Megaloblastic Anemia Associated with Long-Term Tetracycline Therapy

1973 ◽  
Vol 78 (6) ◽  
pp. 910 ◽  
Author(s):  
CARROLL C. JONES
Keyword(s):  
2009 ◽  
Vol 155 (2) ◽  
pp. 295-297 ◽  
Author(s):  
Caterina Borgna-Pignatti ◽  
Milena Azzalli ◽  
Stefania Pedretti

2020 ◽  
Vol 14 (3) ◽  
pp. 247-250
Author(s):  
Edmund Tsui ◽  
Jenna Tauber ◽  
Irene Barbazetto ◽  
Susan K. Gelman

2007 ◽  
Vol 98 (5) ◽  
pp. 1014-1020 ◽  
Author(s):  
Ondine van de Rest ◽  
Jane Durga ◽  
Petra Verhoef ◽  
Alida Melse-Boonstra ◽  
Henny A. M. Brants

Folate is required for 1-carbon metabolism and deficiency in folate leads to megaloblastic anemia. Low levels of folate have been associated with increased risk of vascular disease. To investigate whether RDA of folate are met, habitual folate intake needs to be assessed reliably. We developed a FFQ to specifically measure folate intake over the previous 3 months in elderly people in the Netherlands. Major sources of folate intake, i.e. foods contributing to at least 80 % of the average folate intake, were identified through an analysis of the second Dutch Food Consumption Survey for the sub-population of men and women aged 50–70. In 2000 and 2001, folate intake was estimated with this questionnaire in 1286 individuals aged 50–75 years. Concentrations of serum and erythrocyte folate served as biomarkers with which relative validity of the questionnaire was assessed. The same FFQ was repeated after 3 years in 803 subjects in order to assess long-term reproducibility. Mean folate intake was estimated to be 196 (sd 69) μg/d. Spearman correlation coefficients between folate intake and serum and erythrocyte concentrations were 0·14 (P < 0·01) and 0·05 (P = 0·06) respectively. Spearman correlations between folate intakes measured at baseline and after 3 years were 0·58 (P < 0·01). 47 % of the participants were classified in the same quartiles on the two occasions. Our FFQ showed a weak correlation between folate intake and blood folate concentrations and reproducibility was acceptable. This FFQ is able to rank subjects according to their folate intake.


Diabetes Care ◽  
1998 ◽  
Vol 21 (1) ◽  
pp. 38-41 ◽  
Author(s):  
G. Valerio ◽  
A. Franzese ◽  
V. Poggi ◽  
A. Tenore

Author(s):  
Manali Arora ◽  
Deb Kumar Boruah ◽  
Vishal Thakker ◽  
Sangeeta Bhanwra

Phenytoin is a commonly used anti-epileptic drug for various types of seizure disorders except for absent seizures. Long term dose dependant neurological side effects of phenytoin therapy include cerebellar atrophy, cerebral atrophy and brain stem atrophy. Skull hyperostosis, gum hypertrophy and megaloblastic anemia are other known effects of Long term therapy. We present four cases depicting clinical and neuroimaging findings of Phenytoin induced Toxicity.


2020 ◽  
Author(s):  
Francesco Martino ◽  
Alessandra Magenta ◽  
Maria Letizia Troccoli ◽  
Eliana Martino ◽  
Concetta Torromeo ◽  
...  

Abstract Background: Transcobalamin deficiency is a rare autosomal recessive inborn error of cobalamin transport (prevalence: <1/1000000) which clinically manifests in early infancy. Case presentation:We describe the case of a 30 year old woman who at the age of 30 days presented with the classical clinical and laboratory signs of an inborn error of vitamin B12 metabolism. Family history revealed a sister who died at the age of 3 months with a similar clinical syndrome and with pancytopenia. She was started on empirical intramuscular (IM) cobalamin supplements (injections of hydroxocobalamin 1 mg/day for 1 week and then 1 mg twice a week) and several transfusions of washed and concentrated red blood cells.With these treatments a clear improvement in symptoms was observed, with the disappearance of vomiting, diarrhea and normalization of the full blood count. At 8 years of age injections were stopped for 3 months causing the reappearance of megaloblastic anemia. IM hydroxocobalamin was then restarted sine die. The definitive diagnosis could only be established at 29 years of age when a genetic evaluation revealed the homozygous c.1115_1116delCA mutation of TCN2 gene (p.Q373GfsX38).Currently she is a 30-year old healthy lady taking 1 mg of IM hydroxocobalamin once a week.Conclusions: Our case report highlights that early detection of TC deficiency and early initiation of aggressive IM treatment is likely associated with disease control and an overall favorable outcome.


2012 ◽  
Vol 46 (11) ◽  
pp. 1470-1476 ◽  
Author(s):  
Sarah A Pierce ◽  
Amy H Chung ◽  
Karen Korch Black

BACKGROUND: Metformin can result in vitamin B12 deficiency, potentially leading to complications such as neuropathy. Annual monitoring of vitamin B12 has been suggested; however, it is unknown whether current practice reflects this recommendation. OBJECTIVE: To identify vitamin B12 monitoring patterns in patients on long-term, high-dose metformin. Secondary objective was to determine the frequency of new vitamin B12 deficiency, anemia, and neuropathy documented after initiation of high-dose metformin. METHODS: Electronic medical records of veterans treated at the Veterans Affairs Maryland Healthcare System with high-dose metformin (≥2000 mg/day) as of November 1, 2010, were reviewed. Data regarding metformin treatment, vitamin B12 measurements, and documentation of vitamin B12 deficiency, cyanocobalamin supplementation, anemia, and neuropathy were collected. Subjects treated with metformin for less than 1 year or those with documented peripheral neuropathy, megaloblastic anemia, vitamin B12 deficiency, or a condition associated with vitamin B12 malabsorption prior to metformin initiation were excluded. RESULTS: Subjects (N = 235) had a mean metformin dose of 2050 mg/day and mean duration of treatment of 5.2 years. Sixty percent did not have vitamin B12 measured. Of subjects receiving metformin for 10 years or more, nearly half (46%) never had vitamin B12 measured. New documentation of vitamin B12 deficiency or cyanocobalamin supplementation was found in 5.5% of the population, and anemia was found in 12%. Of the 14% with new neuropathy, 42% did not have vitamin B12 measured. CONCLUSIONS: Vitamin B12 was not routinely monitored in patients on high-dose metformin, even in those at highest risk (≥10 years of therapy), or in those with potential manifestations of vitamin B12 deficiency (neuropathy). Cases of vitamin B12 deficiency and resulting anemia or neuropathy may be undiagnosed and untreated because of lack of monitoring. Prospective studies examining the effect of increased vitamin B12 monitoring on identification and treatment of vitamin B12 deficiency in patients on metformin are warranted.


2019 ◽  
Vol 42 ◽  
Author(s):  
John P. A. Ioannidis

AbstractNeurobiology-based interventions for mental diseases and searches for useful biomarkers of treatment response have largely failed. Clinical trials should assess interventions related to environmental and social stressors, with long-term follow-up; social rather than biological endpoints; personalized outcomes; and suitable cluster, adaptive, and n-of-1 designs. Labor, education, financial, and other social/political decisions should be evaluated for their impacts on mental disease.


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