Intravenous Heroin Abuse Research Articles

1993. Serratia is a rare cause for Infective Endocarditis of the Tricuspid Valve

Abstract Background Serratia marcescens is a Gram-negative motile bacillus that is a facultative anaerobe and non-lactose fermenting. Serratia can be isolated from water, soil, plants, and the intestinal microbiome. Serratia produces a unique Identifying reddish pigment called prodigiosin. Serratia is responsible for only 0.14% of infective endocarditis cases, with a mortality rate of 85%. Methods A 37 YO female with a history of Intravenous heroin abuse was admitted with fevers and dyspnea. Vital signs were BP 76/50, HR 140, RR 26, temp 102 F, and SpO2 98% on room air. She was toxic-appearing. Labs: WBC 26000(4,000 – 11,000 /uL) with 14% bands, Hb 5.6 (12.6 – 17.0 g/dL), PLT 15*10^3(150-372*10^3/uL), creatinine 2.5 (0.50 - 1.60 mg/dL), lactic acid 15.8 (0.5-2.2 mmol/L). We started vancomycin, piperacillin-tazobactam, and norepinephrine for septic shock. A transthoracic echo showed a large mass on the tricuspid valve, and a transesophageal echo depicted it as vegetation. Blood cultures grew Serratia. She underwent excision of anterior and posterior tricuspid valve leaflets with reconstruction and ring annuloplasty. She reported washing her syringes with tab water and reusing them again. Serratia has a predilection for left-side heart valves even in the IVDU population but this patient presented with a tricuspid valve endocarditis. Results Serratia is a rare cause for IE in the ICE study; out of 2.761 definite IE cases identified over five years, only forty-nine instances were due to gram-negative bacilli. Of those, only four cases were due to Serratia. The clinical presentation of Serratia includes constitutional symptoms, new-onset murmur, and cutaneous and neurologic manifestations. Serratia produces multiple pathogenic factors allowing Serratia to result in valvular destruction and perivalvular complications, and distant septic emboli metastasis. Conclusion Serratia is sensitive to third and fourth-generation cephalosporins, monobactams, carbapenems, fluoroquinolones, and aminoglycosides. Treatment is complex due to the production of AmpC B-lactamase, which hydrolyzes third and fourth-generation cephalosporins. The 2005 IDSA suggested a combination of B-lactam and an aminoglycoside for Serratia endocarditis, and these are not guidelines but merely recommendations. Disclosures All Authors: No reported disclosures.

A 54-year-old with dysarthria.

A 54-year-old male with a history of intravenous heroin abuse presented to the emergency department for dysarthria. The patient was initially found down with an unknown last known well time. The patient had a blood pressure of 237/101 mmHg. He was alert with a left-sided gaze preference and right-sided Romberg drift. Labs were remarkable for white blood cell count (WBC) 25.7 103/μl and creatine kinase (CK) 5776. Drug screen was positive for opiates. Computed tomography brain and angiography imaging showed bilateral cerebellar hemispheric ischemia, lateral ventricle dilatation, and a right proximal vertebral artery with non-occlusive diminutive distal flow (Figure 1). Several hours later, the patient subsequently experienced a rapid neurological decline from Glasgow Coma Scale (GCS) 11 (E4V2M5) to GCS7 (E2V1M4), prompting intubation for airway protection. Mannitol and 2% hypertonic saline were administered. External ventricular drain was prepared for potential deterioration. Subsequent magnetic resonance imaging showed stable, bilateral subacute cerebellar infarcts with hydrocephalus (Figure 2) and the patient was ultimately extubated and required prolonged rehabilitation. Bilateral ischemic cerebellar strokes are rare cerebrovascular accidents (CVAs).1 Large volume infarcts have a high risk of developing space-occupying brain edema in the compact posterior fossa—risk of rapid, life-threatening herniation through compression of the brain stem and the fourth ventricle with resultant hydrocephalus.2 Opiate abuse has been described as a rare cause of cerebral ischemia though mechanisms including vasospasm and severe hypoperfusion, rhabdomyolysis via muscle compression, and direct toxicity.3, 4 In our case, stable repeat imaging and an elevated CK suggested a subacute presentation and prompted holding off suboccipital craniectomy given the high likelihood of being outside of the acute edema window for effective surgical intervention.5 A positive drug screen with a known history of intravenous drug abuse point to a rare drug-associated ischemia as a potential etiology. Timing of pathology, repeat imaging and clinical assessment, and maintaining a wide differential, including drug-induced ischemia, in relatively young patients without typical CVA risk factors are essential in management of severe cerebellar strokes with unknown onset.

