Evaluation a renal function of patients with Medication-overuse headache (MOH)

Excessive drug use causes Medication-overuse headache (MOH) which can be manifested of chronic daily headaches, occurring monthly 15 or more days, when the medicament is used redundantly for more than three months. Recent studies concerning the epidemiology of drug-induced disorders suggest that increased risk of nephrotoxicity appears in a group of patients who abuse NSAIDs. The aim is to confirm the early phase of nephrotoxicity in patients with (MOH),were treated with NSAIDs in combination with other drugs (analgesics, triptans and antidepressants) and compared patients treated only with Diclofenac, Piroxicam, Ketoprofen, Paracetamol, Ibuprofen and Celecoxib, Besides conventional markers of renal functioning (serum/urine creatinine determined by Jaffe methods, enzymatic assay for urea serum). Imunoturbodimetric assay for determination of urinary albumin, microalbuminuria and β2-microglobulin will be used. Significant glomerular and tubular damage has been reported, and patients on combination therapy with NSAIDs and other drugs (analgesics, triptans, and antidepressants) have seen more glomerular changes than patients treated with NSAID monotherapy. Keywords: Medication-overuse headache, Nephrotoxicity, Nonsteroidalantiinflammatory drugs

Migraine and the effects of NSAIDS on renal function

Trigeminovascular system (TGV) activation is a basic mechanism for generating pain during a migraine attack. Many experimental results highlight the importance of the cyclooxygenase system in the peripheral arm of TGV and suggest that NSAIDs may be effective in migraine therapy through the action of these peripheral nociceptors. Inhibition of NSAID-mediated prostaglandin synthesis prevents neurogenically mediated inflammation of the trigeminal system and reduces pain, but at the same time inhibition of prostaglandin in the kidney may reduce renal blood flow,speed glomerular filtration retention. and water. The purpose of the study is to follow the renal function, in patients with cefaleamigraine that has been treated for a long period, treated with Diclofenac and Paracetamol.We used Jaffe’s method for the determination of serum/urine creatinine and еnzymatic assays for urea and uric acid in serum and ᵧ glutamyl transferase (ᵧ-GT) in serum and jon selective electrode (ISE) are used for determination of electrolite in serum. We used nephelometry by β2 microglobulin (β2M) and photoelectric colorimetry for microalbuminuria in urine, to monitor glomerular and tubular functioning. Any history of kidney diseases was exclusion criteria to enter the study. In chronic treatment of patients with headache with Diclofenac and Paracetamol in symptomatic headaches, they have been confirmed as renoprotective in their use. Keywords: non-steroidal anti-inflammatory drugs, migraine, renal function, trigeminovascular syste

medication-overuse headache (MOH)

Migraine is a common headache disorder that causes significant disabilities. Headache developed or significantly worsened during medication overuse (for simple analgesics and combination acute medications, intake must be 15 days or more per month for triptans, ergotamines, opioids, and combination analgesics; 10 days per month sufficient to get a diagnosis of Medication-overuse headache-MOH). A recent epidemiologic study on drug-induced disorders demonstrated that excessive drug use can lead to nephrotoxicity. Microalbuminuria was common in patients under the influence of nephrotoxic drugs. Subclinical renal damage cannot be identified by routine tests (serum creatinine), and microalbuminuria is a more sensitive indicator of renal dysfunction. The aim is to confirm the sensitivity of certain biomarkers when comparing patients treated with NSAIDs in combination with other drugs (analgesics, triptans and antidepressants) with patients treated with monotherapy by NSAIDs Besides conventional markers of renal functioning (serum/urine creatinine determined by Jaffe methods), enzymatic assay for urea serum and Jon selective electrode (ISE) are used fordetermination of electrolite in serum. Imunoturbodimetric assay for determination of urinary albumin, microalbuminuria and β2- microglobulin will be used. In the case of combination therapy (analgesics, triptans and antidepressants) a significant effect on the increase of microalbuminuria has been demonstrated. Keywords: Medication-overuse headache, Nephrotoxicity, Microalbuminuria

Comparison of the sensitivity of several biomarkers in patients with medication overuse headache (MOH)

