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)

Thirty-three patients with alcoholic cirrhosis (AC), selected on widely recognized criteria (16, 57), were investigated prospectively for cutaneous manifestations of zinc deficiency. The patients were divided into 3 groups: group A (n = 12): AC without skin lesions; group B (n = 12): AC with skin lesions responsive to a zinc-free topical treatment or resistant to enteral zinc sulfate intake; group C (n = 9): AC with skin lesions cured by oral zinc replacement therapy alone. The lesions observed in group C were studied microscopically. Data concerning zinc metabolism (Zn concentrations in plasma, red cells, urine and hair; alkaline phosphatase values), biochemical criteria of AC (plasma serum-albumin concentration, IgA/transferrin ratio) and a malabsorption test (xylosemia 120 min after oral absorption of D-xylose 25 g) were compared by the variance analysis method. A control group (D, n = 12) was used as reference. Few cases of cutaneous manifestations of zinc deficiency in AC patients have been published. In more than one half of the 15 or so we found in the literature, an aggravating factor (total parenteral nutrition, digestive tract surgery) had to be taken into account. In this prospective study 9 new cases in which AC was the only cause of zinc deficiency are reported. A clinical picture similar to acrodermatitis enteropathica with peribuccal bullous lesions was observed in only one patient. In all other cases the patients presented with a cracked and reticulated eczema on the extensor aspect of the limbs and (often erosive) in the perianal and genital regions. The eczema was associated with cheilitis, glossitis, stomatitis, alopecia and, seldom, ungual Beau's lines. Disorders of behaviour, diarrhoea and bouts of lever regressing under zinc replacement therapy were frequent. Histology was not very specific, except for the presence of necrotic areas in the stratum germinativum, sometimes associated with small subcorneal pustules containing altered polymorphonuclears. In every case, it was the rapid regression of symptoms under zinc sulfate treatment that confirmed the diagnosis. Plasma zinc concentrations were most significantly decreased in all AC groups as compared to controls (61.2 +/- 19.4 vs 97.8 +/- 10.4 micrograms/100 ml) and also in AC patients with skin manifestations of zinc deficiency as compared to the other AC patients (44.4 +/- 9.2 vs 66.5 +/- 18.8 micrograms/100 ml) table V). Changes in serum-albumin levels and in hepatocellular function were parallel to changes in plasma zinc concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cutaneous manifestations of zinc deficiency in ethylic cirrhosis]. 357 31

A 39-year-old woman presented with mild anemia, glossitis, an increased MCV, a low serum cobalamin (Cbl) (vitamin B12), mild tissue deficiency of Cbl, but with neither malabsorption of Cbl, impaired intake, nor deficiency of or inactivity of transcobalamin II (TC II). Because of a persistently low holo-TC II (TC II carrying Cbl as the circulating complex of TC II-Cbl), much of the evaluation was focused on the patient's TC II. Her TC II promoted the uptake of Cbl, reacted with anti-TC II, and bound Cbl in vitro. A test dose of 200 micrograms of cyanocobalamin (CN-Cbl) i.m. increased her holo TC II to levels higher than those in healthy persons, but with a much more abrupt fall to a subnormal level. Two milligrams of CN-Cbl i.m. followed by 100 micrograms i.m. monthly failed to maintain normal amounts of circulating TC II-Cbl or to overcome the tissue deficiency of Cbl. One milligram i.m. weekly or daily p.o. corrected both. The low holo TC II was considered to be responsible for the clinical expression and may have been primary to the reduced amounts of total and holo R binder of Cbl in the circulation. This study of a newly recognized defect points out the need for circulating holo TC II, a rational use of pharmacologic amounts of Cbl, and a possible interrelationship between TC II and the R binder of Cbl.
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PMID:A patient with the inability to maintain in vivo levels of bound cobalamin (Cbl) and manifestations of tissue deficiency of Cbl. 395 67

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.
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PMID:Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy. 1103 77

