Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-eight dogs with iatrogenic hyperadrenocorticism were studied. The most common clinical signs were cutaneous lesions (27/28), polydipsia (21/28), polyuria (19/28), and lethargy (16/28). The most predominant findings on biochemical profile were elevated alkaline phosphatase (ALP, 15/28) and alanine transferase (ALT, 14/28); hypercholesterolemia (14/28); elevated aspartate transferase (AST, 12/28); and elevated triglycerides (12/18). Baseline cortisol levels of all 28 dogs were at the lower end of the reference range and exhibited suppressed or no response to adrenocorticotropic hormone (ACTH) stimulation. The mean time for each dog to show initial improvement of clinical signs after corticosteroid withdrawal was six weeks, with another mean time of 12 weeks to demonstrate complete remission.
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PMID:Iatrogenic hyperadrenocorticism in 28 dogs. 1033 57

Fourteen dogs with enlarged gallbladders and immobile stellate or finely striated bile patterns on ultrasound are described. Smaller breeds and older dogs were overrepresented, with 4/14 Cocker Spaniels. Most dogs presented for nonspecific clinical signs such as vomiting, anorexia and lethargy. Abdominal pain, icterus and hyperthermia were the most common findings on physical examination. All dogs except one had serum elevation of total bilirubin and/or alkaline phosphatase, alanine aminotransferase and gamma glutamyl transferase. All dogs were diagnosed with a gallbladder mucocele upon histologic and/or macroscopic evaluation. Ultrasonographically, mucoceles are characterized by the appearance of the stellate or finely striated bile patterns and differ from biliary sludge by the absence of gravity dependent bile movement. On ultrasound, gallbladder wall thickness and wall appearance were variable and nonspecific. The cystic or common bile duct were normal sized in 5 dogs although all 5 had evidence of biliary obstruction at surgery or necropsy. Loss of gallbladder wall integrity and/or gallbladder rupture were present in 50% of the dogs, all located in the fundus. Gallbladder wall discontinuity on ultrasound indicated rupture whereas neither bile patterns predicted the likelihood of gallbladder rupture. Pericholecystic hyperechoic fat or fluid were suggestive of but not diagnostic for a gallbladder rupture. Cholecystectomy appears to be an appropriate treatment for mucoceles, if not to treat a gallbladder rupture, at least in most dogs to prevent it since gallbladder wall necrosis was identified by histology in 9 of 10 dogs. Mucosal hyperplasia was present in all gallbladders examined histologically. Positive aerobic bacterial culture was obtained from bile in 6 of 9 dogs. Cholecystitis was diagnosed histologically in 5 dogs and 4 dogs had signs of gallbladder infection solely upon bacterial bile culture. Gallbladder infection was not present with all the mucoceles suggesting that biliary stasis and mucosal hyperplasia may be the primary factors involved in mucocele formation. Based on the results of our study, we suggest two alternate courses of action in the presence of a distended gallbladder with an immobile ultrasonographic stellate or finely striated bile pattern: a cholecystectomy when clinical or biochemical signs of hepatobiliary disease are present or a medical treatment (antibiotics and choleretics) and patient monitoring by follow-up ultrasound examinations when the patient does not have clinical or biochemical abnormalities. An aerobic bile culture should be obtained in all patients, by ultrasound-guided fine needle aspirate or at surgery.
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PMID:Ultrasonographic appearance and clinical findings in 14 dogs with gallbladder mucocele. 1085 Aug 78

A newborn girl with hemorrhagic purpura, suspected neonatal sepsis, and pale and dry skin was lethargic with remarkable hepatosplenomegaly, convergent strabismus, severe anemia, and elevated alkaline phosphatase activity. Radiographs showed a generalized increase in bone density, small medullary cavities, sclerosis of the skull and vertebrae, transverse wavy stripes of sclerotic bone in the metaphyses, and bone-in-bone appearance in phalanges of hands and feet. On this basis, she was diagnosed with malignant infantile osteopetrosis. On the first day of life, the infant was given a blood transfusion and vitamin K (1 mg intravenously [iv]). Corticosteroid therapy was started with prednisone (2 mg/kg per day). She showed marked improvement of symptoms. On the 26th day and 42nd day of life, she received additional blood transfusions. On the 49th day, the patient was discharged and corticosteroid therapy was continued at a regimen of 5 mg/day. Subsequent blood sample analyses revealed normal values for age. At 1 year of life, a bone marrow sample showed normal white and red cell lineages. X-ray confirmed attenuation of the bone sclerosis; therefore, bone marrow transplantation (BMT) was not implemented. At the age of 1.5 years, prednisone therapy was discontinued gradually and withdrawn before the age of 2 years. Subsequent follow-up showed normalization of all radiological and hematologic parameters. At present, the patient is 3 years old and appears healthy with apparently complete regression of the disease.
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PMID:Apparent cure of a newborn with malignant osteopetrosis using prednisone therapy. 1176 Aug 52

