Clinical signs and diagnosis of thiamine deficiency in juvenile goshawks (Accipiter gentilis)

2008 ◽  
Vol 163 (7) ◽  
pp. 215-217 ◽  
Author(s):  
M. Carnarius ◽  
H. M. Hafez ◽  
A. Henning ◽  
H. J. Henning ◽  
M. Lierz
Keyword(s):  
Thiamine Deficiency ◽  
Clinical Signs ◽  
Accipiter Gentilis

Subclinical thiamine deficiency in patients with abdominal cancer

2017 ◽  
Vol 16 (4) ◽  
pp. 497-499 ◽  
Author(s):  
Hideki Onishi ◽  
Mayumi Ishida ◽  
Iori Tanahashi ◽  
Takao Takahashi ◽  
Yoshitada Taji ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Thiamine Deficiency ◽  
Storage Capacity ◽  
Clinical Symptoms ◽  
Performance Status ◽  
Clinical Signs ◽  
Medical Emergency ◽  
Wernicke Encephalopathy ◽  
Appetite Loss ◽  
Pancreatic Body Cancer

AbstractObjectiveThiamine is an essential coenzyme for oxidative metabolisms; however, it is not synthesized in the human body, and the average thiamine storage capacity is approximately 18 days. Therefore, thiamine deficiency (TD) can occur in any condition of unbalanced nutrition. If TD is left untreated, it causes the neuropsychiatric disorder Wernicke encephalopathy (WE). Although WE is a medical emergency, it is sometimes overlooked because most patients with WE do not exhibit all of the typical symptoms, including delirium, ataxia, and ophthalmoplegia. If all of the typical clinical symptoms of WE are absent, diagnosis of TD or WE becomes more difficult.MethodFrom a series of cancer patients, we reported three patients who developed TD without the typical clinical symptoms of WE.ResultA 69-year-old woman with pancreatic body cancer receiving chemotherapy with paclitaxel and gemcitabine for six months. Her performance status (PS) was 1. A detailed interview revealed that she had appetite loss for six months. Another 69-year-old woman with ovarian cancer received nedaplatin; her PS was 0. A detailed interview revealed that she had appetite loss for three months. A 67-year-old woman with colon cancer receiving ramucirumab in combination with second-line fluorouracil with folinic acid and irinotecan. Her PS was 1. A detailed interview revealed that she had appetite loss for three weeks. None exhibited typical clinical signs of WE, but they developed appetite loss for six months, three months, and three weeks, respectively. The diagnosis of TD was supported by abnormally low serum thiamine levels.Significance of the resultsThis report emphasizes the possibility of TD in cancer patients even when patients do not develop typical clinical signs of WE. The presence of appetite loss for more than two weeks may aid in diagnosing TD. Patients receiving chemotherapy may be at greater risk for developing TD.

Polioencephalomalacia of Dogs with Thiamine Deficiency

1977 ◽  
Vol 14 (2) ◽  
pp. 103-112 ◽  
Author(s):  
D. H. Read ◽  
R. D. Jolly ◽  
M. R. Alley
Keyword(s):  
Thiamine Deficiency ◽  
Neurological Disease ◽  
Thermal Destruction ◽  
Spastic Paraparesis ◽  
Clinical Signs ◽  
Thiamine Hydrochloride ◽  
Naturally Occurring ◽  
Brainstem Nuclei ◽  
Cooked Meat ◽  
Dietary Deficiency

A naturally occurring neurological disease occurred in six dogs fed cooked meat. Clinical signs were anorexia, progressive spastic paraparesis, recumbency, convulsions and death. The disease was characterized by bilaterally symmetrical spongy change and necrosis of brainstem nuclei with a lesion distribution pattern similar to that in thiamine deficient foxes and cats. An associated thiamine deficiency was evidenced by decreased thiamine levels in the blood of one dog and in the food of another, and rapid remission of clinical signs in a dog given thiamine hydrochloride. Thermal destruction of thiamine through cooking of the foods probably caused the dietary deficiency.

Clinical reasoning in feline vestibular syndrome: which presenting features are the most important?

2020 ◽  
pp. 1098612X2097086
Author(s):  
Nicholas J Grapes ◽  
Frances E Taylor-Brown ◽  
Holger A Volk ◽  
Steven De Decker
Keyword(s):  
Middle Ear ◽  
Clinical Reasoning ◽  
Thiamine Deficiency ◽  
Clinical Presentation ◽  
Clinical Signs ◽  
Binary Logistic Regression ◽  
Clinical Progression ◽  
Feline Infectious Peritonitis ◽  
Clinical Variables ◽  
Regression Modelling

