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   Nephrologie 1983;4(2):69-74
   
[Anomalies of human gonadal function in periodic hemodialysis: role of the
etiology of kidney failure and the role of iron overload].

   [Article in French]
   
    Dueymes JM, Caron P, Pourrat JP, Louvet JP, Conte JJ
    
   Levels of testosterone, free testosterone, oestrogen, LH, FSH,
   prolactin were measured in 39 dialysed men. A LHRH stimulation test
   was performed. This study was analysed in function of the underlying
   renal disease, the duration of hemodialysis, and serum ferritin
   levels. In chronic glomerulonephritis serum gonadotrophins
   concentrations were significantly higher than in chronic interstitial
   nephritis or polycystic disease. A correlation between prolactin and
   ferritin was found, which may reflect the pituitary iron overload.
   Free testosterone levels were significantly lower in patients with
   gynecomastia (23-29 patients). In fact, the most direct relationship
   that we found with gynecomastia in dialysed men was with the free
   testosterone/oestrogen ratio.
   
   PMID: 6877481, UI: 83271729
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   JAMA 1980 Jul 25;244(4):343-5
   
Hemosiderosis in hemodialysis patients. An autopsy study of 50 cases.

    Ali M, Fayemi AO, Rigolosi R, Frascino J, Marsden T, Malcolm D
    
   The distribution of stainable iron stores was investigated in various
   organs of 50 hemodialysis patients with chronic renal disease. Massive
   iron deposits were found in the liver and spleen. Among 18 patients
   with severe hepatosplenic siderosis, iron deposits were abundant in
   the adrenal glands, lymph nodes, and lungs and were sparse in the
   heart, kidneys, and pancreas. There was an absence or scarcity of
   stainable iron in bone marrow of 19 pats. In five of these
   marrow-iron-depleted patients, serum concentrations of ferritin were
   high. In long-term hemodialysis patients, a variety of factors make
   massive iron overloads of various organs a likely occurrence, severe
   hepatosplenic siderosis may occur in marrow-iron-depleted patients,
   and serum ferritin levels in this setting may not always accurately
   reflect the status of marrow iron store.
   
   PMID: 7392125, UI: 80230133
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   Clin Investig 1992 Jul;70(7):566-72
   
Testosterone treatment of men with idiopathic hemochromatosis.

    Kley HK, Stremmel W, Kley JB, Schlaghecke R
    
   Stadtisches Krankenhaus, Singen/Hohentwiel,
   Heinrich-Heine-Universitat, Dusseldorf.
   
   Patients with chronic liver disease usually exhibit low plasma levels
   of testosterone with loss of libido and potency; this is also valid in
   male patients suffering from idiopathic hemochromatosis (IHC), in whom
   nowadays the diagnosis is made at an earlier age. Therefore, the
   effect of testosterone treatment was studied in 10 patients with IHC.
   After the application of 250 mg testosterone enanthate i.m., the
   plasma testosterone (from 2.4 +/- 1.9 to 20.1 +/- 7.4 ng/ml) and
   estradiol (from 17.4 +/- 6.3 to 38.5 +/- 14.2 pg/ml) levels increased
   significantly. The rise of estradiol was in the range of controls and
   smaller than reported in other chronic liver diseases. In a long-term
   study, 250 mg testosterone enanthate was given 4-weekly for 33-96
   months to 5 patients with IHC. General well-being, libido, and potency
   recovered almost immediately. Over a treatment period of 27.3 patient
   years, symptoms of hyperestrogenism (gynecomastia) or (portal vein)
   thrombosis were not seen, both of which had been described in patients
   with alcoholic liver cirrhosis. There was no deterioration of liver
   function. The effect of testosterone treatment on the patients'
   well-being and plasma hormone concentrations remained unchanged over
   the whole period of testosterone treatment. Thus, in male patients
   with IHC and lowered plasma testosterone, treatment with testosterone
   enanthate may be instituted. Because of the positive effects on
   general well-being, liver regeneration capacity, and potency,
   testosterone should especially be administered to younger subjects
   suffering from IHC.
   
