Session

Pharmaceutical and Natural Sciences

Description

Excessive drug use causes Medication-overuse headache (MOH) which can be manifested with 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 an 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), who 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, Nonsteroidal antiinflammatory drugs

Proceedings Editor

Edmond Hajrizi

ISBN

978-9951-550-47-5

First Page

1

Last Page

10

Location

UBT Kampus, Lipjan

Start Date

30-10-2021 12:00 AM

End Date

30-10-2021 12:00 AM

DOI

10.33107/ubt-ic.2021.95

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Oct 30th, 12:00 AM Oct 30th, 12:00 AM

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

UBT Kampus, Lipjan

Excessive drug use causes Medication-overuse headache (MOH) which can be manifested with 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 an 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), who 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.