An Attempted Suicide with Copper Sulphate injected intravenously:Pathopsysiology and Therapy about a case report

Acute copper sulphate poisoning is an unusual event, rarely following parenteral exposure, complicated by toxicological effects as haemolytic anaemia, methaemoglobinaemia , hepato-renal damage and acute rhabdomyolysis. Currently, the therapeutic management ignores unique classes of evidence and is mainly based on supportive and chelation therapies. Case details. This case report describes acute copper sulphate poisoning in a 37-year-old man who attempted suicide by self-injecting an unknown amount of copper sulphate. Within three days the patient developed severe intravascular haemolysis and rhabdomyolysis. Initial therapy relied on intensive supportive care with fluids administration, electrolyte correction and packed red blood cells transfusion. The D-penicillamine (30 mg/Kg/day per os) was prescribed as chelation therapy by the poison control centre. The N-acetilcysteine and ascorbic acid were administered to prevent further oxidative stress. Later on, two sessions of therapeutic plasma exchange were performed in order to support the drug therapy. Haemolysis and rhabdomyolysis reversed throughout the hospital stay. Discussion. In this case the antidotic and antioxidant therapy resulted effective to reverse haemolysis and rhabdomyolysis and to prevent hepatic and renal damage. Moreover, this case underlies that therapeutic plasma exchange should be considered as an additive measure to undertake since the earlier stages of the emergency intervention. Acute copper sulphate poisoning is an event complicated by toxicological effects: haemolytic anaemia, methaemoglobinaemia, hepato-renal damage, acute rhabdomyolysis. The therapeutic management ignores unique classes of evidence and is based on supportive and chelation therapies. In this case: i) the antidotic and antioxidant therapy resulted effective to reverse haemolysis and rhabdomyolysis and to prevent hepatic and renal damage, ii) therapeutic plasma exchange should be considered as an additive measure to undertake

Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD4OL (Spearman's rank correlation coefficient [r(s)], -0.33; P < 0.001), sNox2-dp (r(s), -0.57; P < 0.0001), and urinary excretion of isoprostanes (r(s), -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2 alpha-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Adefovir dipivoxil is a nucleotide analog reverse transcriptase inhibitor used to treat adult patients affected by HBeAg-positive and HBeAg-negative chronic hepatitis B and with clinical evidence of lamivudine-resistant hepatitis B virus (HBV). Adefovir administered at a dosage of 10 mg/day is generally well tolerated, even if renal toxicity, type Fanconi syndrome, was reported during long-term treatments. We report a case of osteomalacia with Fanconi syndrome and pathologic fracture of the femur related to long-time (67 months) adefovir treatment (10 mg/day) in a patient with compensated hepatitis B virus (HBV) cirrhosis (Child 5A) and with a previous normal renal function (estimated Glomerular Filtration Rate before adefovir = 78.26 ml/min/1.73 m2; during adefovir treatment = 57.38 ml/min/1.73 m2). The patient was switched to entecavir at a dose of 1 mg/day, with both suppression of viremia and improvement of osteomalacia and Fanconi syndrome; the patient’s follow-up is still ongoing after 22 months

Adefovir dipivoxil-induced development of osteomalacia and Fanconi syndrome during the treatment of hepatitis B virus (HBV)-related cirrhosis

Adefovir dipivoxil is a nucleotide analog reverse transcriptase inhibitor used to treat adult patients affected by HBeAg-positive and HBeAg-negative chronic hepatitis B and with clinical evidence of lamivudine-resistant hepatitis B virus (HBV). Adefovir administered at a dosage of 10 mg/day is generally well tolerated, even if renal toxicity, type Fanconi syndrome, was reported during long-term treatments. We report a case of osteomalacia with Fanconi syndrome and pathologic fracture of the femur related to long-time (67 months) adefovir treatment (10 mg/day) in a patient with compensated hepatitis B virus (HBV) cirrhosis (Child 5A) and with a previous normal renal function (estimated Glomerular Filtration Rate before adefovir = 78.26 ml/min/1.73 m2; during adefovir treatment = 57.38 ml/min/1.73 m2). The patient was switched to entecavir at a dose of 1 mg/day, with both suppression of viremia and improvement of osteomalacia and Fanconi syndrome; the patient’s follow-up is still ongoing after 22 months

Muscular damage during telbivudine treatment in a chronic hepatitis B patient

Muscle tissue damage might be related to metabolic and mechanical factors. Certain drugs have been associated with increased blood levels of creatin phospho kinase (CPK) and myoglobin that are biochemical markers of musculoskeletal damage. An increase of CPK plasma levels might suggest severe rhabdomyolysis with possible resulting renal failure. Telbivudine is an antiviral drug indicated for the treatment of chronic hepatitis B (CHB) in adult patients. An increase in CPK plasma levels has been recently described in some telbivudine-treated CHB patients without muscle-skeletal symptoms. In this paper we report a CHB patient that developed a severe increase of CPK plasma levels during telbivudine-treatment. Pharmacological evaluation, using the Naranjo probability scale, indicated a probable relationship between telbivudine and CPK increase, so telbivudine was discontinued and replaced with entecavir with a complete resolution of laboratory findings. In conclusion, telbivudine treatment can induce muscular damage in the absence of skeletal injury, therefore we suggest to closely monitor the muscular function of the patients treated with this drug in order to prevent possible major complications

