[Gynecological care among women reporting sexual violence: a qualitative study]. / Recours au soin gynécologique chez les femmes rapportant des violences sexuelles : étude qualitative.

INTRODUCTION: Sexual violence can be followed by different levels of gynecological care. Our objective was to characterise gynecological care and to identify the related factors among women who had reported sexual violence. METHODS: Twenty-five semi-structured interviews were conducted among adult women who reported sexual violence during childhood or as adults. Topics addressed included gynecological health, gynecological care and experienced violence, RESULTS: Interviewed women, aged 20-60, had a good professional integration and a high level of education. The violence had often been committed by a relative or acquaintance. For the women interviewed, the least use of gynecological care was motivated by a desire to avoid the gynecological examination. Among women who had regular check-ups, the desire to conform to the norm explained their need for gynecological check-ups, which was similar to that of women who had never been subjected to violence. Lastly, some care pathways were characterised by multiple recourse of gynecological care for complaints with identical motives. The women interviewed expected professionals to spontaneously identify the violence they had suffered and the gynecological consequences attributed to such violence. CONCLUSION: Individual and interpersonal differences in levels of gynecological care use were related to the characteristics of the violence and its perceived effects on gynecological health. It would be interesting to extend this research by examining the care pathways of women with other socioeconomic characteristics. A quantitative study would measure the association between violence and the use of gynecological care.

Simultaneous determination of methanol, acetaldehyde, acetone, and ethanol in human blood by gas chromatography with flame ionization detection.

BACKGROUND: Methanol, acetaldehyde, acetone, and ethanol, which are commonly used as biomarkers of several diseases, in acute intoxications, and forensic settings, can be detected and quantified in biological fluids. Gas chromatography (GC)-mass spectrometry techniques are complex, require highly trained personnel and expensive materials. Gas chromatographic determinations of ethanol, methanol, and acetone have been reported in one study with suboptimal accuracy. Our objective was to improve the assessment of these compounds in human blood using GC with flame ionization detection. METHODS: An amount of 50 µl of blood was diluted with 300 µl of sterile water, 40 µl of 10% sodium tungstate, and 20 µl of 1% sulphuric acid. After centrifugation, 1 µl of the supernatant was injected into the gas chromatograph. We used a dimethylpolysiloxane capillary column of 30 m × 0.25 mm × 0.25 µm. RESULTS: We observed linear correlations from 7.5 to 240 mg/l for methanol, acetaldehyde, and acetone and from 75 to 2400 mg/l for ethanol. Precision at concentrations 15, 60, and 120 mg/l for methanol, acetaldehyde, and acetone and 150, 600, and 1200 mg/ml for ethanol were 0.8-6.9%. Ranges of accuracy were 94.7-98.9% for methanol, 91.2-97.4% for acetaldehyde, 96.1-98.7% for acetone, and 105.5-111.6% for ethanol. Limits of detection were 0.80 mg/l for methanol, 0.61 mg/l for acetaldehyde, 0.58 mg/l for acetone, and 0.53 mg/l for ethanol. CONCLUSION: This method is suitable for routine clinical and forensic practices.

Impaired redox status and cytochrome c oxidase deficiency in patients with polymyalgia rheumatica.

OBJECTIVE: To evaluate redox status and muscular mitochondrial abnormalities in patients with polymyalgia rheumatica (PMR). METHODS: Prospective evaluation of deltoid muscle biopsy in 15 patients with PMR. Fifteen subjects matched for age and sex, with histologically normal muscle and without clinical evidence of myopathy, were used as controls. Cryostat sections of muscle were processed for conventional dyes, cytochrome c oxidase (COX), usual histochemical reactions, and Sudan black. A total of 300-800 fibres was examined in each case. Blood lactate, pyruvate, and lactate/pyruvate ratio were determined in all patients. RESULTS: Ragged red fibres were found in eight patients with PMR and accounted for 0-0.5% of fibres. Focal COX deficiency was found in 14 (93%) of 15 patients and in nine (60%) of 15 controls. COX deficient fibres were more common in patients with PMR (range 0-2.5%; mean 0.9%) than in controls (range 0-1.2%; mean 0.3%) (paired t test, p=0.001). Seven (47%) of 15 patients had high blood lactate levels (1.50-2.60 mmol/l) or high blood lactate/pyruvate ratios (22-25). CONCLUSIONS: PMR is associated with mitochondrial abnormalities not solely related to the aging process.

