Tako-tsubo transient left ventricular apical ballooning: is intravascular ultrasound the key to resolve the enigma?
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Publications and source records attributed to M Cordoba.
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Rheumatoid neutrophilic dermatitis (RND) is an uncommon, but distinctive manifestation of rheumatoid arthritis (RA). We describe the case of a 35-year-old female who developed RND as an early stage of seronegative RA. Clinically, the lesions were presented by erythematous, slightly tender, papules, 5-10 mm in diameter, on the extensor surface of the left arm. The histopathological findings revealed a dense, dermal, mainly neutrophilic infiltrate, with prominent leucocytoclasia, but without any features of vasculitis. There was fibrinoid degeneration of collagen, resembling the collagen changes present in rheumatoid nodules in a miniaturized form. RND can be a reliable, early clinical sign of RA, as seen in our patient. Furthermore, this case demonstrates that RND may be associated not only with seropositive RA, as described in the literature, but also with seronegative RA, never before reported. The histological findings in our case are remarkable because of the fibrinoid collagen degeneration, which is described here for the first time in RND. Thus, RND may, in fact, be the initial phase of a spectrum that begins with a neutrophilic reaction and mild fibrinoid collagen degeneration, and evolves into rheumatoid nodules at the final stage.
UNLABELLED: A 12-year-old boy presented with a limp and findings suggesting localised myositis of his right calf and a working diagnosis of Behçet disease was made. During 3 years of follow-up, he had another three episodes of calf myositis, all responsive to corticosteroids within days. CONCLUSION: A case of recurrent localised myositis as a main manifestation of Behçet disease is reported. The evolution of incomplete Behçet disease, which is common in children, to the full blown form, with the emphasis on muscle involvement and the importance of early diagnosis of Behçet disease, is discussed.
The histopathological features of the purpuric patch test have been described in individual cases only. We report a series of patients with allergic contact dermatitis, who developed purpuric patch tests at the sites of allergens from the azo dye group. 105 patients were clinically evaluated and tested with the TRUE Test and the textile color & finish series (Chemotechnique Diagnostics) because of suspected clothing dermatitis. Positive results to the latter were found in 31 patients (29.5%). In 9 of these, purpuric patch tests were observed at the sites of the allergens Disperse Blue 124, 106 and 85. 10 biopsies were performed and studied. The histopathological changes of the purpuric patch test included: spongiosis (in 90% of cases), exocytosis (70%), and dilated blood vessels (100%) without signs of vasculitis, surrounded by an inflammatory infiltrate composed mainly of T lymphocytes. Extravasated erythrocytes were seen perivascularly, but also in the interstitium, surrounding the acrosyringium, at the dermoepidermal junction, and in the epidermis. Increased number of mast cells were found in 22.2% of cases. Disperse Blue 124, 106, and 85 are potent allergens that can elicit purpuric patch test reactions. The purpuric patch test in our cases was a manifestation of an allergic reaction, based not only on histopathological changes, but also on evolution and relevance of the patch tests.
