Trifluoperazine (Stelazine)
Research
Chekhonin VP, Kabanov AV, Zhirkov YA, Morozov GV: FATTY ACID ACYLATED FAB-FRAGMENTS OF ANTIBODIES TO NEUROSPECIFIC PROTEINS AS CARRIERS FOR NEUROLEPTIC TARGETED DELIVERY IN BRAIN. FEBS Letters 1991; 287(1-2):149-52.
Summary:
A method for targeted delivery of neuroleptics from blood in brain based on using Fab-fragments of antibodies to antigens of brain glia cells (acid gliofibrillar antigen and alpha 2-glycoprotein) is suggested. The essence of the technique is that the molecule of neuroleptic (trifluoperazine) is conjugated with Fab-fragments of these antibodies. The conjugate thus obtained is modified by stearoylchloride in the system of Aerosol OT reversed micelles in octane. The study of the distribution of 125I-labelled conjugates in the rat organism after intracordial introduction is performed. On the contrary to the nonmodified conjugates and conjugate, containing fatty acylated Fab-fragments of antibodies, nonspecific to the rat brain, the conjugate of trifluoperazine with stearoylated Fab-fragments of antibodies to neurospecific antigens accumulate in brain tissues. The drastic increase of the neuroleptic activity of trifluoperazine resulting from its coupling with stearoylated Fab-fragments of antiglial antibodies is observed.
Turk J, Lask B: PISA SYNDROME IN AN ADOLESCENT ON NEUROLEPTIC MEDICATION. British Journal of Psychiatry 1991; 158:422-3.
Summary:
To our knowledge Pisa syndrome in childhood or adolescence has not previously been described. The syndrome developed in an adolescent girl following administration of neuroleptic medication for psychotic features, and was transiently thought to be abnormal illness behaviour. This case emphasises the need for early diagnosis and rapid effective treatment.
Balzan M, Cacciottolo JM: NEUROLEPTIC MALIGNANT SYNDROME PRESENTING AS HYPEROSMOLAR NON-KETOTIC DIABETIC COMA. British Journal of Psychiatry 1992; 161:257-8.
Summary:
A 50-year-old man presented with hyperosmolar non-ketotic diabetic coma associated with the neuroleptic malignant syndrome (NMS) after intramuscular treatment with haloperidol. It is suggested that NMS may occur as a complication of uncontrolled diabetes mellitus with dehydration. Conversely, NMS might precipitate diabetic coma in patients with previously well controlled blood glucose.
Woodbury MM, Woodbury MA: NEUROLEPTIC-INDUCED CATATONIA AS A STAGE IN THE PROGRESSION TOWARD NEUROLEPTIC MALIGNANT SYNDROME. [REVIEW]. Journal of the American Academy of Child & Adolescent Psychiatry 1992; 31(6):1161-4.
Summary:
Neuroleptic-induced catatonia is reported in an adolescent patient who responded successfully to lorazepam. The authors propose five discrete stages toward the progression of neuroleptic malignant syndrome, each with a separate treatment. [References: 28]
Budd GT, Bukowski RM, Lichtin A, Bauer L, Van Kirk P, Ganapathi R: PHASE II TRIAL OF DOXORUBICIN AND TRIFLUOPERAZINE IN METASTATIC BREAST CANCER. Investigational New Drugs 1993; 11(1):75-9.
Summary:
Pre-clinical and clinical studies have shown that trifluoperazine (TFP) can modulate multidrug resistance. We have performed a Phase II trial of TFP and doxorubicin in doxorubicin-naive patients with metastatic breast cancer. We hypothesized that TFP would inhibit the development of doxorubicin resistance, resulting in an increased rate of complete response or a prolongation in response duration. Twenty patients with metastatic breast cancer were treated every 3 weeks with TFP 5 mg by mouth every 6 hours on days 0-5 and doxorubicin 60 mg/m2/96 hr on days 1-4 by continuous intravenous infusion. The first 5 patients were treated with TFP 15 mg by mouth every 6 hours, but the dose was reduced to 5 mg every 6 hours when grade 3-4 extrapyramidal toxicity was noted in 3 of the first 5 patients. Thereafter, neurologic toxicity was grade 0-2. No complete and 9 partial responses were produced in 20 patients (45%). The median response duration was 17 weeks (range 7-112). The combination of trifluoperazine and doxorubicin did not seem to produce a response rate or duration markedly different than that expected for doxorubicin alone in patients with metastatic breast cancer. Alternative trial designs may be necessary in future clinical trials investigating the inhibition of acquisition of drug resistance.
Buckley C, Thomas V, Lewin J, Harris D, Rustin MH: STELAZINE-INDUCED PIGMENTATION. Clinical & Experimental Dermatology 1994; 19(2):149-51.
Summary:
A case of a West Indian patient is reported who developed abnormal blue-grey pigmentation on exposed areas of skin following treatment with low dose stelazine. Oculocutaneous melanosis is a well-recognized side-effect of prolonged phenothiazine treatment. In this condition the areas of skin exposed to sunlight develop a violaceous, blue-grey or slate-grey colour in more severe cases. These characteristic changes are rarely seen now. We describe the case of a patient who developed pigmentation while taking a low dose of stelazine for 5 years.