How I treat pain in hematologic malignancies safely with opioid therapy.

The field of malignant hematology has experienced extraordinary advancements with survival rates doubling for many disorders. As a result, many life-threatening conditions have since evolved into chronic medical ailments. Paralleling these advancements have been increasing rates of complex hematologic pain syndromes, present in up to 60% of patients with malignancy who are receiving active treatment and up to 33% of patients during survivorship. Opioids remain the practice cornerstone to managing malignancy-associated pain. Prevention and management of opioid-related complications have received significant national attention over the past decade, and emerging data suggest that patients with cancer are at equal if not higher risk of opioid-related complications when compared with patients without malignancy. Numerous tools and procedural practice guides are available to help facilitate safe prescribing. The recent development of cancer-specific resources directing algorithmic use of validated pain screening tools, prescription drug monitoring programs, urine drug screens, opioid use disorder risk screening instruments, and controlled substance agreements have further strengthened the framework for safe prescribing. This article, which integrates federal and organizational guidelines with known risk factors for cancer patients, offers a case-based discussion for reviewing safe opioid prescribing practices in the hematology setting.

Cerebral infarct in a patient with a history of systemic arterial and venous thrombosis from essential thrombocythemia.

Although essential thrombocythemia (ET) may involve thrombotic complications, including arterial or venous thrombosis, there are no reports of major vascular complications, including both arterial and venous thrombosis, in a patient with ET. We report on a patient with a cerebral infarction affecting the right lateral thalamus and a stenotic lesion of the right posterior cerebral artery. This arterial thrombotic event may be related to ET, which was based on results of a bone marrow biopsy specimen. The patient had experienced previous events of thrombosis, splenic infarction with venous thrombosis, and myocardial infarction. The cause of recurrent ischemic events involving both arterial and venous systems may be sustained elevation of platelet counts. Previous thrombosis is an established risk factor for rethrombosis in patients with ET. Efficient cytoreductive therapy with an antiplatelet agent should be considered for the prevention of recurrent thrombosis.

High prevalence of hyperhomocysteinemia due to marginal deficiency of cobalamin or folate in chronic myeloproliferative disorders.

Hyperhomocysteinemia is an established risk factor for thrombosis. In patients with myeloproliferative disorders, thrombotic events are common. Our aim was to investigate whether the increased burden of proliferating cells present in these patients implies a risk of homocysteine (HCY) accumulation secondary to depletion of folate and/or cobalamin. Fifty patients (PV, 25; ET, 10; IMF, 15) and 163 healthy volunteers (HV) participated in the study. The prevalence of hyperhomocysteinemia was 56.0% in PV, 70.0% in ET, 60.0% in IMF, and 34.9% in HV. The mean P-homocysteine (P-HCY) was 13.88 +/- 4.24 micromol/L in PV, 12.78 +/- 3.70 in ET, 11.34 +/- 4.22 in IMF, and 9. 71 +/- 2.76 in HV. In PV and ET, but not in IMF, the mean P-HCY was significantly higher than in the HV group (P < 0.001, P = 0.028, and P = 0.163, respectively). Thirty-three percent of the patients with hyperhomocysteinemia displayed metabolic changes compatible with cobalamin deficiency (P-HCY and P-methylmalonic acid both elevated), while 67% were folate deficient (P-HCY elevated, P-methylmalonic acid normal). Supplementation therapy with the relevant vitamin was implemented in 11 vitamin-deficient patients and led to normalization of metabolite levels in all cases. No correlation between hyperhomocysteinemia and thrombosis was found. Our data indicate that patients with PV, ET, and IMF frequently develop hyperhomocysteinemia due to discrete depletion of cobalamin or folate. Vitamin therapy leads to normalization of P-HCY and should be considered, even though hyperhomocysteinemia does not seem to be of crucial importance for the thrombotic tendency in the myeloproliferative disorders.

[Clinical experience of urological surgery of the patients with hemostatic disorder or hemolytic disease].

This report deals with clinical experience of urologic surgery of patients with hemostatic disorder or hemolytic disease. In the past 5 years from May 1986, 14 operations were conducted in our clinic on 13 patients, consisting of 4 with von Willebrand disease (vWd), 1 with hemophilia B, 4 who had warfarin administration, 3 with essential thrombocythemia and 2 with spherocytosis. Almost all patients were treated hematologically before the urological operations. Except in 1 case, the post-operative course was favorable and under hematologic control. Massive bleeding in 1 case was obviously attributable to over-dosage of warfarin. It is difficult to determine the optimal dose of warfarin under an unstable hemostatic condition during the operation and recovery periods. However, it is possible to carry out urologic surgery for these patients under appropriate hematologic control, and ESWL was safely performed without medical treatment on 3 patients; 1 with vWd, 1 treated with warfarin and 1 with spherocytosis.