Paradoxical and Retrograde Air Embolism from Pressurized Peripheral Bolus

Introduction Cerebral air embolism is a rare, yet serious neurological occurrence with unclear incidence and prevalence. Here, we present a case of fatal cerebral arterial and venous cerebral gas embolism in a patient with infective endocarditis and known large right-to-left shunt and severe tricuspid regurgitation following pressurized fluid bolus administration. Case Presentation. A 32-year-old female was admitted to the medical intensive care unit from a long-term acute care facility with acute on chronic respiratory failure. Her medical history was significant for intravenous heroin and cocaine abuse, methicillin-sensitive Staphylococcus aureus tricuspid valve infective endocarditis on vancomycin, patent foramen ovale, septic pulmonary embolism with cavitation, tracheostomy with chronic ventilator dependence, multifocal cerebral infarction, hepatitis C, nephrolithiasis, anxiety, and depression. After intravenous fluid administration, she became unresponsive with roving gaze, sluggish pupils, and hypotensive requiring vasopressors. CT of the brain showed diffuse arterial and venous cerebral air embolism secondary to accidental air administration from fluid bolus. Magnetic resonance imaging of the brain showed diffuse global anoxic injury and flattening of the globe at the optic nerve insertion. Given poor prognosis, her family chose comfort measures and she died. Conclusions Fatal cerebral air embolism can occur through peripheral intravenous routes when the lines are inadequately primed and fluids administered with pressure. Caution must be exercised in patients with right-to-left shunting as air may gain access to systemic circulation.

OSTEOMYELITIS OF FEMUR IN A DRUG ADDICTED CHILD

One of the serious complications related to intravenous drug use is osteomyelitis. We report a 13-year-old male child with a history of intravenous heroin abuse, who was admitted to the hospital complaining of abdominal pain and pain in the left leg. Anteroposterior roentgenogram and CT scan of the left thigh and femur, confirmed the diagnosis of osteomyelitis. Pus culture was positive for Staphylococcus aureus. Despite extensive antibiotic and anticoagulant therapy, the patient’s clinical status improved very slowly. Surgical procedure was not undertaken. Femoral osteomyelitis due to injection drug use in childhood is an extremely rare and uncommon condition. Intravenous drug abuse, late-onset treatment, and secondary bacterial infection can lead to complications which occurred in the case presented. It is an extremely difficult condition to treat and is a real challenge for physicians. The rapid response and participation of a multidisciplinary team of physicians is of particular importance. Key words: antibiotics, children, femur, osteomyelitis, staphylococcus aureus.