   PMID: 1392425, UI: 93005397
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Subject: thyroid/iron

   Arch Intern Med 143 (10): 1890-1893 (Oct 1983)
   
Thyroid disease in hemochromatosis. Increased incidence in homozygous men.

   
   
    Edwards CQ, Kelly TM, Ellwein G, Kushner JP
    
   
   
   The thyroid function of 49 patients homozygous for the hemochromatosis
   allele was studied by measurement of serum thyroxine and thyrotropin
   concentrations. Of 34 homozygous men, three were found to be
   hypothyroid (thyroxine, less than 3.0 micrograms/dL and thyrotropin,
   greater than 40 ImU/mL) and one was hyperthyroid (thyroxine, 24
   micrograms/dL). All 15 homozygous women had normal thyroid function.
   The hypothyroid patients had elevated titers of antithyroid
   antibodies. Histologic examination of the thyroid at autopsy of one
   hypothyroid patient showed notable iron accumulation and fibrosis with
   modest lymphocytic infiltration. The causative importance of iron
   deposition in thyroid diseases associated with hemochromatosis was
   suggested by the reversal of the usual sex ratio of thyroid
   dysfunction. Men with hemochromatosis had a much greater iron load
   than women, and they also had a surprisingly higher incidence of
   thyroid disease. Iron may have caused injury to the thyroid, followed
   by the development of antithyroid antibodies and hypothyroidism. The
   frequency of thyroid disorders in men with hemochromatosis is about 80
   times that of men in the general population.
   

Subject: Hypothyroid/coffee

 COFFEE: fYI Found a case-control study showing coffee to protect against 
 thyroid
 disease. They found a strong negative association (p<0.05) in 125 patients 
 with
 thyroid disease and matched controls--the more coffee, the less thyroid 
 disease. After
 adjustment for possible confounders, the association remained. They 
 postulate a
 stimulatory effect of caffeine on the intracellular cyclic AMP production, 
 which
 inhibits cell growth. (Linos et al., Does coffee consumption protect 
 against thyroid
 disease? Acta Chir Scand 1989 Jun; 155(607) 317-320.)
 
Subject: thyroid

   
   Eur J Haematol 1997 Aug;59(2):76-81
   
Incidence of endocrine complications and clinical disease severity related to
genotype analysis and iron overload in patients with beta-thalassaemia.

    Jensen CE, Tuck SM, Old J, Morris RW, Yardumian A, De Sanctis V, Hoffbrand
    AV, Wonke B
    
   Department of Obstetrics and Gynaecology, The Whittington Hospital,
   London, UK.
   
   The incidence of endocrine dysfunction in relation to the detailed
   genotype of beta-thalassaemia is investigated in this study. In
   addition, the association of genotype to specific clinical features of
   beta-thalassaemia is examined, together with the relationship between
   serum ferritin levels and endocrine complications. Ninety-seven
   patients were included, all with transfusion dependent
   beta-thalassaemia. Patients were divided into 2 categories; group 1
   consisted of patients with a beta0/beta0 genotype with or without a
   concomitant alpha-globin gene deletion as well as patients with
   beta0/beta+ or beta+/beta+ genotype and normal alpha-globin chain
   synthesis. Group 2 included patients with beta+/beta+ or beta+/beta0
   genotype and one alpha-globin chain deletion and those with a moderate
   amount of beta-globin chain synthesis (beta++) and normal alpha-globin
   chain synthesis. The results showed that group 1 patients were more
   likely to have severe clinical disease (p=0.005). Sixty-four patients
   (66%) had at least 1 endocrine disorder and 39 (40%) had multiple
   endocrinopathies; the most common abnormality was hypogonadotrophic
   hypogonadism (HH). There was a significant association between
   patients with group 1 genotypes and the presence of HH and impaired
   glucose tolerance or diabetes. A positive correlation was demonstrated
   between serum ferritin concentrations and the presence of thyroid or
   parathyroid dysfunction.
   
