Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vertigo in children is rarer than in adults and the examiner in cases showing these symptoms must rely on the parents' or relatives' observations and details. Besides the equilibrium disorders caused by hereditary malabsorption or lesions in the peripheral or central vestibular structures, e.g. ototoxic drugs, tumours in the brain, meningitis, encephalitis, otitis, labyrinthine fistulas or head trauma, we only known of typical diseases, associated with vertigo, that develop during childhood. These are: so-called benign paroxysmal vertigo of childhood, benign paroxysmal torticollis, basilar migraine, spasmus nutans, visual-cliff phenomenon, and kinetosis. Careful examinations are necessary to differentiate these illnesses from vestibular epilepsy, brain tumours, and hereditary episodic vertigo. Neuro-otologic examination in children, especially small children, is a kind of "stepchild" in ENT departments. The reasons are the time-consuming examination necessary in the case of children and by problems connected with a plethora of troublesome individual tests. Additional difficulties arise in cases of sensory, mental, and other impairments. - The paper gives an overview of vestibular disturbances during childhood and diagnostic procedures for determination by means of Frenzel glasses, electronystagmography, cranio-corpography, and posturography.
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PMID:[Equilibrium disorders and their diagnosis in childhood]. 174 79

36 patients with severe neurological diseases (craniocerebral trauma, cerebrovascular insufficiency, meningo-encephalitis, polyneuropathy, paraplegia, intoxication etc.) received for more than 3 months monosaccharides and polyols (Triofusin E 1000) and a 10-%-concentration of crystalline amino acids (Aminofusin L10% kohlenhydratfrei) via the parenteral route in combination with / or exclusively a nutrient-defined diet (Biosorb). Exclusive enteral nutrition was given preference if possible. Numerous laboratory parameters, as for example blood counts, "hepatic enzymes", electrolytes, trace elements, plasma proteins, lipids, urea and creatinine were determined once a week. Substitutions and secondary complications were registered in addition. Iron and plasma proteins had to be substituted most frequently. It could be proved that hypoferremia was caused by insufficient iron supply in case of exclusive/prevailing parenteral nutrition, incorrect application of the iron preparations, inflammatory complications with iron moving into the R.E.S., as well as malabsorption syndromes probably induced by bacteria. Inflammatory complications were also the major cause of protein deficiency syndromes (hypoalbuminemia). In case of relatibely often occurring diarrhea, however, it could clearly be proved that it was not induced by nutrition but was produced by a broad-spectrum antibiosis. Chronically persistent diarrhea with colitis-like colonic changes required enteral feeding with an oligopeptide diet (z.B. Peptisorb) via jejunal feeding tube. Nitrogen balances which were determined after more than 3 months of artificial nutrition formed the basis of a nutritional plan differentiated according to diagnostic groups and stages of disease.
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PMID:[Artificial nutrition in neurology--indications and problems]. 640 43

Microsporidia are ubiquitous in nature. Several clinical syndromes have been associated with microsporidiosis, especially in HIV-infected individuals, and include enteropathy, keratoconjunctivitis, sinusitis, tracheobronchitis, encephalitis, interstitial nephritis, hepatitis, cholecystitis, osteomyelitis, and myositis. Diarrhea and malabsorption are the most common clinical problems. Enterocytozoon bieneusi is the most common microsporidial cause of intestinal disease. A second species, Encephalitozoon intestinalis (originally named Septata intestinalis) is associated with disseminated as well as intestinal disease. Microsporidiosis has been seen worldwide, and is recognized as a frequent enteric infection in patients with AIDS. The pathogenesis of intestinal disease is related to excess death of enterocytes as a result of cellular infection. Clinically, microsporidiosis most often presents with diarrhea and weight loss as a result of small intestinal injury and malabsorption. However, microsporidia have been detected in virtually all organs, and may provoke symptoms related to their specific localization. The diagnosis of microsporidiosis is made histologically, either from tissue biopsies or secretions. While transmission electron microscopy was required for diagnosis in the past, special stains and light microscopy, as well as immunohistochemical and molecular techniques are capable of providing a firm diagnosis. Therapeutic options are limited. Enc. intestinalis responds well to albendazole, while no antiparasitic therapy has documented efficacy in Ent. bieneusi infections.
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PMID:Clinical syndromes associated with microsporidiosis. 955 78