PULMONARY CAVITARY LESION WITH RARE PSEUDOMONAS STUTZERI

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Pseudomonas stutzeri is a gram-negative rod bacterium infrequently associated with clinical infection. We present a case of pulmonary cavitary lesions caused by P.stutzeri. CASE PRESENTATION: A 59-year-old male with history significant for intravenous (IV) heroin abuse (last use 1 week prior), splenectomy and culture negative endocarditis (10 months prior) presented to the hospital with 1 week of chest pain, dyspnea and subjective fevers. Within a few hours of admission, a rapid response was called for altered mental status, chest pain and tachypnea. Computed tomography of the chest revealed a 12cm cavitary left lower lung lesion. He was placed on tuberculosis precautions and subsequently transferred to the Intensive Care Unit (ICU) for further management. Blood cultures were obtained prior to empiric vancomycin plus piperacillin/tazobactam. He required intubation for impending respiratory failure. Bronchoscopy with bronchoalveolar lavage (BAL) was performed demonstrating copious mucus and purulent secretions bilaterally. Approximately 36 hours into his admission, he suffered a PEA (pulseless electrical activity) arrest. Return of spontaneous circulation (ROSC) was achieved after 15 minutes of cardiopulmonary resuscitation (CPR). Physical exam revealed diffuse crepitus, subcutaneous emphysema tracking along posterior thorax extending into left lateral thigh and profound scrotal swelling. Arterial blood gas demonstrated acidemia with hypercarbia. Within less than an hour, he suffered a second PEA arrest. There was concern for ruptured pleural cavitary lesion leading to a tension pneumothorax. Needle decompression performed bilaterally was unsuccessful; surgery at bedside placed left hemithorax chest tube. Again, achieved ROSC after 18 minutes of CPR. Unfortunately, within a few minutes he decompensated into ventricular fibrillation. Further resuscitation efforts a third time were unsuccessful. Post-mortem blood cultures were negative but his BAL cultures were positive for pan-sensitive Pseudomonas stutzeri. All acid-fast bacilli smears and cultures were negative. DISCUSSION: Pseudomonas stutzeri has rarely been reported as a cause of necrotizing pneumonia (1) and may represent only 1% of all clinical Pseudomonas isolates (2). In our patient, the timeline of events, whether the cavitary lesion ruptured from the positive pressure of mechanical ventilation or as a consequence of CPR remains a mystery. CONCLUSIONS: There is debate in the literature regarding the pathogenicity of this organism which is frequently deemed to be colonization rather than pathogenic. However, in the case of this patient, all other infectious work up was negative and no alternative pathogen could be linked to the development of the cavitary lesions. This case emphasizes the necessity of diagnostic testing to identify uncommon pathogens. Reference #1: Lin KH et al, Pseudomonas stutzeri necrotizing pneumonia in pre-existing pulmonary tuberculosis. Intern Med. 2014;53(21):2543-6. 2014 Nov 1. Reference #2: Bisharat, N et al, 10-Years Hospital Experience in Pseudomonas stutzeri and Literature Review. The Open Infectious Diseases Journal, 2012, 6, 21-24. DOI: 10.2174/1874279301206010021 DISCLOSURES: No relevant relationships by Zachary Bugos, source=Web Response No relevant relationships by Brandon Smith, source=Web Response

Ophthalmic Artery Occlusion From Injection of Heroin Into the Forehead

Purpose: To report a case of ophthalmic artery occlusion after injection of heroin into the forehead. Methods: Retrospective case report. Results: A 27-year-old patient with a history of intravenous heroin abuse presented with a left ophthalmic artery occlusion after attempting to inject heroin into a vein in her forehead. Exam was significant for diffuse retinal edema, disc edema, disc hemorrhage, and diffuse retinal hemorrhages. Findings were also noted in the widefield image, optical coherence tomography, and optical coherence tomography angiography of the retina. Conclusions: This patient suffered from a severe form of talc retinopathy resulting in an ophthalmic artery occlusion after injecting heroin into her forehead. To our knowledge, this is the first instance of combined ophthalmic artery occlusion and talc retinopathy resulting from intentional injection into a superficial facial vein.

The Case Files

The Case Files

Basic principles unveil an unusual diagnosis

A 59 year-old man with medical history significant for current intravenous heroin abuse presented with status epilepticus. Cerebrospinal fluid (CSF) showed 317 neutrophils, 45 red blood cells, lactate 6.7 mm/L, protein 140 md/dl, and glucose 24 mg/dl. Glucose CSF/serum ratio was 0.14. Opening pressure was 23 cm of water. Cytology studies and HIV were negative. MRI was performed, illustrated in the figure. What is the most likely diagnosis?A.Streptococcus Meningitis.B.Herpes Simplex Viral Meningitis.C.Candida Meningitis.D.Carcinomatous Meningitis. No financial disclosure to report. Answer on page 221. Basic principles unveil an unusual diagnosisJournal of Clinical NeuroscienceVol. 42PreviewAnswer: C-Candida Meningitis. Full-Text PDF

