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PubMed1986

[Immunosuppression by retroviruses in tumors and immune deficiency diseases].

Most retroviruses are immunosuppressive in vitro and in vivo. They are able to enhance virus-induced tumor development and/or to induce acquired immune deficiency syndromes (AIDS) which are characterized by malignant tumors and opportunistic infections. Experimental evidence for the immunosuppressive properties of several type D viruses derived from human cell lines and other retroviruses is presented.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Porphyria cutanea tarda, or the uroporphyrinogen decarboxylase deficiency diseases.

The term "porphyria cutanea tarda" originally described the dermatological manifestations of various chronic porphyrias. Its usage now is usually restricted to disorders associated with a deficiency of uroporphyrinogen decarboxylase (UROD), for which the term "UROD-deficiency" may be more appropriate. Four etiologic agents have been implicated in this condition: alcohol, oral estrogens, halogenated aromatic hydrocarbons, and iron. An inherited deficiency of UROD is also recognized, with increased susceptibility to these agents. Certain halogenated aromatic hydrocarbons can cause UROD-deficiency in animals and synergism with iron is demonstrable in this model. Neither ethanol nor estrogen has been shown to cause UROD-deficiency in animals. Treatment by venesection to reduce total body iron is safe and effective. The 4-aminoquinoline antimalarial drugs also provide effective treatment, possibly by lysis of affected liver cells. Unlike venesection, they may not reverse the biochemical lesion which causes porphyrins to accumulate. The mechanism of acquired UROD-deficiency is not clear but animal studies suggest a role for the hepatic mixed function oxygenases which initiate iron-dependent inactivation of UROD. Diagnosis is simple, often requiring only appropriate clinical data and testing of a random urine sample. Although not common, the disorder is the most frequently diagnosed disturbance of porphyrin metabolism in many countries, and further insight into its unusual pathogenesis may clarify the hepatotoxic effects of the 4 etiologic agents.

Animals↗
PubMed1981

Tropical pyomyositis, a thiamine-deficiency disease.

On the basis of clinical observations made in Shanghai which confirmed the clinical and experimental findings of Osawa in Japan, it is suggested that thiamine deficiency is an essential contributary factor in producing tropical pyomyositis (TPM). It was found that the majority of patients affected by TPM suffer or have previously suffered from beriberi. The practical disappearance of TPM in Japan in recent years supports the above view. Thiamine deficiency induces a biochemical lesion (Peters) in the pyruvate oxidase system of the muscle, which breaks down its normal resistance to infection and opens the gate to bacterial agents. It is possible that in different parts of the world other or additional factors may play a similar role to that of thiamine deficiency. It is suggested that a wide survey should be undertaken--perhaps by the World Health Organisation--especially in areas in which TPM is endemic, using all relevant methods, to elucidate the factor or factors responsible for the development of TPM.

Adult↗
PubMed1997

Membrane phospholipid alterations in Alzheimer's disease: deficiency of ethanolamine plasmalogens.

The ethanolamine plasmalogens are decreased whereas serine glycerophospholipids are significantly increased in plasma membrane phospholipid in affected regions of brain in Alzheimer's disease. This may be due to stimulation of Ca(2+)-independent plasmalogen-selective phospholipase A2 which was recently discovered in brain. This phospholipase A2 differs from other Ca(2+)-independent phospholipases A2 in response to ATP and various inhibitors. It may be responsible for excess release of arachidonic acid and accumulation of prostaglandins and lipid peroxides in AD. Accumulation of the above lipid metabolites due to abnormal receptor function and signal transduction may contribute to neurodegeneration in AD.

Alzheimer Disease↗
PubMed2004

Effect of controlled zinc release on bone mineral density from injectable Zn-containing beta-tricalcium phosphate suspension in zinc-deficient diseased rats.