   PMID: 9293854, UI: 97438079
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 (HOME) Subject: hormone/osteo/iron/arthritis

   
   Arthritis Rheum 1999 Apr;42(4):799-806
   
Elevated parathyroid hormone 44-68 and osteoarticular changes in patients with
genetic hemochromatosis.

    Pawlotsky Y, Le Dantec P, Moirand R, Guggenbuhl P, Jouanolle AM, Catheline
    M, Meadeb J, Brissot P, Deugnier Y, Chales G
    
   Centre Hospitalier et Universitaire, Rennes, France.
   
   OBJECTIVE: To determine whether the osteoarticular changes associated
   with genetic hemochromatosis could be explained by metabolic
   parathyroid hormone (PTH) disorders. METHODS: The study involved 210
   patients with liver iron overload syndromes. Osteoarticular changes
   were numerically scored as the number of damaged joints. PTH 1-84 and
   44-68 were assayed. RESULTS: An increase in serum PTH 44-68 levels was
   found in one-third of untreated patients who had no calcium or PTH
   1-84 abnormalities. Serum PTH 44-68 levels correlated positively with
   serum ferritin levels. In multivariate analyses, the number of
   affected joints correlated positively with age, serum PTH 44-68
   levels, and serum ferritin levels. CONCLUSION: Liver iron overload
   syndromes, especially genetic hemochromatosis, are associated with
   elevated circulating levels of PTH fragments containing the 44-68
   region, which appears to play a role in osteoarticular changes. This
   increase seems to be a consequence of iron overload.
   
   PMID: 10211896, UI: 99226878
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Subject: thalassemia/iodine

   
   Eur J Endocrinol 2000 Sep;143(3):319-25
   
Increased sensitivity to the inhibitory effect of excess iodide on thyroid
function in patients with beta-thalassemia major and iron overload and the
subsequent development of hypothyroidism.

    Alexandrides T, Georgopoulos N, Yarmenitis S, Vagenakis AG
    
   Endocrine Division, Department of Medicine, University of Patras
   Medical School, Patras, Greece.
   
   [Record supplied by publisher]
   
   OBJECTIVE: Patients with beta-thalassemia frequently develop primary
   hypothyroidism and other endocrine disorders due to iron overload. We
   studied whether administration of excess iodide to patients with
   apparently normal thyroid function could uncover an underlying thyroid
   disease. DESIGN AND METHODS: Twenty-five patients, 10 prepubertal
   (mean age 11+/-3 years) and 15 adults (mean age 23+/-5 years) with
   normal thyroid hormone and TSH levels, a normal response of TSH to TRH
   and negative thyroid peroxidase antibodies received 20mg iodide three
   times daily for three weeks, and thyroid hormone and TSH levels were
   measured weekly during, and for three weeks after, iodide
   administration and every 3 months thereafter for the next 5 years.
   RESULTS: During iodide administration there was a significant decrease
   in thyroid hormone concentrations which remained within normal levels,
   and a significant increase in TSH concentrations which in 14 out of 25
   (56%) patients reached the hypothyroid level. Baseline TSH values were
   higher in those patients who developed subclinical hypothyroidism
   (2.31+/-0.71mU/l vs 1. 34+/-0.64mU/l, P=0.0016). Subclinical
   hypothyroidism developed in 70% of prepubertal and in 47% of adult
   patients. Serum ferritin was elevated in all patients. Nine of the
   fourteen patients (64.3%) who developed subclinical hypothyroidism
   during iodide administration developed hypothyroidism during the
   5-year follow-up compared with only one of the eleven patients with a
   normal response to iodide (P=0.004). CONCLUSIONS: Patients with
   beta-thalassemia should not be exposed to excess iodide due to
   increased sensitivity to its inhibitory effects on thyroid function.
   The susceptible individuals frequently develop permanent
   hypothyroidism in the following years.
   
   Publication Types:
     * Clinical trial
       
   PMID: 11022172, UI: 20478148
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Subject: thyroid/radiology/MRI

   
   AJR Am J Roentgenol 2000 Dec;175(6):1567-9
   
T2 relaxation rate as an index of pituitary iron overload in patients with
beta-thalassemia major.

