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)

A 16-year-old girl was admitted with the complaints of headache, chest pain, low abdominal pain and left hemi-numbness. Her blood pressure was high and plasma renin activity and aldosterone levels were elevated. Renal angiography revealed vascular stenoses and microaneurysms although the renal artery and its main branches were not involved. Polyarteritis nodosa (PN) was strongly suspected and oral prednisolone and intravenous pulse therapy of cyclophosphamide were started. The second renal angiography which was performed 11 days after the therapy was started, showed marked improvement of vascular lesions. This is a case which suggests that the angiographic findings of PN can improve very rapidly with therapy.
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PMID:A young female case of polyarteritis nodosa strongly suspected by typical angiographic findings which improved rapidly after prednisolone and cyclophosphamide therapy. 135 68

A 23-year-old man presented with high fever and left abdominal pain. Ultrasonography, CT scan and angiography visualized a left adrenal cyst. Cyst fluid obtained preoperatively by percutaneous needle puncture under ultrasonographic guidance was purulent, and had a higher level of aldosterone, and lower level of amylase than the plasma. These findings suggested that this cyst originated from the adrenal gland. Histopathological examination of the surgically removed specimen confirmed the adrenal pseudocyst.
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PMID:[Adrenal pseudocyst: a case report]. 163 22

26 children were investigated on an average 11.5 years after partial (n = 13) and total (n = 13) colonic resection. Total colectomy was followed by an increased frequency of gastrointestinal symptoms such as recurrent abdominal pain, flatulence, attacks of diarrhoea, frequent and pasty or liquid stools with strange smell. An increased salt or fluid intake was observed in one half of these patients. Their height and bone age was slightly but significantly reduced. Laboratory investigations revealed no significant deficiencies of electrolyts, vitamins or trace elements. However Renin (mean and 2s-range = 5.2; 2.7-6.8 ng/ml.h, normal values (NV) 1.3; 0.5-4.0 ng/ml.h, p less than 0.02), aldosterone (242.1; 168.4-357.8 pg/ml, NV 78.9; 39.4-168.4 pg/ml, *p less than 0.02), conjugated bile acids (11.3; 5.2-20.0 mumol/1, NV 4.2; 1.5-7.0 mumol/1, p less than 0.01) and serum urea concentration (32.5; 20.8-48.7 mg/dl, NV 14.6; 6.0-22.5 mg/dl, p less than 0.01) were significantly elevated. Three postprandial plasma levels of gastrin, VIP and neurotensin were within normal limits. In patients with partial large bowel resection all signs were less pronounced. According to our results a special diet in children years after colectomy seems not to be required.
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PMID:[Late results following partial and total colectomy in infancy]. 328 87

A 16-year-old woman was admitted to our hospital because of abdominal pain, paresis of extremities, and muscle weakness. Bartter's syndrome was suspected because of the features of the hypokalemia, hyperaldosteronism, hyperreninemia, increased concentration of plasma angiotensin I & II, the defect in distal fractional reabsorption of chloride and normotension. The concentrations of the plasma angiotensin II and aldosterone, however, were decreased to normal levels after admission probably due to a decrease in the salt intake because of the regular hospital diet. Furthermore, the hyperplasia of the juxtaglomerular apparatus was not found. Therefore, at first we thought we were dealing with another disease, that is pseudo-Bartter's syndrome, which is caused by different pathogenesis. Gill et al. reported that the defect in distal fractional reabsorption of chloride was a characteristic feature in the diagnosis of the Bartter's syndrome. Thus, we tried to explain the clinical symptoms and diagnosis of this case as the Bartter's syndrome according to the theory of Gill et al. If the defect of chloride reabsorption was the only pathogenesis of the Bartter's syndrome, other symptoms seen in our case could be thought of as secondary (or new) changes. Therefore, this case could be differentiated from the pseudo-Bartter's syndrome or the "true" Bartter's syndrome because of the clinical symptoms and the defect in chloride reabsorption.
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PMID:[A case of Bartter-like syndrome with abdominal pain, paresis of the extremities and muscle weakness]. 343 14

Hypokalemia with hyperkaliuresis was diagnosed in a 10 1/4-year-old boy, who presented with spontaneously disappearing abdominal pain. The diagnosis of Gitelman-Syndrome (asymptomatic chronic hypokalemia and -magnesemia) was established after detection of hypomagnesemia, renal magnesium losing but normal renin-angiotensin-aldosterone system and glomerular filtration rate. After oral supplementation of potassium hypokalemia persisted and hyperkaliuresis increased. The substitution was discontinued, the hyperkaliuresis diminished and the child remained asymptomatic during a 24 months follow-up. The substitution of potassium and magnesium can be avoided in children with Gitelman-Syndrome as long as they remain asymptomatic.
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PMID:[Asymptomatic hypokalemia and hypomagnesemia with renal cation loss (Gitelman syndrome)]. 361 31

