Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Origin of epidermal urea and the therapeutical possibilities are shown: the waterbinding, keratolytic, epidermal thinning, antipruriginous, and the penetrating-supporting effects. Our clinical studies revealed mild to moderate eczemas and psoriasis capitis to be treated with a 10% urea-, 1% hydrocortisone cream. A 10% urea cream is well indicated for mild palmar and plantar hyperkeratotic dermatitis, the after treatment of contact dermatitis, and senile atrophic skin. Serious hyperkeratotic palmar dermatitis gives better results when handled alternately with triamcinolone-acetonid cream and a 10% urea cream.
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PMID:[Urea and its therapeutic possibilities]. 685 12

The development of topical corticosteroids has enabled many dermatoses to be more effectively treated than previously, but there is also no doubt that misuse of these preparations can lead to troublesome local effects and potentially serious systemic problems. The most effective assay for comparing different compounds has been their vasoconstrictive activity, and this on the whole correlates well with clinical effect. To be effective, corticosteroid must be absorbed and the importance of concentration, occlusion, the type of vehicle, added penetrants such as urea and the anatomical site, on the amount of absorption and therefore on clinical activity has been demonstrated. Ointments have been shown to be more effective than creams but because of the considerable choice of potencies now available most dermatologists tend to prescribe the different formulations according to the wishes of the patient. For the same reason, dilution of the commercially marketed preparations is now not generally recommended. The main therapeutic activity of topical corticosteroids is their nonspecific anti-inflammatory effect, thought to be primarily a result of their action on the chemical mediators of inflammation. They have also been shown to be antimitotic which may well be relevant not only to the treatment of scaling dermatoses but also to their dermal thinning effect resulting from inhibition of fibroblasts. Combinations of corticosteroids with antibacterial and antifungal agents have been shown to be very effective in flexural eruptions and secondarily infected dermatoses. As a general rule, the use of topical corticosteroids in outpatients, unless badly misused, is not associated with any significant risk of adrenal axis suppression, but care must be exercised as to the amount prescribed, especially if large areas of the body are to be treated with highly potent preparations. Certain groups such as young children and patients with liver failure, and certain anatomical sites such as the flexures and face appear much more prone to side effects, and in these cases mild or moderate compounds should be used in preference to the stronger preparations.
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PMID:Topical corticosteroids: clinical pharmacology and therapeutic use. 736 38

Hyperlipidemic rats, which have been described as a useful animal model for focal glomerulosclerosis in humans, were examined at the ages of 17, 20, 24, and 27 weeks for evaluation of spontaneously developed coronary arterial lesions. The mean concentrations of cholesterol, triglyceride, phospholipid, and urea nitrogen were greater than the respective control concentrations at and after the age of 17 weeks. No abnormalities were detected in the blood pressure values. Starting from the age of 24 weeks, the rats had disseminated white spots in the ventricles and septum of the heart. Mean renal weights of hyperlipidemic rats were higher than those of control rats at the ages of 17 and 20 weeks, and the surface of the kidney appeared irregular when rats were 27 weeks old. Histologic examination revealed atrophy of the coronary artery, a decrease in the number of smooth muscle cells, and thinning of the wall, resulting in loss of the normal wall structure. A homogenous eosinophilic substance, the nature and cause of which were unknown, was also seen in the affected arterial walls. Furthermore, white spots observed macroscopically were found to represent myocardial degeneration and necrosis with reactive histiocytic cells and lymphocytes, adventitial fibrosis, and edema associated with the affected arteries. These arterial lesions became evident in rats at and after the age of 24 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary arterial abnormalities in hyperlipidemic rats with renal failure. 802 73

32 patients with chronic lymphoid leukemia (CLL) were examined to specify reasons of renal damage. Measurements were made of blood urea, creatinine, total protein, electrolytes, uric acid. Also, urinary sediment, diurnal loss of protein and creatinine with urine, glomerular filtration rate, concentration ability of the kidneys were studied. Urinary system was assessed by ultrasound. Most CLL patients studied had renal affection characteristic for chronic pyelonephritis with chronic renal insufficiency. The ultrasonic investigation stated reduced size of the kidneys, thinning of the cortex, extension of the renal pelvis and calyces, concrements. The kidneys and ureters were pressed and displaced by enlarged spleen, liver, lymph nodes. The plan of CLL patients' examination must include ultrasonic investigation of the abdominal organs for early detection of renal lesions.
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PMID:[Renal lesions in patients with chronic lymphocytic leukemia]. 1243 39

