Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old woman with hepatitis-B-surface-antigen-positive hepatic cirrhosis presented with weakness and paresthesias over the distal part of the limbs in the course of adenine arabinoside 5'-monophosphate (ARA-AMP) treatment, and recovered spontaneously after several weeks of drug withdrawal. Electrophysiological and histological studies demonstrated axonal neuropathy. Although the patient received a relatively low total dose (120 mg/kg), her age and advanced liver disease may have played a role in the ARA-AMP neurotoxicity.
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PMID:Toxic neuropathy after adenine arabinoside treatment in chronic HBsAg-positive liver disease. 168 32

A 41-year-old man with PPP since in 1982 was admitted in May, 1987, because of the progressive asymmetric sensory disturbance in the hands and feet over 4 months, accompanied by an exacerbation of PPP. On admission, eruptions of PPP were observed in the palms and soles. Asymmetric and mildly decreased sensations of touch and pain were present in the distal part of the four extremities as well as in his trunk, accompanied by paresthesia and dysesthesia. Mild to moderate weakness was noted in the hand muscles, and slight muscular atrophy was present in the right lower leg. A work-up for collagen vascular disease was within normal limits. T lymphocyte subset showed a decreased ratio of OKT 4/OKT 8. Left sural nerve biopsy showed axonal degeneration and moderate decrease of myelinated fibers, and the vasculitis was not found. The neurological signs and symptoms as well as the skin eruptions improved with methylprednisolone 40 mg/day. A causal relationship between the multiple mononeuropathy and PPP of our patient was indicated by the almost simultaneous onset of the neuropathy and the exacerbation of PPP as well as the improvement of these two conditions with corticosteroid therapy. Such combination of multiple mononeuropathy and PPP has not so far been reported.
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PMID:[A case of multiple mononeuropathy associated with pustulosis palmaris et plantaris (PPP)]. 176 52

We reported a case with the superior vena cava syndrome and compression neuropathy of the right brachial plexus after pacemaker implantation. A 27-year-old man with the second degree atrio-ventricular block had underwent pacemaker implantation via the right subclavian vein at the age of 19. Since the age of 25, he occasionally experienced paresthesia and swelling in his right arm after excessive work. These symptoms gradually resolved within a few days by rest. On June 2, 1990, he noticed swelling and paresthesia of his right face, arm and upper trunk after excessive labor. A few days later, weakness of right hand developed. On examination on June 8, the right arm was edematous, but not cyanotic. There were weakness and hypoactive muscle stretch responses in the right upper extremity with hypesthesia of all modalities in the neck, arm and upper trunk of the right side. Venous angiography showed total occlusion of the right brachiocephalic vein and superior vena cava and well-developed collateral channels. We speculate that swelling of the right upper extremity, which became overt when arterial blood supply to that limb outbalanced impaired venous drainage, finally compressed the right brachial plexus.
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PMID:[Superior vena cava syndrome and compression neuropathy of the right brachial plexus following cardiac pacemaker implantation]. 178 66

A 42 year old woman with foot process disease, was treated with corticosteroids for 6 years. She had been suffering, for about 3 years from progressive muscle weakness of the limbs, accompanied by general paresthesia, cramps of the calves and burning muscle pain both at rest and an effort. The clinical, neurophysiological and histochemical examination indicated noninflammatory myopathic damage. The progressive reduction of corticosteroid dosage led rapidly to a distinct improvement, but not to a remission, of symptoms. Clinical and laboratory findings were consistent with those observed in most cases of steroid myopathy described in literature. We discuss the possible pathogenetic role of corticosteroids in this affection.
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PMID:Steroid myopathy: clinical and immunohistochemical study of a case. 179 Nov 35

Recently, a causative association has been made between the ingestion of levotryptophan (L-tryptophan) and the eosinophilia-myalgia syndrome (EMS), a new entity manifested by peripheral blood eosinophilia, myalgias, constitutional symptoms, and cutaneous edema with fibrosis. Contaminated levotryptophan preparations produced at a single manufacturing company between October 1988 and June 1989 have been implicated in all EMS cases. In this study, we analyzed retrospectively 49 patients with cutaneous fibrosis for a history of levotryptophan use. Levotryptophan ingestion prior to the onset of their disease was reported by 11 (65%) of 17 patients with eosinophilic fascilitis (EF), two (20%) of 10 patients with localized scleroderma, and none of 22 patients with systemic sclerosis. The onset of levotryptophan-associated cutaneous disease preceded the availability of contaminated levotryptophan preparations in seven (54%) of 13 patients. One patient with levotryptophan-associated generalized morphea also had lichen sclerosus et atrophicus and acanthosis nigricans, findings not previously reported in patients with EMS. In addition, we compared the clinical and laboratory features of levotryptophan-associated EF and idiopathic EF. Myalgias, muscle weakness, paresthesias, morpheaform plaques, cutaneous ulcers, and livedo reticularis were more common in patients with levotryptophan-associated EF. We conclude that levotryptophan-associated EF and localized scleroderma were present before the presumed date of contaminated levotryptophan availability. The clinical spectrum of cutaneous fibrosis associated with the ingestion of levotryptophan includes generalized morphea and EF, which are similar though not identical to their idiopathic counterparts.
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PMID:Idiopathic and L-tryptophan-associated eosinophilic fasciitis before and after L-tryptophan contamination. 186 73

