side effects from long-term GCS therapy. Vegetable protein should be increased in the diet, and fats and carbohydrates limited. Adequate calcium is imperative, and calcium supplementation is recommended for high-risk osteoporosis patients. Small amounts of vitamin D may be necessary to increase absorption of calcium. Restriction of sodium is also important, as is maintainance of dietary potassium. Supplemental potassium may be necessary in some patients, and a thiazide diuretic might be useful in patients with hypertension, edema, or osteoporosis. Vitamin C can be given to promote wound healing. A good doctor-patient relationship is important in managing the patient on long-term GCS. The patient must return for regular visits and be encouraged to promptly report any adverse reactions to the physician. If these criteria are maintained and the strategies noted previously are followed, problems from long-term therapy with GCS will be minimized.
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PMID:Minimizing complications from systemic glucocorticosteroid use. 878 96

A 35-year-old, previously healthy woman, known to be thyrotoxic, was transferred from a community hospital for "acute abdomen." Abdominal pain, distention, and hyperemesis resolved with placement of nasogastric tube (NGT) and return of 2,600 mL of bilious fluid. Continued high NGT output made oral or NGT administration of antithyroid drugs impossible. We gave propylthiouracil (PTU) by retention enemas with therapeutic serum levels and sublingual saturated solution of potassium iodide (SSKI) with 70% absorption based on 24-hour free iodine urinary excretion. The patient's thyroxine (T4) and triiodothyronine (T3) radioimmunoassays were normal on hospital days 10 and 12, respectively. However, free T4 and T3 resin uptake did not normalize until hospital day 31. On hospital day 32, she tolerated removal of NGT without nausea and 4 days later was taking a regular diet. We conclude that our patient's gastrointestinal symptoms were a prominent feature of her thyrotoxicosis and that rectal PTU and sublingual SSKI are effective in administration of antithyroid drugs.
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PMID:Duodenal obstruction in thyroid storm. 938 60

Gitelman's syndrome was diagnosed in five siblings. The parents were relatives in the third remove. Gitelman's syndrome is a rare autosomal recessive hereditary magnesium reabsorption defect in the distal tubule. It is characterized by episodes of muscle weakness, usually accompanied by abdominal pain and vomiting. Tetany may occur during a febrile illness. Patients are of normal height and weight and have normal blood pressures. Sometimes eczematous skin lesions are found. Biochemically there is hypokalaemia, hypomagnesaemia and alkalosis. Urinary excretion rates of potassium and magnesium are elevated, the excretion of calcium is diminished. Treatment consists of oral suppletion of magnesium, sometimes also with oral potassium. A potassium-sparing diuretic may be used. The prognosis appears to be good.
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PMID:[5 children with hypokalemia, hypomagnesemia and hypocalciuria (Gitelman syndrome) in one family]. 954 87

Sixty-one children with a median age of 6 years (range 1-16) were given prophylaxis/therapy for 78 courses of treatment with liposomal amphotericin (AmBisome) and were reviewed retrospectively. Thirty-six received allogeneic bone marrow, 22 a liver transplant, 2 kidneys and 1 a liver and kidney. AmBisome was given as prophylaxis in 30 episodes, as treatment for suspected invasive fungal infections (IFI) in 33 and for a verified IFI in 15. AmBisome prophylaxis was given for a median of 14 days in a dose of 1 mg/kg/day. The median dose of AmBisome was 2.1 mg/kg/day (range 0.9-5.0). The median duration of therapy was 10 days in children with suspected IFI and 20 days in children with verified IFI. The total dose ranged from 0.025 g up to a maximum of 3.95 g. Proven and probable side effects of AmBisome were a decrease in the level of serum potassium (30/78 cases), renal toxicity (22), an increase in the alkaline phosphatases (24), back pain (2), fever and abdominal pain (2), anaphylactic reaction (1), an increase in the bilirubin level (1), nausea (1), chest pain (1) and fever (1). Of 31 children with suspected IFI, fever disappeared in 21 (68%). In 14 verified or suspected IFI cases treated for 5 days or more, the clinical cure rate was 12 (86%). Eradication of fungi from a deep site was verified in 8/10 and the survival rate from 1 1/2 years to more than 7 years was 7/12 (58%). We conclude that AmBisome was well tolerated as prophylaxis and therapy in transplanted children, few acute toxic side effects were seen and the cure rate in verified IFI was high.
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PMID:Prophylaxis and therapy using liposomal amphotericin B (AmBisome) for invasive fungal infections in children undergoing organ or allogeneic bone-marrow transplantation. 1008 72

