Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a 16-month period children presenting to a pediatric outpatient facility from an area with a high tuberculosis incidence (> 400/100,000) and suspected of having respiratory tuberculosis (TB) were evaluated for close contact with adult pulmonary tuberculosis, weight loss, symptom duration, respiratory signs, lymphadenopathy and hepatosplenomegaly and by chest radiography and tuberculin testing (Mantoux or tine). Probable tuberculosis was diagnosed in 258 children and was confirmed in 109 (42%) patients with a mean age of 31 months by culture of Mycobacterium tuberculosis from gastric aspirate or another source. Eleven children with confirmed TB had a normal chest radiograph. After review of special investigations, clinical course and follow-up of the remaining 149 children, 86 children (58%) with a mean age of 32.4 months were considered to have probable TB and 63 (42%) with a mean age of 27 months not to have TB. Significantly fewer children in the "not TB" group than in the confirmed and probable TB groups had a close adult pulmonary tuberculosis contact (13 (21%) and 95 (49%), respectively; P < 0.01). There was no difference between the "not TB" group and the confirmed and probable TB groups in the proportion presenting with weight loss, cough or other respiratory symptoms, a symptom duration > 2 weeks, the presence of bronchial breathing, wheeze, hepatomegaly or splenomegaly or peripheral lymphadenopathy. Final diagnoses in the "not TB" group included bacterial or viral pneumonia or bronchopneumonia in 37, asthma often accompanied by segmental collapse in 9 and cavitating pneumonia in 3 children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory tuberculosis in childhood: the diagnostic value of clinical features and special investigations. 776 Nov 83

Pooling of blood in the spleen is a frequent occurrence in children with sickle cell diseases, particularly in the first few years of life, resulting in what is termed "splenic sequestration crisis." The spectrum of severity in this syndrome is wide, ranging from mild splenomegaly to massive enlargement, circulatory collapse, and even death. The diagnosis is usually clinical, based on the enlargement of the spleen with a drop in hemoglobin level by > 2 g/dl, and it is rare that imaging studies are ordered. However, in the patient who presents to the emergency department with non-specific findings of an acute abdomen, it is important to recognize the appearance of sequestration on imaging studies. We studied seven patients utilizing contrast-enhanced CT scans and found two distinct patterns--multiple, peripheral, non-enhancing low-density areas or large, diffuse areas of low density in the majority of the splenic tissue. Although radiological imaging is not always necessary to diagnose splenic sequestration, in those situations where this diagnosis is not immediately obvious, it makes an important clarifying contribution.
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PMID:CT imaging of splenic sequestration in sickle cell disease. 1114 89

From 1995-2002, 14 patients with predominantly prehepatic, noncirrhotic portal hypertension were evaluated. At presentation, the eight females and six males had a mean age of 9 years (range 2-18). Seven were admitted with gastrointestinal, mostly esophageal bleeding, three with splenomegaly, three with hepato-pulmonary syndrome, and one with hyperammonemia. Imaging studies showed portal vein obstruction in six patients and non-obstructed but frequently anomalous vascular patterns, including hypoplasia of the portal vein, in the remaining eight patients. At the onset, liver function was marginally abnormal in all patients, but thrombocytopenia of approximately 100 x 10(9)/L was consistently observed, probably reflecting chronic mild consumption coagulopathy and hypersplenism. The most striking and frequent histopathologic finding in 25 liver samples, was the presence of hypoplastic portal triads with collapsed portal vein radicles. In contrast, other triads showed markedly distended and misshapen portal vein radicles and likely lymphatics. These two patterns of collapse and distention presumably reflect areas of impaired versus overloaded intrahepatic portal venous flow. Some of the biopsies showed variable portal/sinusoidal fibrosis. Four patients (two with intestinal bleeding, two with hepatopulmonary syndrome) required liver transplants and are doing well. Eight patients are doing well clinically after surgical or spontaneous vascular shunting. Two patients with intestinal bleeding and hepato-pulmonary syndrome, respectively) who had congenital dyskeratosis, underwent bone marrow transplantation and died of nonhepatic-related complications. It is possible to suggest prehepatic causes of portal hypertension even in needle biopsies when collapsed portal vein radicles are present in portal triads, but more than one biopsy sample with larger bore bioptomes may be required to see the changes. Conversely, identifying these changes may suggest to the clinicians the need to work-up a patient for portal hypertension.
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PMID:Pathology of noncirrhotic portal hypertension: clinicopathologic study in pediatric patients. 1470 35

CASE DESCRIPTION-An 8-year-old castrated male German Shepherd Dog was evaluated because of abdominal distension, retching, and vomiting. CLINICAL FINDINGS-Gastric dilatation-volvulus was suspected on the basis of the dog's signalment, history, clinical signs, and results of clinicopathologic analyses and abdominal radiography. Celiotomy was performed, and gastric dilatation-volvulus was confirmed along with splenomegaly. Gastric invagination was performed over an area of gastric necrosis. The dog was reevaluated 21 days later after an episode of collapse. Findings of physical examination and clinicopathologic analyses were suggestive of internal hemorrhage. Abdominal ultrasonography and subsequent celiotomy revealed severe gastric ulceration at the gastric invagination site, splenic torsion, and a focal splenic infarct. TREATMENT AND OUTCOME-Splenectomy and gastrectomy of the necrotic tissue were performed. The dog was discharged from the hospital, and the owner was instructed to administer gastroprotectants and feed the dog a bland diet. The dog was reported to be healthy 3.25 years after surgery. CLINICAL RELEVANCE-Findings suggest that complications associated with the gastric invagination procedure include severe gastric ulceration that may require subsequent surgery. Prolonged treatment with gastroprotectants following gastric invagination surgery may be necessary to avoid gastric ulceration in dogs.
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PMID:Gastric ulceration subsequent to partial invagination of the stomach in a dog with gastric dilatation-volvulus. 1678 79

