[Pulmonary lymphangitis, an infrequent manifestation of prostatic adenocarcinoma].
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A study was conducted between January 2003 and June 2004 on 19,082 carthorses in 28 towns in Ethiopia to investigate the epidemiology of equine histoplasmosis (EH). Clinical and microscopic examinations were used and an overall prevalence of 18.8% (3579/19082) was recorded. Statistically significant (P<0.001) differences was observed in the average prevalence with high, medium, and low prevalence categories. The highest prevalence (39%) was recorded at Mojo while the lowest (0.0%) was recorded at five towns, namely, Agaro, Bokoji, Debre Berhan, Dinsho, and Sagure. The prevalence of EH was not associated (R=0.08, F=0.15, P=0.71) with the mean annual rainfall but was associated (R=0.64, F=11.5, P<0.01) with the average annual temperature. Statistically significant (R=0.57, F=12.34, P<0.01) association was observed between the altitude of the study towns and the prevalence of EH. Moreover, the number of cases of EH increased significantly (R=0.88, F=90.9, P<0.001) with the horse population in the towns. In general, EH was prevalent in hot and humid towns with an altitude ranging from 1500m above sea level (asl) to 2300masl but was nil or low in cold and in dry and windy towns. It was concluded that EH is prevalent in Ethiopia and warrants the initiation of a control strategy.
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A cross-sectional study was conducted to determine the prevalence of Histoplasma farciminosum in 2,907 carthorses using clinical and microbiological examinations at three towns (Debre Zeit, Mojo and Nazareth), Central Ethiopia, between December 1999 and January 2001. An overall prevalence of 26.2% (762/2,907) was recorded; the highest prevalence (39.1%) being recorded at Mojo whereas the lowest (21.1%) was recorded at Nazareth. The difference in prevalence among the three towns was highly significant (chi(2) = 76.92, P<0.0001). Carthorses found at Mojo [OR =2.4, CI=(1.9-3.0), P<0.0001] and Debre Zeit [OR=1.9, CI=(1.5-2.3), P<0.0001] were at higher risk of infection than those found at Nazareth. The mycelial and yeast forms of the Histoplasma capsulatum variety farciminosum were isolated on the Sabouraud's dextrose agar. The results of the present study showed the rampant occurrence of histoplasmosis farciminosi at the three towns and indicates the need for further nationwide investigation into the disease to design sound control strategy.
The case of a 7 year-old who presented with lymphangitic carcinomatosis revealed by lung biopsy and secondary to renal adenocarcinoma is described. This biopsy was performed because of radiologic and clinical signs associating bilateral interstitial infiltrates, mediastinal adenopathy and gradually increasing respiratory distress. Despite treatment, the child died two weeks later.
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BACKGROUND: Cutaneous lymphangitis carcinomatosis from cervical carcinoma is a very rare form of tumor metastatization; only anecdotal cases are reported in the literature. Most of the patients with skin relapse experienced metastasis as a single or multiple nodules. CASE: A case of cutaneous lymphangitis carcinomatosis mimicking contact dermatitis was diagnosed at our institution in a patient affected by cervical carcinoma stage IIB. Palliative chemotherapy with paclitaxel was started and the patient experienced complete clinical response. The hypothetical mechanism of spread and the unusual manifestation of relapse are described. CONCLUSION: In a woman with a history of cervical cancer, a diffuse pruritic skin eruption should alert the clinician to the possibility of cutaneous carcinomatous lymphangitis. If a lymphangitis carcinomatosis is diagnosed, systemic intravenous chemotherapy should be considered.
Two different types of hereditary late-onset lymphedema are presented. In one family the father and one son had recurrent streptococcal lymphangitis beginning in childhood. In the son there was lymphatic hypoplasia in both legs with the infection having only occurred in one. Prophylaxis with penicillin prevented the recurrent lymphangitis. Because of 30 years of untreated lymphangitis, the father has chronic severe lymphedema. The second type, lymphedema associated with extra eyelashes (distichiasis) and a wide spinal canal, occurred in a woman whose lymphedema began at age 12 but in whom the hereditary nature of the disorder was not recognized until she was 29. Both of these types of late-onset lymphedema, lymphedema with lymphangitis and lymphedema with distichiasis, are due to autosomal dominant genes. Both families would have benefited from early diagnosis of the cause of the lymphedema.
The author describes changes in the skin, lesions in the lymph vessels and changes seen on lymphography. Amongst cutaneous lesions, necrosing lymphangitis or gangrenous lymphangitis are the most serious. In the calf, they develop after an extensive episode of acute erysipelas. In erysipelas, the most common cutaneous lesion, the course varies according to associated disturbances, lymphatic and lymphnode. Combining of these lesions results in the most severe forms of obliterating thrombolymphangitis, capable of simulating venous thromboses of the lower limbs. In abscesses associated wtih severe erysipelas, massive eosinophilia found. Endoarterial therapy is invariably selected. Lymphographic appearances are dependent upon the stage of progression of inflammation. Disappearance, increase in vascular parietal permeability, varicose and ectasic appearance of the lymphatics may be seen in the superficial and deep collecting vessels. During the chronic phase, lesions are more extensive and more obvious. They are characteristic of severe lymphatic stasis. Histopathological studies show lymphangitis and perilymphangitis characterized by polynuclear neutrophil infiltration during the acute phase. At a more advanced stage, obliterating endolymphangitis and acute thrombolymphangitis are followed at the chronic phase by fibrous lymphangitis.
