Comparison of the Effectiveness of Mindfulness-based Stress Reduction Therapy and Emotion Regulation Training on the Distress Tolerance of Adolescent Girls with a Drug-Dependent Parent

Background: The undesirable conditions resulting from addiction can be mitigated with timely diagnosis and effective interventions. Distress tolerance can be promoted in adolescents with a drug-dependent parent. Objectives: The present study aimed to investigate the effectiveness of mindfulness-based stress reduction (MBSR) therapy and emotion regulation training (ERT) on the distress tolerance of adolescent girls with a drug-dependent parent in Ahvaz, Iran. Methods: This clinical trial was performed on the experimental and control groups as the pretest-posttest design with follow-up. The statistical population included all the adolescent girl students with a drug-dependent parent in Ahvaz. The sample consisted of 45 adolescents with a drug-dependent parent selected by cluster sampling. The participants were randomly divided into two experimental groups of MBSR (eight 60-min sessions) and ERT (eight 45-min sessions) and a control group (n = 15 per group). All three groups were followed up after 45 days. The research instrument was the Distress Tolerance Scale (DTS), and data were analyzed using the analysis of covariance. Results: MBSR and ERT enhanced distress tolerance in adolescent girls with a drug-dependent parent (P < 0.001). The effects of the two interventions were not significantly different, and this result persisted in the follow-up stage. Conclusions: MBSR and ERT increased distress tolerance in adolescent girls with a drug-dependent parent. Therefore, these two interventions can be administered to enhance the mental health of adolescents.

Case Report: First Case of Cefotaxime-Sulbactam-Induced Acute Intravascular Hemolysis in a Newborn With ABO Blood Type Incompatibility by the Mechanism of Non-Immunologic Protein Adsorption

BackgroundABO blood type incompatibility hemolytic disease of newborn (ABO-HDN) and drug-induced immune hemolytic anemia (DIIHA) due to non-immunologic protein adsorption (NIPA) mainly cause extravascular hemolysis. All the reported severe DIIHA were caused by drug-induced antibodies, and rare report of acute intravascular hemolysis was caused by the NIPA mechanism or ABO-HDN.Case presentationWe report the first case of acute intravascular hemolysis induced by cefotaxime sodium - sulbactam sodium (CTX - SBT) in a case of ABO-HDN which resulted in death at 55 h after birth. The mother’s blood type was O and RhD-positive, and the newborn’s blood type was B and RhD-positive. No irregular red blood cell (RBC) antibodies or drug-dependent antibodies related to CTX or SBT was detected in the mother’s plasma and the plasma or the RBC acid eluent of the newborn. Before the newborn received CTX - SBT treatment, the result of direct antiglobulin test (DAT) was negative while anti-B was positive (2 +) in both plasma and acid eluent. After the newborn received CTX - SBT treatment, the results of DAT for anti-IgG and anti-C3d were both positive, while anti-B was not detected in plasma, but stronger anti-B (3 +) was detected in acid eluent. In vitro experiments confirmed that NIPA of SBT promoted the specific binding of maternal-derived IgG anti-B to B antigen on RBCs of the newborn, thereby inducing acute intravascular hemolysis.ConclusionThe NIPA effect of SBT promoted the specific binding of mother-derived IgG anti-B in newborn’s plasma to the newborn’s RBC B antigens and formed an immune complex, and then activated complement, which led to acute intravascular hemolysis. Drugs such as SBT with NIPA effect should not be used for newborns with HDN.