An 8-yr-old intact male Grant's zebra (Equus burchelli bohmi) was referred to the Veterinary Medical Teaching Hospital of the University of California-Davis after being found in the owner's pasture obtunded and in lateral recumbency. The animal was hypothermic, weak, and unwilling to rise. There was no evidence of trauma, and the zebra had seemed normal the preceding evening. There was no extensor rigidity, and cranial nerve reflexes were normal. Flexor and extensor reflexes were weak upon initial examination. A complete blood count and serum biochemistry analysis revealed a mild leukocytosis, hyperfibrinogenemia, hypoglycemia, hyponatremia, hypochloremia, hypocalcemia, and hypoalbuminemia. Urinalysis was normal, and a urine toxicology screen for alkaloids was negative. No toxic substance was found in the hay or pasture grasses although the owner reported the presence of yellow star thistle and mushrooms in the pasture. The cerebrospinal fluid cytologic and biochemical analyses were normal, but antibodies to Sarcocystis neurona were detected. The zebra died despite aggressive supportive therapy over a 4-day period. The necropsy demonstrated severe gastrointestinal nematodiasis that could account for hypoalbuminemia and electrolyte abnormalities. Histopathologic examination of the nervous system revealed focal areas of perivascular cuffing in the brainstem that were comprised mainly of lymphocytes, monocytes, and plasma cells. Immunohistochemical staining identified the presence of S. neurona merozoites associated with the lesions. This zebra probably died from severe endoparasitism that resulted in malabsorption, weakness, and recumbency rather than from encephalitis associated with S. neurona merozoites. Equine protozoal myeloencephalitis has not been reported previously in nondomestic equids.
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PMID:Detection of Sarcocystis neurona in the brain of a Grant's zebra (Equus burchelli bohmi). 1088 30

A recalcitrant rheumatoid arthritis patient taking low dose weekly methotrexate was given oral 2-chlorodeoxyadenosine (cladribine) for 8 months in a multicenter trial. He developed dual infections over the course of the trial: disseminated herpes zoster and staphylococcal arthritis of the right elbow. His disseminated herpes zoster started with severe, unremitting abdominal pain caused by a gastric ulcer, followed by disseminated cutaneous herpes, hepatitis, pancreatitis, encephalitis, homonymous hemianopsia, the syndrome of inappropriate secretion of antidiuretic hormone (ADH), and malabsorption. Both the herpes zoster and S. aureus infections required prolonged proper chemotherapies. Serious, complicated viral, bacterial, or other unusual infections should be considered in patients with severe rheumatoid conditions treated with combination immunosuppressive therapy.
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PMID:Disseminated herpes zoster and s. Aureus septic arthritis in a rheumatoid arthritis patient treated with 2-chlorodeoxyadenosine (cladribine) and methotrexate. 1907 80

Along with myasthenia, other paraneoplastic neurological syndromes (PNS) may occur in thymoma. Anti-Hu antibodies and a clinical "anti-Hu syndrome" characterized by encephalitis and/or painful neuropathies have been reported in only three patients at the time of the diagnosis of thymoma. We describe a severe anti-Hu-related autonomic neuropathy with gastrointestinal paresis and intestinal pseudo-obstruction with malabsorption that occurred concomitantly with the worsening of myasthenic symptoms long after the initial diagnosis of thymoma in a young patient. The clinical anti-Hu syndrome preceded the radiological diagnosis of thymoma recurrence. Treatment with plasma exchange led to a transient improvement of neurological symptoms.
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PMID:Thymoma associated with myasthenia and autonomic anti-Hu paraneoplastic neuropathy. 1957 74