Basic principles unveil an unusual diagnosis

Answer: C-Candida Meningitis. Severe hypoglycorrhachia occurs in the setting of subarachnoid hemorrhage, glucose transport defects, infectious meningitis, meningeal carcinomatosis, inflammatory, and autoimmune conditions. Candida’s morphology (small unicellular yeast) allows its spread through the blood–brain barrier into the subarachnoid space and meninges, unlike dimorphic and hyphae organisms. It may present with cerebral micro or macro-abscesses, meningitis, and vascular complications. Our patient’s MRI pattern of nodular pachymeningeal (gray arrow), and leptomeningeal (white arrow) enhancement, along with micro-abscesses (black arrow); and hypoglycorrhachia, and history of active intravenous heroin use suggested a yeast fungal infection [[1]Mathur M. Johnson C.E. Sze G. Fungal infections of the central nervous system.Neuroimag Clin North America. 2012; 22: 609-632Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar]. Specific antifungal therapy was added to the empirical antibiotic coverage initiated in the emergency room, with rapid clinical improvement. Subsequently, CSF smear identified Candida Albicans 12 h after admission. CSF cultures confirmed the diagnosis. An expedient identification of fungal central nervous system infections is critical to minimize their progression and control life-threatening complications (i.e. seizure, stroke, and hydrocephalus) [[2]Sanchez-Portocarrero J. Perez-Cecilia E. Corral O. et al.The central nervous system and infection by Candida species.Diagn Microbiol Infect Dis. 2000; 37: 169-179Abstract Full Text Full Text PDF PubMed Scopus (146) Google Scholar] (Fig. 1). No financial disclosure to report. Basic principles unveil an unusual diagnosisJournal of Clinical NeuroscienceVol. 42PreviewA 59 year-old man with medical history significant for current intravenous heroin abuse presented with status epilepticus. Cerebrospinal fluid (CSF) showed 317 neutrophils, 45 red blood cells, lactate 6.7 mm/L, protein 140 md/dl, and glucose 24 mg/dl. Glucose CSF/serum ratio was 0.14. Opening pressure was 23 cm of water. Cytology studies and HIV were negative. MRI was performed, illustrated in the figure. What is the most likely diagnosis? Full-Text PDF

Rhabdomyolysis: Heroin induced or HCV related

Abstract Rhabdomyolysis is defined as dissolution of skeletal muscle, manifested by the release of myocyte contents into the circulation. It is a well recognized complication of toxins, recreational drugs, and medications. We report a case of a 32 year old man, intravenous heroin abuser who took heroin 2 days before presentation. He presented with oliguria, tea colored urine and painful bilateral lower limb swelling. Evaluation revealed azotemia, dyselectrolytemia (hyperkalemia and hyponatremia), proteinuria and hematuria. Highly elevated serum lactate dehydrogenase and creatinine kinase led to the diagnosis of rhabdomyolysis and acute renal failure. The patient was managed with hydration and haemodialysis, following which he improved appreciably. Rhabdomyolysis in heroin addicts is caused by muscle ischemia, direct myotoxic effects of heroin, skeletal muscle vasoconstriction and immunologic reaction. The patient was also found to have concurrent hepatitis C virus infection (HCV). HCV is known to produce extrahepatic manifestations like myositis. Some studies have proved isolation of HCV RNA from perivascular infiltrative lymphocytes and skeletal muscle fibers, implying that HCV may decrease the threshold for muscle lysis. This case highlights the probable role of HCV in predisposing rhabdomyolysis in an illicit drug abuser, which has not been reported in Indian literature.

Intravenous Heroin Abuse and Acute Myocardial Infarction: Forensic Study.

The purpose of this study was to investigate chronic intravenous heroin abuse and its potential to induce acute myocardial infarction (AMI). It also aims to examine the causative factors and the incidence of heroin-induced myocardial infarction. The hearts of 113 intravenous heroin abusers were studied for a duration exceeding 3 years. The parameters studied included sex, age, time of intravenous heroin abuse, medical history, and body and heart weight. Macroscopic histological studies of the heart were also performed. The histological examination revealed only 1 case of AMI. The victim was an intravenous heroin abuser for the last 7 years. The age and the medical history of the victim do not act as dissuading factors for the potential of an AMI. The incidence of heroin-induced myocardial infarction is rare, and the actual mechanism remains unclear. The increased heart weight in relation to the increased thickness of the heart walls may be an aggravating factor, and thus, it is a fact that should be investigated.

