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The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Onychomycoses represent the most frequently seen nail diseases and are the most difficult to treat of all skin mycoses. They are rare in children and increase in incidence with age. Most cases are caused by dermatophytes, in particular by Trichophyton rubrum, less frequently by T mentagrophytes and Epidermophyton floccosum. Molds may secondarily infect nails already diseased; however, some are probably capable of primary invasion of nail tissues. Yeasts, particularly Candida albicans, are mainly isolated from fingernails in chronic paronychia and onycholysis, and from nails in chronic mucocutaneous candidosis. Mixed infections by dermatophytes, molds, and/or yeasts are not uncommon. Probably, most fungi cannot infect a healthy nail organ, and only predisposing factors such as impaired blood circulation, peripheral neuropathy, diabetes mellitus, damage from repeated minor trauma, and limited immune defects as well as AIDS make the nail susceptible to fungal infection. Most onychomycoses are secondary to a mycosis of the adjacent skin. Distallateral subungual onychomycosis starts at the hyponychium spreading proximally to the nail bed and matrix. In proximal subungual onychomycosis, the fungus infects the cuticle and eponychium to reach the matrix where it becomes enclosed into the nail plate substance. Total dystrophic onychomycosis may result from either form or develop in chronic mucocutaneous candidosis. Superficial white onychomycosis is commonly a culture of T mentagrophytes on the surface of a toenail. Mycotic paronychia and onycholysis are usually due to C albicans. Clinically, onychomycoses have to be differentiated from noninfectious onychodystrophy, nail psoriasis, lichen planus unguium, and chronic nail eczema. Despite a considerable number of effective antifungal drugs, treatment has remained difficult because the predisposing factors are usually not amendable to therapy.
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PMID:Fungal infections of the nail. 201 19

An increase in the capillary permeability to albumin (CPA) has been reported in diabetic patients. We observed this frequently with a non-invasive isotopic test derived from the Landis method, using 99mTc-albumin and measuring residual radioactivity externally after removal of forearm venous compression. Evidence of the independent effects of hypertension and microangiopathy on CPA has already been found. The present work was designed to investigate CPA using the same test on diabetic patients without retinopathy and clinical proteinuria. Some of these patients had objective clinical distal and symmetrical polyneuropathy. Neuropathy was clearly present in 10 of the 11 patients with an abnormal test unexplained by causes other than diabetes and in only one of the 17 patients with a normal test. The most frequent abnormality affected the late radioactivity disappearance curve, which probably reflects an impaired lymphatic wash-out of interstitial albumin. These results strongly suggest a link between peripheral neuropathy and diabetic functional microangiopathy. An elevated blood flow secondary to sympathetic nerve failure may induce an increase in CPA and a saturation of lymphatic pumping which could also be deficient due to impaired lymphatic innervation.
Diabetes Res Clin Pract 1991 Jan
PMID:Increased capillary permeability to albumin and diabetic neuropathy. 201 34

Peripheral neuropathy remains a major complication of diabetes. Numerous etiological theories of metabolic and/or vascular disturbances have been suggested including decreased endoneurial oxygen tension with presumed tissue hypoxia. Increases in the affinity of hemoglobin for oxygen (Hb-O2 affinity) may also produce tissue hypoxia and such Hb-O2 affinity changes have been implicated in the pathogenesis of diabetic microangiopathy. In order to test whether affinity hypoxia might contribute to the development of diabetic peripheral neuropathy, we have utilized a rat model of high and normal Hb-O2 affinity produced by backcrossing animals with increased and decreased levels of 2,3-diphosphoglycerate (DPG). Diabetes was induced in ten high and ten low DPG animals with a tail vein injection of 55 mg/kg streptozotocin (STZ). Five animals in each group were treated with 2.4 U protamine zinc insulin (PZI)/day while the remaining animals were untreated. All rats were killed after 30 days, sections of tibial and sural nerve were rapidly removed and processed for teased fiber analysis. A minimum of 125 axons were assessed per nerve for E degeneration (myelin ovoids) using the classification developed by Dyck et al. Untreated animals, regardless of DPG levels, demonstrated 0% neuropathy. In contrast, all insulin-treated animals showed degeneration (0.4-17%) that inversely correlated with the DPG level (r = -0.59, P less than 0.04). The results of this study suggest that the level of RBC DPG (and presumably the Hb-O2 affinity) with its attendant effect on tissue oxygen release may play a role in the development of peripheral neuropathy in STZ-induced diabetic rats treated with insulin.
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PMID:Oxygen affinity of hemoglobin and peripheral nerve degeneration in experimental diabetes. 203 5

Peripheral neuropathy, infection, and peripheral vascular disease can produce serious problems in diabetic patients, particularly in the lower limbs. Ulceration of the foot may progress to gangrene and ultimately necessitate amputation. Distal symmetric polyneuropathy causes sensory loss. Such loss in patients with peripheral vascular disease creates a high risk for foot ulcers, which are vulnerable to infection. Treatment includes relief of neuropathic pain and antibiotic therapy for infection. Pentoxifylline (Trental) improves microvascular flow and appears to be effective against peripheral vascular disease. Aldose reductase inhibitors are being investigated as therapy for diabetic neuropathy. Prevention is the mainstay of management in these patients. Patient education is essential to help maintain health and prevent the potential adverse effects of diabetes.
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PMID:Lower limb problems in diabetic patients. What are the causes? What are the remedies? 203 95