The effect of external gamma irradiation on the kidneys is well described. However, the mechanisms of radiation nephropathy as a consequence of targeted radionuclide therapies are poorly understood. The functional and morphologic changes were studied chronologically (from 10 to 40 wk) in mouse kidneys after injection with an actinium-225 (225Ac) nanogenerator, a molecular-sized, antibody-targeted, in vivo generator of alpha-particle-emitting elements. Renal irradiation from free, radioactive daughters of 225Ac led to time-dependent reduction in renal function manifesting as increase in blood urea nitrogen. The histopathologic changes corresponded with the decline in renal function. Glomerular, tubular, and endothelial cell nuclear pleomorphism and focal tubular cell injury, lysis, and karyorrhexis were observed as early as 10 wk. Progressive thinning of the cortex as a result of widespread tubulolysis, collapsed tubules, glomerular crowding, decrease in glomerular cellularity, interstitial inflammation, and an elevated juxtaglomerular cell count were noted at 20 to 30 wk after treatment. By 35 to 40 wk, regeneration of simplified tubules with tubular atrophy and loss with focal, mild interstitial fibrosis had occurred. A lower juxtaglomerular cell count with focal cytoplasmic vacuolization, suggesting increased degranulation, was also observed in this period. A focal increase in tubular and interstitial cell TGF-beta1 expression starting at 20 wk, peaking at 25 wk, and later declining in intensity with mild increase in the extracellular matrix deposition was noticed. These findings suggest that internally delivered alpha-particle irradiation-induced loss of tubular epithelial cells triggers a chain of adaptive changes that result in progressive renal parenchymal damage accompanied by a loss of renal function. These findings are dissimilar to those seen after gamma or beta irradiation of kidneys.
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PMID:Renal tubulointerstitial changes after internal irradiation with alpha-particle-emitting actinium daughters. 1598 54

A heterozygous mutation in autosomal Alport genes COL4A3 and COL4A4 can be found in 20 to 50% of individuals with familial benign hematuria and diffuse glomerular basement membrane thinning (thin basement membrane nephropathy [TBMN]). Approximately 1% of humans are heterozygous carriers of mutations in the autosomal Alport genes and at risk for developing renal failure as a result of TBMN. The incidence and pathogenesis of renal failure in heterozygous COL4A3/4 mutation carriers is still unclear and was examined further in this study using COL4A3 knockout mice. In heterozygous COL4A3(+/-) mice lifespan, hematuria and renal function (serum urea and proteinuria) were monitored during a period of 3 yr, and renal tissue was examined by light and electron microscopy, immunohistochemistry, and Western blot. Lifespan of COL4A3(+/-) mice was found to be significantly shorter than in healthy controls (21.7 versus 30.3 mo). Persistent glomerular hematuria was detected starting in week 9; proteinuria of > 0.1 g/L started after 3 mo of life and increased to > 3 g/L after 24 mo. The glomerular basement membrane was significantly thinned (167 versus 200 nm in wild type) in 30-wk-old mice, coinciding with focal glomerulosclerosis, tubulointerstitial fibrosis, and increased levels of TGF-beta and connective tissue growth factor. The renal phenotype in COL4A3(+/-) mice resembled the clinical and histopathologic phenotype of human cases of TBMN with concomitant progression to chronic renal failure. Therefore, the COL4A3(+/-) mouse model will help in the understanding of the pathogenesis of TBMN in humans and in the evaluation of potential therapies.
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PMID:Chronic renal failure and shortened lifespan in COL4A3+/- mice: an animal model for thin basement membrane nephropathy. 1677 36

Argininosuccinicaciduria is a rare metabolic disorder of the urea cycle associated with the inability to excrete nitrogenous waste in the form of urea. Along with low serum arginine, hepatomegaly, and mental retardation, congenital trichorrhexis nodosa is a distinguishing feature of the disorder. We present a 3.5-year-old girl diagnosed with argininosuccinicaciduria who presented to the dermatology clinic with hair thinning and loss since birth. Microscopic evaluation revealed nodular swellings on the hair shafts and frayed cortical fibers consistent with the diagnosis of trichorrhexis nodosa occurring in the setting of argininosuccinicaciduria.
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PMID:Trichorrhexis nodosa secondary to argininosuccinicaciduria. 1730 Jun 44

