This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent.
Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs.
This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome.
Here is a case i have seen
28 year old man, hypertensive since 6 months, non diabetic, non alcoholic, non smoker, unmarried, constructor worker from Nalgonda who was apparently alright, busy working daily at construction sites one day an year back developed high grade fever along with body pains for which he was taken to a RMP and he was given ' tablets for fever ' as the attendant describes it, which got subsided temporarily. By night he again developed fever for which he was taken to Nalgonda Hospital and was admitted for a few days and was discharged.
Since then he was on regular NSAID use for fever and body pains.
After 4 months he again developed fever and he was taken to NIMS where they performed a Renal biopsy and told them his kidneys got affected because of overuse of painkillers.
Biopsy report
2 months later he developed Dyspnea at rest, reduced urine output, non productive cough, he developed even pedal edema which slowly crawled up to his abdomen cause its distension along with facial puffiness. Upon examination they were told that he had hypertension and was started on antihypertensives and that he needed hemodialysis.
During his stay in the hospital a pleural tap was done and his sputum cultures were sent too. They were negative for tuberculosis.
On examination, pallor is present
flat nails are present
Jvp raised
PR - 92 bpm, regular
Bp - 150/8
Afebrile
chest wall retraction are present with a respiratory rate of 20 cpm
Abdomen is distended and umbilicus is everted
Inspiratory crackles present in Bilateral iAA, ISA
Apex beat present in 6th intercostal space
ECG shows
sinus tachycardia and Left ventricular hypertrophy
During his hospital stay, his blood pressure has always been on the higher end and he has been going into Pulmonary edema on and off for which he been put on the following medications :
7am - T Nicardia 20mg
Arkamine 0.1mg
Met XL 50mg
Lasix 80mg
Spironolactone 25mg
At 1:30 - 2pmish
T Arkamine 0.1mg
Nicardia 20mg
6pm
T Lasix 80mg
8pm
T Arkamine 0.1mg
Met XL 50
Lasix 80mg
Spironolactone 25mg
Nicardia 20mg
He has also been started on emperical ATT even though his sputum turned out to be negative because of the long standing history of fever, cough and around 10 kgs of weight loss in 7 months.
After initiating ATT, his blood pressure couldn't be under control.
On reviewing this literature as suggested by one of my senior PGs,a decision was made to put Rifampicin on hold
Link to the article :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015508/
24 patients enrolled had controlled hypertension (BP ≤140/90 mmHg) with stable anti-HT drug requirement for ≥4 weeks before recruitment. All patients were receiving regular thrice-weekly MHD. Patients were excluded if they were receiving concomitant drugs which could influence CYP450 metabolism; had a current history of smoking or alcohol abuse; were inadequately dialyzed; had fluid overload, or were poorly compliant to treatment.
A Single-center, prospective observational cohort study conducted at a tertiary care hospital in India between September 2012 and December 2013.
Serum levels of amlodipine besylate, metoprolol succinate, and prazosin hydrochloride were measured using high-performance liquid chromatography (HPLC) technique. Blood samples for estimation were drawn at baseline (day 0) and days 3, 7, 10, and 14 days after starting rifampicin.
All 24 patients in the study had worsening of hypertension after rifampicin and 83.3% required increase in drugs to maintain BP <140/90 mmHg. Serial amlodipine levels were estimated in 16 patients; metoprolol and prazosin in four patients each. Drug levels declined by >50% in all patients and became undetectable in 50-75%. Drug requirement increased from 4.5 ± 3.6 to 8.5 ± 6.4 units (P < 0.0001). Mean time to first increase in dose was 6.5 ± 3.6 days. Eleven (46%) patients experienced a hypertensive crisis at 9.1 ± 3.8 days. Three of them had a hypertensive emergency with acute pulmonary edema. In two patients, rifampicin had to be discontinued to achieve BP control. In conclusion, rifampicin caused a significant decrease in blood levels of commonly used anti hypertensives. This decrease in levels correlated well with worsening of hypertension.
Rifampicin, a first-line antitubercular drug, exhibits pharmacokinetic interactions with numerous drugs. It is a potent inducer of cytochrome P450 (CYP)