Objectives The aim of this study was to evaluate whether clinical variables from the history, clinical presentation, and physical and neurological examinations of cats with vestibular syndrome were statistically predictive of the underlying diagnosis. Methods In total, 174 cats presenting with vestibular syndrome between January 2010 and May 2019 were investigated. Univariate statistical analysis of clinical variables was performed and those statistically associated with a diagnosis were retained for multivariable binary logistic regression modelling. Results The seven most prevalent diagnoses represented 95% of vestibular presentations, which included: otitis media/interna (n = 48), idiopathic vestibular syndrome (n = 39), intracranial neoplasia (n = 24), middle ear polyp (n = 17), feline infectious peritonitis (n = 13), thiamine deficiency (n = 13) and intracranial empyema (n = 11). Idiopathic vestibular syndrome was commonly associated with non-purebred cats and had 17.8 times the odds of an improving clinical progression (95% confidence interval [CI] 1.3–250.0; P = 0.03). Intracranial neoplasia was associated with older age and chronic onset of clinical signs, and was significantly more likely to have a central vestibular neuroanatomical localisation (95% CI 8.5–344349142.0; P = 0.015) with postural deficits on neurological examination. Thiamine deficiency was more common in female cats, with 52.6 times the odds of a waxing and waning clinical progression (95% CI 1.2–1000; P = 0.038) and 6.8 times the odds of presenting with bilateral vestibular signs (95% CI 1.0–45.7; P = 0.047) and wide excursions of the head (95% CI 1.0–45.7; P = 0.047). Middle ear polyps were associated with 8.8 times the odds of presenting with Horner syndrome (95% CI 1.5–50.0; P = 0.015). Conclusions and relevance Although it may be difficult to identify the underlying diagnosis in cats with vestibular syndrome from the presenting features alone, there are instances in which discrete clinical features may help to guide clinical reasoning when evaluating cats with vestibular presentations.

Alteration of Mitochondria in Oxythiamine-Induced, Acute Thiamine Deficiency in the Mouse

1976 ◽  
Vol 34 ◽  
pp. 284-285
Author(s):  
Itaru Watanabe ◽  
Dante G. Scarpelli
Keyword(s):  
Electron Microscopy ◽  
Adult Male ◽  
Thiamine Deficiency ◽  
Light And Electron Microscopy ◽  
Fatty Change ◽  
Deficient Diet ◽  
Subcutaneous Injections ◽  
Swiss Mice ◽  
Time Period ◽  
Ad Libitum

Acute thiamine deficiency was produced in mice by the administration of oxythiamine, a thiamine analogue, superimposed upon a thiamine deficient diet. Adult male Swiss mice (30 gm. B.W.) were fed with a thiamine deficient diet ad libitumand were injected with oxythiamine (170 mg/Kg B.W.) subcutaneously on days 4 and 10. On day 11, severe lassitude and anorexia developed, followed by death within 48 hours. The animals treated daily with subcutaneous injections of thiamine (300 μg/Kg B.W.) from day 11 through 15 were kept alive. Similarly, feeding with a diet containing thiamine (600 μg/Kg B.W./day) from day 9 through 17 reversed the condition. During this time period, no fatal illness occurred in the controls which were pair-fed with a thiamine deficient diet.The oxythiamine-treated mice showed a significant enlargement of the liver, which weighed approximately 1.5 times as much as that of the pair-fed controls. By light and electron microscopy, the hepatocytes were markedly swollen due to severe fatty change and swelling of the mitochondria.

A rapid method for the direct identification of paramyxovirus in canine CSF by ultracentrifugation and negative staining as a rule out for distemper

1990 ◽  
Vol 48 (3) ◽  
pp. 594-595
Author(s):  
W.L. Steffens ◽  
M.B. Ard ◽  
C.E. Greene ◽  
A. Jaggy
Keyword(s):  
Subacute Sclerosing Panencephalitis ◽  
Clinical Signs ◽  
Viral Disease ◽  
Etiologic Agent ◽  
Mucosal Inflammation ◽  
Worldwide Distribution ◽  
Negative Stain ◽  
Viral Particles ◽  
Systemic Manifestations ◽  
Rule Out

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.

Hormone Replacement Therapy and Voice

2019 ◽  
Vol 4 (4) ◽  
pp. 607-614
Author(s):  
Jean Abitbol
Keyword(s):  
Replacement Therapy ◽  
Symptom Severity ◽  
Low Dose ◽  
Hormone Replacement ◽  
Clinical Signs ◽  
Female Voice ◽  
Fat Cells ◽  
High Pitch ◽  
Endocrine Effects ◽  
The Voice

The purpose of this article is to update the management of the treatment of the female voice at perimenopause and menopause. Voice and hormones—these are 2 words that clash, meet, and harmonize. If we are to solve this inquiry, we shall inevitably have to understand the hormones, their impact, and the scars of time. The endocrine effects on laryngeal structures are numerous: The actions of estrogens and progesterone produce modification of glandular secretions. Low dose of androgens are secreted principally by the adrenal cortex, but they are also secreted by the ovaries. Their effect may increase the low pitch and decease the high pitch of the voice at menopause due to important diminution of estrogens and the privation of progesterone. The menopausal voice syndrome presents clinical signs, which we will describe. I consider menopausal patients to fit into 2 broad types: the “Modigliani” types, rather thin and slender with little adipose tissue, and the “Rubens” types, with a rounded figure with more fat cells. Androgen derivatives are transformed to estrogens in fat cells. Hormonal replacement therapy should be carefully considered in the context of premenopausal symptom severity as alternative medicine. Hippocrates: “Your diet is your first medicine.”

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