Over the past decade, attention has been paid to the role of visceral sensitivity in the pathophysiology of functional bowel disorders, especially irritable bowel syndrome, and visceral hypersensitivity is the most widely accepted mechanism responsible for both motor alterations and abdominal pain. Inflammatory mediators sensitize primary afferents, especially C-fibre polymodal nociceptors, favouring the recruitment of silent nociceptors that give rise to secondary spinal sensitization. After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors. Among the intermediary structures activated by inflammatory mediators and susceptible to the release of proalgesic substances, mast cells and platelets play a crucial role; however, immunocytes such as macrophages and neutrophils or sympathetic nerve terminals are also candidates. Moreover, events likely to activate synthesis of mediators by mast cells, such as stress and septic shock, also trigger colonic hypersensitivity. Prolonged visceral hyperalgesia may also depend on spinal sensitization. A number of substances are candidates to play a role at the spinal cord level in mediating painful and nonpainful sensations. Among them, substance P, dynorphins and glutamate play a pivotal role in postsynaptic sensitization, particularly during and after gut inflammation. Finally, despite the complexity of the relationship between inflammatory mediators and gut hypersensitivity, numerous results strongly suggest that alteration neuroimmune communications at the gut level may trigger a series of events that give rise to chronic changes in visceral sensitivity.
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PMID:Effects of inflammatory mediators on gut sensitivity. 1020 8

Trimebutine [2-dimethylamino-2-phenylbutyl-3,4,5-trimethoxybenzoate hydrogen maleate (TMB)] has been demonstrated to be active for relieving abdominal pain in humans. To better understand its mechanism of action, we have tested TMB; nor-TMB, its main metabolite in humans; and their respective stereoisomers for their affinity toward sodium channels labeled by [3H]batrachotoxin, their effect on sodium, potassium, and calcium currents in rat dorsal root ganglia neurons, and their effect on veratridine-induced glutamate release from rat spinal cord slices. TMB has also been tested in an animal model of local anesthesia. TMB (Ki = 2.66 +/- 0.15 microM) and nor-TMB (Ki = 0.73 +/- 0.02 microM) displaced [3H]batrachotoxin from its binding site with affinities similar to that of bupivacaine (Ki = 7.1 +/- 0.9 microM). nor-TMB was found to block veratridine-induced glutamate release with an IC50 value of 8.5 microM, which is very similar to that of bupivacaine (IC50 = 8.2 microM); the effect of TMB was limited to 50% inhibition at 100 microM. TMB and nor-TMB blocked sodium currents in sensory neurons from rat dorsal root ganglia (IC50 = 0.83 +/- 0.09 and 1.23 +/- 0.19 microM, respectively), whereas no effect was observed on calcium currents at the same concentrations. A limited effect was observed on potassium currents (IC50 = 23 +/- 6 at 10 microM) for TMB. In vivo, when tested in the rabbit corneal reflex, TMB displayed a local anesthetic activity 17-fold more potent than that of lidocaine.
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PMID:Pharmacological properties of trimebutine and N-monodesmethyltrimebutine. 1033 31

The case described here is that of a 48-year-old lady who presented with abdominal pain and fever; at a later stage she was found to have hyperkalaemia of uncertain origin. Blood examination revealed there to be marked elevation of the platelets (thrombocytosis) on some occasions. It was then realised that there was correlation between the platelet levels and serum potassium values. During the clotting process the release of potassium from the increased number of platelets caused the serum potassium to be elevated on account of an in vitro effect. The important point is that the raised serum potassium levels were not due to an in vivo phenomenon and, therefore, the patient did not need treatment for this; however, the presence of thrombocytosis was itself a clue to the diagnosis--which was eventually recognised as being due to an infection. At operation a tubo-ovarian abscess was discovered to be the cause of the problem.
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PMID:Lessons to be learned: a case study approach: pseudohyperkalaemia due to thrombocytosis in a case of tubo-ovarian abscess. 1051 60

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to correct potassium quickly in severe cases, because acute reduction of potassium may decrease aldosterone. Today, ACEI is a common drug for CHF, so we should pay attentions that ACEI could cause such acute changes. To prevent such acute changes, excessive restriction of water and sodium intake should be avoided. If possible, NSAID and potassium sparing diuretics also should be avoided. Steroid therapy must be introduced rapidly when needed.
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PMID:[Electrolyte abnormalities and metabolic acidosis in two Duchenne muscular dystrophy patients with advanced congestive heart failure]. 1100 25


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