    Argyropoulou MI, Metafratzi Z, Kiortsis DN, Bitsis S, Tsatsoulis A,
    Efremidis S
    
   Department of Radiology, School of Medicine, University of Ioannina,
   45110, Ioannina, Greece.
   
   OBJECTIVE: In transfusion-dependent ss-thalassemia major, increased
   iron deposition in the pituitary gland has a cytotoxic effect, leading
   mainly to hypogonadotropic hypogonadism. Early detection and
   quantification of iron in the pituitary gland are of particular
   importance for successful treatment. The purpose of this study was to
   evaluate the T2 relaxation rate (1/T2) as a marker of pituitary
   siderosis. SUBJECTS AND METHODS: In 29 patients with ss-thalassemia
   major and 40 controls, we assessed the 1/T2 of the pituitary gland in
   a 1.5-T MR unit, using a multiecho spin-echo sequence. In all
   patients, an extensive endocrine evaluation was performed, including
   measurements of spontaneous and stimulated levels of gonadotropins,
   thyroid hormones, growth hormone, insulinlike growth factor, and
   adrenal hormones. RESULTS: A positive correlation was found between
   the 1/T2 and the serum ferritin level (r = 0.73, p < 0.001). The 1/T2
   was higher in patients (mean, 0.020 msec(-1); SD, 0.006) compared with
   that of controls (mean, 0.011 msec(-1); SD, 0.001; p < 0.001). The
   1/T2 was higher in patients with hypogonadotropic hypogonadism (mean,
   0.024 msec(-1); SD, 0.006) in comparison with that of patients without
   any pituitary dysfunction (mean, 0.017 msec(-1); SD, 0.004; p < 0.05).
   CONCLUSION: The T2 relaxation rate could be used as an index of
   pituitary iron overload, and it might be of value to monitor treatment
   with deferoxamine in patients with ss-thalassemia major.
   
   PMID: 11090376, UI: 20544695
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Subject: thyroid/early/children

   
   J Pediatr Endocrinol Metab 2000 Jun;13(6):651-6
   
Early onset of endocrine abnormalities in beta-thalassemia major in a
developing country.

    Gulati R, Bhatia V, Agarwal SS
    
   Department of Genetics, Sanjay Gandhi Postgraduate Institute of
   Medical Sciences, Lucknow, India.
   
   Endocrine complications in patients with thalassemia major in
   developing countries may be frequent due to suboptimal iron chelation.
   Data from developing countries are scant. We prospectively evaluated
   growth, growth hormone (GH), insulin-like growth factor I, thyroid
   hormone, cortisol and glucose tolerance in 84 patients over one year.
   Height standard deviation (SD) score of patients > 8 years (-2.2 +/-
   1.5 against National Center for Health Statistics references) was
   significantly lower than that of normal controls (-1.0 +/- 0.7, p <
   0.001). 51% of patients had GH deficiency, 13% hypocortisolism and
   7.9% diabetes/impaired glucose tolerance. Ten of 11 adolescents/young
   adults had hypogonadism. Of 54 preadolescent children who underwent
   dynamic testing, 18 (33%) had at least one endocrine deficiency other
   than short stature. We conclude that hypogonadism and hypocortisolism
   form important causes for morbidity in our thalassemic children.
   Thalassemic patients in developing countries may be at risk for
   endocrine deficiencies at younger ages.
   
   PMID: 10905390, UI: 20361325
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Subject: Blackfan/thyroid

   
   J Pediatr Endocrinol Metab 2000 Mar;13(3):325-8
   
Multiple endocrine abnormalities in a child with Blackfan-Diamond anemia and
hemochromatosis. Significant improvement of growth velocity and predicted adult
height following growth hormone treatment despite liver damage.

    Lanes R, Muller A, Palacios A
    
   Pediatric Endocrine Unit, Hospital de Clinicas Caracas, Erythrocyte
   and Leucocyte Laboratory, Centro de Quimioterapia, Oncologia y
   Hematologia and Clinica Avila, Caracas Venezuela.
   
