Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old woman was admitted to our hospital because of tingling numbness in the trunk and upper extremities. She was well until 18 days earlier, when she began to feel tingling numbness on the ulnar side of the left arm. During the next two weeks it spread gradually over the trunk and ulnar side of the bilateral arms. She had also progressive difficulty in taking hold of objects. On neurological examination she was alert and cooperative with normal articulation. The neck was supple. The cranial nerves were intact. Superficial sensation was bilaterally hypesthetic in the distribution from the 7th cervical through 12th thoracic segments. Mild weakness was distally noted in the upper extremities. Deep tendon reflexes were reduced or absent without laterality. Plantar responses were bilaterally flexor. Coordination and gait were normal. Routine laboratory examinations including blood counts, blood chemistries and urinalysis were unremarkable. Serum angiotensin converting enzyme (ACE) was slightly elevated. A lumbar puncture yielded clear, colorless cerebrospinal fluid (CSF) containing 22 white cells/mm3 and protein of 106 mg/dl. Conventional nerve conduction studies were normal. F-wave conduction studies revealed elevated F-ratios for the upper and lower extremities. Studies of short-latency somatosensory evoked potential showed mild prolongation of N13 recorded after stimulation of the right median nerve. An X-ray film of the spine was unremarkable except for mild narrowing of the C5-6 intervertebral disk space. Postcontrast magnetic resonance imaging of the spine with gadolinium-DTPA was unrevealing as well as a precontrast study. A myelogram disclosed enlarged lateral filling defects corresponding to cervical nerve roots from C6 through C8 bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of sarcoid polyradiculopathy with nerve roots swelling demonstrated by myelography]. 133 26

A case of sarcoidosis presenting ataxic hemiparesis was reported. A 25-year-old man was admitted to Kanto Teishin Hospital because of slight weakness and dysesthesia in the right side of his body. His physical findings were normal. Neurological findings disclosed mild right hemiparesis (MMT 4+), cerebellar signs and mild dysesthesia in the same side. Laboratory findings were within normal limits except for elevated serum ACE and lysozyme. Chest roentgenogram showed bilateral hilar lymphadenopathy and TBLB disclosed sarcoid granuloma. Though brain CT, brain MRI and cerebral angiography were within normal limits, the neurological features were thought to be due to sarcoidosis. They disappeared along with the decrease of ACE and lysozyme. This is the first report of ataxic hemiparesis due to sarcoidosis, and it is interesting in that ataxic hemiparesis, which is one of signs of diseases in central nervous system, is the first manifest clinical feature of sarcoidosis.
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PMID:[A case of sarcoidosis presenting ataxic hemiparesis as an initial clinical manifestation]. 258 93

Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.
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PMID:Zinc, copper and selenium in reproduction. 803 70

Ramipril is a long-acting nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor introduced for clinical use about a decade ago. Ramipril is a prodrug that undergoes de-esterification in the liver to form ramiprilat, its active metabolite. Ramipril rapidly distributes to all tissues, with the liver, kidneys and lungs showing markedly higher concentrations of the drug than the blood. After absorption from the gastrointestinal tract, rapid hydrolysis of ramipril occurs in the liver. In the therapeutic concentration range, protein binding of ramipril and ramiprilat is 73 and 56%, respectively. Ramiprilat binds to ACE with high affinity at concentrations similar to that of the enzyme and establishes equilibrium slowly. Although ramipril is metabolised by hepatic and renal mechanisms to both a glucuronate conjugate and a diketopiperazine derivative, most of the drug is excreted in the urine as ramiprilat and the glucuronate conjugate of ramiprilat. Elimination from the body is characterised by a relatively rapid initial phase with a half-life of 7 hours and a late phase with a half-life of about 120 hours. No clinically significant pharmacokinetic interactions between ramipril and other drugs have been reported. The drug has been generally well tolerated with the most prevalent adverse effects being dizziness (3.4%), headache (3.2%), weakness (1.9%) and nausea (1.7%). Ramipril is an effective and well tolerated drug for the treatment of hypertension and congestive heart failure in all patients, including those with renal or hepatic dysfunction, and the elderly.
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PMID:Clinical pharmacokinetics of ramipril. 813 99

