Effect of multi-nutrient insufficiency on markers of one carbon metabolism in young women: response to a methionine load.

BACKGROUND/OBJECTIVES: Multi-nutrient insufficiencies as a consequence of nutritional and economic factors are common in India and other developing countries. We have examined the impact of multi-nutrient insufficiency on markers of one carbon (1C) metabolism in the blood, and response to a methionine load in clinically healthy young women. SUBJECTS/METHODS: Young women from Pune, India (n=10) and Cleveland, USA (n=13) were studied. Blood samples were obtained in the basal state and following an oral methionine load (50 mg/kg of body weight in orange juice). Plasma concentrations of vitamin B12, folate and B6 were measured in the basal state. The effect of methionine load on the levels of methionine, total homocysteine, cysteine, glutathione and amino acids was examined. RESULTS: Indian women were significantly shorter and lighter compared with the American women and had lower plasma concentration of vitamins B12, folate and B6, essential amino acids and glutathione, but higher concentration of total homocysteine. The homocysteine response to methionine load was higher in Indian women. The plasma concentrations of glycine and serine increased in the Indian women after methionine (in juice) load. A significant negative correlation between plasma B6 and homocysteine (r= -0.70), and plasma folate and glycine and serine levels were observed in the Indian group (P<0.05) but not in the American group. CONCLUSIONS: Multi-nutrient insufficiency in the Indian women caused unique changes in markers of whole body protein and 1C metabolism. These data would be useful in developing nutrient intervention strategies.

Neuromyopathy of cyanide intoxication due to "laetrile" (amygdalin). A clinicopathologic study.

A 67-year-old woman with lymphoma presented with a neuromyopathy following "laetrile" (amygdalin) treatment. She had significant elevation of blood and urinary thiocyanate and cyanide levels. Sural nerve biopsy specimen revealed a mixed pattern of demyelination and axonal degeneration, the latter being prominent. Gastrocnemius muscle biopsy specimen showed histochemically a mixed pattern of denervation and myopathy with Type II atrophy. It is concluded that cyanide toxicity secondary to laetrile therapy and nutritional deficiency caused the neuromyopathy, as the changes in peripheral nerve are similar to changes described in ataxic polyneuropathy occurring in Nigeria attributed to high cyanide content in the diet and nutritional deficiency. Although this patient received vincristine initially, the development of the neuromyopathy had no temporal relationship to its administration. The clinical profile, as well as peripheral nerve and muscle changes were not similar to either vincristine neuromyopathy or neuromyopathy due to paraneoplastic manifestation of lymphoma. Clinical improvement following discontinuation of "laetrile" by the patient further supports the toxic etiologic results for the neuromyopathy in this patient.

Syndrome of inappropriate secretion of antidiuretic hormone in patients treated with psychotherapeutic drugs.

We report two patients in whom the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) developed during the administration of psychotherapeutic drugs. In one, the syndrome occurred after administration of a phenothiazine drug and in the other, a butyrophenone. Both the patients were diagnostically studied for evidence of other disorders, either neurologic or systemic, which could cause this syndrome with negative results. They responded to fluid and free water restriction with remarkable recovery and no sequelae. It is stressed that psychotherapeutic drug administration must be considered as one of the iatrogenic causes of SIADH.

Hypokalemic vacuolar myopathy of chronic alcoholism. A histological and histochemical study.

Recent reports have emphasized the occurrence of a myopathy in chronic alcoholism associated with hypokalemia. This report of hypokalemic myopathy in a chronic alcoholic, emphasizes the primary myopathic nature of the condition and attributes it to a possible non-specific effect of the hypokalemia on skeletal muscle. It is pointed out, that histological and histochemical changes of muscle in this type of myopathy are indistinguishable from other types of hypokalemic myopathies like periodic paralysis. It is conjectured that in alcoholic myopathy, the underlying disorder might be related to a primary disturbance of potassium metabolism, though in most cases, serum potassium is normal. It is likely that studies aimed at studying total body potassium content and turnover in alcoholic myopathy would help in understanding its pathogenesis and possible relationship to disturbed potassium metabolism.

Early onset myotonic dystrophy in association with polyneuropathy.

A patient with early onset of myotonic dystrophy, with associated neuropathy and epilepsy, is presented. It is postulated that his disorder was inherited through a recessive, pleomorphic gene. His differential diagnosis is discussed and the literature reviewed. The clinical variability of myotonic dystrophy is stressed and the diagnostic difficulties encountered in the younger age group.

Bulbar paralysis in chronic alcoholism with recovery. A case report with discussion of possible etiologic factors.

A 47-year-old chronic alcoholic with acute onset of spastic bulbar paralysis and quadriparesis with recovery has been reported. The differential diagnosis of occurrence of bulbar symptoms in an alcoholic has been discussed. It is postulated that on anatomical and clinical grounds this case probably represents the occurrence of central pontine myelinolysis with recovery. Attention has been drawn to recent literature in which the importance of vascular insufficiency, hypotension and disturbance of fluid and electrolyte balance in the occurrence of irreversible myelinolytic lesions has been stressed. It is postulated that the recovery of this patient from a seemingly inexorably progressive lesion was the result of prompt reversal of etiologic factors which result in central pontine myelinolysis-like, fluid and electrolyte imbalance, hypotension and vascular insufficiency.