Tropical sprue is a disease that causes progressive villus atrophy in the small intestine, similar to nontropical (celiac) sprue. The loss of intestinal villi profoundly affects intestinal absorptive function, and patients with tropical or nontropical sprue present with malabsorption. Whereas the etiology of celiac sprue has been elucidated in considerable detail, the etiology of tropical sprue remains obscure. The favored hypothesis is that the disease is either initiated or sustained by a still-undefined infection. Patients with tropical sprue typically present with macrocytic anemia due to malabsorption of folate and/or vitamin B(12). Treatment of tropical sprue with folic acid replacement was introduced more than 50 years ago and has become standard medical treatment. Vitamin B(12) replacement is usually added if there is evidence of B(12) deficiency or malabsorption. Treatment of tropical sprue with folate and B(12) cures the macrocytic anemia and the accompanying glossitis, and often results in increased appetite and weight gain. However, even prolonged treatment with these vitamins fails to restore villus atrophy, and malabsorption usually persists. The benefit of antibiotic treatment of tropical sprue was first documented during World War II, when sulfonamides were used to treat epidemics of tropical sprue in British and Italian troops in India. Antibiotic treatment has since become the standard treatment, and tetracycline has replaced sulfonamides. The recommended length of treatment with tetracycline is 6 months and it is given in combination with folate. The treatment has been shown to normalize mucosal structure in the small intestine and resolve malabsorption in most patients with tropical sprue. However, there is a substantial relapse rate in treated patients who return to, or remain in, endemic areas in the tropics.
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PMID:Tropical Sprue. 1472 33

Cobalamin deficiency is a common finding. In the elderly the prevalence is 10-20%, but only 5-10% of these are clinically symptomatic. Typical clinical symptoms include macrocytic anemia, neuropsychiatric symptoms and glossitis. In many cases this triad is lacking, however. The serum cobalamin assay is the best first line test, but the results must be carefully interpreted, since a normal level does not exclude deficiency. Markers of cobalamin activity, such as serum homocysteine or methylmalonic acid may be helpful in this situation. The main cause of cobalamin deficiency is atrophic gastritis. It is either caused by an autoimmune process which leads to achlorhydria and severe intrinsic factor deficiency ("classical pernicious anemia") or by atrophic gastritis from other causes, in particular helicobacter pylori infection. In the latter cases the lack of gastric acid does not allow separation of cobalamin from proteins, but intrinsic factor, although low, is sufficient for cobalamin protection (food cobalamin malabsorption). Helicobacter pylori eradication may cure some of these patients. While in food cobalamin malabsorption syndrome small doses of oral cobalamin are effective, parenteral therapy or high oral doses are required for treatment of pernicious anemia. While almost all patients respond hematologically, only half of the patients with neurological signs, and a small minority of psychiatric patients respond to treatment. Patients with pernicious anemia and atrophic gastritis have a greatly increased long-term risk for gastric carcinoids.
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PMID:[Vitamin B12 deficiency. New data on an old theme]. 1639 86

Zinc is an essential micronutrient for human metabolism that catalyzes more than 100 enzymes, facilitates protein folding, and helps regulate gene expression. Patients with malnutrition, alcoholism, inflammatory bowel disease, and malabsorption syndromes are at an increased risk of zinc deficiency. Symptoms of zinc deficiency are nonspecific, including growth retardation, diarrhea, alopecia, glossitis, nail dystrophy, decreased immunity, and hypogonadism in males. In developing countries, zinc supplementation may be effective for the prevention of upper respiratory infection and diarrhea, and as an adjunct treatment for diarrhea in malnourished children. Zinc in combination with antioxidants may be modestly effective in slowing the progression of intermediate and advanced age-related macular degeneration. Zinc is an effective treatment for Wilson disease. Current data do not support zinc supplementation as effective for upper respiratory infection, wound healing, or human immunodeficiency virus. Zinc is well tolerated at recommended dosages. Adverse effects of long-term high-dose zinc use include suppressed immunity, decreased high-density lipoprotein cholesterol levels, anemia, copper deficiency, and possible genitourinary complications.
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PMID:Zinc: an essential micronutrient. 2014 Oct 96