STIR magnetic resonance imaging: a noninvasive method for detection and follow-up of dermatomyositis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M David.
Explore the source record for details and available documents.
Radiation chimeras, generated by transplantation of SCID bone marrow into C3H/HeJ mice, show lethal susceptibility to staphylococcal enterotoxin B (SEB), thus constituting a valid murine model for SEB shock. This SEB sensitivity is due to the ability of the irradiated host to restore residual T cell populations, since the SCID donor bone marrow is unable to generate T cells. SCID bone marrow transplanted into irradiated nude mice does not generate SEB-sensitive chimeras, as a consequence of the inability of the recipient nude mice to develop mature T cells. Thymectomy of normal recipient mice prior to bone marrow transplantation does not affect the development of susceptibility to SEB, suggesting that postthymic, residual T cells of the host probably mediate this SEB sensitivity. In vivo depletion experiments show that CD4+ T cells are required for the SEB-triggered shock, while CD8+ cells suppress it. A further examination of the T helper subpopulations in the SEB-sensitive mice reveals a prevalence of CD4+ CD45RB(dim) cells over CD4+ CD45RB(bright) cells. This T helper balance was statistically significant when correlated with SEB-induced mortality. Our model provides a possible explanation for the SEB resistance of normal mice: they have a prevalence of CD4+ CD45RB(dim) over CD4+ CD45RB(bright) cells.
Intravenous drug abuse is a risk for alloimmunization in pregnancy. One case is presented of a nulliparous Rhesus-negative parturient who shared her Rhesus-positive partner's needles for the injection of heroin; she subsequently developed elevated antepartum anti-D titers despite routine anti-D prophylaxis.
OBJECTIVE: Our purpose was to compare birth complications and fetal outcome in hospitals and birth centers. METHOD: We retrospectively compared all 801 deliveries between 1992 and 1994 from two free-standing birth centers against 3271 hospital deliveries in Berlin. The hospital collective was selected according to the same risk criteria of the birth centers. RESULTS: The birth center group had significantly fewer medical interventions, with a similar cesarean section rate (3.0% vs. 4.6%, P = 0.057) and occurrence of severe perineal lesions. The episiotomy rate was significantly higher (P < 0.001) in the clinics for first-time and multiple births. The perinatal mortality was not significantly different ( < 0.1 per 1000). One-minute Apgar scores less than 7 were found significantly more often in the birth center group. CONCLUSION: When birth centers employ thorough risk selection and significant early referral rates to nearby hospitals, there is no evidence of increased maternal or perinatal risk compared to hospital deliveries.
The toxicity of interferon (IFN) alfa-2b therapy was prospectively evaluated in 53 children treated from 1991 to 1996 in 2 successive studies of IFN alfa therapy for severe hemangiomas at Sainte-Justine Hospital. Toxicity was generally mild and transient, with grade 1 toxicity occurring in 100% of patients, grade 2 toxicity in 89%, grade 3 toxicity in 58%, and grade 4 toxicity in 17%. Ten of 43 patients available for evaluation had an abnormal neurologic examination. Severe neurotoxicity in the form of spastic diplegia occurred in one patient. In conclusion, IFN alfa therapy is generally well tolerated in children. However, it may rarely be associated with severe toxicity and must be used with caution.
A prospective study was carried out to assess the occurrence and character of adverse cutaneous reactions in patients receiving ticlopidine hydrochloride to prevent subacute thrombosis after having undergone placement of coronary stents. During a 1-year period such patients were requested to report any adverse cutaneous reactions, and those with skin reactions were referred for dermatological evaluation. Among the 136 patients who underwent stent placement by one of the authors, 20 were referred for dermatological evaluation. Of these, 16 (11.8%) fit the case definition of ticlopidine-associated cutaneous reactions. In the first 8 consecutive patients ticlopidine was withdrawn (in 2 of these a rechallenge test was later performed); in the next 8 patients ticlopidine was not discontinued before completion of the intended 4-week period of treatment. Patients remained under weekly follow-up and underwent a weekly blood count. Skin biopsies were obtained in 5 patients with different types of eruptions. The skin reactions appeared from 2 to 21 days after commencement of ticlopidine (mean, 10 days), lasting from 2 to 30 days (mean, 5 days). Only 3 patients had other adverse effects: neutropenia in 1 and abdominal pain and nausea in 2. The most common presentations were urticaria, pruritus, and maculopapular eruption. In 3 patients there were previously unreported reactions: fixed drug eruption, erythromelalgia-like eruption, and erythema multiforme-like eruption. Of note was the rapid clearing of the skin eruption in most cases even when the drug was not withdrawn. It was concluded that adverse cutaneous reactions are relatively common in association with ticlopidine treatment but that serious reactions are rare and the disappearance of the signs and symptoms is rapid, suggesting that discontinuation of the drug is not usually imperative.
