"Cervical cytology: perspectives from both sides of the Atlantic".
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Biomedical subjects
Publications and source records attributed to C M Lombard.
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Solitary fibrous tumors are rare neoplasms that most commonly involve the pleura, mediastinum, and lung. Because they lack distinctive histologic features, immunologic staining has frequently been employed to exclude other neoplasms in the differential diagnosis. Their reported phenotype to date is generally negative, notably for muscle-type actins, desmin, keratin, and S-100 protein. Although this testing is of some help, it does not serve to distinguish all processes in the differential diagnosis, and when it does, it places too great an emphasis on a negative finding to make a diagnosis. We report here that CD34 monoclonal antibodies reacted with 11 of 14 solitary fibrous tumors in paraffin sections. Thus, they provide a positive marker that distinguishes the solitary fibrous tumor from most elements in the differential diagnosis.
Pathologic findings in eight patients with the eosinophilia-myalgia syndrome, secondary to L-tryptophan ingestion, are reported. Tissue was obtained by biopsy alone in six patients, by biopsy and autopsy in the seventh patient, and by autopsy alone in the eighth patient. Muscle biopsies in five patients demonstrated an inflammatory infiltrate composed predominantly of lymphocytes, histiocytes, plasma cells, and a few eosinophils. The inflammation involved the perimysial and epimysial connective tissue, the walls of some small blood vessels, the perineurium of small nerve twigs, muscle spindles, and fibrous septae of subcutaneous adipose tissue. In two patients with peripheral neuropathy and one patient without overt neuropathy, denervation atrophy of muscle and perimysial and epimysial fibrosis were present. Sural nerve biopsy tissue taken from two patients displayed prominent axonopathy in one, and minimal changes in the second. Pulmonary changes in the two autopsied patients included endothelial cell damage, endovasculitis and fibromyxoid intimal change im arteries and veins, and interstitial pneumonitis with fibrosis.
Bacillary angiomatosis, a recently characterized pseudoneoplastic vascular proliferation caused by a bacterium identical or related to the cat-scratch disease bacillus, usually presents as cutaneous lesions. We report the histologic findings of this disease involving the lymph nodes of two immunocompromised patients. The lymph nodes showed patchy involvement by coalescent nodules of proliferated blood vessels lined by plump endothelial cells with pale cytoplasm. There were foci exhibiting mild to moderate nuclear atypia. Although neutrophil infiltration was prominent in one case, it was minimal in the other. The interstitium was formed by pink-staining material in hematoxylin-eosin-stained sections, and this proved to be aggregated bacilli on Warthin-Starry stain. Recognition of this potentially fatal disease is important because it is curable with antibiotics.
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Opportunistic infection with the causative agent of cat scratch disease may be responsible for an unusual vascular proliferative lesion, referred to as bacillary epithelioid angiomatosis, previously described only in human immunodeficiency virus (HIV)-infected patients. We present a case of an HIV-infected patient with bacillary epithelioid angiomatosis involving the liver and bone marrow causing progressive hepatic failure. We also report a case of a cardiac transplant recipient with hepatic and splenic bacillary epithelioid angiomatosis manifesting as a fever of unknown origin, a previously unreported event in a non-HIV-infected patient. These cases represent the first documentation of bacillary epithelioid angiomatosis with visualization of cat scratch-like organisms involving internal organs.
It is widely believed that thoracotomy is necessary to obtain biopsy specimens adequate for the histopathologic demonstration of pulmonary Wegener's granulomatosis (WG). We report five patients with WG who were diagnosed by transbronchial biopsy (TBB). In three cases, a diagnosis of WG was made by TBB alone. In the other two patients, subsequent open lung biopsies confirmed the TBB findings but did not add essential diagnostic information. Our experience suggests TBB may be appropriate as the initial diagnostic procedure in selected cases of suspected WG. This approach requires an understanding of the diverse histologic features of WG and the correlation of clinical and pathologic data.
We report the findings of lung biopsies from five patients with anti-basement membrane antibody-associated Goodpasture's syndrome (ABMA-GS). In four patients, pulmonary capillaritis with hemorrhage was found on lung biopsy, confirming that pulmonary capillaritis can be found in ABMA-GS. Although alveolar hemorrhage was the dominant pathologic finding in four of our five patients, all five patients had evidence of injury at the level of the alveolar wall, manifested by hyaline membranes and widening of alveolar walls by edematous connective tissue. In one of our patients, alveolar hemorrhage was only focal, and diffuse alveolar damage was the dominant pathologic finding. This pattern of lung disease has not been previously described in ABMA-GS.
