Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomized, placebo-controlled, double-blind, crossover study in 40 lumbar spinal stenosis patients with a 1-year follow-up showed that calcitonin had beneficial effects on the patients' symptoms without producing any notable side effects. Calcitonin had a clear analgesic effect. The mean of walking distance increased, but the crossover trend was not as good as the analgesic effect. Side effects such as erythema and nausea were usually mild and transient. Calcitonin therapy can be used as a conservative treatment in selected cases of lumbar spinal stenosis. When rest pain was mild or the walking distance was under 200-300 m because of neurogenic claudication, the effect of calcitonin seemed to be poor.
 ...
PMID:Calcitonin treatment in lumbar spinal stenosis: a randomized, placebo-controlled, double-blind, cross-over study with one-year follow-up. 159 76

The reports of the effect of calcitonin on pituitary function are confusing and often refer to uncontrolled studies. We have now carried out a double-blind placebo-controlled trial of intravenous and subcutaneous salmon calcitonin on anterior pituitary function in 17 healthy volunteers. Visual analogue scores for the nausea and vomiting seen after salmon calcitonin correlated with the rise in ACTH and, secondarily, cortisol. Calcitonin had no effect on growth hormone, prolactin, thyrotrophin, luteinizing hormone or follicle stimulating hormone. It is concluded that the stimulation of ACTH secretion following a single dose of salmon calcitonin is probably the result of the stress of nausea rather than a direct effect on the pituitary.
 ...
PMID:The effects on anterior pituitary hormone secretion of salmon calcitonin in healthy volunteers. 165 86

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
 ...
PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

Synthetic human calcitonin was used in the treatment of 26 patients over a period of 1-14 months. 17 patients had Paget's disease of the bone, 6 postmenopausal osteoporosis and 3 Sudeck's syndrome. Subjective improvement (reduction of pain, improvement of mobility) was found in 15 patients with Paget's disease, in 4 females with postmenopausal osteoporosis and in all 3 patients with Sudeck's syndrome. Radiographic improvement of bone changes developed only very slowly. These results were confirmed by diminution of the exchangeable calcium pool indicating reduction of rates of osseous degradation. Calcitonin tolerance was acceptable. Transitory nausea and occasional vomiting occurred in 3 patients.
 ...
PMID:[Synthetic human calcitonin in Paget's disease of bone and osteoporosis (author's transl)]. 616 31

Hypercalcemia is a common, life-threatening metabolic disorder that can be associated with cancer. Its pathophysiology includes enhanced osteoclastic bone resorption and decreased renal excretion of extracellular calcium. Symptoms of hypercalcemia include nausea, vomiting, bone pain, polyuria, renal insufficiency, bradycardia, and arrhythmia. The goals of medical therapy are to inhibit bone resorption and promote renal calcium excretion. Hydration is the first step in management. Treatments for hypercalcemia include phosphates, calcitonin, bisphosphonates, and gallium nitrate. Although intravenous phosphates prevent intestinal calcium absorption and inhibit mineral and bone matrix resorption, serious adverse events include renal failure, hypotension, extraskeletal calcification, and severe hypocalcemia. Calcitonin has a rapid onset of action and can lower serum calcium concentrations within hours, but its usefulness is limited by its short duration of effect and the development of tachyphylaxis. Bisphosphonates are effective inhibitors of bone resorption but appear to have decreased response rates in hypercalcemic patients with high levels of parathyroid-related protein. Gallium nitrate, an antitumor agent noncytotoxic to osteoclasts and bone cells, appears to be more effective than pamidronate, etidronate, and calcitonin in the treatment of cancer-related hypercalcemia. Importantly, unlike bisphosphonates, gallium nitrate is effective in both parathyroid-related protein-mediated and non-parathyroid-related protein-mediated hypercalcemia.
 ...
PMID:Treatment of cancer-related hypercalcemia: the role of gallium nitrate. 1277 55

Severe hypercalcemia is a life-threatening medical emergency. It is most commonly caused by malignant tumors, but can also be caused by primary hyperparathyroidism or less often by a dysregulated production of active vitamin D in granulomatous disorders. Symptoms include nausea, vomiting, renal insufficiency, severe dehydration, lethargy, confusion, and even coma. Severity of symptoms, calcium concentrations, and the overall status of the patient are important considerations in selecting appropriate therapy. Hydration to correct volume depletion is the cornerstone of acute therapy. Loop diuretics may be added to saline hydration after extracellular fluid volume has been replenished to enhance urinary calcium excretion and mitigate fluid overload from rehydration. Calcitonin and intravenous infusion of bisphosphonates reduce serum calcium levels by interfering with calcium release from the skeleton. Dialysis with a low or zero calcium dialysate is reserved for patients who are refractory to these measures. Corticosteroids are effective with hypercalcemia due to increased vitamin D levels and in multiple myeloma.
 ...
PMID:[Hypercalcemic crisis]. 1468 84