BACKGROUND: IgA pemphigus of the subcorneal pustular dermatosis (SPD) type is characterized by subcorneal acantholysis and by an abundance of neutrophils, making colchicine a reasonable pharmacologic option for treatment. OBJECTIVE: We attempted to determine the efficacy of colchicine in the treatment of SPD-type IgA pemphigus. METHODS: Two patients with SPD-type IgA pemphigus were treated with colchicine 1.5 mg/day as monotherapy. RESULTS: A sustained clinical response was achieved within 2 to 3 weeks of therapy. Relapses were noted each time colchicine was stopped. CONCLUSION: Colchicine should be considered in the treatment of SPD-type IgA pemphigus.
OBJECTIVE: To assess risk factors for mortality in cardiac surgical adult patients as part of a study to develop a European System for Cardiac Operative Risk Evaluation (EuroSCORE). METHODS: From September to November 1995, information on risk factors and mortality was collected for 19030 consecutive adult patients undergoing cardiac surgery under cardiopulmonary bypass in 128 surgical centres in eight European states. Data were collected for 68 preoperative and 29 operative risk factors proven or believed to influence hospital mortality. The relationship between risk factors and outcome was assessed by univariate and logistic regression analysis. RESULTS: Mean age (+/- standard deviation) was 62.5+/-10.7 (range 17-94 years) and 28% were female. Mean body mass index was 26.3+/-3.9. The incidence of common risk factors was as follows: hypertension 43.6%, diabetes 16.7%, extracardiac arteriopathy 2.9%, chronic renal failure 3.5%, chronic pulmonary disease 3.9%, previous cardiac surgery 7.3% and impaired left ventricular function 31.4%. Isolated coronary surgery accounted for 63.6% of all procedures, and 29.8% of patients had valve operations. Overall hospital mortality was 4.8%. Coronary surgery mortality was 3.4% In the absence of any identifiable risk factors, mortality was 0.4% for coronary surgery, 1% for mitral valve surgery, 1.1% for aortic valve surgery and 0% for atrial septal defect repair. The following risk factors were associated with increased mortality: age (P = 0.001), female gender (P = 0.001), serum creatinine (P = 0.001), extracardiac arteriopathy (P = 0.001), chronic airway disease (P = 0.006), severe neurological dysfunction (P = 0.001), previous cardiac surgery (P = 0.001), recent myocardial infarction (P = 0.001), left ventricular ejection fraction (P = 0.001), chronic congestive cardiac failure (P = 0.001), pulmonary hypertension (P = 0.001), active endocarditis (P = 0.001), unstable angina (P = 0.001), procedure urgency (P = 0.001), critical preoperative condition (P = 0.001) ventricular septal rupture (P = 0.002), noncoronary surgery (P = 0.001), thoracic aortic surgery (P = 0.001). CONCLUSION: A number of risk factors contribute to cardiac surgical mortality in Europe. This information can be used to develop a risk stratification system for the prediction of hospital mortality and the assessment of quality of care.
The aetiology of mycosis fungoides (MF) and Sézary syndrome (SS) is unknown. A pathogenic role for the human T-cell lymphotropic virus type 1 (HTLV-1) has been suggested but remains controversial. We used an animal model to test the possibility that peripheral blood mononuclear cells (PBMC) obtained from MF patients harbour the HTLV-1 virus which may be infective. The polymerase chain reaction (PCR) was used to detect HTLV-1 proviral DNA sequences in PBMC of 27 MF patients and one SS patient of non-Iranian origin. Positive results were found in six of the patients. Twelve of the 28 patients tested by Western blot showed HTLV-1 antibodies. Twenty-eight immunosuppressed inbred Fisher F344 rats were inoculated intravenously with cultures of PBMC obtained from the 28 patients. Eight of these 28 rats showed antibodies to HTLV-1 while the proviral genome was demonstrated in the blood of only two of the rats. PBMC from two MF patients, in spite of showing negative results for the proviral genome by PCR, still induced HTLV-1 antibody formation in the F344 rat model. None of 10 control rats inoculated with normal donor PBMC showed antibodies to HTLV-1, nor the proviral genome. The present study suggests that HTLV-1 plays a cofactor role in MF/SS patients.