Huge Recurrent Fungal (Candida parapsilosis) Aortic Prosthetic Valve Endocarditis in a Patient with Intravenous Drug Abuse

Prosthetic valve endocarditis (PVE) is a frequent complication of valve replacement surgery, accounting for 9.5-15% of all endocarditis cases. Fungi cause a small proportion of PVE and contribute to 4-6% of all etiology. Fungal PVE in drug addicts is a rare, but challenging and disastrous disease. We describe the case of a 49-year old patient with intravenous heroin abuse, Hepatitis C and HIV infection, suffering from extreme fungal aortic PVE caused by Candida parapsilosis five month after valve replacement due to endocarditis caused by Enterococcus faecalis. Predisposed patients under immunosuppression might benefit from aggressive endocarditis prophylaxis to avoid PVE.

ENDOGENOUS ENDOPHTHALMITIS ASSOCIATED WITH INTRAVENOUS DRUG ABUSE

To describe demographics, characteristics, and management of eyes with endogenous endophthalmitis (EE) in intravenous drug abusers. Retrospective chart review of patients with EE who presented to University Hospital, New Jersey Medical School between January 2005 and October 2012. Thirty-four patients presented with a clinical diagnosis of EE during this time period. Eighteen patients (53%) had a history of intravenous drug abuse with at least 15 of the 18 patients reporting intravenous heroin abuse. Average age was 43 years (24-61 years), 13 were men. Three patients had bilateral involvement. Mean time from the onset of symptoms to presentation was 10 days (range, 1-42 days). Presenting vision in the affected eye ranged from 20/100 to no light perception; the majority of patients had vision of counting fingers or worse. All patients were admitted to the hospital for intravenous antimicrobials and further workup. Final best-corrected visual acuity at the last follow-up ranged from 20/20 to no light perception, with most patients having final vision of 20/400 or worse. We reviewed 21 eyes of 18 patients with EE and concurrent intravenous drug abuse over an 8-year period; our study shows extremely poor visual prognosis associated with EE in this setting.

Retinal Neovascularization and Endogenous Fungal Endophthalmitis in Intravenous Drug Users

Intravenous heroin abuse in persons aged 12 or older has nearly doubled between the years of 2002 and 2012.1 Intravenous drug users (IVDU) are a high-risk group for developing endogenous fungal endophthalmitis (EFE), with Candida albicans being the most commonly identified causative organism.2 EFE is a potentially blinding disease in which the causative organism reaches the eye through hematogenous dissemination. The frequency of chorioretinitis and endophthalmitis in patients with documented fungemia ranges from 2–26% and 0–6%, respectively.3 Factors contributing to poor visual outcomes include macular involvement, subretinal and choroidal neovascularization, retinal detachment, and insufficient or delayed treatment.4,5 However, to our knowledge, this is the first case series characterizing retinal neovascularization as a potentially blinding complication of EFE in IVDU.

Polymicrobial Endocarditis in Intravenous Heroin and Fentanyl Abuse

Infective endocarditis is a life threatening condition with a high mortality rate. Intravenous Drug Abusers (IVDA) are more likely to acquire endocarditis. Most of the cases of infective endocarditis are caused by a single pathogen; cases of polymicrobial endocarditis are rare and they are associated with a reported mortality rate of more than 30%. Only 21 cases of N. sicca endocarditis have been described in the literature since 1918, and only 15 reported cases of endocarditis which involved Actinomyces species have been reported since 1939. We are reporting a case of a 49-year-old male with intravenous heroin and fentanyl abuse, who presented with infective endocarditis caused by Neisseria sicca/subflava(N. sicca), Actinomyces, Streptococcus mitis, and Haemophilus parainfluenzae, complicated by septic emboli to the lungs and skin, ARDS , splenic infarct and immunocomplex mediated proliferative glomerulonephritis.

