Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 35-year-old female developed cervical adenopathy and mediastinal tumor in 1988. A lymph node biopsy specimen showed nodular sclerosing Hodgkin's disease. She received combination chemotherapy with cyclophosphamide, vincristine, adriamycin and prednisolone, and radiotherapy for mediastinal tumor. She had a complete remission (CR). In September 1990, she developed swelling of the left hip and felt pain in the left hip and thigh. She also noticed swelling of the left inguinal lymph nodes. MRI T2-weighted images showed enlargement and destruction of the fascia and hyperintense signal of the left iliac and gluteus muscle. A biopsy specimen of the inguinal lymph node showed recurrence of Hodgkin's disease of mixed cellularity. She received salvage therapy with ifosfamide, methotrexate, etoposide and procarbazine, and achieved a second CR. The clinical appearance of the skeletal muscle involvement by lymphoma is uncommon, especially in Hodgkin's disease.
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PMID:[Massive skeletal invasion in Hodgkin's disease observed by MRI]. 813 11

Hodgkin's disease (HD) is rarely considered in the differential diagnosis of gastrointestinal (GI) disorders. We report eight cases of GI HD. The patients, ages 16-64, all with stage IV disease of varied histologic subtypes and GI symptoms including pain, upper or lower GI bleeding and/or obstruction. There was diffuse gastric fold thickening in one case, a large submucosal mass along the proximal greater curvature in another case, and a large ulcerating mass along the lesser curvature in the third case. Two cases of jejunal disease manifested as either a short or long segment of luminal narrowing with prominent mucosal nodularity. Another case exhibited a short area of complete mucosal destruction, irregular cavitation and intraluminal filling defect. In one additional case there was diffuse jejunal nodularity. Colonic involvement (two cases) presented as a solitary polypoid mass in transverse colon in one patient and severe narrowing of the descending colon with adjacent mesenteric mass on CT in another. We conclude that although rare in Hodgkin's disease, GI involvement should be considered, particularly in patients with stage IV disease.
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PMID:Hodgkin's disease of the gastrointestinal tract. 778 34

Since its first description in Hodgkin's disease, alcohol-induced pain has subsequently been described both in other neoplasms and in various non-malignant conditions. There seems little doubt that ethyl alcohol itself is responsible, although the mechanism for producing pain remains elusive. We report a case of alcohol-induced pain in a patient with enlarged lymph nodes on the right side of the neck. This symptom led us to make a preliminary diagnosis of Hodgkin's disease, which was subsequently disproved by biopsy, and tuberculous adenitis was established. We have been able to find only one other record of alcohol-induced pain and tuberculous adenitis in a patient reported by Bastin in 1957.
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PMID:Alcohol-induced pain in tuberculous adenitis. 817 40

The purpose of this study was to determine if a radiolabeled murine monoclonal antibody (EOS) directed against eosinophil peroxidase would localize specifically to tumor sites in patients with lymphomas infiltrated by eosinophils. Ten patients with Hodgkin's disease and eosinophilia, three patients with non-Hodgkin's lymphomas and eosinophilia and five control patients received an intravenous injection of 3-10 mg of EOS antibody radiolabeled with 74-155 MBq (2.0-4.2 mCi) of 111In. At intervals of 24, 48 and 72 hr after injection, gamma camera images were obtained along with blood and urine specimens and the imaging results were correlated with the results of other staging modalities. As early as 24 hr after antibody injection, there was clear visualization of identifiable sites of lymphoma with eosinophilia greater than 1 cm in size, including the spleen, bone marrow and lymph nodes. Although EOS also localized nonspecifically to the liver and, in some patients, to the nasopharynx, there was no appreciable uptake in normal bone marrow, spleen, uninvolved lymph nodes, lymphomas without eosinophilia or various other pathologic conditions without eosinophilia. Except for transient pain at tumor sites in three patients, no adverse reactions were noted. We conclude that a radiolabeled monoclonal antibody directed against eosinophil peroxidase localizes to lymphoma sites infiltrated by eosinophils.
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PMID:Radioimmunodetection of Hodgkin's disease and non-Hodgkin's lymphomas with monoclonal antibody to eosinophil peroxidase. 832 80