   We evaluated a short, prepubertal 13.9 year-old boy with
   Blackfan-Diamond anemia and significant liver iron stores due to
   multiple blood transfusions and found him to have several endocrine
   abnormalities, including hypothyroidism, hypoparathyroidism, primary
   and secondary hypogonadism and IGF-I insufficiency. Growth velocity
   was poor despite treatment with levothyroxine, calcitriol, calcium and
   aggressive therapy with chelating agents. After 25 months of treatment
   with rhGH his growth velocity, height for age and PAH increased
   significantly, suggesting a degree of sensitivity to GH despite his
   liver damage.
   
   PMID: 10714760, UI: 20177242
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Subject: thyroid

   
   Acta Clin Belg 1999 Dec;54(6):334-45
   
[Endocrine complications of genetic hemochromatosis].

   [Article in French]
   
    Paris I, Hermans M, Buysschaert M
    
   Service d'Endocrinologie et Nutrition, Cliniques Universitaires St
   Luc, Bruxelles, Belgique.
   
   The authors report the prevalence and severity of endocrine
   complications in a cohort of 115 patients suffering form genetic
   hemochromatosis and followed since two decades. Already 40% of them
   had developed diabetes at the time of diagnosis of hemochromatosis,
   which was made at the age of 50 +/- 12 years (m +/- SD). Hypogonadism
   was evidenced in 42% of the patients. In most of them, it was
   considered as secondary to pituitary lesions as assessed by GnRH
   tests. No other endocrine complications, in particular thyroid
   disease, were evidenced during follow up. On the other hand, it was
   also of interest to note that liver cirrhosis was observed in 52% of
   the patients at the time of hemochromatosis diagnosis. A relationship
   between cirrhosis, diabetes and hypogonadism was also assessed in
   these patients. We conclude to the still high prevalence of endocrine
   complications in genetic hemochromatosis.
   
   PMID: 10686706, UI: 20151322
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Subject: thyroid/aplastic anemia

   
   Acta Paediatr Jpn 1995 Aug;37(4):534-6
   
Hypothyroidism and hypoparathyroidism in an 11 year old boy with
hemochromatosis secondary to aplastic anemia.

    Himoto Y, Kanzaki S, Nomura H, Araki T, Takahashi Y, Seino Y
    
   Department of Pediatrics, Fukuyama Municipal Hospital, Japan.
   
   This is the first reported case, to our knowledge, of
   hypoparathyroidism and hypothyroidism due to secondary hemochromatosis
   with onset during childhood. The patient was a boy with refractory
   aplastic anemia in whom primary hypothyroidism and hypoparathyroidism
   became apparent at the age of 10 and 11 years old, respectively. He
   had received a total of 100 L of transfused blood by the age of 10
   years. The patient showed poor annual height gain due to primary
   hypothyroidism, together with hypocalcemia, cataract and intracranial
   calcification due to hypoparathyroidism. The early appearance of both
   thyroid and parathyroid dysfunction in this patient may have been due
   to the delay of initiation of iron-chelating agents and liver
   dysfunction due to hepatitis type C.
   
   PMID: 7572161, UI: 96054163
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Subject: thyroid/idiopathic/child

   
   Hepatology 1981 Jan-Feb;1(1):58-64
   
Idiopathic neonatal iron storage involving the liver, pancreas, heart, and
endocrine and exocrine glands.