A 10-year-old spayed female mixed-breed dog was presented to the Purdue University Veterinary Teaching Hospital (PUVTH) with complaints of persistent anemia with occasional exacerbations, anorexia, and lethargy. The dog had been presented to the referring veterinarian 2 months prior with multiple bite wounds received during a fight with 3 Pit Bull Terriers. The dog was discharged after the wounds were cleaned and surgically closed. Upon admission to the PUVTH, blood was collected for a complete blood count and biochemical analysis. Microscopic examination of peripheral blood smears revealed intraerythrocytic protozoal parasites consistent with Babesia gibsoni. Molecular analysis confirmed that the organism was B. gibsoni and that its 18S ribosomal RNA sequence was identical to that of other B. gibsoni isolates from Oklahoma, North Carolina, and Okinawa, Japan. Hematologic changes included moderately severe, regenerative, macrocytic, normochromic anemia, with poikilocytosis, polychromasia, anisocytosis, and a marked increase in nucleated RBCs. Biochemical changes included increased serum alanine aminotransferase, alkaline phosphatase, and gamma-glutamyltransferase activities. The dog was treated with imidocarb, but despite initial clinical improvement, the dog died 2 weeks after the first dose. A necropsy was not performed. The infection in this dog is the first reported case of B. gibsoni infection in Indiana. Because of the widespread geographical distribution of the organism, veterinarians and veterinary clinical pathologists throughout the United States should carefully examine Romanowsky-stained blood smears from patients with acute hemolytic anemia for small intraerythrocytic babesial parasites.
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PMID:Babesia gibsoni infection in a dog from indiana. 1202 99

A 13-year-old, crossbreed dog presented with a history of recent onset polydipsia, progressive lethargy, weakness and reduced appetite. Blood tests showed raised concentrations of alkaline phosphatase and alanine aminotransferase with marginally low serum potassium. There was a leucocytosis with a mature neutrophilia and no eosinophils. Endocrine tests showed a normal aldosterone concentration and an exaggerated adrenocorticotropic hormone (ACTH) stimulation test, consistent with a diagnosis of hyperadrenocorticism (HAC). A diagnosis of adrenal-dependent HAC was made, based on the presence of a calcified mass involving the left adrenal gland, and hepatomegaly, on radiography and ultrasonography. The owners declined surgical adrenalectomy. Medical management with trilostane rapidly improved the clinical signs and normalised the serum chemistry. ACTH stimulation tests showed an improvement in post-ACTH cortisol concentrations and were used to make dose adjustments where necessary. At the time of writing, no adverse side effects had been seen and the dog remained well after 80 weeks of treatment.
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PMID:Trilostane treatment of a dog with functional adrenocortical neoplasia. 1265 28

In this retrospective study, we describe 14 cats diagnosed with hepatic abscesses. The objective of the study was to report the clinical signs, physical examination findings, clinicopathologic findings, and outcomes in affected cats. These findings were then compared with those previously reported in dogs and humans. Clinical signs were vague and included anorexia, lethargy, and weight loss. Only 23% of cats had fever, whereas 31% were hypothermic. Increases in serum activities of alanine aminotransferase and alkaline phosphatase were found in 45 and 18%, respectively, of the 11 cats that had laboratory work performed. Abdominal ultrasound examinations were performed in 7 cats, and abnormalities were found in 71% of them. Four cats had solitary abscesses, all of which were located in the right liver lobes. The other 10 cats had multifocal small abscesses or microabscesses, and all of these cats had clinical signs suggestive of sepsis. Cytologic evaluation of samples obtained by abdominocentesis indicated septic inflammation in 67% of cats in which peritoneal fluid was analyzed. Hepatic abscess cultures yielded polymicrobial growth in 66% of the cats: Escherichia coli was the most commonly cultured organism. Overall mortality rate was 79%. All survivors underwent exploratory laparotomy for partial hepatectomy to resect the abscess followed by medical management. Hepatic abscesses should be considered in cats with signs consistent with sepsis. More routine use of ultrasonography may aid in earlier diagnosis of hepatic abscesses, potentially improving prognosis and outcome.
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PMID:Hepatic abscesses in cats: 14 cases (1985-2002). 1518 14

Babesia felis, originally identified in wild cats in the Sudan, was subsequently found to cause clinical disease in domestic cats. Although babesiosis in domestic cats has been reported sporadically from various countries, as a significant disease it appears to be a distinctly South African phenomenon. Apart from an inland focus, feline babesiosis is reported regularly only from coastal regions. The infection is assumed to be tick-borne, but the vector has not been identified. Feline babesiosis tends to be an afebrile, chronic, low-grade disease. The most frequently reported complaints by owners are anorexia and lethargy. The main clinical findings are anemia, depression, and occasionally icterus. Concurrent infections (e.g., Mycoplasma haemofelis, FeLV, FIV) may contribute to the clinical picture. Laboratory findings commonly include regenerative anemia, elevation of alanine transaminase (but not alkaline phosphatase) and total bilirubin concentrations, and a variety of electrolyte disturbances. Secondary immune-mediated hemolytic anemia can be seen occasionally. Drugs effective against other Babesia species give variable and questionable results. The drug of choice is primaquine phosphate, which effects a clinical cure but does not sterilize the infection. Repeated or chronic therapy may be required.
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PMID:Feline babesiosis in South Africa: a review. 1560 90

