Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the progression of heterotopic ossification (HO) in 17 spinal cord injury patients by comparing radiographs, quantitative radionuclide bone scans, and serum alkaline phosphatase levels. Evidence of maturation of HO appeared earlier (3 months to 6 years post injury) in radiographs, whereas, during the same time frame, radioactive nuclide assessment showed continued progression of HO in 10 out of the 17 patients. The evolution of HO appeared to take place over a period ranging between 3 and 80 months. We believe that stabilization of HO may be reasonably defined in terms of uptake ratios of 2.0 or less in patients with initial uptake ratios over 3.0 but below 5.0, and of ratios of 3.0 or less when the initial values are over 5.0.
Paraplegia 1992 Nov
PMID:Computerized quantitative radionuclide assessment of heterotopic ossification in spinal cord injury patients. 148 34

A 37-year-old female was admitted to our hospital because of progressive dementia and gait disturbance. She was healthy until 34 years of age when she had difficulty in walking and memory disturbance with personality changes. At age 36, she developed urinary incontinence and dementia. The neurological examination demonstrated euphoric mental state, emotional incontinence, severe dementia, paraplegia, dysmetria, choreic movements in both arms and urinary incontinence. Diffuse hyperreflexia and bilateral Babinski signs were observed. Routine laboratory examination showed slightly increased erythrocyte sedimentation rate and alkaline phosphatase. Electroencephalogram revealed diffuse irregular slow waves. X-ray film of the ulnar bone revealed osteoporotic and cystic lesions. The biopsy of the left tibial bone showed a specific membranous cystic structure. Computerized tomography (CT) of the brain showed symmetric, diffuse low density areas in the cerebral white matter and severe atrophy of the cerebellum. T2-weighted magnetic resonance imaging (MRI) revealed diffuse high intensity areas in the cerebral white matter. The present case is characterized by diffuse changes in cerebral white matter and cerebellar atrophy, which have been never reported in Nasu-Hakola disease. The diffuse cerebral white matter changes shown by CT and MRI appear to indicate that this patient is the first case of leukodystrophy of sudanophilic type since the original case reported by Nasu et al.
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PMID:[A case of membranous lipodystrophy (Nasu) with diffuse cerebral white matter involvement and cerebellar atrophy on brain CT and MRI]. 208 28

The blood chemistry was studied in 140 spinal cord injury (SCI) patients (acute injury ward), including 18 patients who developed heterotopic ossification (HO). Comparisons between the HO and non-HO groups were made to determine if the alkaline phosphatase (AP), inorganic phosphorus (P), or calcium (Ca) levels were of diagnostic value. The results showed that AP, P, and Ca by themselves were of little help in the diagnosis of HO. However, the combination of elevated AP and P was significant, especially if both were consistently elevated. There were no significant differences between the HO and non-HO groups concerning completeness or level of spinal injury.
Paraplegia 1990 Sep
PMID:Serum alkaline phosphatase and inorganic phosphorus values in spinal cord injury patients with heterotopic ossification. 212 34

A retrospective study of serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxalacetic transaminase (SGOT) was performed on eighteen previously healthy patients with acute spinal cord lesions C1 to L1 and no abdominal trauma. The SGPT rose in 13 of the 17 (76%). The SGOT rose in 8 of the 17 (47%). The SGPT and SGOT values for the entire group were significantly elevated over the upper limits of normal (p less than 0.01). The mean and median days of onset of elevated SGPT after trauma were 22 and 18, respectively. The mean and median days to normalization after trauma were 67 and 64. The mean and median days of onset of elevated SGOT were 26 and 19 respectively. The mean and median days to normalization were 42 and 43. The alkaline phosphatase were elevated in all but eight patients. The bilirubin was elevated in only three patients. Seventy-six percent of the quadriplegics and 60% of the paraplegics had elevated transaminases. The elevations are probably related to liver injury but the mechanism is unclear.
J Am Paraplegia Soc 1989
PMID:Liver enzyme abnormalities in spinal cord injury. 260 May 93