Migraine is a common headache disorder that causes significant disabilities. Headache developed or significantly worsened during medication overuse (for simple analgesics and combination acute medications, intake must be 15 days or more per month for triptans, ergotamines, opioids, and combination analgesics; 10 days per month sufficient to get a diagnosis of Medication-overuse headache-MOH). A recent epidemiologic study on drug-induced disorders demonstrated that excessive drug use can lead to nephrotoxicity. Microalbuminuria was common in patients under the influence of nephrotoxic drugs. Subclinical renal damage cannot be identified by routine tests (serum creatinine), and microalbuminuria is a more sensitive indicator of renal dysfunction. The aim is to confirm the sensitivity of certain biomarkers when comparing patients treated with NSAIDs in combination with other drugs (analgesics, triptans and antidepressants) with patients treated with monotherapy by NSAIDs Besides conventional markers of renal functioning (serum/urine creatinine determined by Jaffe methods), enzymatic assay for urea serum and Jon selective electrode (ISE) are used for determination of electrolyte in serum. Imunoturbodimetric assay for determination of urinary albumin, microalbuminuria and β2-microglobulin will be used. In the case of combined therapy with NSAIDs and other medications (analgesics, triptans and antidepressants), a significant effect on the increase of microalbuminuria has been demonstrated, which signals us for a more sensitive indicator in compared to β2M which as specific bioindicator did not show a measured sensitivity for the detection of early changes in the tubular level. Significant glomerular damage has been reported in patients with combination therapy than patients treated with NSAID monotherapy. Following the levels of specific biomarkers, we can use them as signals for early detection of nephrotoxicity, especially in patients treated with combination therapy requiring special attention when administering them

Comparison of the adverse renal effects of Ketoprofen and Piroxicam in patients with headaches

Migraine is a common headache disorder that causes significant disability. Ketoprofen is one of the world's most widely-prescribed NSAIDs for treatment of headaches. Piroxicam is another NSAID that was approved in the last several years, with different mechanisms of action on cyclooxygenase inhibition. Theoretically, this approach can lead to various adverse effects on the kidneys. Relatively, little is known about comparative nephrotoxicity of NSAIDs. Therefore, the present study was designed to compare the adverse renal effects, of Ketoprofen and Piroxicam in patients with headaches. We used venous urine and blood from cephalic-migraine in 10 patients treated with Ketoprofen with a total dose of up to 100 mg per day, and 10 with Piroxicam 20 mg after 12 months of therapy, patients in comparison with the control group of examinees. Besides conventional markers of renal function (serum/urine creatinin determined by Jaffe methods enzymatic assay for urea in serum), we used nephelometry by β2 Microgloglobulin (β2 M) and photoelectric colorimetry for microalbuminuria in urine, to monitor glomerular and tubular functioning. Any history of kidney disease was exclusion criteria to enter the study. The standard metrics to follow the progression of AKI, like serum creatinine and blood urea levels, are inconvenient and depend on kidney injury. That’s why we must use specific markers for early detection. Following the levels of specific biomarkers in urine we can use them as signals for early detection of nephrotoxicity, we can recommend constant monitoring of renal functions during use of different groups of NSAIDs and be careful while using analgesic -anti-inflammatory drugs. Keywords: adverse renal effects, non-steroidal anti-inflammatory drugs, migrain

Comparison of the adverse renal effects of different types of NSAID based on COX inhibition in patients with headaches

Migraine is a common headache disorder that causes significant disabilities. Non-selective COX inhibitors (Piroxicam, Ketoprofen and Ibuprofen) are most widely-prescribed NSAIDs treatment of headaches. Celecoxib is another NSAID therapy that has been approved in the last several years, with different mechanisms of action. The purpose of the study is to follow the renal function and comparisons of nephrotoxicity of different types of NSAID based on COX inhibition, in patients with cefalea-migraine that has been treated for a long period. Besides conventional markers of renal function (serum/urine creatinin determined by Jaffe's methods of enzymatic assay for urea in serum), we used nephelometry by β2 Microglobulin (β2 M) and photoelectric colorimetry for microalbuminuria in urine, to monitor glomerular and tubular functioning. Any history of kidney diseases was an exclusion criteria to enter the study. The results show that the greatest deviations are observed in β2 microglobulin in terms of its increase in all patients treated with Piroxicam and Ketoprofen, in 91.7% patients treated with Ibuprofen, and in 50% of patients treated with Celecoxib. The most frequent decrease was shown in creatinine values in urine, in 50% of patients of Piroxicam-treated group, 66.7% of the group treated with Ketoprofen and Ibuprofen, and 75% of the patients treated with Celecoxib. Following the levels of specific biomarkers in urine we can recommend constant monitoring of renal functions during usage of different groups of NSAIDs and be careful while using analgesic -anti-inflammatory drugs