BACKGROUND: Purpuric lesions have been described as an uncommon manifestation of allergic contact dermatitis in individual case reports. OBJECTIVE: We describe a series of patients who developed purpuric allergic contact dermatitis to textile dyes and resins in their personal clothing. Our purpose was to study the patients clinically and histopathologically and to define the most frequent allergens, which cause purpuric allergic contact dermatitis. METHODS: One hundred and three patients were clinically evaluated and tested with the Textile Color & Finish Series (TCFS) (Chemotechnique Diagnostics) and Standard Series (TRUE Tests) because of suspected allergic contact dermatitis (ACD) to clothing. The patients with clinical features of purpura as presenting sign of ACD were studied. Biopsies from the purpuric lesions were performed in three patients. RESULTS: Thirty of the 103 patients (29.1%) had positive reaction to an allergen from the TCFS. Clinically purpuric ACD was observed in 8.7% of all the cases studied (n = 9 of 103). Nine of the 30 patch-positive patients to the TCFS (30%) demonstrated purpuric macules, papules and patches. Patch testing of the nine patients with purpuric contact dermatitis, with the TCFS, resulted in 26 positive patch test results. The major causative allergens were the following: Disperse Blue 106 and Disperse Blue 124 in 26.9% each, Disperse Blue 85 in 11.5%, and ethyleneurea melamine formaldehyde in 7.7%. Positive patch tests were observed to dimethylol dihydroxyethyleneurea, dimethylol propyleneurea, tetramethylol acetylenediurea, urea formaldehyde, melamine formaldehyde, Disperse Red 17, and Basic Red 46 3.8% in each. Purpuric patch test reaction was observed in five cases. The patch test results had present relevance in all the cases. Lesional biopsies demonstrated acanthosis, spongiosis and parakeratosis. The blood vessels were dilated, without signs of vasculitis. The inflammatory infiltrate was composed of lymphocytes and erythrocytes. The extravasated erythrocytes had a perivascular and interstitial distribution in the superficial and deep plexus and were observed at the dermo-epidermal junction as well as in the epidermis. CONCLUSION: Purpuric contact dermatitis is not an uncommon clinical form of ACD to textile dyes and resins. New allergens, which can evoke the development of purpuric allergic contact dermatitis and have not been described in the literature until now include: ethyleneurea melamineformaldehyde, dimethylol dihydroxyethyleneurea, tetramethylol acetylenediurea, urea formaldehyde, melamine formaldehyde and Disperse Red 17.
Low energy helium-neon (He-Ne) laser irradiation has been shown to induce various therapeutic effects. We investigated its effect on the viability of skin flaps in the rat. Thirty rats underwent skin flap elevation and were then divided into three equal groups. Group I (control) was not irradiated. Groups II and III were irradiated for 5 days postoperatively, Group II to the transition zone (between the live and expected necrotic areas) and Group III to the transitional and distal zones; total energy, 2.9 J/cm(2)for each rat. Ten days after the last treatment larger surviving areas were demonstrated macroscopically in Groups II and III (P< 0.01 and 0.001, respectively). Histological examination showed tremendous proliferation of capillaries (P</= 0.05) and fibroblasts in the responsive irradiated areas. In conclusion, postoperative low-energy (2.9 J/cm(2)) He-Ne laser irradiation of the expected ischaemic zone of the rat flap can enlarge the surviving area. Irradiation of the whole expected ischaemic zone seems to be superior to irradiating the transition zone alone.
To assess whether a higher cumulative tamoxifen dose is associated with increased incidence of various types of endometrial pathologies, we compared cumulative dose of tamoxifen treatment as well as demographic characteristics, risk factors for endometrial cancer, transvaginal ultrasonographic endometrial thickness, and various treatments for the primary breast cancer between 159 postmenopausal breast cancer tamoxifen-treated patients without endometrial pathologies (group I) and 67 similar patients with endometrial pathologies (group II). A similar comparison was made between group I patients and similar patients with proliferative endometrium (group IIa), with endometrial hyperplasia (group IIb), with endometrial polyps (group IIc), and with endometrial cancer (group IId). Overall cumulative tamoxifen dose was significantly higher in group II as compared to group I (27.4+/-33.4 and 17.4+/-20.2, respectively; P<0.0252). Transvaginal ultrasonographic endometrial thickness was significantly higher in group II than in group I patients (16.3+/-11.3 mm and 12.1+/-6.3 mm, respectively; P<0.0147). The frequency of diabetes mellitus, of previous postmenopausal bleeding, and of previous exposure to hormone replacement therapy was significantly higher in group II than in group I patients (P<0.001, P<0.0001 and P<0.001, respectively). There were no significant differences in all parameters tested between group I, group IIa, group IIb, group IIc, and group IId. However, there was an obvious trend for higher cumulative tamoxifen dose in patients with benign endometrial pathologies as compared to those without endometrial pathologies or to those with endometrial cancer (Group I = 17.4+/-20.2 g, group IIa = 22.5+/-18.5 g, group IIb = 28.1+/-20.3 g, group IIc = 31.4+/-42.7 g and group IId = 10.4+/-12.6 g). Endometrial pathologies, except for endometrial cancer, are associated with a high cumulative dose of tamoxifen in postmenopausal breast cancer patients.