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.
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PMID:Two fatal cases of selenium toxicity. 1689 Oct 71

Envenomation by a spotted black snake (Pseudechis guttatus), following multiple bites on the buccal mucosa of a captive maned wolf (Chrysocyon brachyurus), caused the animal's collapse, hemolysis, rhabdomyolysis, local tissue necrosis, hepatic and renal failure, and subsequent death. The wolf died despite intensive supportive care including antivenom administration, fluid support, and a blood transfusion. Gross necropsy findings included myocardial and intestinal hemorrhage, pulmonary congestion, hepatomegaly, and splenomegaly. Microscopic examination of formalin-fixed tissues demonstrated pulmonary and abdominal visceral hemorrhage, acute nephrosis with casts, multifocal hepatic necrosis, and splenic congestion.
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PMID:Spotted black snake (Pseudechis guttatus) envenomation in a maned wolf (Chrysocyon brachyurus). 1793 61

In 2006 an outbreak of canine distemper affected 14 young domestic ferrets in Barcelona, Spain. Their clinical signs included a reduced appetite, lethargy, dyspnoea, coughing, sneezing, mucopurulent ocular and nasal discharges, facial and perineal dermatitis, diarrhoea, splenomegaly and fever. Late in the course of the disease, general desquamation and pruritus, and hyperkeratotic/crusting dermatitis of the lips, eyes, nose, footpads, and perineal area were observed. None of the ferrets developed neurological signs. Non-regenerative anaemia and high serum concentrations of alpha- and beta-globulins were the most common laboratory findings. Most of the animals died or were euthanased because of respiratory complications. Postmortem there were no signs of lung collapse. Distemper was diagnosed by direct immunofluorescence of conjunctival swabs or pcr of several organs, and histology revealed the characteristic eosinophilic intracytoplasmic and intranuclear inclusion bodies of canine distemper virus in several organs. The minimum incubation periods calculated for six of the ferrets were 11 to 56 days, and in 13 of the ferrets the signs of disease lasted 14 to 34 days. Inclusion bodies compatible with infection by herpesvirus were found in the lungs of one of the ferrets.
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PMID:Outbreak of canine distemper in domestic ferrets (Mustela putorius furo). 1872 66

Case reports of severe idiopathic portal hypertension (IPH) requiring liver transplantation are very rare. We report the case of a 65-year-old woman who was diagnosed as having IPH. At the age of 60 years, her initial symptom was hematemesis, due to ruptured esophageal varices. Computed tomography of the abdomen showed splenomegaly and a small amount of ascites, without liver cirrhosis. She was diagnosed as having IPH and followed-up as an outpatient. Five years later, she developed symptoms of a common cold and rapidly progressive abdominal distension. She was found to have severe liver atrophy, liver dysfunction, and massive ascites. Living donor liver transplantation was then performed, and her postoperative course was uneventful. Histopathological findings of the explanted liver showed collapse and stenosis of the peripheral portal vein. The areas of liver parenchyma were narrow, while the portal tracts and central veins were approximate one another, leading to a diagnosis of IPH. There was no liver cirrhosis. The natural history of refractory IPH could be observed in this case. Patients with end-stage liver failure due to severe IPH can be treated by liver transplantation.
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PMID:Acute deterioration of idiopathic portal hypertension requiring living donor liver transplantation: a case report. 1897 82

A 4-year-old male, castrated Saint Bernard was evaluated for acute onset of lethargy and collapse. Moderately severe anemia and splenomegaly were noted. Immune mediated hemolytic anemia was initially suspected. Abdominal ultrasound demonstrated an absence of splenic blood flow. Splenic torsion was confirmed on exploratory laparotomy and a splenectomy was performed.
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PMID:A case of splenic torsion with progressive anemia and thrombocytopenia. 2067 99

Rickesttsial diseases are a group of diseases caused by obligate intracellular gram negative bacilli and transmitted to man by arthropod vectors (except Q fever). It is increasingly realised that rickesttsial diseases are underdiagnosed. It is now well documented that rickettsial disease is prevalent all over India, in pockets. The hallmark of rickettsial infection is microvasculitis, causing microinfarcts in various organs. Usually the patients present with classical triad of Fever, Headache & Rash. Apart from this, pain in legs, oedema, Gastro-intestinal symptoms, hepato-splenomegaly, anaemia, necrotic rash, gangrene of digits, toes, earlobes, scrotum, painless eschar and lymphadenopathy are other manifestations. Complications include encephalitis, ARDS, pneumonia, Myocarditis, Renal failure and Vascular collapse. Endocarditis is seen in Q fever. Gold standard test for confirmation of diagnosis is I.F.A. Weil felix test is widely available but unacceptable for accurate diagnosis. Weil Felix test can be used in developing countries where other tests are not available. ELISA Should be preferred and is now available in India. The drug of choice for all age group is doxycycline. Rickettsia are potentially dangerous pathogens and unfortunately, specific serological tests are available in only a few specialized laboratories. Hence, it is imperative to have a high index of suspicion for Rickettsial diseases and make a clinical diagnosis based on prudent history taking and appropriate physical findings. A therapeutic trial with a specific agent in these patients is justified because a delay in initiating treatment may prove fatal. A rapid and favorable response is suggestive of a correct diagnosis.
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PMID:Childhood rickettsiosis. 2096 15


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