We report a series of five patients with nonalcoholic chronic pancreatitis who underwent abdominal radiotherapy for Hodgkin's disease (n = 4) or seminoma (n = 1) at doses ranging from 3600 to 4050 rads, 6 to 20 years (median, 7 years) before the onset of pancreatitis. Patients were in complete remission for their malignant disease. Other causes of chronic pancreatitis were excluded. The manifestations of chronic pancreatitis (median follow-up after the diagnosis of pancreatitis, 5 years) were pancreatic pain (n = 5), acute pancreatitis (n = 3), pseudocysts (n = 3), common bile duct stenosis (n = 2), duodenal stenosis (n = 1), splenic vein obstruction (n = 1), diabetes mellitus (n = 4), steatorrhea (n = 4), and pancreatic calcifications (n = 1). Other abdominal radiation injuries were severe chronic ulcer of the genu superius (n = 1), stenosis at the junction of the right and left hepatic ducts (n = 1), and splenic and left renal atrophy (n = 1). In one patient, pathological examination of the pancreas showed signs of chronic pancreatitis, severe fibrous endarteritis, and lack of inflammation. Abdominal radiotherapy should be added to the list of causes of chronic pancreatitis. We suggest that the physiopathology of postradiotherapy chronic pancreatitis is a vascular process.
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PMID:Abdominal radiotherapy is a cause for chronic pancreatitis. 803 46

Epidural spinal cord disease (ESCD), an infrequent complication of systemic non-Hodgkins lymphoma (NHL), can occur at diagnosis or at relapse, and is usually treated with radiotherapy, or infrequently surgical decompression. We retrospectively analyzed 140 patients with intermediate-grade NHL (IG-NHL) who were treated on a dose-intense protocol using doxorubicin, vincristine, and high-dose cyclophosphamide (NHL-15). There were seven episodes of ESCD in six (4.3%) patients. Five episodes were asymptomatic at presentation; one patient had back pain, leg numbness, and tingling; and one had radicular pain and mild leg weakness. None had malignant cells in the CSF. One patient received high-dose dexamethasone after laminectomy for diagnostic biopsy; otherwise, dexamethasone was used only as an anti-emetic prior to chemotherapy. Patients who developed ESCD at diagnosis received the planned course of NHL-15 chemotherapy as treatment for ESCD, and those treated with NHL-15 who developed ESCD at relapse were given a regimen containing ifosfamide, carboplatin, and etoposide (ICE). After chemotherapy alone, five of seven episodes showed radiographic resolution of ESCD and improvement of neurologic deficits. One patient received consolidation radiotherapy (2,700 cGy) to the spine after ICE for relapsed ESCD and had a complete response. One patient had progression of systemic lymphoma and ESCD despite chemotherapy. These data suggest that chemotherapy may be effective as initial treatment of ESCD in IG-NHL and may reduce the potential complications of spinal surgery and radiotherapy.
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PMID:Chemosensitive epidural spinal cord disease in non-Hodgkins lymphoma. 864 45

After being successfully applied to other intraabdominal organs, the laparoscopic approach has been applied to the spleen since 1991. The experience with 17 cases of laparoscopic splenectomy performed due to immune thrombocytopenia purpura (10 instances), hereditary spherocytosis (2 cases), and Hodgkin's disease where the staging was done according to Standford (5 cases), have been reported. With the patient in anti-Trendelenburg position, and the surgeon between the patient's legs, four or five trocars are introduced into the upper abdominal quadrants and the spleen hilum is isolated. Hilar vessels are dissected and ligated with a surgical stapler. A plastic bag is introduced into the abdomen cavity and the spleen is slipped inside; it is then extracted through an umbilical incision after morcellation. Advantages of the open operation include a decrease in postoperative pain, a decrease in pulmonary sequelae, a reduced incidence of subphnic abscesses, and cosmetic advantages. The decrease of postoperative sequelae reduces hospitalization and costs, which are higher for the operation itself (materials and staff's training).
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PMID:Laparoscopic splenectomy in the management of hematological diseases. Surgical technique and outcome of 17 patients. 866 83