Asymptomatic spleen rupture in patient with endocarditis

A 50-year-old Caucasian male presented to the emergency department with worsening abdominal pain more than 6 h associated with nausea and dizziness. The pain was dull in nature periumbilical with no radiation. He denied hematemesis, hematochezia, trauma, fever or change in urine/bowel habits. Past medical history was positive for diabetes, hypertension and intravenous (IV) heroin abuse. On arrival, he was lethargic and vital signs were remarkable for sinus tachycardia 122 per min, 61/40 mm Hg blood pressure and respiratory rate of 25 cycles per minute. Abdominal examination showed generalized tenderness more prominent in the left upper quadrant with no rebound. Apart from faint …

Duration dependent effect of intravenous heroin intake on morphological changes in the liver

Intravenous heroin intake leads to significant morphological changes in the liver tissue (vesicular changes, fatty changes, chronic hepatitis and cirrhosis). The intensity of these changes increases with the duration of heroin use. Direct hepatotoxic effects of heroin are vesicular changes in hepatocytes, fatty changes are the result of chronic influence of alcohol, whereas the rest of the morphological liver lesions are the result of the interaction of heroin, viral infection and alcohol. In the present study, we analyzed a total of 50 autopsies, 40 from the group of intravenous heroin users and 10 from the control group (dead bodies of young and healthy people with mechanical injuries that did not affect the liver). For ease of analysis, all autopsy cases of intravenous heroin abuse were divided into 4 groups according to the duration of intravenous heroin intake: up to 2 years, between 2 and 5 years, between 5 and 10 years, and longer than 10 years.

The reduction of glycogen in the liver induced by chronic intravenous heroin abuse

Introduction. The liver plays a key role in the removal of lipophyllic substances from the plasma, including both morphine and its derivative heroin. Intravenous heroin abuse leads to liver damages, so that the effects of heroin intake are the most marked and characteristic in the liver. Objective. A histochemical and ultrastructural study of the liver, particularly hepatocyte glycogen content, should provide a precise insight into the type and degree of liver damage induced by intravenous heroin abuse. Methods. The study included the analysis of 50 autopsies, 40 from the group of intravenous heroin abusers and 10 control autopsies. Paraffin sections, 5 µm thick, were stained by PAS method for deposited glycogen staining. The ultrastructural investigation was performed on transmission electron microscope. Results. Glycogen amount was reduced proportionally to the severity and distribution of degenerative and necrotic hepatocytic lesions. Regarding deposited glycogen depletion in particular acinar zones, glycogen was most preserved in zone 1 (30% of studied cases), then in zone 3 (preserved in 25%), while the depletion was most significant in intermediary zone (preserved in 5%). In the intravenous heroin abusers group of up to 2 years glycogen was preserved in the acinar zones 1, 2 and 3 in 43%, 30% and 57%, respectively; in the group of over 10 years glycogen preservation in zone 1 was 25% and in other zones 0%. Conclusion. Intravenously administered heroin directly influences glycogen reduction in the hepatocytes, and the effect is potentiated by morphologic changes in the liver due to intravenous heroin abuse. Glycogen depletion in the hepatocytes reduces energy reserves in these cells and causes cell death, which is an important segment of general liver injury in intravenous heroin abusers. The degree of reduction of glycogen depositions is proportional to the duration of intravenous heroin abuse

Evaluation of Circulating Immune Complexes and Anti-phospholipid Antibodies (anti Beta 2 Glycoprotein 1) in Heroin Addicts and their Clinical Significance