    Goldfischer S, Grotsky HW, Chang CH, Berman EL, Richert RR, Karmarkar SD,
    Roskamp JO, Morecki R
    
   Autopsy studies of two infants, one a newborn, the other 4 months old,
   revealed massive amounts of iron in lysosomes of hepatocytes and
   pancreatic acinar cells. Iron, which had been transported across the
   placenta, accumulated in the same cell types as in adults with primary
   and secondary hemochromatosis. Hemosiderin was found in cardiac muscle
   cells, gastric and intestinal glands, and endocrine and exocrine
   organs including pituitary, thyroid, adrenals, islets of Langerhans,
   and sublingual and sweat glands. The liver was the most affected organ
   and the normal hepatic architecture was replaced by hepatocytes which
   were arranged in cluster, pseudoacinar structures, and multinucleated
   giant cells embedded in a collagen matrix. The islets of Langerhans
   were hyperplastic and hypertrophic. Ten similar cases, in five
   families, have been described; no patients liver longer than 4 months.
   Neonatal iron storage disease is clinically and pathologically
   distinct from Zellweger's cerebrohepatorenal syndrome and
   hypermethioninemia (tyrosinemia) neonatal diseases in which large
   stores of iron are present in hepatocytes. No abnormalities in serum
   iron, ferritin, or transferrin concentrations were detected in five
   parents of the affected children.
   
   PMID: 7286889, UI: 82029068
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Subject: thyroid/hemodialysis

   
   Clin Nephrol 1992 Aug;38(2):105-9
   
Primary hypothyroidism and multiple endocrine failure in association with
hemochromatosis in a long-term hemodialysis patient.

    Shirota T, Shinoda T, Aizawa T, Mizukami T, Katakura M, Takasu N, Yamada T
    
   Department of Geriatrics, Endocrinology and Metabolism, Shinshu
   University School of Medicine, Matsumoto, Japan.
   
   A 56-year-old male patient on chronic hemodialysis developed liver
   cirrhosis. He received a total of 20 liters of blood transfusion.
   Bronze pigmentation of the skin and iron deposition to the liver,
   spleen, pancreas and thyroid gland, which was demonstrated by computed
   tomography and magnetic resonance imaging studies, and histological
   demonstration of iron deposition to the thyroid gland, bone marrow and
   gastric mucosa established a diagnosis of secondary hemochromatosis.
   Endocrine work-up revealed the presence of diabetes mellitus with
   minimum insulin secretory response, primary (or thyroprivic)
   hypothyroidism, hypoparathyroidism and hypogonadotropic hypogonadism.
   A wide-spread endocrine involvement as seen in this patient is a rare
   clinical feature of hemochromatosis secondary to massive blood
   transfusion in hemodialysis patients. Particularly, primary
   hypothyroidism due to iron deposition to the thyroid gland was quite a
   rare feature of hemochromatosis.
   
   PMID: 1516278, UI: 92386797
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Subject: thyroid/ferrous sulfate

   
   South Med J 1997 Jun;90(6):637-9
   
Ferrous sulfate-induced increase in requirement for thyroxine in a patient with
primary hypothyroidism.

    Shakir KM, Chute JP, Aprill BS, Lazarus AA
    
   Department of Internal Medicine, National Naval Medical Center,
   Bethesda, MD 20889-5600, USA.
   
   Recent studies have shown that under experimental conditions ferrous
   sulfate may reduce the gastrointestinal absorption of orally
   administered levothyroxine sodium in patients with primary
   hypothyroidism. We describe a patient who became hypothyroid while
   taking ferrous sulfate. The hypothyroid status was corrected by
   increasing the dose of levothyroxine. Subsequently, when ferrous
   sulfate was discontinued, the patient became hyperthyroid while taking
   the higher dose of thyroid hormone preparation. Since both
   hypothyroidism and iron deficiency anemia may coexist, additional
   thyroid function testing is recommended in patients treated
   concurrently with ferrous sulfate and L-thyroxine.
   
   PMID: 9191742, UI: 97335076
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Subject: thyroid/pruritus

   
   Schweiz Med Wochenschr 1995 Nov 18;125(46):2244-50
   
[Pruritus--also a challenge in internal medicine].

   [Article in German]
   
    Brunner W
    
   Medizinische Klinik, Kantonsspital Chur.
   