The pharmacokinetics and pharmacodynamics of the ACE inhibitor quinaprilat have been studied in six chronic haemodialysis (HD) patients and in six patients undergoing continuous ambulatory peritoneal dialysis (CAPD) after a single oral dose of 2.5 mg quinapril. Mean tmax and Cmax values (SEM) for quinaprilat in interdialytic HD patients were 4.0 (0) h and 84 (8.4) ng.ml-1 respectively, and they did not differ significantly from those in CAPD patients (4.7 (0.7) h and 64 (5.7) ng.ml-1). Elimination half lives were 30 (10.1) h (HD) and 34 (7.3) h (CAPD). Cmax, tmax, t1/2, and AUC were increased and CL was decreased compared to data reported previously after giving 2.5 mg to healthy subjects. Peritoneal clearance was calculated as 0.1 (0.1) ml.min-1, thus less than 0.5% of the dose were removed within 24 h by CAPD. ACE activity was suppressed by more than 93% between 4 and 24 h postdose (P < 0.001). It decreased in both groups with increasing plasma quinaprilat levels. Angiotensin II concentration compared to baseline was significantly decreased at 4 hours (-30.4 +/- 10%) and 24 h (-30 +/- 9.9%) (P < 0.05, n = 11), while active plasma renin concentration was still significantly increased at 48 h postdose (+ 60.2 +/- 14.5%, P < 0.01). Mean arterial pressure 24 h postdose was significantly (P < 0.05) decreased in HD (-12 mmHg) and CAPD patients (-20 mm Hg). Only two patients reported unwanted effects (fatigue, dizziness, nausea, and weakness). In conclusion, due to its long lasting effect on ACE activity and on blood pressure in terminal renal failure a starting dose of quinapril 2.5 mg o.d. may be used in hypertensive HD and CAPD patients.
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PMID:Pharmacokinetics and pharmacodynamics of quinaprilat after low dose quinapril in patients with terminal renal failure. 838 27

We report two siblings with sarcoidosis; the younger sister had symptoms of central nervous system, and both sisters had subcutaneous mass lesions in the gluteal region. Case 1. A 30-year-old woman presented with two episodes of right leg paresis. On admission, neurological examination revealed right leg weakness, spasticity of both legs, increased deep tendon reflexes in all extremities, urinary disturbance and hearing loss of the right ear, but she had no meningeal signs. Serological studies were normal including angiotensin converting enzyme. Cerebrospinal fluid revealed elevated protein to 340 mg/dl, mild pleocytosis, decreased glucose. CSF culture was negative, and cytology showed no malignant cells. Enhanced MR imaging showed diffuse leptomeningeal enhancement in both the brain around basal meninges and the whole spinal cord. Case 2. A 34-year-old woman (the elder sister of Case 1) presented with visual disturbance. She had been diagnosed to have bilateral iritis at Hiroshima Red Cross Hospital before visiting our hospital. Neurological examination and serological studies were normal. In both cases, left gluteal subcutaneous mass was detected and its biopsy revealed characteristic sarcoid nodules and confirmed the diagnosis of sarcoidosis. A tendency of familial occurrence and positive associations of the specific HLA antigens in sarcoidosis have been reported. Though the diagnosis of neurosarcoidosis has been difficult without extraneurological signs, sarcoidosis should be considered as a differential diagnosis in all the patients with myelopathy, and enhanced MRI and measure of CSF angiotensin converting enzyme seem to be useful for diagnosis and evaluation of drug effect during the course of steroid therapy.
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PMID:[Two siblings with sarcoidosis diagnosed by younger sister's central nervous symptoms]. 904 58

Sarcoidosis presenting solely as a granulomatous colitis is rare and appears identical to Crohn's disease. A 56-yr-old woman developed a Crohn's-like illness, which remitted after 5-ASA therapy. Two months later, she developed fever, adenopathy, muscle weakness, and peripheral neuropathy. A diagnosis of sarcoidosis was made after an extensive search for an infectious or rheumatological cause. This case illustrates the utility of serum angiotensin converting enzyme level in differentiating sarcoidosis from Crohn's disease.
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PMID:Sarcoidosis presenting as granulomatous colitis. 977 62