Earlier studies have reported that heroin might cause the structural and antigen changes on numerous tissues, organs and subsequent development of autoimmune reactions (production of antibodies and creation of immune complexes) as a result the immunotoxic effect of heroin. The aims of our study were to: a) Evaluate CIC and antibeta2GP1 in heroin addicts; b) Correlate between the values of the obtained CIC and antibeta2GP1 (stratified by the duration and route of heroin application); c) Compare the CIC and antibeta2GP1 in heroin addicts and the control group and d) Assess the clinical importance of CIC and antibeta2GP1 in heroin addicts. This was a cross-sectional study performed at the University Clinic of Toxicology and the Institute of Transfusiology, Skopje, Republic of Macedonia. Patients referred to the Clinic for clinical examinations who met the inclusion criteria were analyzed. Protocol for work was the following: 1.) detailed anamnestic data, 2.) a whole set of laboratory biochemical blood and urine analyses, 3.) examination with the Schiller's twelve-channel ECG; 4.) toxicological analyses for opioids in a urine sample; circulating immune complexes and 5.) antiphospholipid antibodies (antibeta2GP1, fractions: IgA, IgG, IgM). The obtained results were statistically analyzed. We included 37 heroin addicts and a control group of 27 healthy subjects. Male abusers predominated over female in--28 (76%) subjects; mean age being 26 +/- 5.06. The results which refer to the increased values of circulating immune complexes have shown a high statistically significant dominance of heroin addicts, in comparison with the control group (p < 0.01) and increased values above the reference ones of IgG antibeta2GP1, alone in the group of intravenous heroin abusers (p < 0.025). The mean duration of the heroin use in intravenous abusers was 6.21 +/- 3.25 years, whereas in those snorting heroin was 5.15 +/- 2.26 years. Duration of heroin application was in a positive correlation with IgG antibeta2GP1 (p = 0.35). Our data showed that heroin-dependent patients in our study had increased values of circulating immune complexes and changes in IgG and IgM antibeta2GP1 with significantly increased values of IgG antibeta2GP1 in the intravenous heroin abusers. The duration of heroin application is in direct proportional relationship with IgG antibeta2GP1. Heroin addicts had significantly higher values of circulating immune complexes and statistically significant difference in IgG antibeta2GP1, in comparison with the control group. Changes in the fractions of antibeta2GP1 and CIC suggest a possible relation with the somatic changes found in heroin addicts (i.e. thrombocytopenia, reduced renal clearance, etc).

Amyloidosis, change in macrophage number, and dysplasia in the liver of intravenous heroin users

Apart from the usual morphological changes in the liver of intravenous heroin users such as vesicular and fatty changes, various forms of viral hepatitis and development of cirrhosis, the onset of amyloidosis, the change in the number of hepatic sinusoidal macrophages, and dysplastic changes are of particular significance from the forensic point of view since they can indicate heroin abuse, probably associated with alcohol effects, and they can also be a factor for the occurrence of severe morphological liver damage with a possible lethal outcome. A histopathologic and morphometric study of changes in the liver of heroin users aimed to show the presence of rarer morphologic changes in the liver as the indicators of heroin abuse, additional alcohol effects and viral infections. The present study included 40 autopsies of intravenous heroin users and 10 control autopsies. In order to facilitate the investigation, all autopsies of intravenous heroin users were grouped according to the duration of intravenous heroin intake into 4 groups: up to 2 years, 2-5 years; 5-10 years; over 10 years. Paraffin sections 5 µm thick, were stained by hematoxylin method (HE), van Gieson and Congo red. Morphometric investigation of sinusoidal macrophages in the liver was done using the M42 test system. Liver tissue samples taken to be tested for ultrastructural changes were fixed in glutaraldehyde and epon-embedded, and the analysis was done using transmission electron microscopy JEM 100 CX JEOL. Amyloidosis localized in portal tracts, mostly underneath the endothelium of the smaller branches of the hepatic artery was established in 9 cases (22,5%), out of which in 78% (in 7 of 9) the duration of intravenous intake lasted longer than 5 years. In 55,5% of cases (in 5 of 9), amyloidosis was associated with fatty alcohol changes. There was a statistically significant change in the number of sinusoidal macrophages in relation to the controls only in cases with chronic active hepatitis regardless of coexisting cirrhosis, whereas the other cases with established fatty alcohol changes showed no significantly higher number of these cells in relation to controls. Severe dysplastic changes were established in three cases with vesicular and fatty changes complicated with viral hepatitis, two of which were with coexisting cirrhosis; in all three cases (100%), the duration of intravenous heroin abuse lasted longer than 5 years. Long duration of heroin abuse is a condition for the occurrence of liver amyloidosis and dysplastic changes in the liver. The high percentage of association of amyloidosis with fatty alcohol changes in the liver points to the conclusion that the inactivation of hepatic sinusoid macrophages and the reduction of their enzymatic capacities occur due to additive, immunosuppressive effect of alcohol which may enable the onset of liver amyloidosis.