Eight dogs from western Washington State suspected of being infected with Anaplasma phagocytophilum because of the finding of morulae in peripheral blood neutrophils were studied for determination of the etiologic agent of disease. All cases were diagnosed between April 2003 and April 2004. Six of the eight dogs had no travel history during the 6 months prior to presentation. Two dogs had traveled within the Northwest United States and Canada. Fever, lethargy, and anorexia were the most common clinical signs in the dogs. Lymphopenia, thrombocytopenia, and an elevated activity of alkaline phosphatase in the serum were the most common laboratory findings. All dogs tested during the acute phase of clinical signs were seropositive for A. phagocytophilum antibodies but negative for Ehrlichia canis antibodies. PCR amplification and direct sequencing of portions of the 16S rRNA gene from the whole blood of all seven dogs that were tested yielded A. phagocytophilum after a comparison to bacterial sequences available in the GenBank database. Five genetic variants were identified based on one or two nucleotide differences in the 16S rRNA gene sequences at nucleotide positions 54, 84, 86, and 120. Individual dogs were infected with more than one variant. Treatment with doxycycline or tetracycline resulted in a rapid resolution of clinical signs. The occurrence of canine granulocytic anaplasmosis in western Washington State suggests that A. phagocytophilum infection should be considered in differential diagnoses of dogs presenting with lethargy, anorexia, fever, and lameness, particularly in the context of lymphopenia, thrombocytopenia, and increased serum alkaline phosphatase. The zoonotic importance of A. phagocytophilum should support an increase in surveillance for horses and people residing in this area.
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PMID:Genetic variants of Anaplasma phagocytophilum infecting dogs in Western Washington State. 1569 82

A 7-year-old, intact male Dachshund was presented to the Lyon veterinary school for lethargy and anorexia of several weeks duration. The main clinical signs were pale and icteric mucous membranes, hepatomegaly, splenomegaly, and lymphadenopathy. Results of a CBC and plasma biochemistry tests revealed severe nonregenerative anemia, thrombocytopenia, and increased alanine aminotransferase and alkaline phosphatase activities. Blood smear evaluation and cytologic examination of lymph node and bone marrow aspirate specimens revealed a large population of poorly differentiated blast cells with morphologic features suggesting megakaryocytic lineage. A low number of well-differentiated but dysplastic megakaryocytes also were observed in lymph node and bone marrow smears. A few blast cells were erythrophagocytic. Blast cells were positive for glycoprotein IIIa, factor VIII-related antigen, and factor XIII using immunocytochemistry. The dog was euthanized and necropsied. Histologic findings consisted of diffuse, massive infiltration of lymph nodes, liver, and spleen by megakaryoblasts and atypical megakaryocytes, with widespread thrombosis. This case confirms the usefulness of immunochemistry, including for factor XIII, in the diagnosis of megakaryoblastic leukemia, and demonstrates the unique features of tumor cell erythrophagocytosis and marked fibrinous thrombosis, which have not been reported previously in dogs.
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PMID:Acute megakaryoblastic leukemia with erythrophagocytosis and thrombosis in a dog. 1573 19

Ten dogs with neuroendocrine carcinoma of the liver were selected for inclusion in the study. Clinical signs were anorexia (7), vomiting (5), polydipsia/polyuria (3), icterus (2), lethargy (2), weight loss (2), paresis (1), ataxia (1), weakness (1), collapse (1), and urinary tract infection (1). Hematologic and biochemical abnormalities included anemia (2/8), leukocytosis (4/8), high liver enzyme activity (serum alkaline phosphatase, 7/9; alanine transaminase, 7/9; aspartate transaminase, 8/9), and high total bilirubin (6/9). Grossly, the tumors were diffuse, involving all liver lobes in six dogs, and two dogs had various-sized nodules in addition to diffuse involvement. Histologically, there were eight tumors with solid or trabecular pattern (group A), one tumor with cords or rows of neoplastic cells (group B), and one tumor with multiple rosette-like structures (group C). Immunohistochemical studies revealed that all 10 neoplasms were positive for at least one of the endocrine markers used: neuron-specific enolase (NSE; 8/10), synaptophysin (5/10), and chromogranin-A (3/10). A panel of NSE, chromagranin-A, and synaptophysin detected 100% of the tumors in our series. Electron microscopy confirmed the diagnosis by the presence of intracytoplasmic neurosecretory granules in the two examined cases. Our results show that neuroendocrine markers commonly used in humans can be used for the diagnosis of hepatic neuroendocrine carcinoma in dogs, preferably a panel of synaptophysin, chromagranin-A, and NSE because chromogranin-A alone is not as useful in dogs as in humans.
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PMID:Canine hepatic neuroendocrine carcinoma: an immunohistochemical and electron microscopic study. 1575 67


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