A 70-year-old man admitted to a local hospital because of facial muscle weakness, tinnitus and facial pain in left side, was then given corticosteroid with a tentative diagnosis of Bell's palsy and his symptoms gradually improved. Since these symptoms recurred six months later, he was referred to our neurological service. As his brain CT revealed diffuse thickening and enhancement of the dura mater, he was thought to have hypertrophic pachymeningitis (HP). Intravenous antibiotics were started for aspiration pneumonia and his neurological symptoms gradually improved. HP caused by bacterial infection was thus likely and antibiotics, rifampicin and metronidazole, were administered orally as an outpatient. However, one month later, these symptoms were worsened with headache and double vision. He was then rehospitalized. MR imagings of the head with gadolinium disclosed diffuse meningeal thickening and enhancement, especially of the left-sided cerebellar tentorium. Erythrocyte sedimentation rate and C-reactive protein were moderately elevated. Serum angiotensin converting enzyme was within normal range. The test for cytoplasmic antineutrohil cytoplasmic antibody (ANCA) in the serum was negative, however, that for perinuclear ANCA was positive at a titer of 99 EU. Lumbar puncture showed normal findings and negative culture results for bacteria, fungi or mycobacteria. Dural biopsy specimens showed non-specific granulomatous inflammation of the dura with epithelioid histiocytes and Langerhans type multinuclear giant cells with caseous necrosis, however, with no presence of fungi or tubercle bacilli. After the oral administration of cyclophosphamide (100 mg, daily) and prednisolone (40 mg, daily), his neurological symptoms and laboratory findings have been gradually improved and he is well one year after discharge. This case together with previous reports suggests that ANCA positive HP without evidence of other organ involvements may belong to the limited form Wegener's granulomatosis. In the literatures of idiopathic HP, the treatment effect with corticosteroid alone is initially favorable, but transient. On the other hand, using the combined therapy of cyclophosphamide and prednisolone, the remission has been achieved in more than 90% of patients with WG. These data suggest that P-ANCA positive HP should be treated with a combination of corticosteroid and cyclophosphamide.
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PMID:[An old man presenting with fluctuating bilateral multiple cranial nerve palsies and positive test for perinuclear antineutrophil cytoplasmic antibody]. 1051 63

Although the carbonic anhydrase inhibitors have been used in the treatment of the primary periodic paralyses (PPs), their efficacy has not been demonstrated in double-blind, placebo-controlled trials. Therefore, we tested the efficacy of dichlorphenamide (DCP; Daranide), a potent carbonic anhydrase inhibitor, in the treatment of episodic weakness in the primary PPs. We performed two multicenter, randomized, double-blind, placebo-controlled crossover trials, one involving 42 subjects with hypokalemic periodic paralysis (HypoPP) and the other involving 31 subjects with potassium-sensitive periodic paralysis (PSPP). In each trial, two 8-week treatment periods were separated by an active washout period of at least 9 weeks. The primary outcome variable in the HypoPP trial was the occurrence of an intolerable increase in attack severity or frequency (end point). The primary outcome variable in the PSPP trial was the number of attacks per week. In the HypoPP trial, there were 13 subjects who exhibited a preference (in terms of the end point) for either DCP or placebo, and 11 of these preferred DCP. In the PSPP trial, DCP significantly reduced attack rates relative to placebo. DCP also significantly reduced attack rates relative to placebo in the HypoPP subjects. We conclude that DCP is effective in the prevention of episodic weakness in both HypoPP and PSPP.
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PMID:Randomized trials of dichlorphenamide in the periodic paralyses. Working Group on Periodic Paralysis. 1063

Spinal neurosarcoidosis is rare (0.43 p. 100 of all sarcoidosis) and can be the initial manifestation of the disease. A 43-year-old right handed African man developed a progressive dorsal neck pain, slowly worsened paresthesia weakness in the legs and a gait disturbance. Magnetic resonance imaging (MRI) scan of the cervical and thoracic spinal cord (sagittal T(1)- weighted image) revealed diffuse enlargement of the cord from C2 to T7 with intense intramedullary enhancement from C2 to T3 after administration of contrast material on sagittal T(1)- weighted image. Cranial MRI scan was normal. Radiographs of the chest revealed bilateral symmetric hilar mediastinal lymphadenopathy with no pulmonary infiltrates. Bronchial biopsy demonstrated non caseating granulomas with langerhans giant cells. The serum angiotensin converting enzyme level was elevated. The patient received corticosteroid with good progressive response. His neurologic symptoms improved markedly and twenty months post-treatment MRI showed no abnormality on enhanced T(1)- weighted images. Two years later he had no relapse. Only 6 to 10 p. 100 of patients with neurosarcoidosis have spinal cord involvement, which may account for the first clinical manifestation of the disease. Most patients with neurosarcoidosis have associated extraneurologic abnormalities. The diagnosis is supported usually by extraneurologic biopsies. Spinal cord biopsy needs to be considered on case-by-case basis.
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PMID:[Spinal cord involvement revealing systemic sarcoidosis]. 1103 20


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