Focal neurological complications of handcuff application.

The application of handcuffs may result in compression neuropathies at the wrist. The frequency of these complications is unknown. Twelve of 190 (6.3%) consecutive subjects kept in police custody presented distal neurological symptoms possibly related to handcuff application. The duration of handcuffing was significantly longer in patients with neurological symptoms than in patients without neurological symptoms (mean +/- SD: 3.7+/-5.2 h vs. 1.8+/-2.6 h, P = 0.02). A long duration of handcuff application and, possibly, the existence of somnolence or acute alcohol intoxication could be predisposing factors to handcuff neuropathy. A prospective study of clinical and electrophysiological detection and follow up is needed.

Macrophagic myofasciitis lesions assess long-term persistence of vaccine-derived aluminium hydroxide in muscle.

Macrophagic myofasciitis (MMF) is an emerging condition of unknown cause, detected in patients with diffuse arthromyalgias and fatigue, and characterized by muscle infiltration by granular periodic acid-Schiff's reagent-positive macrophages and lymphocytes. Intracytoplasmic inclusions have been observed in macrophages of some patients. To assess their significance, electron microscopy was performed in 40 consecutive cases and chemical analysis was done by microanalysis and atomic absorption spectrometry. Inclusions were constantly detected and corresponded to aluminium hydroxide, an immunostimulatory compound frequently used as a vaccine adjuvant. A lymphocytic component was constantly observed in MMF lesions. Serological tests were compatible with exposure to aluminium hydroxide-containing vaccines. History analysis revealed that 50 out of 50 patients had received vaccines against hepatitis B virus (86%), hepatitis A virus (19%) or tetanus toxoid (58%), 3-96 months (median 36 months) before biopsy. Diffuse myalgias were more frequent in patients with than without an MMF lesion at deltoid muscle biopsy (P < 0.0001). Myalgia onset was subsequent to the vaccination (median 11 months) in 94% of patients. MMF lesion was experimentally reproduced in rats. We conclude that the MMF lesion is secondary to intramuscular injection of aluminium hydroxide-containing vaccines, shows both long-term persistence of aluminium hydroxide and an ongoing local immune reaction, and is detected in patients with systemic symptoms which appeared subsequently to vaccination.

Cytochrome c oxidase deficiency in the muscle of patients with zidovudine myopathy is segmental and affects both mitochondrial DNA- and nuclear DNA-encoded subunits.

Zidovudine (AZT) can induce a mitochondrial disorder associated with mitochondrial (mt) DNA depletion affecting skeletal muscle, heart, and liver. Zidovudine myopathy is characterized by ragged-red fibers and partial cytochrome c oxidase (COX) deficiency. We evaluated at a single fiber level the expression of COX II (mtDNA-encoded) and COX IV (nuclear DNA-encoded) subunits in 12 HIV-infected patients with zidovudine myopathy. We also evaluated COX activity on longitudinal muscle sections in one patient. In all patients, evaluation of the expression of COX II and COX IV subunits showed focal deficiency. All fibers negative for COX II or COX IV were negative by COX histochemistry; 32-92% (median 61%) of COX-negative fibers were negative for COX II antigens, and 7-58% (median 28%) were negative for COX IV antigens. One hundred and thirty-nine of 317 COX-negative fibers 139 (43.8%) were selectively negative for COX II; 28 of 317 (8.8%) COX-negative fibers were selectively negative for COX IV. A study of longitudinal distribution of COX activity demonstrated that COX deficiency was segmental with blurred borders, as previously observed in patients with myoclonus epilepsy with ragged-red fibers. We conclude that proteins encoded by mtDNA are predominantly, but not exclusively, involved in zidovudine myopathy. Our results confirm the value of single muscle fiber evaluation in the assessment of mitochondrial abnormalities related to zidovudine.

Declining autopsy rate in a French hospital: physician's attitudes to the autopsy and use of autopsy material in research publications.