   Generalized or localized itch without primary skin manifestations may
   be the presenting symptom of serious internal diseases. Five
   characteristic cases of pruritus are discussed: Hodgkin's disease,
   primary sclerosing cholangitis, polycythemia vera, iron deficiency
   (with pica), and uremia. Other important causes must be considered;
   all forms of cholestasis, including primary biliary cirrhosis,
   drug-induced, pregnancy-related, and extrahepatic cholestasis; other
   hematologic and malignant disorders such as non-Hodgkin's lymphoma,
   leukemia, multiple myeloma, solid tumors, and myelodysplastic
   syndromes; metabolic and endocrine diseases, most notably diabetes
   mellitus, hyperthyroidism, hypothyroidism, and carcinoid syndrome;
   focal neurologic diseases such as brain tumors, cerebral infarctions
   and multiple sclerosis; adverse drug reactions without rash;
   infectious diseases, especially parasitic and HIV infections. A
   diagnostic laboratory screening for pruritus of undetermined origin is
   suggested.
   
   PMID: 8525344, UI: 96091969
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Subject: ZINC/IRON/TESTOSTERONE



APPLIED NUTRITIONAL INVESTIGATION

  Zinc Status and Serum Testosterone Levels of Healthy Adults
  
    ANANDA S. PRASAD, MD, PHD, CHRIS S. MANTZOROS, MD, FRANCES W. J. BECK, PHD,
    JOSEPH W. HESS, MD, AND GEORGE J. BREWER, MD
    
      From the Department of Internal Medicine, Division of
      Hematology-Oncolgoy, Wayne State University School of Medicine, Detroit,
      Michigan, Departments of Human Genetics and Division of Endocrinology,
      Department of Internal Medicine, Beth Israel Hospital, Harvard Medical
      School, Boston, Massachusetts, USA
      
        ABSTRACT
        
   Zinc deficiency is prevalent throughout the world, including the USA.
   Severe and moderate deficiency of zinc is associated with hypogonadism
   in men. However, the effect of marginal zinc deficiency on serum
   testosterone concentration is not known. We studied the relationship
   between cellular zinc concentrations and serum testosterone
   cross-sectionally in 40 normal men, 20 to 80 y of age. In four normal
   young men (27.5±0.5 y), we measured serum testosterone before and
   during marginal zinc deficiency induced by restricting dietary zinc
   intake. We also measured serum testosterone in nine elderly men (64±9
   y) who were marginally zinc deficient before and after 3 to 6 mo of
   supplementation with 459 umol/ d oral zinc administered as zinc
   gluconate. Serum testosterone concentrations were significantly
   correlated with cellular zinc concentrations in the cross-sectional
   study (lymphocyte zinc versus serum testosterone, r = 0.43, p = 0.006;
   granulocyte zinc versus serum testosterone, r = 0.30, p = 0.03).
   Dietary zinc restriction in normal young men was associated with a
   significant decrease in serum testosterone concentrations after 20
   weeks of zinc restriction (baseline versus post-zinc restriction
   mean±SD, 39.9±7.1 versus 10.6±3.6 nmol/L, respectively; p = 0.005).
   Zinc supplementation of marginally zinc-deficient normal elderly men
   for six months resulted in an increase in serum testosterone from
   8.3±6.3 to 16.0±4.4 nmol/L (p = 0.02). We conclude that zinc may play
   an important role in modulating serum testosterone levels in normal
   men. Nutrition 1996 12:344-348
   
   Key words: zinc, serum testosterone, elderly
   
   
     _________________________________________________________________

Subject: zinc/iron


   Yip R, Reeves JD, Lonnerdal B, et al., "Does Iron Supplementation
   Compromise Zinc Nutrition in Healthy Infants?", (Oct 1985), The
   American Journal of Clinical Nutrition, 42 (4), pp: 683-7.

Subject: zinc/DNA/iron

     _________________________________________________________________

   J. Biol. Chem. 271: 5125-5130 (1996)[96214945]

In vivo and in vitro iron-replaced zinc finger generates free radicals and
causes DNA damage.



    D. Conte, S. Narindrasorasak & B. Sarkar



   Department of Biochemistry Research, The Hospital for Sick Children,
   Toronto, Ontario M5G 1X8, Canada.

