(BMJ)—A 51-yo man had a painful nodule on his R medial calf x4 days. He’d had varicose veins bilaterally on the lower limbs for >4y. No trauma hx or other sx. Exam: tender, red-purple ~2x2-cm nodule with surrounding rash. U/S confirmed the dx. What is it?
Superficial venous thrombosis
Abscess with cellulitis
Angiokeratoma
Deep vein thrombosis
Hematoma
You are correct. U/S showed engorged superficial veins with echogenic substances and absence of color Doppler flow, consistent with superficial vein thrombosis (SVT). SVT is usually benign and self-limited. Systemic anticoagulation is preferred in SVT with nonvaricose trunk involvement, thereby reducing thromboembolic complications such as DVT/PE.

U/S findings of cellulitis include increased echogenicity and edema with cobblestone appearance of the SC tissue. Hematoma, however, can be acute to chronic in duration, and the echotexture will vary from hyperechoic to hypoechoic.

The patient underwent Diotech varicose vein closure of the R great saphenous vein and ligation of the communicating vein. He was asymptomatic at follow-up 1mo later.

Emergency Medicine Journal 2023;40:47-60
(BMJ)—A man in his 60s had blurred vision and bilateral eye redness x3y. Slit-lamp exam: bilateral peripheral dense corneal deposits with snowflake-like needle-shaped crystals extending centrally. Labs: calcium WNL, elevated uric acid. What’s the cause?
Streptococcus viridans infection
Multiple myeloma
Uric acid crystal deposition
Schnyder crystalline corneal dystrophy
Cystinosis
You are correct. Corneal deposits of uric acid crystals are a manifestation of hyperuricemia. This patient had corneal transplantation, and his visual acuity improved.

BMJ 2022;379:e071402
(epocrates)—A 63-yo female w/ HTN, hyperlipidemia, CHF, afib, and peripheral vascular dz initially presented w/ general malaise, an episode of weakness at home, knee pain, and stinging skin pain in her arms and legs, w/ AST 351 units/L and ALT 131 units/L. Atorvastatin was discontinued, and 4 days later, the pt presented w/ dark urine, generalized weakness, increased muscle and skin pain throughout her body, and creatine kinase (CK) 58,349 units/L (>50x the upper limit of normal). She was diagnosed w/ rhabdomyolysis and hospitalized for tx.

Meds: atorvastatin, carvedilol, digoxin, furosemide, spironolactone, rivaroxaban, and sacubitril/valsartan.

Which drug combo most likely caused the rhabdomyolysis?
digoxin and atorvastatin
furosemide and atorvastatin
carvedilol and sacubitril/valsartan
atorvastatin and sacubitril/valsartan
You are correct. Rhabdomyolysis has been reported in pts receiving atorvastatin and sacubitril/valsartan. Sacubitril (an OATP1B1 and OATP1B3 inhibitor) inhibits the uptake of atorvastatin (an OATP1B1 and OATP1B3 substrate) into the liver, leading to increased systemic atorvastatin exposure; therefore, coadministration w/ sacubitril requires monitoring of CK and myopathy sx, due to the increased risk of adverse effects.

More info on Entresto is available in epocrates.

Sources:

1. Faber ES, Gavini M, Ramirez R, Sadovsky R. Rhabdomyolysis After Coadministration of Atorvastatin and Sacubitril/Valsartan (Entresto™) in a 63-Year-Old Woman. Drug Saf Case Rep 2016;3(1):14. Free, full-text article in PubMed® Central

2. Entresto [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2019. Entresto package insert at DailyMed
(PubMed)—A 57-yo man w/ HIV and COPD presented w/ recurrent rib fractures, centripetal adiposity, and abdominal and inguinal striae. Dx: Cushing syndrome. Meds include ritonavir-containing HAART regimen, aspirin, clopidogrel, fluticasone/salmeterol, niacin, omeprazole, and pravastatin.