Nine patients with follicular cutaneous T-cell lymphoma (CTCL), a recently described variant of lymphoma, are presented. On the basis of clinical manifestations and disease course, three groups of patients were distinguished: (i) two patients with follicular CTCL not associated with conventional lesions of mycosis fungoides (MF) and showing no evolution towards MF in follow-up periods of 3 and 6 years; (ii) one patient with follicular CTCL that evolved into conventional MF within 3 years; (iii) six patients showing conventional MF lesions either before or concurrently with the follicular lesions and thus representing follicular CTCL of the true MF type. The follicular lesions included hair-devoid patches or plaques with spiky hyperkeratotic papules (four patients), keratosis pilaris-like lesions (four), comedo-like lesions (four), follicular papules with alopecia (three) and milia-like lesions (three). Histopathological examination showed perifollicular and intrafollicular lymphocytes, without mucin deposition and with minimal or no involvement of the overlying epidermis. Significant syringotropism was also observed in three cases. Immunohistochemical analysis showed the predominance of CD4 + T cells, deletion of CD7 in some cases, Ki-67 + lymphocytes confined mainly to the follicular epithelium, and expression of keratinocyte intercellular adhesion molecule-1 exclusively in the hair follicle. T-cell receptor gamma gene rearrangement was positive in the one case studied from each group. Different treatment modalities were employed, the most commonly used as monotherapy being phototherapy: psoralen ultraviolet A in four patients, two of whom showed a complete clinical and histopathological remission, and ultraviolet B in one patient, who showed a complete remission (both clinical and histopathological). This study indicates that follicular CTCL is more common than reflected in the literature, has heterogeneous clinical manifestations, and is either an expression of or closely related to MF. The influence of the follicular involvement on the therapeutic response remains to be clarified. However, our therapeutic experience clearly suggests that some patients with follicular CTCL can benefit from phototherapy.
Granuloma annulare and localized morphoea are both well described in the dermatological literature. We now present two patients with both of these diseases, a comorbidity rarely described. A possible pathogenic relationship is discussed.
Explore the source record for details and available documents.
AIMS: The purposes of this study were to determine the clinical features and to identify prognostic factors of abscesses associated with infective endocarditis. METHODS AND RESULTS: During a 5-year period from January 1989, 233 patients with perivalvular abscesses associated with infective endocarditis were enrolled in a retrospective multicentre study. Of the patients, 213 received medical surgical therapy and 20 medical therapy alone. No causative microorganism could be identified in 31% of cases. Sensitivity for the detection of abscesses was 36 and 80%, respectively using transthoracic and transoesophageal echocardiography. Surgical treatment consisted of primary suture of the abscess (38%), insertion of a felt aortic or mitral ring using Teflon or pericardium (42%), or debridment of the abscess cavity (20%). The 1 month operative mortality was 16%. Actuarial rates for overall survival at 3 and 27 months in operated patients were 75 +/- 10% and 59 +/- 11%, respectively. Increasing patient age, staphylococcal infection, and fistulization of the abscess were found to be independent risk factors in both 1 month and overall operative mortality. Renal failure was a risk factor predictive of operative mortality at 1 month, whereas uncontrolled infection and circumferential abscess were regarded as risk factors predictive of overall operative mortality. CONCLUSION: The data determined prognostic factors of abscesses associated with infective endocarditis.
In many neoplasms, the finding p53 immunoreactivity correlates with striking cytologic atypia, a high tumor cell proliferation rate, and poor prognosis. The literature regarding p53 and Ki-67 (a nuclear proliferation-associated antigen) immunoreactivity in Kaposi's sarcoma is limited. We aimed to: (1) evaluate the role of p53 in the development of Kaposi's sarcoma; (2) determine whether there is a correlation between p53 and Ki-67 protein expression; and (3) determine possible differences between classical Kaposi's sarcoma, known usually to have a benign course, and iatrogenic Kaposi's sarcoma, the course of which is unpredictable, by studying the differential expression of p53 and Ki-67. Among 26 cases of classic KS and 19 of iatrogenic KS, 12 were classified histopathologically as early type and 33 as mixed or spindle-cell type. P53 and Ki-67 immunoreactivity correlated significantly with the histopathologic stage of KS (r=0.63, p=0.0001; r=0.42, p=0.0084, respectively). P53 was not detected in any of the cases in an early histopathologic stage but was present in 55% of the cases in a more advanced stage. The spindle cells increased in proportion with the histopathologic progression and were more often positive (p=0.019) and displayed more extensive staining than the endothelial cells (p=0.0001). There was a strong positive correlation between p53 and Ki-67 protein expression (r=0.43, p=0.0087). There was no correlation between the expression of either p53 or Ki-67 and the extent of the eruption. The expression of p53 and Ki-67 was significantly lower in iatrogenic cases than in the classic cases (p=0.009, p=0.0014, respectively), although no statistical difference was found between the histopathologic stages in the two clinical forms of KS. P53 immunoreactivity was detected in 79% of the cases of classic Kaposi's sarcoma in the mixed or spindle cell stage but in only 21.5% of the iatrogenic cases showing the same histopathologic stage (p=0.001), and the percentage of spindle cells as well as the endothelial cells expressing p53 was higher in the classic cases than in the iatrogenic cases (p=0.0032, p=0.0142, respectively). We conclude that p53 immunoexpression is a marker of tumor progression in classic Kaposi's sarcoma but not in most cases of iatrogenic Kaposi's sarcoma. The proliferative activity of the tumor cells in classic Kaposi's sarcoma is much higher than in iatrogenic Kaposi's sarcoma. Our work implies that the molecular steps involved in classic and iatrogenic Kaposi's sarcoma differ.
