Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Head trauma (HT) and whiplash injury (WI) is followed by a posttraumatic headache (PH) in approx. 90% of patients. The PH due to common WI is located occipitally (67%), is of dull-pressing or dragging character (77%) and lasts on average 3 weeks. Tension headache is the most frequent type of PH (85%). Besides posttraumatic cervicogenic headache or symptomatic, secondary headache due to SDH, SAB, ICB or increased ICP, migraine- or cluster-like headache can be observed in rare cases. Prolonged application of analgetics (> 4 weeks) can cause a drug induced headache. In 80% of patients PH following HT shows remission within 6 months. Chronic PH lasting at least 4 years occurs in 20%. Unfavorouble prognostic factors include an age higher than 40 yrs, a low intellectual, educational and socio-economic level, previous HT or a history of alcohol abuse. A prolonged PH due to WI can be expected in patients with initially severe headache, with an extensive decrease of mobility of the cervical spine, with subjective impediment, with depressive mood, with somatic-vegetative complaints, with a history of pretraumatic headache and with increased age. Acute PH is treated with analgesics, antiphlogistics and/or muscle relaxants; chronic PH with thymoleptics (e.g. Amitryptiline or Amitryptiline oxide). Additional physical therapy (e.g. wearing a cervical collar for a short time, hydrocollator pack), physiotherapy incl. muscle relaxation techniques (Jacobson) and psychotherapy can be performed. Medico-legal issues should be solved as soon as possible.
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PMID:[Post-traumatic headache]. 944 Dec 48

The recent genetic discoveries in CP support the hypothesis that inappropriate intrapancreatic activation of zymogens by trypsin results in autodigestion and pancreatitis. Two different protective mechanisms prevent activation of the pancreatic digestive enzyme cascade. First, SPINK1 inhibits up to 20% of potential trypsin activity and, second, trypsin itself activates trypsin-like enzymes readily degrading trypsinogen and other zymogens. Pancreatitis may therefore be the result of an imbalance between proteases and their inhibitors within the pancreatic parenchyma. The discovery of PRSS1 mutations in families with CP was the first breakthrough in the understanding of the underlying genetic mechanisms. Enhanced trypsinogen activation may be the common initiating step in pancreatitis caused by these mutations. The discovery of SPINK1 mutations underlines the importance of the protease inhibitor system in the pathogenesis of CP. Thus, gain-of-function in the cationic trypsinogen resulting in an enhanced autoactivation, or loss-of-function mutations in SPINK1 leading to decreased inhibitory capacity, may similarly disturb the delicate intrapancreatic balance of proteases and their inhibitors. The recent findings of SPINK1, CFTR, and PRSS1 mutations in CP patients without a family history have challenged the concept of idiopathic CP as a non-genetic disorder and the differentiation between HP and ICP. There is a clear mode of autosomal dominant inheritance for some mutations (R122H, N291, possibly MIT), whereas the inheritance pattern (autosomal recessive, complex, or modifying) of other mutations (A16V, N34S) is controverted or unknown. The lack of mutations in the above-mentioned genes in many patients suggests that CP may also be caused by genetic alterations in yet unidentified genes. Evaluation of CP patients without an obvious predisposing factor, e.g. alcohol abuse, should include genetic testing even in the absence of a family history of pancreatitis. Finally, identification of further disease-causing genes will create a better understanding of pathogenesis and may help to develop specific preventive and therapeutic strategies.
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PMID:Genetic aspects of chronic pancreatitis: insights into aetiopathogenesis and clinical implications. 1177 91

Carbohydrate-deficient transferrin (CDT) is a specific biomarker of alcohol abuse, and for diagnosis of chronic alcohol, abuse is often determined using isoelectric focusing (IEF) and chromatographic techniques. To allow this method to be used for the diagnosis of alcohol abuse, inferences of various physical and chemical factors with the detection of CDT have been investigated. However, few reports have focused thus far on whether different metal ions have different binding affinities to CDT and HTf variants or further interfere in the detection of CDT. Here, in order to figure out whether and how metal ions such as Pb(2+) and Cu(2+) bind to holo-human serum transferrin (holo-HTf) and further interfere in CDT detection, the binding characteristics and the binding parameters of holo-HTf with metal ions such as Pb(2+) and Cu(2+) were investigated using UV-visible spectroscopy, Fluorescence spectroscopy, and ICP-MS. Moreover, whether the metal ions such as Pb(2+) and Cu(2+) will reduce the diagnostic accuracy of CDT in clinic was investigated using IEF. The present study demonstrates that Pb(2+) and Cu(2+) have different binding affinities to holo-HTf variants and produce different changes in the relative amounts of each glycosylation isoforms of HTf. Accordingly, the glycosylation chains of HTf will affect the binding affinities of glycosylation isoforms with Pb(2+) and Cu(2+), causing further interferences in CDT detection.
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PMID:Different binding affinities of Pb2+ and Cu2+ to glycosylation variants of human serum transferrin interfere with the detection of carbohydrate-deficient transferrin. 2179 95