Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042024 (incontinence)
 13,409 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 52-year-old male patient with Shy-Drager syndrome (SDS) complicated by an occurrence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The patient first developed impotence at the age of 48, accompanied by urinary incontinence, and episodes of dizziness while standing. The following year, the patient had developed a staggering gait and speech became monotonous. At age 52, the patient was admitted to the hospital after experiencing frequent episodes of syncope associated with complete loss of consciousness. Upon examination, blood pressure was 100/70 in a recumbent position, and 80/60 when standing. The pulse rate varied from 60 per minute to 62. The patient was alert. The alternating Horner sign was observed, and a paucity of facial movements was visible. His speech was slow and monotonous. Muscle tone was increased bilaterally. There was incoordination. A laboratory examination revealed reduced serum sodium levels of 127 mEq/L and increased sodium excretion with plasma hypoosmolality (262 mOsm/kg/H), urine hyperosmolality and low serum renin activity (0.2 ng/ml/h). Renal functions were normal and the levels of adrenocortical and thyroid hormones were normal. There were no abnormalities observed in the chest roentgenogram taken. The level of antidiuretic hormone (ADH) was unreasonably high (5.74 pg/ml). A water-load test demonstrated failure of both water diuresis and inhibition of ADH secretion. These data suggested that hyponatremia in this case was caused by SIADH. The correlation between plasma osmolality and the concentration of ADH suggested that osmolality that initiates ADH release appeared to have been reset to around 230 mOsm/kg lower than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Shy-Drager syndrome and the syndrome of inappropriate secretion of antidiuretic hormone]. 161 76

A case of allergic granulomatous angiitis showing various symptoms of the central nervous system is reported. A 29-year-old female was admitted to our hospital because of severe headache and urinary incontinence. Consciousness was drowsy, and right IIIrd cranial nerve palsy was observed. CT scan revealed subarachnoid hemorrhage, hydrocephalus and arachnoid cyst. Since no aneurysm or arteriovenous malformation was detected by angiography, continuous ventricular drainage was performed. Marked hypertension due to renal vascular origin was suggested by means of laboratory data about serum renin etc., so renal as well as cerebral angiography was carried out by Seldinger's method. There revealed aneurysms of the left renal artery and a branch of the left anterior cerebral artery. Then, ventriculo-peritoneal shunt and resection of left frontal aneurysm were done. Microscopic finding of the excised aneurysm was necrotizing angiitis with infiltration of eosinophil. Six days after the operation, CT scan showed asymptomatic subcortical hematoma at the right occipital lobe. The patient was in good condition and had no cerebral or other complication following steroid therapy. The present case was considered as a very rare one because no case with subarachnoid hemorrhage and cerebral aneurysm due to allergic granulomatous angiitis was reported in the previous literature.
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PMID:[Allergic granulomatous angiitis with subarachnoid hemorrhage--a case report]. 339 97

The present study determined the effects of the angiotensin-converting enzyme (ACE) inhibitor captopril and angiotensin II receptor subtype 1 (AT1-R) antagonist losartan on the internal anal sphincter pressures (IASP) in spontaneously hypertensive rats (SHR) versus normotensive Wistar-Kyoto rats (WKY). The SHR had significantly higher IASP (21.7 +/- 0.8 mm Hg) than the WKY (14.7 +/- 0.9 mm Hg), which was associated with the higher levels of angiotensin II (Ang II) in plasma (50.3 +/- 0.9 pg/ml) and in muscle bath perfusates (72.7 +/- 11.8 pg/ml) compared with the WKY (p < 0.05). Captopril and losartan decreased the IASP in SHR and WKY, but they were more potent in SHR. Captopril and losartan normalized the IASP in the SHR, whereas these agents may compromise rectoanal continence in the WKY. Reverse transcriptase-polymerase chain reaction and Western blots showed higher levels of angiotensinogen, renin, ACE, and AT1-R in the internal anal sphincter (IAS) of SHR. Ang II caused concentration-dependent contraction of IAS smooth muscle strips from WKY (pEC50 = 8.5 +/- 0.1) and SHR (pEC50 = 8.6 +/- 0.2). Losartan (100 nM) significantly (p < 0.05) inhibited this effect. From these data, we conclude that 1) hypertensive IAS in SHR is primarily the result of renin-angiotensin system up-regulation, 2) ACE inhibitors and AT(1)-R antagonists simply relieve the hypertensive IAS, and 3) the differential effect of these inhibitors in the hypertensive versus the normotensive IAS may explain the lack of incontinence as a side effect in hypertensive patients receiving ACE inhibitors and AT1-R antagonists.
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PMID:Angiotensin-converting enzyme and angiotensin II receptor subtype 1 inhibitors restitute hypertensive internal anal sphincter in the spontaneously hypertensive rats. 1664 68