The purpose of this study was to evaluate the efficacy of zinc (Zn)-containing beta-tricalcium phosphate (Zn-TCP) in correcting the bone mineral deficiency noted in osteoporosis using ovariectomized rat model. Four rats were used for each of the four experimental groups: D0, D10, D20, and N10. The rats in D0, D10, and D20 groups were ovariectomized, and fed a vitamin D-, Ca-, and Zn-deficient diet, and induced Zn-deficient osteoporoses for 9 weeks. In contrast, the N10 group was the normal rats fed normal healthy diet for 9 weeks. D0 group was injected with pure beta-TCP suspension, D10 and D20 groups were injected with suspensions containing 10 mg of 10 mol % (6.17 wt % Zn) and 20 mol % (12.05 wt % Zn) Zn-TCP, respectively, and the healthy group, N10 were injected with 10 mol %. Zn-TCP suspensions. Injections were administered intramuscularly in the left thigh once a week in all rats, and fed a vitamin D- and Zn-deficient diet for 9 weeks. The plasma calcium (Ca) and Zn levels, plasma alkaline phosphatase activity (ALP) and bone mineral density (BMD) of the lumbar vertebra and femora were measured. The plasma Zn levels in all the rats were between 1.1 and 2.8 microg/mL. The areas under the curves for the Ca, Zn, and ALP (Ca-AUC, Zn-AUC, and ALP-AUC) levels between 0 and 63 days were calculated. Results for the AUCs were as follows: (1) the Zn-AUCs were in the order of N10 = D20 > D10 > D0; (2) the Ca-AUCs for D0, D10 groups were significantly lower than that for the N10 group; (3) the ALP-AUCs for the D10 and D20 groups were significantly higher than that for the N10 group, and that of the D0 group was in between those. The body weight of D10 and D20 groups significantly increased with time, that of the D0 group increased slightly, and that of the N10 group remained unchanged for the entire experimental period. The BMD of the lumbar vertebrae of the D10 and D20 groups (about 100 mg/cm(2)) was significantly higher than that of the D0 group but lower than that of the N10 group. The BMD of the left femur increased more than that of the right femur with the increase in the amount of Zn in the suspension. The results of this study suggest that the local effect on BMD was more pronounced than the effect on the whole body.

Alkaline Phosphatase↗
PubMed1980

The immune system: primary immune deficiency diseases.

Table 1 summarizes the major IDD and the methods used for their diagnosis and treatment. The clue to the diagnosis of IDD remains a high index of suspicion when one encounters a child or an adult with recurrent infections. IDD must be relatively common in Lebanon because of the high rate of interfamily marriages. With a heightened awareness and few easily available laboratory methods (underlined in table 1) the primary physician should be able to make the diagnosis of most of these diseases.

Complement System Proteins↗
PubMed2004

Search for poliovirus carriers among people with primary immune deficiency diseases in the United States, Mexico, Brazil, and the United Kingdom.

OBJECTIVE: To estimate the rate of long-term poliovirus excretors in people known to have B-cell immune deficiency disorders. METHODS: An active search for chronic excretors was conducted among 306 persons known to have immunoglobulin G (IgG) deficiency in the United States, Mexico, Brazil, and the United Kingdom, and 40 people with IgA deficiency in the United States. Written informed consent or assent was obtained from the participants or their legal guardians, and the studies were formally approved. Stool samples were collected from participants and cultured for polioviruses. Calculation of the confidence interval for the proportion of participants with persistent poliovirus excretion was based on the binomial distribution. FINDINGS: No individuals with long-term excretion of polioviruses were identified. Most participants had received oral poliovirus vaccine (OPV) and almost all had been exposed to household contacts who had received OPV. Polioviruses of recent vaccine origin were transiently found in four individuals in Mexico and Brazil, where OPV is recommended for all children. CONCLUSION: Although chronic poliovirus excretion can occur in immunodeficient persons, it appears to be rare.

Adolescent↗
PubMed1982

[Chronic cholestasis and progressive neuromyopathy. Diagnostic problems and therapeutic possibilities in a vitamin E deficiency disease (author's transl)].

A 15-year-old female developed a slowly progressive gait disturbance starting from the age of two. She was suffering from congenital choleostatic jaundice. Neurological examination revealed cerebellar ataxia, hyporeflexia and hyposensitivity. The initial vitamin E level in serum was extremely low with 0.4 mcg/ml (normal 5-20 mcg/ml). Muscle biopsy changes were similar to those in experimental vitamin E deficient animals. Pathological data of children with longstanding choleostatic jaundice showed degeneration of the posterior column and selective loss of large-caliber, myelinated axons in peripheral nerves. Similar to one other report in the literature the only effective treatment was the intramuscular injection of 50-100 mg Vitamin E twice a week which normalized the serum levels, stopped the progression of the disease and showed improvement of some neurological functions after half a year. A very early treatment seems to be important to keep these children walking.

Adolescent↗
PubMed1977

Acquired zinc deficiency disease of skin.

Two patients, who were on long term parenteral hyperalimentation, developed skin lesions similar to those seen in acrodermatitis enteropathica. Both patients were treated with oral zinc sulphate and their skin lesions cleared completely. These patients are presented as an acquired zinc deficiency syndrome.

Female↗
PubMed1989

[Xerophthalmia caused by self-induced deficiency disease].

Xerophthalmia is no longer seen in Europe since the 19th century. We report the case of a female patient, aged 33, of french nationality, who presented a clinical picture of major vitamin A deficiency, self-induced and with ocular complications. An untreated long standing depressive condition appeared to be the major etiologic factor. Perforation of a desmetocele necessitated penetrating keratoplasty. Histologic corneal and conjunctival aspects are reported. Oral prescription of vitamin A resulted in considerable clinical improvement. Only 3 similar cases have been previously reported. Clinical manifestations of xerophthalmia are described along with preventive and curative therapy.

Adult↗