Carfilzomib-induced thrombotic microangiopathy. A case report

Introduction Drug-induced thrombotic microangiopathy (DITMA) is an acquired condition resulting from exposure to a drug that induces the formation of platelet-rich thrombi in small arterioles or capillaries secondary to drug-dependent antibodies or direct tissue toxicity. Carfilzomib is a selective proteasome inhibitor approved to treat selected patients with Multiple Myeloma (MM). It is one of the drugs with the strongest evidence for a causal association with non-antibody-mediated DITMA. Case Report A 75-year-old man presented to the emergency department for the outbreak of vomit, asthenia, oliguria and dark stool emission. He was recently diagnosed with multiple myeloma, treated with lenalidomide, dexamethasone and carfilzomib. Laboratory exams were significant for microangiopathic haemolytic anaemia, thrombocytopenia and new-onset renal failure. ADAMTS-13 levels were in range, and no infectious signs were found both in blood nor in stool test. Management & Outcome A carfilzomib induced thrombotic microangiopathy was soon suspected. Thus, since daily haemodialysis and supportive care did not seem to get a fast enough recovery, the patient was treated with eculizumab with a good general outcome. Discussion Drug-induced thrombotic microangiopathy is a rare and often life-threatening acquired condition whose diagnosis can be challenging and whose therapy is not always limited to supportive treatment and drug avoidance. Carfilzomib, along with other proteasome inhibitors, is one of the described potential drugs which can trigger such a manifestation.

Drug Abuse Patterns of Combined Amphetamine-Type Stimulants and Opioid Dependence in Malay Male Subjects in Kota Bharu, Kelantan, Malaysia

The objective of this study was to examine the socio-demographic characteristics and drug abused patterns of combined amphetamine-type stimulants (ATS) and opioid dependence in Malay Male subjects in Kota Bharu, Kelantan, Malaysia. Seventy drug dependent subjects who were diagnosed using Diagnostic and Statistical Manual-IV (DSM-IV), and 87 control subjects who fulfilled the inclusion and exclusion criteria were interviewed using a questionnaire.The median age (IQR) for drug dependent group was 28.0 (7.68) years old while median age for control group was 24.0 (10.55). The mean (SD) initiation age for ATS was 27.39 (9.79) while the mean (SD) initiation age for opioid was 22.20 (7.19). 57.1% of the drug dependent subjects used injections as their method of opioid ingestion, while 65.7% preferred chase to ingest ATS. Most of the subjects were HIV negative (61.4%). Majority have not sought any treatment regarding their drug usage (71.4%). Most of the drug dependent subjects have been arrested and convicted for drug use (88.6%). However, majority demonstrated no history of arrest or conviction for non-drug related crime (77.1%). This study provides an update on the socio-demographic and drug abuse patterns of combined amphetamine-type stimulants and opioid dependence subjects that may help in combating the alarming increase of the drug abuse.

Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3

Acute myeloid leukemia (AML) with mutations in the FMS-like tyrosine kinase (FLT3) is a clinically unresolved problem. AML cells frequently have a dysregulated expression and activity of epigenetic modulators of the histone deacetylase (HDAC) family. Therefore, we tested whether a combined inhibition of mutant FLT3 and class I HDACs is effective against AML cells. Low nanomolar doses of the FLT3 inhibitor (FLT3i) AC220 and an inhibition of class I HDACs with nanomolar concentrations of FK228 or micromolar doses of the HDAC3 specific agent RGFP966 synergistically induce apoptosis of AML cells that carry hyperactive FLT3 with an internal tandem duplication (FLT3-ITD). This does not occur in leukemic cells with wild-type FLT3 and without FLT3, suggesting a preferential toxicity of this combination against cells with mutant FLT3. Moreover, nanomolar doses of the new FLT3i marbotinib combine favorably with FK228 against leukemic cells with FLT3-ITD. The combinatorial treatments potentiated their suppressive effects on the tyrosine phosphorylation and stability of FLT3-ITD and its downstream signaling to the kinases ERK1/ERK2 and the inducible transcription factor STAT5. The beneficial pro-apoptotic effects of FLT3i and HDACi against leukemic cells with mutant FLT3 are associated with dose- and drug-dependent alterations of cell cycle distribution and DNA damage. This is linked to a modulation of the tumor-suppressive transcription factor p53 and its target cyclin-dependent kinase inhibitor p21. While HDACi induce p21, AC220 suppresses the expression of p53 and p21. Furthermore, we show that both FLT3-ITD and class I HDAC activity promote the expression of the checkpoint kinases CHK1 and WEE1, thymidylate synthase, and the DNA repair protein RAD51 in leukemic cells. A genetic depletion of HDAC3 attenuates the expression of such proteins. Thus, class I HDACs and hyperactive FLT3 appear to be valid targets in AML cells with mutant FLT3.