A 43-year-old woman presented with complaints of exfoliation of the skin and mottled pigmentation all over the body, intolerance to sunlight for the last 14 years, and swelling on the lower one-third of the neck for 15 years. She was apparently well until the age of 29 years when she noticed redness on her shins which later progressed to involve the upper limbs, chest, and face. Three months later, she observed multiple, small, brownish plaques over the erythematous areas, which gradually spread to the sun-exposed areas, namely the face, forearms, hands, and nape of the neck. The erythema disappeared within 5 months of onset. The patient experienced redness of the face, intolerance to the sun, and reduced sweating, particularly during the summer. There was no history of bullous eruption, difficulty during deglutition, tremors, or pedal edema. She suffered five miscarriages and, ultimately, was successful in delivering a normal boy who is now 16 years of age. She had menarche at the age of 14 years and her menstrual cycle was regular. There was no history of similar illness in the family. On cutaneous examination, the skin on the face, neck, trunk, buttocks, and limbs was found to be dry, lusterless, thin, and covered with fine scales. Mottled hyperpigmentation was observed all over the body. Atrophy and telangiectasia were seen over the neck (Fig. 1), face (Fig. 2), nape of the neck, upper and lower limbs, back, and chest. Mild erythema was observed over the face, nose, ears, and forearms. The hair on the scalp, eyebrows, axillae, and pubic area was sparse and thin. The teeth were loose and discolored due to caries, and a foul odor emanated from the mouth. The nails were lusterless and centrally depressed. The thyroid gland was enlarged, smooth, nontender, and moved with deglutition. No bruit was heard over it. No ocular abnormality was detected. The patient had a haemoglobin level of 7.6 g%, total serum iron binding capacity of 70 micromol/L (normal, 45-66 micromol/L), and serum ferritin level of 10 microg/L (normal, 15-200 microg/L). Peripheral blood smear showed hypochromic microcytic red blood cells. Total and differential leukocyte counts, erythrocyte sedimentation rate (ESR), blood glucose, serum electrolytes, total and differential serum proteins, liver function tests, blood urea, and microscopic examination of urine and stools were within normal limits. The thyroid profile and complement C3 and C4 levels were within normal limits. Rheumatoid factor, antinuclear factor and LE cells were absent. Abdominal ultrasonogram was normal. Fine needle aspiration cytology from the thyroid gland showed features suggestive of colloid goiter. Skin biopsy revealed thinning of the epidermis, flattening of the rete ridges, and hydropic degeneration of the basal cell layer. The dermis was edematous with dilated capillaries, melanophages, and a band-like mononuclear infiltrate. The sweat glands were reduced in number.
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PMID:Late-onset Rothmund-Thomson syndrome. 1747 79

Renal TB is difficult to diagnose, because many patients present themselves with lower urinary symptoms which are typical of bacterial cystitis. We report a case of a young woman with renal TB and ESRD. She was admitted with complaints of adynamia, anorexia, fever, weight loss, dysuria and generalized edema for 10 months. At physical examination she was febrile (39 degrees C), and her abdomen had increased volume and was painful at palpation. Laboratorial tests showed serum urea = 220 mg/dL, creatinine = 6.6 mg/dL, hemoglobin = 7.9 g/dL, hematocrit = 24.3%, leukocytes = 33,600/mm(3) and platelets = 664,000/mm(3). Urinalysis showed an acid urine (pH = 5.0), leukocyturia (2+/4+) and mild proteinuria (1+/4+). She was also oliguric (urinary volume < 400 mL/day). Abdominal echography showed thick and contracted bladder walls and heterogeneous liquid collection in the left pelvic region. Two laparotomies were performed, in which abscess in pelvic region was found. Anti-peritoneal tuberculosis treatment with rifampin, isoniazid and pyrazinamide was started. During the follow-up, the urine culture was found to be positive for M. tuberculosis. Six months later the patient had complaints of abdominal pain and dysuria. New laboratorial tests showed serum urea = 187 mg/dL, creatinine = 8.0 mg/dL, potassium = 6.5 mEq/L. Hemodialysis was then started. The CT scan showed signs of chronic nephropathy, dilated calyces and thinning of renal cortex in both kidneys and severe dilation of ureter. The patient developed neurologic symptoms, suggesting tuberculous meningoencephalitis, and died despite of support measures adopted. The patient had ESRD due to secondary uropathy to prolonged tuberculosis of urinary tract that was caused by delayed clinical and laboratorial diagnosis, and probably also due to inadequate antituberculous drugs administration.
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PMID:End-stage renal disease due to delayed diagnosis of renal tuberculosis: a fatal case report. 1762 50

Alpha-synuclein (alpha-Syn) fibrils are the major component of Lewy bodies that are closely associated with the pathogenesis of Parkinson's disease, but the mechanism for the fibril assembly remains poorly understood. Here we report using a combination of peptide truncation and atomic force microscopy (AFM) to elucidate the self-assembly and morphology of the alpha-Syn fibrils. The results show that protease K significantly slims the fibrils from the mean height of approximately 6.6 to approximately 4.7 nm, whereas chaotropic denaturant urea completely breaks down the fibrils into small particles. The in situ enzymatic digestion also results in thinning of the fibrils, giving rise to some nicks on the fibrils. Moreover, N- or C-terminally truncated alpha-Syn fragments assemble into thinner filaments with the heights depending on the peptide lengths. A nine-residue peptide corresponding to the homologous GAV-motif sequence can form very thin (approximately 2.2 nm) but long (>1 microm) filaments. Thus, the central sequence of alpha-Syn forms a fibrillar core by cross-beta-structure that is flanked by two flexible termini, and the orientation of the fibril growth is perpendicular to the beta-sheet structures.
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PMID:Assembly of alpha-synuclein fibrils in nanoscale studied by peptide truncation and AFM. 1823 Mar 46


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