In 48 patients suffering from diabetes I and diabetes II cardiovascular reflexes were tested in order to detect autonomic nervous system lesions of the heart. We measured the beat to beat variation in heart rate during deep breathing and the response of heart rate to change in posture (30:15 ratio). These tests were performed to prove the parasympathic function. To detect sympathic lesions the blood pressure changes were observed as response to change in posture (Schellong-Test). The patients under investigation showed a high prevalence of autonomic dysfunction depending on duration of diabetes and manifestations of other diabetic lesions. More often and earlier destructions of the parasympathic system were observed. Autonomic nervous lesions were correlated to the peripheral neuropathy. The diabetic polyneuropathy is a common complication of long term diabetes mellitus.
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PMID:[Diabetes mellitus in autonomic neuropathy of the heart]. 205 52

Clinical signs of spinal cord involvement in diabetes mellitus have gained very little attention in the past four decades. On the other hand many pathological studies have shown spinal cord lesions in diabetic patients. We report 12 diabetic patients with clinical signs of myelopathy which, per exclusion, could be explained only as related to diabetes mellitus. Posterior column lesions were more common than corticospinal tract involvement. All our patients had combined peripheral sensory polyneuropathy with myelopathic signs. The combination of peripheral neuropathy, disturbed sense of position and/or vibration with pyramidal signs is highly suggestive of diabetic myelopathy with polyneuropathy. Even though myelopathy is not common in diabetic patients, it is one of the most debilitating neurological complications of diabetes mellitus. We believe that there is enough pathological and clinical evidence to accept the concept of diabetic myelopathy, especially with its prognostic and rehabilitative implications.
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PMID:Myelopathy as a complication of diabetes mellitus. 206 Oct 17

Biotin in high doses was given for 1-2 years to three diabetic patients suffering from severe diabetic peripheral neuropathy. Within 4-8 weeks there was a marked improvement in clinical and laboratory findings. It is suggested that in diabetes may exist a deficiency, inactivity or unavailability of Biotin, resulting in disordered activity of biotin-dependent enzyme, pyruvate carboxylase, leading to accumulation of pyruvate and/or depletion of aspartate, both of which play a significant role in nervous system metabolism. Based on our good results, regular biotin administration could be suggested for every diabetic patient for the prevention and management of peripheral neuropathy although extensive randomised clinical trials are required.
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PMID:Biotin for diabetic peripheral neuropathy. 208 65

The role of microvascular disease in the aetiology of diabetic peripheral neuropathy remains controversial. Muscle capillary basement membrane thickening (MCBMT) and increased albumin excretion rates (AER) are features of generalized diabetic microangiopathy and may relate to the severity of neuropathy. We have studied 19 patients with neuropathy of greater than 12 months duration and assessed relationships between the severity of neuropathy and MCBMT, AER, presence of retinopathy, age and duration of diabetes. Nine patients had retinopathy and 10 did not. The two groups of patients were well matched for age, type of diabetes and HbA1% but diabetic patients with retinopathy had significantly longer duration of diabetes (median duration 22 yr, range 3-42 yr compared with patients without retinopathy (6 yr range 1-20 yr p less than 0.05). The group with retinopathy had significantly greater median MCBMT 3,077 A (range 741-10,732 A) than their age matched non-diabetic controls 2,256 A (1,290-4,406 A p less than 0.02) or the 10 diabetic patients without retinopathy 1,599 A (805-5,152 A). The patients with retinopathy also had greater median AER 88 micrograms/min (range 8-200 micrograms/min) compared with patients without retinopathy 8 micrograms/min (2-63 micrograms/min p less than 0.05), and had significantly more severe neuropathic features on a 12 point neurophysiological ranking scale (p less than 0.05). This study showed an association between retinopathy and severity of neuropathy but there were no associations between severity of neuropathy or AER with MCBMT. Severe chronic peripheral neuropathy is associated with microangiopathic complications.
Diabetes Res 1990 Feb
PMID:Impact of microangiopathy on chronic symptomatic peripheral neuropathy. 209 70

The present report concerns investigations of detrusor muscle adrenergic innervations in patients affected by bladder neuropathy secondary to diabetes without obstructive disturbances. Detrusor contractile activity evoked by NE is markedly reduced which can probably be attributed to receptor deficit. Urodynamic evaluation demonstrated a prevalence of sensory peripheral neuropathy than a motor conduction abnormality. In vitro study demonstrated that motor conduction abnormality of detrusor contractile activity is present early without bladder disturbances. Therefore early urodynamic measurements are necessary to evaluate bladder dysfunction and neuropathy in diabetic patients.
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PMID:[Evaluation of the activity of the bladder detrusor muscle and analysis of bladder function in subjects with diabetes mellitus under insulin treatment]. 209 34


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