Which drug combo could have caused Cushing syndrome?
fluticasone and clopidogrel
clopidogrel and ritonavir
fluticasone and ritonavir
You are correct. Cushing syndrome and adrenal suppression have been reported in pts receiving ritonavir and inhaled or intranasal fluticasone. Ritonavir (a strong CYP3A4 inhibitor) inhibits the metabolism of fluticasone (a CPY3A4 substrate), leading to increased systemic exposure; therefore, coadministration w/ ritonavir is not recommended because of the increased risk of adverse effects.

More info is available, including the free full-text SpringerPlus article PDF at PubMed Central.

Source article: Epperla N, McKiernan F. Iatrogenic Cushing syndrome and adrenal insufficiency during concomitant therapy with ritonavir and fluticasone. SpringerPlus. 2015;4(1):455. doi: 10.1186/s40064-015-1218-x.
(Epilepsy Behav Case Rep)—A 44-yo man w/ hx of Marfan syndrome, mechanical mitral valve replacement, and tx-resistant epilepsy presented for an INR check 4wk after starting a new medication for intractable seizures. His INR had increased from 2.2 (before the new agent was added) to 6.7, leading the primary care physician to adjust the warfarin dosage to maintain an INR w/in a therapeutic range of 2 to 3.

Current meds: warfarin, cannabidiol, lamotrigine, levetiracetam.

Which drug was most likely to have resulted in the increased INR?
lamotrigine
cannabidiol
levetiracetam
You are correct. Cannabidiol (predicted to cause clinically significant interactions w/ CYP1A2, CYP2C8, and CYP2C9 substrates) may inhibit the metabolism of warfarin (a CYP1A2, CYP2C8, and CYP2C9 substrate), leading to increased systemic exposure. Monitor INR in pts taking warfarin w/ cannabidiol because of the increased risk of adverse effects, including bleeding.

More info is available in the free, full-text Epilepsy Behav Case Rep article PDF at PubMed Central.

Source article: Grayson L, Vines B, Nichol K, Szaflarski JP; for the UAB CBD Program. An interaction between warfarin and cannabidiol, a case report. Epilepsy Behav Case Rep. 2018;9:10-11.
(Ment Health Clin)—A 58-year-old White female with a BMI of 33.6 kg/m2 and hx of recurrent major depression, generalized anxiety disorder, restless leg movements, onychomycosis, and alcohol use disorder presented with intensification of severe depression, intolerable anxiety, and restlessness. A commercial pharmacogenetic testing platform classified the patient as a normal metabolizer for CYP3A4 and CYP2D6. Her serum trough aripiprazole level was 207.5 ng/mL, which is 18% higher than the guideline-based dose-related reference concentration.

Meds: albuterol inhaler prn, aripiprazole, aspirin, cholecalciferol, ferrous sulfate, fluticasone/umeclidinium/vilanterol, lisinopril, lorazepam prn, metoprolol, pantoprazole, and terbinafine.

Which drug combo could have caused the elevated aripiprazole levels and akathisia?
aripiprazole and pantoprazole
aripiprazole and lorazepam
aripiprazole and terbinafine
aripiprazole and lisinopril
You are correct. Terbinafine, a strong CYP2D6 inhibitor, may inhibit the metabolism of aripiprazole, resulting in increased aripiprazole levels and risk of adverse effects in this CYP2D6 normal-metabolizer patient. Adjust aripiprazole dosage in patients taking concomitant CYP3A4 or CYP2D6 inhibitors or in patients who are poor CYP2D6 metabolizers. Of note, both aripiprazole and terbinafine have long elimination half-lives; thus, tx-emergent adverse events from aripiprazole may not present immediately.

More info is available in the free, full-text Ment Health Clin article PDF at PubMed Central.

Source article: McGrane IR, Lindbloom TJ, Munjal RC. Possible inhibitory effects of terbinafine on aripiprazole metabolism: Two case reports. Ment Health Clin. 2021 Sep 24;11(5):297-300. doi: 10.9740/mhc.2021.09.297