Patients with systemic necrotizing vasculitis frequently present as diagnostic dilemmas. In previous series of patients with polyarteritis nodosa, less than one third were diagnosed antemortem. Although current clinical awareness of systemic necrotizing vasculitis is greater than in the past and procedures for the diagnosis of these diseases have improved, patients commonly present with atypical features. The diagnosis of a systemic necrotizing vasculitis frequently remains unsuspected or unproven until an involved tissue is biopsied. We report an unusual case of systemic necrotizing vasculitis in which the diagnosis was confirmed by a transbronchial biopsy of the lung which demonstrated pulmonary capillaritis with hemorrhage.
Four cases of an unusual histologic variant of Wegener's granulomatosis, diagnosed by open lung biopsy, are described. In addition to pathergic necrosis, granulomatous inflammation, and vasculitis, intense stromal eosinophilia was observed in the absence of peripheral blood eosinophilia or clinical asthma. A microangiitis was also present in all four cases. Clinically, all patients presented with systemic disease and responded to immunosuppressive therapy including steroids and cyclophosphamide. This form of Wegener's disease poses problems in its distinction from allergic angiitis and granulomatosis, and the differential diagnosis of these two entities is discussed.
We report 3 new cases of phyllodes type of atypical prostatic hyperplasia. This lesion is characterized by epithelial and stromal proliferation. Stromal changes are the most characteristic finding in phyllodes type of atypical prostatic hyperplasia, which show atypical cells with enlarged, hyperchromatic sarcomatoid nuclei. Mitotic figures are not present. Although the histological appearance may mimic that of cystosarcoma phyllodes of the breast, this pattern is present only focally or not at all in phyllodes type of atypical prostatic hyperplasia. On computerized tomographic imaging phyllodes type of atypical prostatic hyperplasia has a distinct appearance. These patients can be expected to have a benign clinical course and distant metastases have not been reported. Treatment is by surgical excision as in benign prostatic hyperplasia.
Two cases of pulmonary eosinophilia associated with coccidioidal infections are reported. Pulmonary eosinophilia in these cases represents a hypersensitivity reaction to the fungus. Histologically, the pulmonary eosinophilia in these cases closely mimicked or appeared identical to idiopathic chronic eosinophilic pneumonia. Coccidioides immitis organisms were rare or absent in the areas of pulmonary eosinophilia. Recognition of this phenomenon is important for proper care of the patient.
We report three cases of pulmonary veno-occlusive disease which developed following treatment for malignant neoplasms. Two patients received single agent BCNU chemotherapy for malignant gliomas. The third patient underwent combination radiation and chemotherapy for Hodgkin's disease. Isolated case reports of pulmonary veno-occlusive disease following therapy for malignant disease are reviewed and clinical features summarized. Pulmonary veno-occlusive disease in this setting is thought to be rare. However, the diagnosis is rarely suspected clinically and is difficult to diagnose pathologically. Therefore, the true incidence of this complication is unknown and may be higher than believed. It is important that both clinician and pathologist be aware of this entity; otherwise, elastic tissue stains may not be performed and the diagnosis missed.
Four patients who developed both pulmonary histiocytosis X and carcinoma of the lung are described. Some authors have hypothesized that patients with pulmonary histiocytosis X-associated scarring are also at increased risk of developing lung carcinoma. However, case reports of this phenomenon are rare. The cases presently reported may support this hypothesis, although additional factors, such as cigarette smoking, may better explain the association.
We describe a case of polyarteritis nodosa in a 66-year-old woman who presented with multiple neurologic complaints. The case remained perplexing to the clinicians caring for her until a total abdominal hysterectomy and bilateral salpingo-oophorectomy were performed for a right adnexal mass noted on physical examination and computed tomography scan. Although unsuspected polyarteritis nodosa has been diagnosed on examination of other tissues removed at surgery, this is the first case of polyarteritis nodosa diagnosed following total abdominal hysterectomy and bilateral salpingo-oophorectomy reported in the English literature.
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A delayed hemolytic transfusion reaction (DHTR) occurring in a 30-year-old Caucasian man is described. His blood groups were B, CDe/cDE (R1R2, f-) K-, S-s+, Fy (a + b-), and Jk (a + b +). Eight days after receiving two units of packed red blood cells, his urine was strongly positive for hemoglobin; serum-free hemoglobin was 125 mg/dl. Serum contained a clearly reactive Rh antibody of anti-f specificity and a weakly reactive anti-Kell. The DHTR was probably caused by an anti-f alloantibody appearing as an anamnestic response to transfusion of seemingly compatible, but f-positive blood.