Attempted suicide with intravenous copper sulphate: a case report

Acute Copper Sulphate Poisoning (ACuSP) usually results from oral ingestion with suicidal purpose, rarely from parenteral exposure: only few cases of parenteral ACuSP have been reported. Case report: a 37-year-old man was admitted at ED three hours after an attempted suicide by self-injecting intravenously an unknown amount of a copper sulfate solution. The patient had a history of heroin and cocaine abuse. At the admission, he was conscious, GCS 15, T 36.5°C, RR 18 breaths/min, SpO2 96% on room air, BP 105/75 mmHg, HR 120 beats/min. He presented tremors and diffuse myalgia. Biochemical tests were normal. One day later, serum copper levels reached 263 μ/dL (normal range 70-140 μ/dL). On day 3, he was oriented and febrile (T 38°C). Physical examination revealed pallor, jaundice, brown to red urines, signs of extravasation by the antecubital area of both arms. He was complaining epigastric pain. Laboratory findings showed normochromic normocytic anaemia (Hb 7.40 g/dL) with signs of intravascular haemolysis, methaemoglobin 6.3% and rhabdomyolysis. The patient received fluids therapy, electrolyte correction, and 4 units of RBC transfusion. N-acetilcysteine (150 mg/Kg over 120 minutes + 300 mg/Kg/day) and D-penicillamine (30 mg/Kg/day per os) were started. Piperacillin/tazobactam and clindamycin were administered for peri-injection cellullitis. As critical condition was persisting, Therapeutic Plasma Exchange (TPE) was performed on day 5 and 6. On day 7 he was transferred to the ICU, then to the surgery unit for wounds toilet. On day 12 he was moved to the psychiatric unit, on day 13 D-penicillamine was discontinued due to increasing liver function tests. On day 32 he was discharged asymptomatic with normal laboratory values. ACuSP is uncommon and insidious. Clinical picture is mainly characterized by massive haemolysis associated with slight extracellular methaemoglobin. The management is symptomatic and supportive. Chelation therapy is safe and effective. Haemodialysis is indicated only in case of persistent renal failure. The TPE should be considered as an addictive measure

Erratum to: Portal vein thrombosis relevance on liver cirrhosis: Italian Venous Thrombotic Events Registry (Intern Emerg Med, 10.1007/s11739-016-1416-8)

In the original publication, the second author name was incorrectly published as Roberto Gino Corazza. The correct name should read as \u201cGino Roberto Corazza\u201d. Also, the PRO-LIVER Study Collaborator, Dr. Gabriella Carnevale Maff\ue8 has not been included in the Appendix by mistake. The name of Dr. Carnevale Maffe` should read in the Appendix as follows: Bergamaschi Gaetano, Carnevale Maff\ue8 Gabriella, Masotti Michela, Costanzo Filippo (I\ub0 Clinica Medica, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy)

Incidence and Recurrence of Portal Vein Thrombosis in Cirrhotic Patients

Cirrhosis has been long considered a risk factor for bleeding due to the co-existence of the so-called \u2018coagulopathy\u2019. More recently, however, compelling evidences have been provided on the occurrence of thrombotic events in the portal and systemic circulation.3\u20135 Portal vein thrombosis (PVT) is predominantly observed in patients with moderate to severe liver failure with a variable prevalence ranging from 0.6 to 25%. Only fewstudies have provided a longitudinal assessment of the PVT incidence and its sequelae, including recurrence and survival.9\u201314 Due to the variability of PVT incidence and the paucity of data regarding recurrence and survival,15\u201320 we prospectively analysed the incidence and the recurrence of PVT in the population of Portal vein thrombosis Relevance On Liver cirrhosis: ItalianVenous thromboticEventsRegistry (PROLIVER), a multi-centre study,8 which involved 43 enrolling centres in Italy (ClinicalTrials.gov Identifier: NCT01470547)

Platelet Count Does Not Predict Bleeding in Cirrhotic Patients: Results from the PRO-LIVER Study.

OBJECTIVES: Thrombocytopenia is a hallmark for patients with cirrhosis and it is perceived as a risk factor for bleeding events. However, the relationship between platelet count and bleeding is still unclear. METHODS: We investigated the relationship between platelet count and major or clinical relevant nonmajor bleedings during a follow-up of ∼4 years. RESULTS: A total of 280 cirrhotic patients with different degrees of liver disease (67% males; age 64±37 years; 47% Child-Pugh B and C) were followed up for a median of 1,129 (interquartile range: 800-1,498) days yielding 953.12 patient-year of observation. The annual rate of any significant bleeding was 5.45%/year (3.57%/year and 1.89%/year for major and minor bleeding, respectively). Fifty-two (18.6%) patients experienced a major (n=34) or minor (n=18) bleeding event, predominantly from gastrointestinal origin. Platelet counts progressively decreased with the worsening of liver disease and were similar in patients with or without major or minor bleeding: a platelet count ≤50 × 103/μl was detected in 3 (6%) patients with and in 20 (9%) patients without any bleeding event. Conversely, prothrombin time-international normalized ratio was slightly higher in patients with overall or major bleeding. On Cox proportional hazard analysis, only a previous gastrointestinal bleeding (hazard ratio (HR): 1.96; 95% confidence interval: 1.11-3.47; P=0.020) and encephalopathy (HR: 2.05; 95% confidence interval: 1.16-3.62; P=0.013) independently predicted overall bleeding events. CONCLUSIONS: Platelet count does not predict unprovoked major or minor bleeding in cirrhotic patients