Although hypercalcemia is a frequent event during the course of many malignancies it has only rarely been described with patients with chronic lymphocytic leukemia. Review of the literature revealed only eleven such case reports. The mechanism of the hypercalcemia in these patients was generally unclear although one patient was found to have a parathyroid adenoma and in another patient tested the level of osteoclast activating factor was high. Two additional chronic lymphocytic leukemia patients with hypercalcemia are described in this report and in each a parathyroid adenoma was found. The patient in whom the diagnosis was made ante mortem had an excellent response to parathyroidectomy. Osteoclast activating factor level was measured in one patient and found to be within normal limits. Since three of the thirteen reported cases of chronic lymphocytic leukemia with hypercalcemia have demonstrated parathyroid adenomas, it is suggested that consideration be given to that possibility in such patients so that appropriate surgery may be done.
CommentAlthough the explanation for the arrhythmias cannot be defined with certainty, several possibilities exist. Cardiopulmonary arrest with subse¬ quent idioventricular rhythm and ventricular tachycardia has been de¬ scribed in the spectrum of nonanaphylactic reactions to penicillin G procaine.1 In the present case, howev¬ er, the symptoms of the nonanaphylactic reactions described previously were not present; moreover, there was no evidence that the drug was given intravenously. The nurse administer¬ ing the drug had aspirated in the usual manner, with no evidence of entry into a venous channel. The absence of neurological and behavio¬ ral changes argues against the in vivo release of toxic quantities of procaine that have been reported following intramuscular injection." However, a toxic reaction to procaine cannot entirely be ruled out.Although skin testing to procaine was negative and there were no signs of anaphylaxis, the possibility of procaine or a derivative acting as a hapten, which resulted in a hypersen¬ sitivity reaction, cannot be excluded. A third explanation for the ventricu¬ lar irritability might be a hypersensi¬ tivity reaction to the penicillin alone, although clinically there was no evidence of true anaphylaxis. A final possibility is a cardiotoxic or hyper¬ sensitivity reaction from the penicil¬ lin G procaine molecule itself, which is pharmacologically distinct from either procaine or penicillin.5Regardless of the cause, the neces¬ sity for skin testing patients with any adverse reaction temporally related to penicillin G procaine administra¬ tion is underscored by the present case. Bell5 reported several cases of patients who were thought to have had adverse reactions to the procaine portion of penicillin G procaine. When these patients were given peni¬ cillin without procaine, both anaphy¬ laxis and death occurred. One cannot exclude true penicillin hypersensitivi¬ ty clinically manifested by or coexist¬ ing with a nonanaphylactic reaction to penicillin G procaine.In contrast with Galpin et al,1 we would not administer penicillin to patients who previously had any adverse reaction to penicillin G pro¬ caine. The positive skin tests to both major and minor penicillin determi¬ nants have precluded the subsequent administration of penicillin to this patient. We also recommend that any subjective complaints or objective findings following penicillin use be assessed and evaluated by proper skin testing.
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