Patients who are receiving multiple medications must be screened for significant drug interactions. The specific mechanism of a drug interaction determines whether the patient may experience a subtherapeutic effect or a potentially toxic reaction. Three cases of relative warfarin resistance, possibly related to high-dose nafcillin, are described in this report. Several reports have suggested that penicillinase-resistant penicillins, such as nafcillin and dicloxacillin, exert an important enzyme-inducing effect in patients receiving warfarin. This potential interaction must be appropriately recognized and managed in order to maintain adequate anticoagulation in this patient population.

Decreased chloride, potassium, and sodium with ticarcillin disodium-c1avulanate potassium TO THE EDITOR: Hypokalemia is a reported side effect of ticarcillin disodium-c1avulanate potassium (Te). 1-3 To date there have not been any reports of TC causing other electrolyte imbalances; however, I wish to report two cases where TC may have been implicated in decreased serum potassium, chloride, and sodium levels.Patient I isa 75-year-old femaleadmitted withchills,fever, cough, and shortness of breath. A chest X-ray confirmed the diagnosis of pneumonia. Past medical historyis significant for left mastectomy, hypothyroidism(not severe), and hypertension. The patient was receivingatenolol 50 mg bid prior to and duringadmission.TC was initiated on admission at 3.1 g iv q6h. Serum potassium,chloride, and sodium levelson admission were 3.9,89, and 124mEq/L, respectively. Electrolytesweredrawn on day 7 ofTC therapy and werefound to havedropped to 3.3, 71, and 113 mEq/L, respectively, and TC was discontinued at this time. The patient receivedpotassiumchloride supplementationand electrolytes returned to the normal range.Patient 2 is a 60-year-old male admitted with a chief complaint of right leg pain. Admission diagnosis was possible right femoral artery stenosis. The patient was started on TC 3.1 g iv q6h on admission for cellulitis. His past medical historyis significantfor chronic obstructive pulmonary disease,peptic ulcer disease, peripheral vascular disease, and cerebrovascular accident. Admission medications were prednisone 10 mg/d, potassium chloride 8 mEq tid, transdermalnitroglycerin5 mg/d, ranitidine 150mg bid, clonidine0.1 mg bid, and furosemide 80 mg/d. Admission serum electrolytes for potassium, chloride, and sodium were as follows: 3.1, 94, and 137mEq/L, respectively. The potassiumchloride was discontinuedon hospital day 2. Electrolyteswere rechecked on day 3 and the serum potassium, chloride, and sodium had droppedto 2.4,80, and 127mEq/L, respectively. Values wereverifiedby repeat testing.TC wasdiscontinuedat this timeand the patient wassupplementedwith potassiumchloride 80mEq/d ivon days 3 and 4. The patient also received four dosesof potassiumchloride 20mEq po on day 5. Four daysafter the discontinuation of TC his electrolyteswere4.1 mEq/L (potassium), 101 mEq/L (chloride),and 140mEq/L (sodium).It should be noted that neither of the patients had diarrhea or vomiting as a cause of electrolyte loss. Although patient 2 was receiving furosemide, which can inhibit sodium reabsorption, potassium supplementation was also a part of the medication regimen. The hypokalemia associated with penicillin therapy appears to be related to the fact that penicillins act as nonabsorbable anions in the distal renal tubules and thus promote urinary loss of potassium. The report of hyponatremia is of particular interest since one might expect to see hypernatremia with TC due to ticarcillin's disodium salt. Other causes of hyponatremia, such as salt-wasting nephropathy, nephrotic syndrome, congestive heart failure, and dilutional hyp...

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