CONTEXT: Autopsy rates have been declining throughout the world, although preservation of the autopsy is considered a fundamental principle of medical care. In France, the 1994 bioethics law requires physicians to inform relatives before performing an autopsy. OBJECTIVE: To analyze the following factors that potentially influence hospital autopsy rates: legal constraints, autopsy reporting times, opinions of physicians requesting autopsies and pathologists regarding the usefulness of autopsy in patient care, and use of autopsy material in research publications. DESIGN: Record of the annual numbers of deaths and autopsies during a 10-year period (1988-1997). Record of the delays for transmission of final autopsy report to the requesting physician. Questionnaire analyzing the possible factors influencing autopsy rate. Categorization of articles published by pathologists according to the use of autopsy material. SETTING: A 1000-bed, university teaching hospital in the Paris, France, area. PARTICIPANTS: Questionnaire addressed to physicians, head nurses, and mortuary staff. RESULTS: A total of 1454 autopsies were reviewed. The autopsy rate declined from 15.4% in 1988 to 3.7% in 1997. This decline was marked after 1994 and tended to be slower for neurologic indications than for other indications. The final report had not been communicated within 180 days in 620 (42.6%) of 1454 autopsies. Fifty-five of 105 respondents considered that the bioethics law was one cause of the recent decrease of autopsy rate. Considering the contribution of autopsy to medical research, 94 (81%) of 116 articles dealing with central nervous system but only 28 (6%) of 464 articles dealing with other organs used autopsy-derived material. CONCLUSIONS: The 1994 bioethics law seems to contribute to the decline of autopsy. Inadequate delays for communicating autopsy results are frequent. Except for neuropathologists, autopsy is a minor source of research material.

Muscle disorders associated with cyclosporine treatment.

Alone or as part of a multidrug immunosuppressive regimen, cyclosporine A (CsA) has been reported in isolated case studies as a cause of muscle disorders. We reviewed the current knowledge on muscle toxicity of CsA and discussed the possible role of mitochondrial dysfunction in the genesis of CsA-associated myopathy. A systematic review using Medline(R) and Current Contents(R) databases combined with a manual literature search allowed us to select 56 references. We identified 34 patients with muscle disorders possibly related to CsA, usually manifesting by myalgia or muscle weakness and plasma creatine kinase elevation. Only 2 of 34 patients were treated with CsA alone. Experimental studies have shown that administration of CsA to rats reduces capillary density in extensor digitorum longus, skeletal muscle mitochondrial respiration, and endurance exercise capacity. Cyclosporine has been shown to inhibit the mitochondrial permeability transition pore. Whether identified interactions between CsA and mitochondria can explain CsA-associated myopathy is still unclear.

MRI of intralesional hemolysis in focal nodular hyperplasia of the liver.

A case of Kasabach-Merritt syndrome caused by focal nodular hyperplasia of the liver is presented with atypical magnetic resonance findings due to intratumoral hemosiderin deposition. The high sensitivity of magnetic resonance imaging for iron served to identify the site of hemolysis in this patient with Kasabach-Merritt syndrome.

Choreic movements and MRI abnormalities in the subthalamic nuclei reversible after administration of coenzyme Q10 and multiple vitamins in a patient with bilateral optic neuropathy.

A 37-year-old man developed choreic movements of the limbs over a few months. His medical history included bilateral visual loss detected at the age of 9 and worsening at age 20. Visual field testing showed a central scotoma. Fundus examination showed atrophy of the optic disks and narrowing of vessels. The diagnosis of Leber hereditary optic neuropathy (LHON) was considered. There was no family history of visual loss or movement disorders. Blood lactate:pyruvate ratio was moderately elevated. Skeletal muscle biopsy was normal. Magnetic resonance imaging showed bilateral hypointense lesions on T1-weighted sequences in the subthalamic nuclei and in the lateral part of the substantia nigra. Linear hyperlucencies in the pyramidal tract facing the lateral part of the ruber nuclei were also demonstrated on T2-weighted sequences. Nine LHON-associated mutations were ruled out by RFLP analysis. Treatment with 250 mg coenzyme Q10 per day and multiple vitamins was initiated. Gradual recovery in movement disorders occurred over 1 year. Lactate to pyruvate ratio normalized. No change of visual function was observed. On magnetic resonance imaging performed 3 years later, lesions of the subthalamic nuclei almost completely disappeared. We think the patient might have an unusual, genetically uncharacterized mitochondrial disorder, combining optic neuropathy and chorea.