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AIMS: To evaluate whether endometrial pathology is more likely to be diagnosed in gynaecologically symptomatic rather than in gynaecologically asymptomatic postmenopausal breast cancer patients with tamoxifen treatment; and to evaluate the possible influence of various clinical factors on the incidence of endometrial pathology. METHODS: Endometrial histological findings, transvaginal ultrasonographic endometrial thickness, demographic characteristics, health habits, and risk factors for endometrial cancer were compared between 14 gynaecologically symptomatic (group I) and 224 gynaecologically asymptomatic (group II) postmenopausal breast cancer patients with tamoxifen treatment. RESULTS: Overall, 28.6% of the study population had endometrial pathology. The incidence of overall positive endometrial histological findings was significantly higher in group I than in group II (92.9% v 24.6%, p < 0.0001). Atrophic endometrium was more common in group II than in group I (75.3% v 7.1%, p < 0.0001). Most other endometrial pathology was significantly more common in group I than in group II (endometrial hyperplasia, 35.7% v 5.6%, p < 0.0001; endometrial polyps, 35.7% v 13.4%, p < 0.0111; endometrial carcinoma, 21.5% v 0.9%, p < 0.0001). Endometrial pathology appeared considerably later in the gynaecologically asymptomatic patients than in gynaecologically symptomatic patients (p = 0.0002). Vaginal bleeding or spotting occurred exclusively in group I. The incidence of endometrial pathology in the entire study population was consistent with that reported elsewhere, and higher than that reported for healthy postmenopausal women. CONCLUSIONS: Endometrial pathology is more likely to be diagnosed in gynaecologically symptomatic postmenopausal breast cancer patients with tamoxifen treatment, and after a shorter duration of time, than in gynaecologically asymptomatic patients.
Histological findings of endometrial specimens collected by hysteroscopy from 261 postmenopausal breast cancer patients with tamoxifen treatment (group I) and from endometrial specimens obtained following hysterectomy from 40 similar patients (group II) were compared. This comparison was performed in order to assess whether endometrial pathologies are more frequently diagnosed in specimens collected by hysterectomy than by those collected during hysteroscopy in such patients. Overall positive endometrial histological findings were significantly more common in group II patients than in group I patients (82.5 and 24.5%, respectively; p < 0.0001). Atrophic endometrium was significantly more common in group I patients than in group II patients (75.5 and 15.0%, respectively; p < 0.0001). All other different endometrial pathologies, except for proliferative endometrium, were significantly more common in group II patients than in group I patients (endometrial hyperplasia = 17.5 and 4.2%, respectively; p < 0.0003; endometrial polyps = 30.0 and 11. 5%, respectively; p < 0.006; endometrial polyps with hyperplasia = 17.5 and 4.2%, respectively; p < 0.0003; endometrial carcinoma = 15. 0 and 0.4%, respectively; p < 0.0001). These findings suggest that in postmenopausal breast cancer patients treated with tamoxifen, the frequency of various endometrial histological findings and of overall positive endometrial histological findings were significantly higher in specimens collected by hysterectomy than in specimens obtained by hysteroscopy.
We describe the first case of catastrophic antiphospholipid syndrome triggered by trauma. In contrast to reports that emphasize the devastating nature of the syndrome, our patient's course is less dramatic and more elusive. A possible pathophysiological explanation to the association of antiphospholipid syndrome and trauma is discussed.