Piperacillin–Tazobactam-Induced Immune Thrombocytopenia: A Case Report

Drug-induced immune thrombocytopenia is an isolated thrombocytopenia caused by accelerated platelet destruction from drug-dependent, platelet-reactive antibodies. Heparin-induced thrombocytopenia is the most common drug-induced immune thrombocytopenia. Common implicated antibiotics for drug-induced immune thrombocytopenia include ceftriaxone, trimethoprim–sulfamethoxazole, vancomycin, and penicillin. The platelet nadir can be less than 20 × 10 (9)/L and typically occurs within 1 to 2 weeks of exposure to the inciting drug. Although rare, drug-induced immune thrombocytopenia can be fatal. Diagnosis is made by excluding other causes of thrombocytopenia. Laboratory testing for drug-dependent antiplatelet antibodies is often helpful but not required. Thrombocytopenia typically improves within 1 to 2 days of drug discontinuation and platelet count returns to normal within a week. Identifying and discontinuing the implicated medication is key to prevention of serious complications. A patient case of drug-induced immune thrombocytopenia is described after initiation of empiric piperacillin–tazobactam for refractory right foot cellulitis in the setting of right fourth toe diabetic ulcer.

A CLINICO-COMPARATIVE STUDY ON THE EFFECT OF LASHUNA SIDDHA TAILPANA POORVAK VAMANA KARMA AND NITYA VIRECHANA BY GOMUTRA HARITAKI IN THE MANAGEMENT OF HYPOTHYROIDISM

Hypothyroidism is a condition in which thyroid gland doesn’t produce enough thyroid hormone. This is more prevalent among women. Management through levothyroxine is safe & may bring the value of Thyroid stimulating hormone and thyroxine to normal range but the increased dosage and continuous medication are cost expensive and make the patient into drug dependent till the end of mortal life. So, better, therapy is needed for the society through the heritage of Ayurveda especially with Shodhana therapy. Aim of Clinico-comparative study was to evaluate and compare the efficacy of Lashuna siddha Tailpana Poorvak Vamana Karma and Nityavirechana by Gomutra Haritaki in the management of Hypothyroidism. Study was conducted at Govt. Akhandanada Ayurvedic hospital, Ahmedabad, Gujarat. This study was Open labelled parallel randomized control trial. 15 patients were treated with Lashuna siddha Tailpana Poorvak Vamana Karma in group A. 15 patients was treated with Nitya Virechana by Gomutra Haritaki in group B. Washout period was 14 days. Triiodothyronine and thyroxine were compared at the end of treatment by paired t-test and Mann Whitney-U test. Lashuna siddha Tailpana Poorvak Vamana Karma was more beneficial than Nitya Virechana by Gomutra Haritaki. Insignificant difference was found on subjective and objective parameters (Weight gain, Basal metabolic rate, Serum triiodothyronine) but significance difference found on objective parameters (Thyroid stimulating hormone, Serum thyroxine).

Severe vancomycin-induced thrombocytopenia in a patient with meningitis

Vancomycin is a widely used antibiotic and rarely can cause drug-induced thrombocytopenia. A patient with hospital-acquired meningitis after neurosurgery was treated with systemic and intrathecal vancomycin. On 9th day of antibiotic treatment, the patient’s platelets dropped to 0.68×109/L. Multiple platelet transfusions had minimal influence on platelet count. After cessation of vancomycin therapy, platelets returned to normal values without any additional interventions. Diagnosis of vancomycin-induced thrombocytopenia was confirmed by detection of drug-dependent antiplatelet IgG antibodies.