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PubMed1983

Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction.

Three Basenji dogs with renal tubular dysfunction were studied. Hyposthenuria and diminished urine concentrating ability, indicative of nephrogenic diabetes insipidus, were documented. Metabolic acidosis, hyperchloremia, and reduction in glomerular filtration rate also were detected in all dogs. In addition, an exaggerated response to the adrenocorticotropin test and hyperaldosteronism, believed to be secondary to decreased effective circulating blood volume, were detected in all 3 dogs. Thyroxine values were decreased in all dogs and could be correlated with histopathologic changes of the thyroid gland in 2 dogs. Gastropathy and hypergastrinemia were identified in 2 dogs. Diffuse lymphocytic-plasmacytic enteritis was evident in 2 dogs. It was concluded that a urine concentrating defect that may be secondary to hypercortisolism exists in Basenji dogs with renal tubular dysfunction.

Animals↗
PubMed1994

Lipid patterns in patients with chronic occlusive arterial disease affecting lower limbs.

114 consecutive patients with chronic occlusive arterial disease of lower limbs (COADL) had their serum lipid pattern compared with that of 62 controls. 53 had abnormal lipids and 36 multiple abnormalities emphasising the common prevalence of atherosclerosis among patients with COADL in Sri Lanka. 48.6% of patients under 40 years had a lipid abnormality. Smoking and lipid disorders were the main risk factors in the under 50 age group. 14 of 16 patients with aortic occlusions and five of eight patients under 45 years with iliac disease had lipid disorders. 21 of 50 patients with femoropopliteal occlusive disease also had lipid disorders. A consistent dominant lipid disorder affecting most, was not found. Total cholesterol/HDL cholesterol ratio was found to be the commonest abnormality. Serum lipid studies are advocated for those with aortoiliac and femoropopliteal disease.

Adolescent↗
PubMed1993

Multiple chromosome abnormalities in patients with acute leukemia after autologous bone marrow transplantation using total body irradiation and marrow purged with mafosfamide.

Cytogenetic follow-up studies such as those reported after allogeneic bone marrow transplantation are not available in patients submitted to an autologous bone marrow transplantation (ABMT). Of 114 patients with acute leukemia (69 acute myelocytic AML, 43 acute lymphocytic ALL, 2 undifferentiated) who underwent an ABMT in our institution in the period from February 1983 to December 1989, 66 had evaluable cytogenetic data post-transplant. They all received a pretransplant regimen consisting of cyclophosphamide (CY) and total body irradiation (TBI) followed by reinfusion of marrow purged with mafosfamide. Twenty patients showed chromosomal damage at some time; of these, six relapsed early post-ABMT, one died while in persisting remission at 81 months post-ABMT from overwhelming pneumococcal sepsis related to a previous splenectomy, and 13 are still alive and well at 13 to 88 months post-transplant. The bone marrow cytogenetic abnormalities were complex: they included various numbers of clonal aberrations or variations or combination of those; they affected all but the Y chromosome, with a predominance however for chromosomes 1, 3, 6, and 7; they were often transitory and in some instances became modified with time. None of these chromosomal abnormalities was connected with the initial leukemia, even in the 6 patients who relapsed early. In the other 14 patients, these abnormalities have so far had no detectable unfavourable implication. The origin of these abnormalities is unknown: both the pretransplant regimen (CY and/or TBI) and/or marrow purging with mafosfamide can be incriminated. Additional studies in patients autografted with pretransplant regimen not containing TBI and/or with unpurged marrow are necessary to discriminate between these two possibilities.

Antineoplastic Agents↗
PubMed1996

Cyclic vomiting: association with multiple homeostatic abnormalities and response to ketorolac.

Cyclic vomiting is a rare syndrome that over the years has variously been ascribed to psychogenic causes, sensory seizures, abdominal migraine, and more recently, to mechanical or electrical disturbances in gastric physiology. We describe the case of a 65-year-old white diabetic female with a 10-yr history of recurrent episodes of nausea and vomiting, occurring every 10-12 days and lasting approximately 1-3 days at a time. These episodes were accompanied by edema, mild temperature elevations, and remarkable elevations in blood pressure. In between these episodes, the patient remained asymptomatic. Initial screening tests were also negative except for moderate gastroparesis. However, antral motility was found to be normal, as was an electrogastrogram. Detailed neurological and psychiatric evaluations were negative. Trials of erythromycin, metoclopramide, naloxone, ondansetron, and amitryptiline were unsuccessful. Serial endocrinological testing revealed that an episode of vomiting was always preceded by an abnormal elevation in at least one of the following: serum adrenocorticotropic hormone, serum cortisol, or urinary cortisol. In the midst of an episode, all three values were exceedingly high (e.g., > 10-fold increases in 24-hr urinary cortisol levels). Fluctuations of a milder degree, though still abnormally high, were also noted in between cycles at times when the patient was completely asymptomatic. High-dose dexamethasone suppressed these hormonal surges completely but not the clinical symptoms, which continued undisturbed. The patient was finally given a trial of intramuscular ketorolac during one of her episodes, which produced prompt and sustained relief. During the next few weeks, she was given this drug each time her symptoms commenced, and each time it appeared that her cycle had been aborted. She has since been able to terminate her episodes promptly and completely by self-administration of ketorolac. We speculate that her syndrome is caused by a poorly characterized disorder of endogenous prostaglandin release, resulting not only in derangements in the hypothalamic pituitary system but also in nausea and vomiting.

Adrenocorticotropic Hormone↗
PubMed1996

Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities.

PU.1 is a member of the ets family of transcription factors and is expressed exclusively in cells of the hematopoietic lineage. Mice homozygous for a disruption in the PU.1 DNA binding domain are born alive but die of severe septicemia within 48 h. The analysis of these neonates revealed a lack of mature macrophages, neutrophils, B cells and T cells, although erythrocytes and megakaryocytes were present. The absence of lymphoid commitment and development in null mice was not absolute, since mice maintained on antibiotics began to develop normal appearing T cells 3-5 days after birth. In contrast, mature B cells remained undetectable in these older mice. Within the myeloid lineage, despite a lack of macrophages in the older antibiotic-treated animals, a few cells with the characteristics of neutrophils began to appear by day 3. While the PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutely required for the normal differentiation of B cells and macrophages.

Animals↗
PubMed2005

Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

The objective of this report was to develop a case definition of distal symmetric polyneuropathy to standardize and facilitate clinical research and epidemiologic studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetric polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiologic studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach to defining distal symmetric polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiologic research studies will ensure greater consistency of case selection.

Clinical Protocols↗
PubMed2005

Distal symmetrical polyneuropathy: definition for clinical research.

The objective of this report was to develop a case definition of "distal symmetrical polyneuropathy" to standardize and facilitate clinical research and epidemiological studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetrical polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiological studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach for defining distal symmetrical polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiological research studies will ensure greater consistency of case selection.

Electrodiagnosis↗
PubMed2005

Distal symmetrical polyneuropathy: a definition for clinical research. A report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

The objective of this report was to develop a case definition of "distal symmetrical polyneuropathy" to standardize and facilitate clinical research and epidemiologic studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetrical polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiologic studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach to defining distal symmetrical polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiologic research studies will ensure greater consistency of case selection.

Electrodiagnosis↗
PubMed1995

Targeted disruption of mouse EGF receptor: effect of genetic background on mutant phenotype.

Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.

Abnormalities, Multiple↗