   The estrogen receptor (ER) is a ligand-activated transcription factor
   whose DNA-binding domain (ERDBD) has eight cysteines, which coordinate
   two zinc atoms, forming two zinc finger-like structures. We
   demonstrate the capability of iron to replace zinc in zinc finger
   (hereby referred to as iron finger) both in vivo (using Escherichia
   coli BL21 (DE3)) and in vitro. Iron has the ability to substitute for
   zinc in the ERDBD as demonstrated by mobility shift and methylation
   interference assays of iron finger, which show specific recognition of
   the estrogen response element. The DNA binding constants for both in
   vivo and in vitro iron-replaced zinc fingers were similar to that of
   the native finger. Atomic absorption analysis revealed a ratio of 2:1
   iron atoms/mol of ERDBD protein, as found for zinc in the crystal
   structure of native ERDBD. More importantly, we demonstrate that iron
   finger in the presence of H2O2 and ascorbate generates highly reactive
   free radicals, causing a reproducible cleavage pattern to the
   proximate DNA, the estrogen response element. The deoxyribose method,
   used to detect free radical species generated, and the resultant
   cleaved DNA ends, caused by iron finger, suggest that the free
   radicals generated are hydroxyl radicals. Due to the close proximity
   of the zinc finger to DNA, we postulate that iron-substituted zinc
   finger may generate free radicals while bound to genetic regulatory
   response elements, leading to adverse consequences such as
   iron-induced toxicity and/or carcinogenesis.

   MeSH Terms:
     * Base Sequence
     * Cloning, Molecular
     * Comparative Study
     * DNA Damage*
     * DNA-Binding Proteins/metabolism
     * DNA-Binding Proteins/biosynthesis
     * DNA, Bacterial/metabolism
     * DNA, Bacterial/chemistry
     * Escherichia coli/metabolism
     * Escherichia coli/growth & development
     * Free Radicals/metabolism
     * Human
     * Iron/pharmacology
     * Kinetics
     * Methylation
     * Models, Molecular
     * Molecular Sequence Data
     * Nucleic Acid Conformation
     * Oligodeoxyribonucleotides
     * Protein Structure, Secondary
     * Receptors, Estrogen/metabolism
     * Receptors, Estrogen/biosynthesis
     * Recombinant Proteins/metabolism
     * Recombinant Proteins/biosynthesis
     * Support, Non-U.S. Gov't
     * Time Factors
     * Zinc/physiology
     * Zinc Fingers*



   Substances:
     * Zinc
     * Iron
     * Recombinant Proteins
     * Receptors, Estrogen
     * Oligodeoxyribonucleotides
     * Free Radicals
     * DNA, Bacterial
     * DNA-Binding Proteins


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Subject: zinc/iron

     _________________________________________________________________
   
Effects of Trace Elements Supplementation on Measures of Nutritional Status

   Effects of supplementation with zinc (30.4 mg/d), copper (3.4 mg/d),
   and chromium (241 ug/d) on alkaline phosphatase, serum ferritin,
   hemoglobin, and plasma and erythrocyte copper, iron, and zinc were
   examined in apparently healthy adults over the age of 50. Differences
   were found between males and females within supplement groups. Serum
   ferritin decreased significantly during and following zinc
   supplementation in males. Total hemoglobin increased significantly
   from baseline to four weeks post supplementation in chromium and
   copper supplemented females. Alkaline phosphatase decreased from
   baseline to four weeks post supplementation in all groups. The
   decrease was significant in the mineral supplement groups except for
   females receiving zinc--but not in the placebo group. Plasma zinc
   increased significantly in zinc supplemented males and during
   supplementation and in copper supplemented females from the end of
   supplementation to four weeks post supplementation. In the copper
   group, plasma copper decreased during supplementation in females but
   was not significantly different over time in males, while in the
   chromium supplemented females plasma copper increased at eight weeks
   of supplementation. These results support the importance of examining
   the interactive effects of minerals in both males and females.
   
   Sponsor: Agricultural Experiment Station
   PI: Andrea Arquitt
   
   
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