Various procedures have been recommended for the treatment of cubital tunnel syndrome. Simple decompression in situ, medial epicondylectomy, subcutaneous transposition, intramuscular transposition, and submuscular transposition all have their advocates. The results of the surgical treatment for cubital tunnel syndrome are related to the severity of the compressive neuropathy at the time of diagnosis and to the adequate decompression of the nerve at all sites of potential compression at the time of surgical treatment. Fourteen patients who had previously undergone surgical treatment for cubital tunnel syndrome were evaluated because of persistent pain, paresthesia, numbness, and motor weakness. All patients had documented persistent compression of the ulnar nerve on clinical and electromyographic evaluation. The indication for repeat surgical exploration in all patients was unremitting pain despite nonoperative treatment. All patients had been treated by neurolysis and submuscular transposition of the ulnar nerve as described by Learmonth. The causes of continued pain after initial surgery included retention of the medial intermuscular septum, dense perineural fibrosis of the nerve after intramuscular and subcutaneous transposition, adhesions of the nerve to the medial epicondylectomy site, and recurrent subluxation of the nerve over the medial epicondyle after subcutaneous transposition. Revision surgery was found to be highly successful for relief of pain and paresthesias; however, the recovery of motor function and return of sensibility were variable and unpredictable.
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PMID:The failed ulnar nerve transposition. Etiology and treatment. 186 38

A 40-year-old man was admitted to our hospital because of paresthesia and weakness of the limbs. At the age of 38, he was diagnosed as having an idiopathic thrombocytopenic purpura (ITP) which have been refractory to oral administration of prednisolone and splenectomy. Platelet-associated IgG was elevated markedly at that time. It was, however, only mildly elevated on this admission. He showed polyneuritis, generalized pigmentation, hirsutism, and marked edema on the legs. The bone X-ray disclosed a lytic lesion in the left iliac bone, which was confirmed as a plasmacytoma by bone biopsy. Axonal degeneration with marked loss of myelinated figure was seen on sural nerve biopsy. Serum immunoelectrophoresis revealed his monoclonal IgG was lambda type. Then, he was diagnosed as having a Crow-Fukase syndrome associated with ITP. Plasma exchange, pulse therapy, and irradiation to plasmacytoma resulted in a slight improvement of the polyneuritis and the skin symptoms, and a disappearance of edema. However, ITP has not responded to these therapies. Although the same autoimmune mechanism is suggested in these conditions, we could not clarify how this monoclonal IgG produce both polyneuritis and ITP.
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PMID:[A case of Crow-Fukase syndrome associated with idiopathic thrombocytopenic purpura]. 188 77

Two clinical cases of women with primary hyperaldosteronism are reported. The patients presented with arterial hypertension, muscular weakness and paresthesia. Severe hypokalemia was found which was resistant to intravenous infusions of potassium but was successfully treated with low daily doses (100-200 mg) of spironolacton, an aldacton antagonist, in the course of 3-4 days. In one of the patients the primary hyperaldosteronism was related to aldosterone secretion by the cells of a malignant corticosteroma, proved histologically. A successful operation led to full recovery of the patient. In the other patient there was an idiopathic form of primary hyper aldosteronism caused by bilateral hyperplasia of the suprarenal cortex. Contemporary diagnostic and therapeutic possibilities in primary hyperaldosteronism as well as the importance of the examination of potassium serum level and kaliuria in the patients with arterial hypertension for the timely and successful diagnosis and treatment of primary hyperaldosteronism are pointed out.
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PMID:[2 cases of primary hyperaldosteronism]. 189 92

Three members of a family developed eosinophilic myelomeningoencephalitis following ingestion of Pila snails. They were father, daughter and son and had similar clinical presentations. Two days after ingestion of snails, they developed a generalized itchy maculopapular rash followed by myalgia, marked paresthesia, fever and headache. Two days later there was weakness of the extremities which was progressive in severity involving the legs more than the arms. They later developed urine retention and cloudiness of consciousness. Two patients progressed to coma, one of whom died after 3 weeks and the other died at home 9 months after the onset. Autopsy of the fatal case revealed multiple tracks and cavities with the presence of Angiostrongylus cantonensis in the brain and various levels of the spinal cord.
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PMID:Eosinophilic myelomeningoencephalitis caused by Angiostrongylus cantonensis: a report of three cases. 194 89

We describe a 34-year-old man from southern Florida with a history of intravenous drug use, dually infected with human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type II (HTLV-II), who developed a myelopathy clinically indistinguishable from HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). This myelopathy was characterized by spastic lower extremity weakness, distal paresthesias, sensory loss with a discrete thoracic level to pinprick, back pain, impotence, and sphincter disturbances. Nerve conduction studies revealed an associated mixed axonal and demyelinative neuropathy. Despite a lack of response to 10 months of zidovudine therapy, the myeloneuropathy improved dramatically 2 years after its onset in the absence of any therapeutic intervention.
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PMID:Tropical spastic paraparesis-like illness occurring in a patient dually infected with HIV-1 and HTLV-II. 198


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