Influence of handling procedures on rat plasma creatine kinase activity.

Ten-week-old Sprague-Dawley rats were held behind the front legs before and during anesthetic injection of sodium pentobarbital (group 1, 12 rats), or lifted by the base of the tail before and during injection (group 2, 12 rats). Creatine kinase (CK) values were higher (P = 0.004) in group 1 (median 564 IU/L) than in group 2 (median 272 IU/L). Handling rats by holding them behind the front legs may reduce the usefulness of CK activity as a measure of muscular disorders.

Zidovudine-induced mitochondrial disorder with massive liver steatosis, myopathy, lactic acidosis, and mitochondrial DNA depletion.

Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied. A 57-year-old man with AIDS, who had been treated with zidovudine for 3 years, developed fatigue and weight loss. Serum creatine kinase and hepatic enzyme levels were high. Lactic acidosis was present. Liver biopsy showed diffuse macrovacuolar and microvacuolar steatosis. After withdrawal of zidovudine, creatine kinase, aspartate aminotransferase, and alanine aminotransferase levels normalised within 5 days, and lactacidaemia decreased. Acidosis persisted. The patient became confused and febrile and died 8 days after detection of high blood lactic acid. A muscle sample obtained at autopsy showed mitochondrial abnormalities with ragged-red fibres and lipid droplet accumulation. Southern blot analysis showed depletion of mitochondrial DNA, affecting skeletal muscle and liver tissue. No depletion was found in myocardium and kidney. This case emphasises that zidovudine treatment can induce mitochondrial multisystem disease, as revealed in our case by myopathy, liver steatosis and lactic acidosis.

Pitfalls in the diagnosis of child sexual abuse.

Case 1: nurses in charge of a 6-year-old girl in a holiday camp noticed some blood spots on the girl's underwear. The possibility of sexual abuse was considered and the girl alleged that her father was responsible. The father was arrested. A surgeon was asked to examine the girl and planned to do it under general anesthaesia. Meanwhile, the girl was brought to the Forensic Medicine Unit. We found a normal hymen and no detectable anal lesions. The girl complained of dysuria and pollakiuria. Urinalysis revealed the presence of blood, leukocytes, and nitrite. Antibiotic treatment for lower urinary tract infection was initiated and all symptoms improved rapidly. The father was released. Case 2: a 7-year-old boy complained of having been sexually assaulted 24 h before. The boy did not report any pain or bleeding during or after the assault. Examination of the perianal region and of the anal sphineter were normal. Proctoscopy did not show any evidence of trauma to the anal canal. Tests to detect spermatozoa in the rectum were positive. The assailant was arrested. The present cases illustrate that: (i) psychological and social consequences of the biased interpretation of common symptoms may be dramatic in the case of child sexual abuse; (ii) both questioning and examining a child may be difficult for non-specialized practitioners; and (iii) tests to detect spermatozoa should be systematically performed in the case of a suspected or alleged recent assault, even in the absence of any clinical lesions.

[Mitochondrial DNA and Parkinson disease. Methodologic review]. / ADN mitochondrial et maladie de parkinson. Revue méthodique.