Laparoscopic splenectomy in children has been shown to be safe, to reduce postoperative pain and hospital stay, and to accelerate return to full activities. We describe our experience with a four-port "lateral" approach in 18 patients. Patients were placed in the lateral decubitus position and the table was flexed to separate the left subcostal margin and iliac crest. The camera port was inserted at the umbilicus and additional ports were placed in the epigastrium and left lower quadrant. After mobilization of the splenic flexure a port was inserted in the left flank below the 12th rib for elevation of the spleen. A 30 degrees laparoscope was used and the splenic vessels were controlled with an endo-GIA and/or clips. The spleens were placed in a bag, morcellated, and extracted through a port site. Eight females and 10 males with a median age of 12.5 years (5-17 years) and weight of 55.5 kg (17-124 kg) underwent splenectomy of idiopathic thrombocytopenia purpora (10), spherocytosis (6), elliptocytosis (1), and Hodgkin's disease (1). The median operating time was 160 min (90-300 min) and median blood loss was 105 ml (5-350 ml). Accessory spleens were removed in four cases. Three patients required extensions of a port site to remove large spleens which could not be placed in a bag. The sole complication was a transient pancreatitis with associated pleural effusion. The median postoperative hospital stay was 2 days (1-11 days) and time to full activities was 8 days (3-25 days). The lateral approach affords excellent visualization of the splenic vessels, pancreas, and accessory spleens. This approach is safe and reliable and is our preferred approach for laparoscopic splenectomy in children.
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PMID:Pediatric laparoscopic splenectomy using the lateral approach. 869 57

Fifteen patients with refractory Hodgkin's disease were treated in a phase I/II trial with the natural killer (NK)-cell-activating bispecific monoclonal antibody HRS-3/A9, which is directed against the Fc(gamma)-receptor III (CD16 antigen) and the Hodgkin's-associated CD30 antigen, respectively. Median counts of NK cells and of all lymphocyte subsets were considerably decreased in the patients before therapy. HRS-3/A9 was administered 4 times every 3 to 4 days, starting with 1 mg/m2. The treatment was well tolerated, and the maximum tolerated dose was not reached at 64 mg/m2, the highest dose administered because of the limited amounts of HRS-3/A9 available. Side effects were rare and consisted of fever, pain in involved lymph nodes, and a maculopapulous rash. A total of 9 patients developed human antimouse Ig antibodies, and 4 patients developed an allergic reaction after attempted retreatment. A total of 1 complete and 1 partial remission (lasting 6 and 3 months, respectively) [corrected], 3 minor responses (1 to 11+ months), and 1 mixed response were achieved. There was no clear-cut dose-side effect or dose-response correlation. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the murine bispecific antibodies.
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PMID:Treatment of refractory Hodgkin's disease with an anti-CD16/CD30 bispecific antibody. 905 26

Neuropathic pain may result from sustained firing of sensory neurones. The questions are what initiates and what stops that firing? Spontaneous firing of a modified Hodgkin-Huxley model axon is induced here by: (1) a depolarizing shift in the K+ channel activation parameter; and (2) a positive change in the K+ equilibrium potential. The duration and pattern of spontaneous discharge is seen to be critically dependent on the level and kinetics of Na+ channel slow inactivation. Slow inactivation of voltage-gated ion channels could be major factors in the induction and treatment of neuropathic pain.
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PMID:Slow Na+ channel inactivation and bursting discharge in a simple model axon: implications for neuropathic pain. 913 79


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