Adenomyosis is an ectopic endometrial tissue located in the myometrium. It has been reported to develop at a higher rate among postmenopausal breast cancer patients on tamoxifen (TAM) treatment than in untreated patients. It has also been reported to be stimulated by estrogen. Assessing receptor levels in adenomyotic tissue may indicate the adenomyotic cell's potential to interact with TAM. In the present study the estrogen receptor (ER) and progesterone receptor (PR) were analyzed by an immunohistochemical technique in adenomyotic and the corresponding endometrial tissues of 14 postmenopausal breast cancer patients treated with TAM and in 15 healthy postmenopausal patients who served as controls. All TAM-treated patients had normal postmenopausal serum estradiol levels. Overall the ER and PR contents in adenomyotic tissue (42.9 and 71.4%) and in the endometriotic tissue (64.3 and 78.6%) obtained from the study patients were similar to those obtained from the control group (adenomyosis, ER and PR = 46.7 and 86.7%; endometrium, ER and PR = 40 and 73.3%; p = NS). In the study group, the ER content was lower in the adenomyotic (42.9%) than in the endometriotic tissue (64.3%). No correlation was found between the duration of TAM therapy, the TAM dosage level or the ER or PR content in the adenomyotic or endometrial tissues. The finding of a relatively low ER content in the adenomyotic tissue than in the endometriotic tissue in postmenopausal TAM-treated patients without endogenous estrogens, similar to that observed in healthy premenopausal women, may be attributed to the estrogen-like effect of TAM.
In order to assess possible ovarian cell potential for interaction with tamoxifen, thus demonstrating possible effects of this agent on the development of ovarian pathologies through growth stimulation and cell proliferation, we measured estrogen receptors (ER) and progesterone receptors (PR) by immunohistochemical method in 16 benign ovarian tumors removed from 11 postmenopausal breast cancer patients treated with tamoxifen (study group). The results were compared with those measured in 7 similar ovarian tumors obtained from 5 similar patients without tamoxifen treatment (control group I), and in 9 similar tumors removed from 9 age-matched postmenopausal women (control group II). There were no significant differences with regard to ER or PR expression between the study group and control group I and II (ER = 18.75, 0.0 and 11%, respectively; PR = 43.75, 28.5 and 44%, respectively; p = NS). There were also no significant statistical differences between the three groups when subdividing the ovarian pathologies according to different histological types. From the results obtained in this study, it seems that tamoxifen probably does not have any direct influence on the ovaries of menopausal breast cancer patients.
Tamoxifen administration to postmenopausal women has been described as being associated with various endometrial and other gynecological pathologies. However, different coexisting gynecological pathologies in such patients have not yet been described. In the present study, we assessed the histopathological conditions diagnosed in endometrium, myometrium, and ovaries of 28 postmenopausal breast cancer patients who were treated with tamoxifen (study group) and compared the findings to those obtained from 14 similar patients without tamoxifen treatment (control group I) and from 28 age-matched healthy postmenopausal controls (control group II). All specimens were removed by total abdominal hysterectomy and bilateral salpingo-oophorectomy for various indications. The overall incidence of two or more different coexisting gynecological pathologies was significantly higher among the study group (92.9%) than in control group I or in control group II (42.9 and 50%, respectively; p = 0. 0001). There was no significant statistical difference between the control groups. Overall endometrial (and endometrial-like) origin of pathological conditions was significantly more common in the study group (92.6%) than in control group I (50%; p = 0.00072) and control group II (32.1%; p = 0.0000), while there was no significant difference between the latter two groups. These findings suggest that there might be an association between postmenopausal tamoxifen exposure and the development of such different coexisting or specific single gynecological pathologies originating from the endometrium.