OBJECTIVE: To report a case of erlotinib-induced breast cancer regression. CASE SUMMARY: A 38-year-old woman developed bilateral locoregional malignant cutaneous lymphangitis following a right subcutaneous mastectomy and 3 months of adjuvant chemotherapy. After several systemic chemotherapy regimens, the lymphangitis worsened rapidly, with progressive skin ulceration. Morphine and dexamethasone were given, with suboptimal pain control. A chemotherapy regimen of gemcitabine and vinorelbine was started. After 2 full-dose administrations, while lymphangitis continued to worsen, erlotinib 150 mg/day was added to the regimen. After 10 weeks of treatment, pain subsided and analgesics were discontinued. Physical examination revealed a partial regression of malignant cutaneous lymphangitis and pulmonary metastases, with resolution of ulceration. DISCUSSION: There has been increased interest in epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in the treatment of breast cancer. Gefitinib has shown a low level of efficacy, while preliminary clinical data on erlotinib were not conclusive and suggested lack of clinical activity. Molecular analysis of the tumor in our patient revealed a profile predictive of response to EGFR selective inhibitors in some patients with lung cancer. CONCLUSIONS: The addition of erlotinib to our patient's chemotherapy regimen resulted in antitumor activity in breast cancer in which an activated EGFR pathway was demonstrated. This finding is consistent with available preclinical and clinical data on EGFR tyrosine kinase inhibitors across tumor types and supports the efforts to optimize EGFR selective inhibitors in treating breast cancer and other malignancies.
INTRODUCTION: It is unanimously acknowledged that the aetiopathogenesis of Crohn's disease (CD) is still a mystery despite the fact that almost 70 years have elapsed since it nosological identification. Another mystery and major problem of CD of the bowel is its histopathology, which has yet to be clarified; consequently, we do not know what kind of disease it is, that is to say, which process, among the ones known to us, it actually corresponds to. MATERIAL AND METHODS: The present paper presents the results of a new histopathological interpretation of the disease on the basis of 100 surgical cases of Crohn's ileitis and ileocolitis. RESULTS AND CONCLUSIONS: The disease is not a form of enteritis, but a lymphoedema of the intestinal wall, caused by a congenital lack of patency of the mesenteric lymphatic collectors, giving rise to stasis of lymph in the lymphatic network of the corresponding bowel segment and consequently to hypertension which dilates the lymph vessels in the intestinal wall. The lymph, which cannot be reabsorbed by the veins, because the venous wall denies entry to protein macromolecules, accumulates in the interstitial space with the result that the intestinal wall thickens considerably. Since the process takes place in the intestine perfused by a continuous flow of septic matter, the process is complicated by the development of lymphocytic lymphangitis, which occurs throughout almost the entire lymphatic network, obstructing the dilated lumen, limiting the dispersion of lymph and preventing gross spread of the intestinal contents into the dilated lymphatic vessels. The lymphocytic lymphangitis causes "transparietal phlogosis", which is rightly regarded as a characteristic of the disease, but is wrongly interpreted by those who have studied it. This transparietal phlogosis is neither excessive nor disproportionate to its task of obstructing the intestinal contents; it is transparietal because the lymphatic network where it takes places is itself transparietal. The reactive lymphocytic lymphangitis prevents the gross spread of the intestinal contents into the dilated lymphatic network, as stated above, but cannot prevent the limited uptake of dissolvable toxic bacterial substances (FMLP, PG-PS, LPS) conjugated in immuno-complexes. The immuno-complexes developing in the lymphatic network undergo lymph- and blood-borne spread, causing; obstructive lymphangitis in branches of the mesenteric lymphatic collectors which are still patent, increasing the degree of lymphatic obstruction and thus the extent of the intestinal lesions; general complications of so-called "metastatic Crohn's disease", which were once interpreted as autoimmune processes, but actually correspond to forms of vasculitis which may be localised in any of the organs or apparatuses of the body, sometimes proving extremely serious. Lymph dispersion in the intestinal lumen, causes not only diarrhoea, but often also lymphocytopenia and hypoproteinaemia, and therefore an immunodepression syndrome, which in the long term may give rise to intestinal and extraintestinal cancer.
The natural history of lymphatic disease in human filariasis remains unclear, but recurrent episodes of acute lymphangitis are believed to constitute a major risk factor for the development of chronic lymphoedema and elephantiasis. Prospective analysis of 600 patients referred to the filariasis clinic of the Centro de Pesquisas Aggeu Magalhães/FIOCRUZ in Recife, Brazil, indicated that 2 distinct acute syndromes accompanied by lymphangitis occur in residents of this filariasis-endemic area. One syndrome, which we call acute filarial lymphangitis (AFL), is caused by the death of adult worms. It is relatively uncommon in untreated persons, usually is asymptomatic or has a mild clinical course, and rarely causes residual lymphoedema. The second syndrome, of acute dermatolymphangioadenitis (ADLA), is not caused by filarial worms per se, but probably results from secondary bacterial infections. ADLA is a common cause of chronic lymphoedema and elephantiasis in Recife as well as in other areas of Brazil where lymphatic filariasis is not present. The syndromes of AFL and ADLA can be readily distinguished from each other by simple clinical criteria.
The lungs of 34 patients who had died of carcinoma of the breast and pulmonary lymphangitis carcinomatosa were prepared by air insufflation and then examined radiologically and histologically. The results were compared with x-ray examination performed just before death. The interstitial pattern of lymphangitis is due to tumour cell infiltration of septal, peri-vasal and peri-bronchial lymphatics, and to fibrosis. Pleural effusions developed in 17 patients and were twice as frequent on the side of the breast tumour. Hilar lymph node enlargement was found in only five cases, although histological involvement was proven in 19. Theories concerning the mode of propagation of pulmonary lymphangitis carcinomatosa are discussed.