Lead poisoning associated with progressive osteoporosis in patients who have been previously lead poisoned has been described but poorly documented. We managed a 4-year-old child with a prior history of plumbism who developed recurrent blood lead elevations (as high as 70 mcg/dl), requiring multiple courses of EDTA, after acute paraplegia from transverse myelitis. The patient was hospitalized throughout these periods of chelation. No exogenous sources of lead were found. Calcium, phosphate, magnesium, alkaline phosphatase and parathyroid hormone levels remained normal while vitamin D levels were depressed. Metabolic studies revealed negative calcium balance with an elevated urinary calcium:creatinine ratio. Long-bone radiographs were remarkable for progressive osteoporosis with no evidence of metallic foreign bodies. This case illustrates that bone, the major repository of lead, can become a source of significant lead level elevations in conditions associated with accelerated resorption.
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PMID:Recurrent lead poisoning in a child with immobilization osteoporosis. 314 14

The purpose of this study is to investigate the use of a three-phase bone scan for early detection of HO formation and as a method of evaluating Didronel treatment. A marked vascular blush and blood pool was noted about the hips sometimes with a normal bone scan and normal X-ray of the hips. This appeared to represent the precursor phase of HO formation since, on repeat scans, the bone scan showed accumulation of the bone-seeking radionuclide usually in 2 to 4 weeks and the X-ray revealed ossification. Fifty-two patients treated with Didronel between October 1978 and December 1979 were reviewed to determine the value of Didronel treatment. There were 23 patients in the series who either showed HO by X-ray on admission or developed HO on follow-up X-rays before beginning Didronel therapy. A three-phase bone scan revealed increased vascularity and accumulation of radioactivity on the bone scan in all areas of ossification on the X-ray and in some areas that did not appear to be involved. The other 29 patients had serial three-phase bone scans, X-ray study, and an alkaline phosphatase determination at approximately 2-week intervals. Didronel treatment was started as soon as the precursor phase of HO was demonstrated on the three-phase bone scan in most of these patients. Nine have not developed ossification that could be seen in X-rays during 3 months of continuing study. Six patients seen at follow-Up during the past year had known HO of 4 to 7 years duration. The three-phase bone scan was used to predict the maturity of HO in these patients. Our study in indicates that increased vascularity precedes rather than being secondary to HO formation as is suggested in the literature. Didronel treatment appears to be most effective if initiated during this precursor phase.
Paraplegia 1982 Aug
PMID:The use of the three-phase bone scan in the early diagnosis of heterotopic ossification (HO) and in the evaluation of Didronel therapy. 621 9

The aim of this study was to determine the ability of disodium dichloromethylene diphosphonate (Cl2MDP) to reduce the hypercalcemia secondary to skeletal metastases and induced by stimulation of bone resorption by malignant cells. Five patients with hypercalcemia due to bone metastases of breast or renal cancer were treated orally for 4 wk with 3,200 mg of Cl2MDP and 4 wk with a placebo in a double blind, crossover study. During the Cl2MDP period of administration four patients experienced a rapid and significant decrease in serum calcium and urinary calcium excretion together with an increase in alkaline phosphatase. In the remaining patient who developed a sudden paraplegia at the onset of the therapy followed by a marked increase in serum calcium levels and urinary calcium excretion, Cl2MDP was able to reverse this worsening of hypercalcemia or to reduce serum and urinary calcium to normal values. For all patients, urinary hydroxyproline excretion was unchanged during the Cl2MDP period when compared with the prestudy or placebo periods. From these results, and because of the rapid relapse of hypercalcemia during the placebo period or after withdrawal of the treatment, we can conclude that Cl2MDP is capable of reducing excessive mobilization of calcium resulting from bone metastases.
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PMID:Effects of disodium dichloromethylene diphosphonate on hypercalcemia produced by bone metastases. 644 55

In order to determine the impact of extremely large doses of methylprednisolone, naloxone, or of spinal cord injury itself, on liver enzymes, we examined the results of SGOT, SGPT, alkaline phosphatase and total bilirubin tests obtained 24 hours, 3 and 10 days after the end of the study drug infusions in spinal cord injured patients entered in the National Acute Spinal Cord Injury Study. The mean values of four liver enzymes, the amount of change between 24 hours and 3 and 10 days post infusion, and the proportion of liver enzyme levels considered to be abnormal did not appear to be affected by either drug protocol. Even when controlling for drug protocol and severity of injury (complete vs incomplete), variation in enzyme levels appeared to be the result of the spinal cord injury, not study drugs. Spinal cord injury is routinely treated with the NASCIS dose of methylprednisolone in many countries. It is reassuring to find no evidence of compromised liver function from this steroid protocol.
Paraplegia 1994 Apr
PMID:The effect of methylprednisolone, naloxone, and spinal cord trauma on four liver enzymes: observations from NASCIS 2. National Acute Spinal Cord Injury Study. 802 33