A unique case with diffuse mixed malignant lymphoma was investigated for gene rearrangement on the level of T-cell receptor (TCR), heavy chain immunoglobulin (Ig), and both light chains. Cell phenotype was examined with immunofluorescence techniques using antibodies against surface immunoglobulins (SIg) and the kappa and lambda light chains. Monoclonal antibodies were used against CD3, CD4, CD5, CD8, CD10, CD19, CD22, HLA-DR, and TdT. Gene rearrangement analysis for monoclonality determination was carried out with restricted DNA (EcoR I and Hind III) hybridized with one of the following 32P-labelled probes: T-cell receptor (TCR beta), immunoglobulin heavy chain (JH), k light chain, and lambda light chain. Phenotyping of the cell population from the excised lymph node (LN) revealed the presence of 66% B-cells and 35% T-cells. Most of the B cells (94%) expressed mu heavy chain only. Expression of both light chains was negligible (k = 7% and lambda = 2%). Gene rearrangement, which indicates monoclonality, was positive on the level of TCR, Ig heavy chain, and both light chains. The data obtained suggests a neoplastic transforming event in lymphoid stem cells, which preceded the subsequent differentiation process into either B or T lymphoma.
A prospective study was performed to assess the efficacy of sonohysterography (SHG) in identifying endometrial pathologies among asymptomatic, postmenopausal breast cancer patients treated with tamoxifen. In this study the uterine cavity of 68 such patients with endometrial thickness of > or = 8 mm was prospectively evaluated by SHG. Forty-six (67.6%) patients in whom SHG did not identify any findings in the uterine cavity (negative group) were followed by diagnostic hysteroscopy. Another 22 (32.4%) who were identified by SHG to have abnormal endometrial findings, such as an echogenic or polypoid mass (positive group), were followed by operative hysteroscopy and by postoperative SHG. In the positive group the basal transvaginal sonogram revealed an endometrial echogenic mass in only 10 (45.5%). In the remaining 12 (54.5%) patients, the transvaginal sonogram identified only thick endometrium. In these latter 12 patients, histological assessment confirmed endometrial polyps in 8 (66.7%) and fibroid in 1 (8.3%). Four (18.2%) patients in the positive group had no histological endometrial pathology. Two (50%) of them had a uterine septum as diagnosed during hysteroscopy, in one (25%) operative hysteroscopy failed to resect the endometrial polyp, and in another (25%) there was a false-positive SHG diagnosis. Overall, SHG accurately diagnosed endometrial and/or other intrauterine pathology in 95.5% of these patients. In the 46 patients with "negative" basal SHG features, diagnostic hysteroscopy confirmed this diagnosis. Thus, there was no SHG false-negative diagnosis. Comparing the results of the basal SHG with those of operative hysteroscopy and/or the histopathological findings in the positive group, the sensitivity of SHG was 1.0, the specificity 0.0, positive predictive value 95.5%, and negative predictive value 0.0. It is suggested that SHG is a useful diagnostic tool for the assessment of specific endometrial pathologies in asymptomatic postmenopausal breast cancer patients treated with tamoxifen who were diagnosed by transvaginal sonography to have thick endometrium.
Postmenopausal breast cancer patients who were treated with tamoxifen and progestogens showed a uniform decidual reaction of the endometrium. It is well established that progestogens antagonize the estrogen effect on the endometrium by reducing its receptors in the endometrium. To assess in vivo such a possible effect of progestogens on endometrium primarily exposed to tamoxifen, we analyzed estrogen and progesterone receptors (ER, PR) on endometrial specimens showing decidualization from nine postmenopausal breast cancer patients on tamoxifen and progestogen treatment and on endometrial polyps with areas of decidualization from two other similar patients. ER was weakly detected in the endometrial glands of four (36.4%) patients and in the endometrial stroma of one (9.1%) patient. PR was detected in the endometrial gland of only one (9.1%) patient. No PR was detected in the endometrial stroma. There was no correlation between the length of tamoxifen treatment, the tamoxifen dosage, or the length of progestogen treatment and the ER or PR content, although progestogens were administered for more than 3 consecutive months in all patients. This relatively very low ER and PR content may be attributed to the antagonistic effect of progestogens on the "priming" estrogen-like effect of tamoxifen on the endometrium.