We have previously shown that nitric oxide (NO) and cyclic guanosine monophosphate (GMP) may cause headache and migraine. However, not all findings in previous studies can be explained by an activation of the NO-cGMP pathway. Calcitonin gene-related peptide (CGRP) causes headache and migraine in migraine patients, but CGRP receptor activation causes an increase in cyclic adenosine monophosphate (cAMP). In order to investigate the role of cAMP in vascular headache pathogenesis, we studied the effect of cilostazol, an inhibitor of cAMP degradation, in our human experimental headache model. Twelve healthy volunteers were included in a double-blind, randomized, crossover study. Placebo or cilostazol (200 mg p.o.) was administered on two separate study days. Headache was scored on a verbal rating scale (0-10) and mechanical pain thresholds were measured with von Frey hairs. The median peak headache score 0-16 h postdose was 0 (range 0-2) after placebo and 3.5 (range 0-7) after cilostazol (P = 0.003). The median headache curve peaked at 6-9 h postdose. The headaches induced were usually bilateral and pulsating. Nausea occurred in two volunteers, photo- and phonophobia were not seen. Two volunteers had a headache that fulfilled International Headache Society criteria for migraine without aura after cilostazol. No change in mechanical pain thresholds in the forehead was seen (P = 0.25). The headache after cilostazol was equal to or more severe than headache induced by glyceryl trinitrate in previous experiments. The present study thus indicates that increased levels of cAMP may play a role in headache and migraine pathogenesis.
 ...
PMID:The headache-inducing effect of cilostazol in human volunteers. 1705 37

A migraine is a disabling neurovascular disorder characterized by a unilateral throbbing headache that lasts from 4 to 72 h. The headache is often accompanied by nausea, vomiting, phonophobia and photophobia, and may be worsened by physical exercise. The trigeminovascular system (TVS) is speculated to have an important role in migraines, although the pathophysiology of this disorder remains to be elucidated. Trigeminal ganglion (TG) and spinal trigeminal nucleus caudalis (TNC) are important components of the TVS. Several clinical cases have provided evidence for the involvement of the brainstem in migraine initiation. Electrical stimulation of the trigeminal ganglion (ESTG) in rats can activate TVS during a migraine attack. Calcitonin gene-related peptide (CGRP) is an important vasoactive compound produced following TVS activation. Numerous studies have revealed that adenosine and its receptors have an important role in pain transmission and regulation process. However, only a few studies have examined whether adenosine A2a receptor (A2aR) and adenosine A1 receptor (A1R) are involved in migraine and nociceptive pathways. In the present study, CGRP, A2aR and A1R expression levels were detected in the TG and TNC of ESTG models through reverse transcription-quantitative polymerase chain reaction and western blot analysis. Tianshu capsule (TSC), a type of Chinese medicine, was also used in the ESTG rat models to examine its influence on the three proteins. Results demonstrated that CGRP, A2aR and A1R mediated pain transmission and the regulation process during migraine and the expression of the three proteins was regulated by TSC.
 ...
PMID:Expression of calcitonin gene-related peptide, adenosine A2a receptor and adenosine A1 receptor in experiment rat migraine models. 2699 80

<P>Background and Objective: Migraine is a neurovascular syndrome associated with unilateral, throbbing headache accompanied with nausea, vomiting and photo/phonophobia. Several proteins are involved in the etiopathogenesis of migraine headache. The aim of the present review is to give an insight into the various target proteins involved in migraine headache pertaining to the development of a potential anti-migraine drug molecule. Proteins/receptors such as serotonin (5-HT), Calcitonin Gene Related Peptide (CGRP), Transient Receptor Potential Vanilloid (TRPV1), cannabinoid, glutamate, opioid and histamine receptors play various roles in migraine. The nature of the proteins, their types, binding partner membrane proteins and the consequences of the reactions produced have been discussed. The studies conducted on animals and humans with the above mentioned target proteins/receptors and the results obtained have also been reviewed. <P> Conclusion: Calcitonin Gene Related Peptide (CGRP), a G protein coupled receptor (GPCR) significantly contributed to the progression of migraine. CGRP antagonist inhibits the release of CGRP from trigeminal neurons of trigeminal ganglion. Based on the study results, the present review suggests that the inhibition of CGRP receptor might be a successful way to treat migraine headache. Currently, researchers across the world are focussing their attention towards the development of novel molecules to treat migraine headache by targeting CGRP receptor which can be attributed to its specificity among the several proteins involved in migraine.</P>.
 ...
PMID:A Review on the Potential Receptors of Migraine with a Special Emphasis on Cgrp to Develop an Ideal Antimigraine Drug. 3283 28

Migraine is a common and debilitating neurological disorder characterized by recurrent attacks of moderate to severe throbbing headache accompanied by nausea, vomiting and photophobia/phonophobia. Because of its high prevalence, migraine causes a considerable financial burden on the society as well as impaired quality of life in individual patients. Scientific evidence shows that migraine is a quite complex neurological disorder that involves not only the trigeminovascular and autonomic systems but also the hypothalamus and cerebral cortex. Calcitonin gene-related peptide (CGRP) was originally discovered as a 37-amino acid neuropeptide derived from a calcitonin gene splicing variant. CGRP is found to be expressed in trigeminal ganglion neurons. Much attention has been attracted to this molecule since CGRP was found to be released from trigeminal terminals in animal migraine models. Subsequent studies demonstrated that CGRP administration induced migraine-like headache attacks specifically in migraineurs, thus highlighting a pivotal role of CGRP in the development of migraine attacks. Several CGRP receptor antagonists were shown to be efficacious for the treatment of acute migraine. Among them, telcagepant, was shown to exert a significant migraine prophylactic action as well. Nevertheless, the development of most of these agents were discontinued due to hepatotoxicity. Currently, newer CGRP receptor antagonists are being developed. On the other hand, monoclonal antibodies targeting CGRP and its receptor showed consistent efficacy for migraine prophylaxis with excellent safety profiles in Phase III clinical trials. Furthermore, emerging data support the long-term safety and efficacy of these antibodies. In this review article, the development and perspective of anti-migraine therapeutic strategies using CGRP-related antibodies are discussed.
 ...
PMID:[Novel migraine treatment with CGRP-related monoclonal antibodies]. 3289 46


1