UNLABELLED: Parkinson's disease (PD), a disorder of unknown etiology, is associated with the degeneration of dopaminergic neurons in nigro-striatal pathways. MPTP, a meperidine analog, causes parkinsonism in human and nonhuman primates. MPP+, the active metabolite of MPTP, inhibits the activity of respiratory chain complex I. In patients with PD, a reduced complex I activity was found in substantia nigra, skeletal muscle, and platelets. Because complex I is partially encoded by the mitochondrial genome, several studies have searched for mitochondrial (mt) DNA abnormalities in patients with PD. Our aim was to answer the following questions: (1) are there some abnormalities of mtDNA in PD? (2) if there are some, what are these abnormalities? and (3) what is the pathogenic role of these abnormalities? METHODS: The literature review was performed using Medline [National Library of Medicine, Washington] and Current Contents [Institute for Scientific Information, Philadelphia] databases. Periods screened were 1966-March, 1998 (Medline) and March 17, 1997-March 9, 1998 (Current Contents). Keywords were: "Parkinson" or "Parkinson's", and "mitochondrial DNA" or "mtDNA". We limited our research to articles in English and French. RESULTS: Medline search provided 59 articles. Current Contents search provided 22 articles. Twelve articles were found in both databases. Thirty-eight of the 69 articles were either reviews about mitochondrial diseases (19 articles) or original articles not related to mtDNA (19 articles). Our final selection included the remaining 31 articles.

[Medical examination of sexually abused children and adolescents]. / L'examen médical de l'enfant et de l'adolescent victime d'agression sexuelle.

Medical examination of sexually-abused children or adolescents aims: 1) to identify clinical evidence of genital or extragenital lesions, 2) to diagnose sexually-transmitted infections or pregnancy, 3) to evaluate the needs for medical care, psychological support, and social investigation. The amount of laboratory evidence depends on the history. Laboratory investigations usually include tests for sperm, bacteriological cultures from all sites, testing for HIV, HCV and HBV antibodies, and the detection of pregnancy. Careful writing of a descriptive medical certificate is an important part of the medical intervention.

Cellular and mitochondrial toxicity of zidovudine (AZT), didanosine (ddI) and zalcitabine (ddC) on cultured human muscle cells.

Zidovudine (AZT), didanosine (ddI) and zalcitabine (ddC) are the reference antiretroviral therapy in patients with AIDS. A toxic mitochondrial myopathy can be observed in patients treated with AZT, but not with ddI and ddC. All 3 compounds can inhibit mitochondrial (mt)DNA polymerase and cause termination of synthesis of growing mtDNA strands and mtDNA depletion. The propensity to injure particular target tissues is unexplained. In our work, cultured muscle cells prepared from human muscle biopsies, were exposed to various concentrations of AZT (4-5000 micromol/l), ddI (5-1000 micromol/l) and ddC (1-1000 micromol/l) for 10 days. We evaluated cell proliferation and differentiation and measured lipid droplet accumulation, lactate production and respiratory chain enzyme activities. All 3 compounds induced a dose-related decrease of cell proliferation and differentiation. AZT seemed to be the most potent inhibitor of cell proliferation. AZT, ddI and ddC induced cytoplasmic lipid droplet accumulations, increased lactate production and decreased activities of COX (complex IV) and SDH (part of complex II). NADHR (complex I) and citrate sinthase activities were unchanged. Zalcitabine (ddC) and, to a lesser extent, ddI, were the most potent inhibitors of mitochondrial function. In conclusion, AZT, ddI and ddC all exert cytotoxic effects on human muscle cells and induce functional alterations of mitochondria possibly due to mechanisms other than the sole mtDNA depletion. Our results provide only a partial explanation of the fact that AZT, but not ddI and ddC, can induce a myopathy in HIV-infected patients. AZT myopathy might not simply result from a direct mitochondrial toxic effect of crude AZT.

[Muscular complications in HIV infection]. / Complications musculaires de l'infection par le VIH.

Skeletal muscle involvement may occur at all stages of HIV-infection and represents the first manifestation of the disease into some patients. We usually classify muscle involvement in HIV-infected patients in one of the following categories: HIV-associated myopathy, a myopathy that meets the criteria for polymyositis in a majority of patients, and those for acquired nemaline myopathy in some cases (1); zidovudine myopathy, a reversible mitochondrial myopathy (2); HIV-wasting syndrome and other AIDS-associated cachexias (3); opportunistic infections and tumor infiltrations of the skeletal muscle (4); vasculitic processes and iron pigment deposits (5); HIV-associated myasthenia gravis (6) and rhabdomyolysis (7). Immunohistology for major histocompatibility complex class I antigen and histochemical reaction for cytochrome coxidase are helpful in the correct classification of a myopathy as HIV polymyositis or zidovudine myopathy.