Paraneoplastic syndromes

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Dual paraneoplastic syndromes in a patient with small cell lung cancer: a case report...

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Paraneoplastic syndromes dĩ nhiên thấy trong ung thư, và có khi xuất hiện hàng tháng truớc khi ung thư hiện ra. Oncologists nhiều khi nhận consultation từ các y sĩ khác hỏi: "bnhân mất ký, có phải paraneoplastic hay không". Những trường hợp này, tôi làm work up (đi tìm bệnh) như sau (dĩ nhiên là đã phải hỏi history và physical exam một cách cẩn thận - để dễ nói chuyện, cứ cho là history và physical không tìm ra cái gì lạ): Đếm máu như thường lệ (đi tìm leukopenia, leukocytosis, anemia, thrombocytosis, thrombocytopenia) (thrombocytosis có khi...

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Paraneoplastic Encephalomyelitis and Focal Encephalitis The term encephalomyelitis describes an inflammatory process with multifocal involvement of the nervous system, including brain, brainstem, cerebellum, and spinal cord. It is often associated with dorsal root ganglia and autonomic dysfunction. For any given patient, the clinical manifestations are determined by the area or areas predominantly involved, but pathology almost always reveals abnormalities (inflammatory infiltrates, neuronal loss, gliosis) beyond the symptomatic regions. ...

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Encephalitis and Encephalomyelitis: Treatment Most types of paraneoplastic encephalitis and encephalomyelitis respond poorly to treatment. Stabilization of symptoms or partial neurologic improvement may occasionally occur, particularly if there is a satisfactory response of the tumor to treatment. The roles of plasma exchange, IVIg, and immunosuppression have not been established. Approximately 30% of patients with anti-Ma2-associated encephalitis respond to treatment of the tumor (usually a germ-cell neoplasm of the testis) and immunotherapy.

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Paraneoplastic myelitis may present with upper or lower motor neuron symptoms, segmental myoclonus, and rigidity. This syndrome can appear as the presenting manifestation of encephalomyelitis and may be associated with SCLC and serum anti-Hu, anti-CV2/CRMP5, or anti-amphiphysin antibodies. Paraneoplastic myelopathy can also produce several syndromes characterized by prominent muscle stiffness and rigidity.

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Vasculitis of the nerve and muscle causes a painful symmetric or asymmetric distal sensorimotor neuropathy with variable proximal weakness. It predominantly affects elderly men and is associated with an elevated erythrocyte sedimentation rate and increased CSF protein concentration. SCLC and lymphoma are the primary tumors involved. Pathology demonstrates axonal degeneration and T cell infiltrates involving the small vessels of the nerve and muscle. Immunosuppressants (glucocorticoids and cyclophosphamide) often result in neurologic improvement.

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Specific Paraneoplastic Neurologic Syndromes (Table 97-3) Table 97-3 Antibody-Associated Paraneoplastic and Nonparaneoplastic Syndromesa Antibodies Paraneoplastic Syndrome Frequent t Infrequen stic Nonparaneopla Limbic encephalitis Ma2, Hu, CV2/CRMP5, anti-NR1/NR2 of NMDA receptor Tr, VGKC VGKC Cerebellar degeneration Yo, Tr, mGluR1; Gliadin, GAD P/Q VGCC, Hu, MAZ Zic, CV2/CRMP5, Ma1-2 Ri, Hypothalamic, brainstem encephalitis Ma2, Hu P5 CV2/CRM Encephalomye litis Hu, Zic P5, CV2/CRM Ri, amphiphysin Chorea P5 CV2/CRM Opsoclonusmyoclonus Ri Yo, Hu, Ma2, Stif...

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Pathogenesis Most PNDs are mediated by immune responses triggered by neuronal proteins (onconeuronal antigens) expressed by tumors. In PNDs of the central nervous system (CNS), many antibody-associated immune responses have been identified (Table 97-2). These antibodies usually react with the patient's tumor, and their detection in serum or cerebrospinal fluid (CSF) strongly predicts the presence of cancer. The target antigens are usually intracellular proteins with roles in neuronal development and function.

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PND of the Central Nervous System and Dorsal Root Ganglia When symptoms involve brain, spinal cord, or dorsal root ganglia, the suspicion of PND is usually based on a combination of clinical, radiologic, and CSF findings. In these cases, a biopsy of the affected tissue is often difficult to obtain, and although useful to rule out other disorders (e.g., metastasis, infection), neuropathologic findings are not specific for PND. Furthermore, there are no specific radiologic or electrophysiologic tests that are diagnostic of PND. ...

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Neuronal cell-surface antigens can be the target of antibodies in some patients with paraneoplastic encephalitis. A few of these antigens have been identified, including the NR1/NR2 subunits of NMDA receptors (Fig. 97-1) and voltage-gated potassium channels (VGKC). These disorders are more responsive to immunotherapy than those associated with immune responses to intracellular antigens. Figure 97-1 Antibodies to NR1/NR2 subunits of the NMDA receptor in a patient with paraneoplastic encephalitis and ovarian teratoma.

