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Biomedical subjects

J Claus-Walker

Publications and source records attributed to J Claus-Walker.

36 records · Page 2Linked to original sources
PubMed1977

Metabolic effects of sodium restriction and thiazides in tetraplegic patients.

The metabolic effects of sodium restriction, alone or with thiazide, were studied in 12 healthy subjects, in 24 tetraplegics during the intial 8 months of paralysis (early) and in 16 others during the subsequent period (late). The diuresis caused by both treatments led to more haemoconcentration in early than in late patients. In contrast with the healthy subjects on low sodium, the tetraplegics had a delayed urinary sodium retention and no fall in calciuria. During thiazide, urinary sodium depletion occurred early and the urine calcium fell after 3 days in all tetraplegics. During both treatments, aldosterone and renin increased more in early patients than in the other groups. The clinical implications of inducing dehydration and a sustained stimulation of the renin-angiotensin-aldosterone axis in recently injured tetraplegics with severe orthostatic hypotension are discussed.

Adolescent↗
PubMed1977

Immediate endocrine and metabolic consequences of traumatic quadriplegia in a young woman.

Onset of paralysis by cervical spinal cord injury led immediately to temporary adrenocortical activation and, within 2 days, to sustained skin and bone breakdown. Urine cAMP was increased, blood parathyroid hormone, renin activity, and electrolytes were normal, and fluid and electrolytes balance became negative during the initial 6 days of paralysis.

17-Hydroxycorticosteroids↗
PubMed1977

Steady state hormonal secretion in traumatic quadriplegia.

Physiologically complete cervical spinal cord transection results in motor and sensory quadriplegia and interruption of the sympathetic neural pathways; this condition leads to metabolic deficiencies suggestive of abnormal endocrine function. An investigation of the non-stimulated secretion of some of the hormones influencing metabolism was undertaken by evaluating thyroxine, iodothyronine binding index, testosterone, growth hormone, calcitonin, and parathyroid hormone in venous blood of fasting healthy subjects and quadriplegic patients. The effect of the duration of the paralysis was examined by repeating the evaluations at different periods after onset. The results show that 1) thyroxine was low for 2 months after onset in 21 patients and normal thereafter in 53 patients, 2) testosterone was low throughout the study in 62 patients; the decrease is greatest during the first 2 months, 3) growth hormone was often increased in 46 patients for 8 months after onset, and nearly normal afterward in 25 patients, 4) calcitonin was normal in 22 patients throughout the study, and 5) parathyroid hormone was normal in relation to normal serum calcium as early as 6 days after onset in 79 out of 83 patients. These data do not preclude a parathyroid hormone increase at onset or alterations in the patterns of circadian secretion and in the responses to specific stimulation for the hormones evaluated. Therefore, it may be concluded only that the steady state secretion of these hormones is not altered by traumatic quadriplegia per se, but is temporarily modified by the original insult to the nervous system, and by changes in life pattern and the heavy sedation that follows. The results suggest that the minor endocrin changes occurring in quadriplegic patients during the early period of paralysis will be rapidly overcome by rehabilitation to an active life pattern.

Calcitonin↗
PubMed1977

The urinary excretion of collagen degradation products by quadriplegic patients and during weightlessness.

Urinary total hydroxyproline, peptide-bound hydroxyproline, hydroxylysine glycosides, and calcium were measured in three healthy individuals subjected to weightlessness for eighty-four days and in three young quadriplegic patients. The former group had significant calciuria but no evidence of collagen degradation. The latter group, however, had conspicuous calciuria and also excreted large amounts of collagen breakdown products. This documented degradation of matrix may be related to the continuous calciuria, osteoporosis, and cutaneous dystrophic changes occurring in quadriplegics.

Calcium↗
PubMed1975

Bone metabolism in quadriplegia: dissociation between calciuria and hydroxyprolinuria.

Relationships between duration of paralysis, recumbency, muscular activity, and urinary loss of calcium (Cau), phosphorus (Pu), and hydroxyproline (OHPu) were studied daily in 32 traumatic quadriplegic patients during comprehensive rehabilitation and randomly in those readmitted for treatment. Within days after onset, quadriplegic patients had increases in Pu, then OHPu, and finally, Cau. Patients actively engaged in rehabilitation exercises showed a steady fall in OHPu, whereas CAU remained high for up to 18 months. Patients paralyzed for over 18 months (late) had low Cau, Pu and OHPu; but if the patients were kept in bed, OHPu increased rapidly. Patients with early quadriplegia have an increased bone remodeling, suggesting that the excess OHPu and Cau are derived from resorbed bone. Patients with late quadriplegia have little bone remodeling, therefore the excess OHPu occurring during recumbency may be derived from the resorption of new collagen produced during the removal of weight bearing without further change in muscular activity. Resorbed new collagen is excreted in part as large, OHP-containing polypeptides; these were found in the urine of quadriplegic patients, and therefore were present in blood and may play a role in initiating ectopic bone and renal calculi. The presence of OHP in 11 bladder calculi from quadriplegic patients tends to support this hypothesis. These studies indicate that muscular activity and weight bearing influence the bone metabolism of quadriplegic patients and suggest that the presence in body fluids of increased catabolic products from bone may have a role in bone-related complications.

Adolescent↗