A fragment of a fractured Telectronics Atrial Accufix 330-801 lead asymptomatically perforated the adjacent bronchus and was detected on routine chest X-ray. The metallic fragment was located by chest CT scan and bronchial fluoroscopy to lie between the right lobar bronchus and the pulmonary artery, confirming bronchial perforation. The foreign body was removed without complication by direct visualisation with rigid bronchoscopy.
Pigmented contact dermatitis has been found to be caused by fragrances, cosmetics, washing powders, azo dyes in textiles, and rubber products in selected groups of patients. The aim of this study was to run screening patch tests in an unselected group of patients with pigmented contact dermatitis (n=29) encountered in our center over a 2-year period. The test series included the European standard, cosmetics, fragrance, Scandinavian photo, and personal products. 21 patients had a positive reaction in at least 1 of the series (total, 29 reactions): 16 - standard, 3 - cosmetics, 1 fragrance, 9 photo, and 1 - personal products; 16 (55%) had relevant results. We conclude that the highest yield for screening for pigmented contact dermatitis is achieved with the standard and photo series.
Reports from Jamaica have indicated that some patients with infective dermatitis or atopic dermatitis (AD) are seropositive for antibodies to human T-lymphotropic virus type 1 (HTLV-1). We describe a 32-year-old Israeli woman with long-term AD and paresthesia in the distal parts of the extremities. Neurological examination revealed a positive Babinski's sign. HLA typing demonstrated that this patient has the common HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and infective dermatitis haplotype for DRB1* DQB1*. The presence of HTLV-1 was demonstrated with polymerase chain reaction; HTLV-1-antibodies were detected by the Western blot method and by inoculation of the patient's peripheral blood mononuclear cells into F344 rats. This study confirms the presence of HTLV-1 antibodies and proviral genome in a patient with AD which later evolved into HAM/TSP. We cannot yet conclude whether these two diseases are associated or coincidental disorders.
Fetal male sexual differentiation is driven by two testicular hormones: testosterone (synthesized by interstitial Leydig cells) and antimüllerian hormone (AMH; produced by Sertoli cells present in the seminiferous tubules). Intersex states result either from gonadal dysgenesis, in which both Leydig and Sertoli cell populations are affected, or from impaired secretion or action of either testosterone or AMH. Until now, only Leydig cell function has been assessed in children with ambiguous genitalia, by means of testosterone assay. To determine whether serum AMH would help in the diagnosis of intersex conditions, we assayed serum AMH levels in 107 patients with ambiguous genitalia of various etiologies. In XY patients, AMH was low when the intersex condition was caused by abnormal testicular determination (including pure and partial gonadal dysgenesis) but was normal or elevated in patients with impaired testosterone secretion, whereas serum testosterone was low in both groups. AMH was also elevated during the first year of life and at puberty in intersex states caused by androgen insensitivity. In 46,XX patients with a normal male phenotype or ambiguous genitalia, in whom the diagnosis of female pseudohermaphroditism had been excluded, serum AMH levels higher than 75 pmol/L were indicative of the presence of testicular tissue and correlated with the mass of functional testicular parenchyma. In conclusion, serum AMH determination is a powerful tool to assess Sertoli cell function in children with intersex states, and it helps to distinguish between defects of male sexual differentiation caused by abnormal testicular determination and those resulting from isolated impairment of testosterone secretion or action.