A 74-year-old man developed bilateral arterial thrombosis of the lower limbs related to heparin-associated thrombocytopenia syndrome (HATS). On day 4 after thrombectomy of both limbs, abdominal pain, fever, hypotension, abdominal tenderness appeared. Acute acalculous cholecystitis was suspected and cholecystectomy was carried out although the gallbladder was not imflamed. Later on, hyponatremia in addition to the aforesaid signs suggested the diagnosis of adrenal insufficiency. Diagnosis was confirmed by low cortisol and aldosterone plasma concentration and by CT scan, which showen two enlarged adrenal glands. HATS might explain two unexpected facts: occurrence of adrenal hemorrhage during heparin therapy with coagulation tests within the therapeutic range and paradoxical thrombosis in the central vein of adrenal gland. HATS must be regarded as one cause of adrenal hemorrhage necrosis.
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PMID:Heparin-associated thrombocytopenia syndrome: an underestimated etiology of adrenal hemorrhage. 829 32

A total of 42 cases of large symptomatic parapelvic or pararenal lymphatic cysts has been reported since 1890, of which 54% were associated with hypertension and 14% were bilateral. We report on a patient in whom during a 3-month period abdominal pain and distention developed successively on both sides associated with hypertension. Initially, ultrasound and computerized tomography revealed a large multicystic pararenal lymphatic mass on the right side and small parapelvic hilus lesions on the left side. Two months after resection and marsupialization of the large cyst on the right side the small hilus lesions on the left side developed into large pararenal cysts requiring the same therapeutic measures. Hypertension was reversible after surgery in both instances; at the second operation high preoperative and lower postoperative renin activity, active renin, total renin, aldosterone and atrial natriuretic factor in plasma were noted. Immunoreactive active and total renin levels in the lymph fluid were elevated, a finding that may be explained by the renal origin of the lymph. Marsupialization is a kidney preserving measure that reverses all symptoms of large pararenal cysts, including Page kidney hypertension.
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PMID:Hygroma renale: pararenal lymphatic cysts associated with renin-dependent hypertension (Page kidney). Case report on bilateral cysts and successful therapy by marsupialization. 834 18

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

We administered the aromatase inhibitor fadrozole to 16 girls with gonadotropin-independent precocious puberty due to the McCune-Albright syndrome. The girls' ages ranged from 3.2-9.7 yr, and their bone ages ranged from 5.75-14.25 yr. After baseline evaluations, fadrozole was started at a dose of 240 microg/kg.d (equivalent to the dose recommended for therapy of estrogen-dependent breast cancer) for 12-21 months and increased to 480 microg/kg.d for an additional 12 months in 10 girls. During treatment, seven girls had evidence of central precocious puberty; hence, the GnRH agonist deslorelin (4 microg/kg.d sc) was added to their regimen. One girl was on a long-acting GnRH agonist from the start of treatment. Patients were evaluated at 2-6-month intervals throughout treatment. After the first 6-12 months of treatment, fadrozole showed some benefits in 10 girls, including decrease in frequency of menses and/or rates of linear growth and bone maturation; however, fadrozole had no significant benefit in the group as a whole. The seven girls with evidence of central precocious puberty had no slowing in the progression of their puberty during the combined fadrozole and GnRH analog treatment. Adverse effects of fadrozole included inhibition of cortisol and aldosterone biosynthesis at the dose of 480 microg/kg.d, without clinical evidence of adrenal insufficiency. In addition, three patients complained of nonspecific abdominal pain during fadrozole treatment. In one patient, this resolved with a reduction in dose from 480 to 240 microg/kg.d; in two patients, it resolved spontaneously. One girl had muscle weakness and constipation on the 480 microg/kg.d. This resolved after discontinuation of the drug. We conclude that fadrozole is not sufficiently potent to block estrogen synthesis in most girls with gonadotropin-independent precocious puberty due to the McCune-Albright syndrome and may impair the adrenocortical stress response.
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PMID:Lack of efficacy of fadrozole in treating precocious puberty in girls with the McCune-Albright syndrome. 1467 Nov 60

Mercury intoxication is a rare cause of severe hypertension. A case of mercury intoxication presented with severe hypertension and erythromelalgia was reported. A 10-year- and -5-month-old girl presented with recurrent rash and painful hands for 2 months, with seizure attack and episodic loss of consciousness for one hand half months. The girl was found to have red painful hands, a blood pressure 170/120 mm Hg(1 mm Hg=0.133 kPa), tachycardia and hypokalemia (2.83-3.25 mmol/L, reference value 3.5-5.5 mmol/L). An extensive investigation ensued. Elevated renin-angiotensin and aldosterone were demonstrated in plasma. Cranial MRI T2 weighed images showed widespread white matter signal abnormalities, which particularly involved parietal, occipital and frontal lobes. With hypertension controlled, white matter signal abnormalities weakened. Other symptoms included insomnia, nausea and paroxysmal abdominal pain. The girl was found to have a raised concentration of mercury in urine (0.171 mg/L, reference value< 0.01 mg/L), and she had been exposed to elemental mercury for several days. After chelating therapy, the girl's blood pressure returned to normal, erythromelalgia ameliorated, all other symptoms disappeared. So, mercury intoxication should be considered in the differential diagnosis of hypertension with erythromelalgia.
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PMID:[Hypertension and erythromelalgia as prominent manifestations of mercury intoxication]. 1765 63


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