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Tumor-Induced Hypoglycemia Caused by Excess Production of IGF-II (See also Chap. 339) Mesenchymal tumors, hemangiopericytomas, hepatocellular tumors, adrenal carcinomas, and a variety of other large tumors have been reported to produce excessive amounts of insulin-like growth factor type II (IGF-II) precursor, which binds weakly to insulin receptors and strongly to IGF-I receptors, leading to insulin-like actions. The gene encoding IGF-II resides on a chromosome 11p15 locus that is normally imprinted (that is, expression is exclusively from a single parental allele).

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Hematologic Syndromes: Introduction The elevation of granulocyte, platelet, and eosinophil counts in most patients with myeloproliferative disorders is caused by the proliferation of the myeloid elements due to the underlying disease rather than a paraneoplastic syndrome. The paraneoplastic hematologic syndromes in patients with solid tumors are less well characterized than the endocrine syndromes because the ectopic hormone(s) or cytokines responsible have not been identified in most of these tumors (Table 96-2).

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Granulocytosis Approximately 30% of patients with solid tumors have granulocytosis (granulocyte count 8000/µL). In about half of patients with granulocytosis and cancer, the granulocytosis has an identifiable nonparaneoplastic etiology (infection, tumor necrosis, glucocorticoid administration, etc.). The other patients have proteins in urine and serum that stimulate the growth of bone marrow cells.

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Clinical Manifestations Patients with cancer who develop deep venous thrombosis usually develop swelling or pain in the leg, and physical examination reveals tenderness, warmth, and redness. Patients who present with pulmonary embolism develop dyspnea, chest pain, and syncope, and physical examination shows tachycardia, cyanosis, and hypotension. Some 5% of patients with no history of cancer who have a diagnosis of deep venous thrombosis or pulmonary embolism will have a diagnosis of cancer within 1 year.

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Harrison's Internal Medicine Chapter 97. Paraneoplastic Neurologic Syndromes Paraneoplastic Neurologic Syndromes: Introduction Paraneoplastic neurologic disorders (PNDs) are cancer-related syndromes that can affect any part of the nervous system (Table 97-1). They are remote effects of cancer, caused by mechanisms other than metastasis or by any of the complications of cancer such as coagulopathy, stroke, metabolic and nutritional conditions, infections, and side effects of cancer therapy. In 60% of patients the neurologic symptoms precede the cancer diagnosis.

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Ectopic hormone production would only be an epiphenomenon associated with cancer if it did not result in clinical manifestations. Excessive and unregulated production of hormones such as ACTH, PTHrP, or vasopressin can lead to substantial morbidity and can complicate the cancer treatment plan. Moreover, the paraneoplastic endocrinopathies are sometimes the presenting feature of underlying malignancy and may prompt the search for an unrecognized tumor.

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Harrison's Internal Medicine Chapter 96. Paraneoplastic Syndromes: Endocrinologic/Hematologic Paraneoplastic Syndromes: Endocrinologic/Hematologic: Introduction In addition to local tissue invasion and metastasis, neoplastic cells can produce a variety of peptides that that can stimulate hormonal, hematologic, dermatologic, or neurologic responses. Paraneoplastic syndromes refer to the disorders that accompany benign or malignant tumors but are not directly related to mass effects or invasion.

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Etiology Humoral hypercalcemia of malignancy (HHM) occurs in up to 20% of patients with cancer. HHM is most common in cancers of the lung, head and neck, skin, esophagus, breast, genitourinary tract, and in multiple myeloma and lymphomas. Several distinct humoral causes of HHM occur, most commonly overproduction of PTHrP. In addition to acting as a circulating humoral factor, bone metastases (e.g., breast, multiple myeloma) may produce PTHrP, leading to local osteolysis and hypercalcemia.

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Etiology Vasopressin is an antidiuretic hormone normally produced by the posterior pituitary gland. Ectopic vasopressin production by tumors is a common cause of the syndrome of inappropriate antidiuretic hormone (SIADH), occurring in at least half of patients with SCLC. Compensatory mechanisms, such as decreased thirst, suppression of aldosterone, and production of atrial natriuretic peptide (ANP), may mitigate the development of hyponatremia in patients who produce excessive vasopressin.

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Rarely, corticotropin-releasing hormone (CRH) is produced by pancreatic islet tumors, SCLC, medullary thyroid cancer, carcinoids, or prostate cancer. When levels are high enough, CRH can cause pituitary corticotrope hyperplasia and Cushing's syndrome. Tumors that produce CRH sometimes also produce ACTH, raising the possibility of a paracrine mechanism for ACTH production. A distinct mechanism for ACTH-independent Cushing's syndrome involves ectopic expression of various G protein–coupled receptors in the adrenal nodules.

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