Urinary tract infection occurs more commonly, is more virulent and proves more difficult to eradicate in spinal cord injury persons than in the neurologically intact. In order to find out the peculiarities of the neuropathic bladder which make it vulnerable to recurrent cystitis, we studied the proliferation status of the urothelium in spinal cord injured persons. Eleven consecutive, unselected male spinal cord injury patients (aged 18-73 years) were included in the study. Those with, or undergoing treatment for acute urinary tract infection were excluded. All patients underwent cystoscopy and cold cup bladder biopsy from the trigone and bladder dome. Immunocytochemical analysis was performed using defined, commercially available antibodies for PCNA (PCNA 10, DAKO) and MIB-1 (raised against recombinant DNA defined segment of Ki-67 antigen DAKO) streptavidin/biotin and alkaline phosphatase immunocytochemistry (for MIB-1 with microwave-enhanced antigen retrieval) were used to demonstrate the presence of cell cycling-associated nuclear proteins. Foci of lymphocytic aggregations present in the sections served as in-section controls for antigen preservation. Ten patients showed labelling of 20-70% of cells for PCNA in basal cell layers of dome lining. Higher urothelial layers showed a variable, but generally reduced degree of labelling. Of these 10 patients, three showed complete absence of MIB-1 activity in the basal and other layers of dome urothelium and two demonstrated only a very occasional positive nucleus. MIB-1 labelling was < 5% in four others and it was between 5% and 10% in one.(ABSTRACT TRUNCATED AT 250 WORDS)
Paraplegia 1995 Sep
PMID:Vesical urothelium proliferation in spinal cord injured persons: an immunohistochemical study of PCNA and MIB.1 labelling. 852 5

We report a 65-year-old woman with HAM who showed rapid progression of the clinical symptoms. The initial symptom was lumbago and she became unable to walk within 4 months after the onset of the lumbago. When seen on admission, she had flaccid paraplegia and areflexia was seen in the lower extremities with positive Babinski and Chaddock reflexes. She had numbness below the level of the navel, vibratory sensation was decreased in both lower limbs, and there was a hyperesthesic zone at the tenth thoracic vertebral level. She had a difficulty in urination and defecation. Laboratory examination revealed elevated anti-HTLV-I antibody titers both in serum (4,096x by PA method) and in cerebrospinal fluid (CSF) (4,096x). The levels of IgG and neopterin in CSF were also increased to 16.6 mg/dl (normal: < 5 mg/dl) and 360.3 pmol/ml (normal: < 30 pmol/ml), respectively. HTLV-I messenger RNA positive cells were detected in 0.1% to 0.01% of cells in CSF by in situ hybridization using an oligonucleotide probe labelled with alkaline phosphatase. Spinal cord MRI detected neither spinal cord compression nor vascular diseases. She was treated with 1,000 mg methylprednisolone for 3 days intravenously, followed by 60 mg oral prednisolone therapy. In several days after receiving the treatments, her muscle tonus became spastic and deep tendon reflexes in the legs became brisk. The hyperesthesia at the tenth thoracic vertebral level and numbness below the level of the navel were also gradually improved. Subsequently, her clinical features were consistant with those of the typical HAM. Therefore, the patient was diagnosed as rapidly progressive HAM. The initial phase of rapidly progressive HAM patients had been described only from clinical history. These patients had common characteristic clinical features, such as older age at onset, relatively severe motor dysfunction, high titers of anti-HTLV-I antibody in CSF, and increased levels of neopterin and IgG in CSF, when compared with those of other HAM patients. The clinical course and laboratory findings in the present patient were compatible with those in the previous cases reported as rapidly progressive HAM. This patient showed flaccid paraplegia and areflexia which have rarely been seen in HAM patients. However, these symptoms were changed to spastic and hyperactive after prednisolone therapy. We speculate that inflammation in the spinal cord in this patient was severe enough to spread to the dorsal root, and disturbed the afferent pathway from the peripheral to the central nervous system. This inflammatory reaction might be suppressed by prednisolone to facilitate the recovery of the afferent pathway, which led to the typical clinical symptoms of HAM.
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PMID:[A case of rapidly progressive HTLV-I-associated myelopathy (HAM)]. 943 Sep 94


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