No abstract available.
Humans ; Infant, Newborn ; Meningitis, Bacterial*

No abstract available.
Humans ; Infant, Newborn* ; Respiration, Artificial ; Survival Rate ; Ventilators, Mechanical*

Myocardial infarction is almost regularly associated with severe and widespread obstructive coronary artery disease. Recently, there have been some reports of myocardial infarction with normal of near normal coronary arteries on cineangiography. The following report concerns 6 cases (4% of a series of 142 consecutively studied patients with myocardial infarction) of myocardial infarction proved on clinical grounds with normal or near normal coronary arteries at coronary angiography obtained several months later. The clinical data was shown in Table 1 and Table 2. All 6 patients were male. Three were in the fifth, two in the sixth, and one in the seventh decade. Multiple risk factors were present in only one patient. Areas of localized dyskinesia or hypokinesia were demonstrated in five on the left ventricular cineangiography. The left ventricular end-diastolic pressure was greater than 12 mmHg in all 6 patients. One patient had hypertrophic cardiomyopathy and the remaining 5 patients had no underlying heart diseases. One patient had moderate congestive heart tailure. It is possible that prolonged, localized coronary artery spasm or platelet thrombi that subsequently resolved are a part of the pathogenic mechanism.
Blood Platelets ; Cardiomyopathy, Hypertrophic ; Cineangiography ; Coronary Angiography ; Coronary Artery Disease ; Coronary Vessels* ; Dyskinesias ; Estrogens, Conjugated (USP) ; Heart ; Heart Diseases ; Humans ; Hypokinesia ; Male ; Myocardial Infarction* ; Risk Factors ; Spasm

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

BACKGROUND: Pustular eruptions due to drugs are uncommonly reported. We studied the characteristics of clinical and histopathologic findings of pustular drug eruption. OBJECTIVE: We observed th.e causative agents, clinical featurs and histopathologic findings of pustular drug eruption and identified differential points of generlized pustular eruption. METHODS: We evaluated t,he clinical and histopathologic findings of 8 patients with pustular drug eruption and reviewed the literatures reported cases of pustular drug eruption. RESULTS: All patients diagnosed pustular drug eruption suffered from generalized pustular eruption associated with systemic symptoms such as fever, headachened myagia one to three days after treatment with causative agents. The causative agents of putular drug eruption are antibiotics such as ceftriaxone, analgesics and antipyretics. The pustule resolved after a few days of treatment with systemic corticosteroids and antihistamines. Laboratory findings revealed leukocytosis, neutrophilia, and analevated erythrocyte sedimentation rate, On histopatologic findings, we observed subcorneal pustuls containing neutrophils, eosinophils and some lymphocytes and spongiosis, exocytosis of acute iiflammatory cells. Perivascular infiltration of lymphocyte ancl edema of papillary dermis was also bserved in the dermis. CONCLUSION: Pustular drug eruption is characterized by generalized pustular eruption associated with systemic symptoms and histopathologic findings of that are sterile subcorneal pustules. Therefore differential diagnosis of other generalized pustular erupticns are relatively easy by careful history of medication, clinical and histopathologic findings.
Adrenal Cortex Hormones ; Analgesics ; Anti-Bacterial Agents ; Antipyretics ; Blood Sedimentation ; Ceftriaxone ; Dermis ; Diagnosis, Differential ; Drug Eruptions* ; Edema ; Eosinophils ; Exocytosis ; Fever ; Histamine Antagonists ; Humans ; Leprosy ; Leukocytosis ; Lymphocytes ; Neutrophils

BACKGROUND: Pustular eruptions due to drugs are uncommonly reported. We studied the characteristics of clinical and histopathologic findings of pustular drug eruption. OBJECTIVE: We observed th.e causative agents, clinical featurs and histopathologic findings of pustular drug eruption and identified differential points of generlized pustular eruption. METHODS: We evaluated t,he clinical and histopathologic findings of 8 patients with pustular drug eruption and reviewed the literatures reported cases of pustular drug eruption. RESULTS: All patients diagnosed pustular drug eruption suffered from generalized pustular eruption associated with systemic symptoms such as fever, headachened myagia one to three days after treatment with causative agents. The causative agents of putular drug eruption are antibiotics such as ceftriaxone, analgesics and antipyretics. The pustule resolved after a few days of treatment with systemic corticosteroids and antihistamines. Laboratory findings revealed leukocytosis, neutrophilia, and analevated erythrocyte sedimentation rate, On histopatologic findings, we observed subcorneal pustuls containing neutrophils, eosinophils and some lymphocytes and spongiosis, exocytosis of acute iiflammatory cells. Perivascular infiltration of lymphocyte ancl edema of papillary dermis was also bserved in the dermis. CONCLUSION: Pustular drug eruption is characterized by generalized pustular eruption associated with systemic symptoms and histopathologic findings of that are sterile subcorneal pustules. Therefore differential diagnosis of other generalized pustular erupticns are relatively easy by careful history of medication, clinical and histopathologic findings.
Adrenal Cortex Hormones ; Analgesics ; Anti-Bacterial Agents ; Antipyretics ; Blood Sedimentation ; Ceftriaxone ; Dermis ; Diagnosis, Differential ; Drug Eruptions* ; Edema ; Eosinophils ; Exocytosis ; Fever ; Histamine Antagonists ; Humans ; Leprosy ; Leukocytosis ; Lymphocytes ; Neutrophils

BACKGROUND: Xerosis is a relatively common disorder, especially in the elderly. The condition is characterized by fine scaling and is associated with generalized pruritus. OBJECTIVE: The purpose of this study was to evaluate the clinical efficacy, safety and tolerability of Zalsming cream in patients with xerosis and pruritus. METHODS: Thirty patients were treated with Zalsming cream. Clinical efficacy, as measured by the score of subjective symptom and objective signs, transepidermal water loss(TEWL) and electron microscopic finding, were asessed at 2, 4, and 6 weeks after topical application of the cream. RESULTS: The scores of clinical signs and TEWL showed statistically significant improvements. No one developed any local or systemic side effects. CONCLUSION: Topical application of Zalsming cream was found to be effective and safe for patients suffering from xerosis and pruritus.
Aged ; Humans ; Pruritus*

Common adverse effects due to topical therapy with DPCP(Diphenyprone) are severe contact dermatitis, dermographism, urticaria, generalized pruritus, lymphadenoiathy, and dermatitis on the remote areas. Rarely, DPCP can induce vitiligo or dyschromia in confetias side effects on the pigmentary system. It is not clear yet whither DPCP induced the vitiligcbatoxic effect of phenol ring in DPCP or by koebner phenomenon clue to repeated contact dermatitis in cases where vitiligo was in latent subclinical condition. We describe a patient with alopecia areatairho developed vitiligo due to topical therapy with DPCP. A 20-year-old woman developed alopecia areata with a loss of eye shows and eyelashes. After sensitization, DPCP was topically applieid to the scalp every week. Vitiligo, confirmed by electron microscopic study, appeared 4 month. after the beginning of treatment and was localized only to the areas of topical application. Both alogecia aieata and vitiligo are improving now under systemic and topical corticosteroid therapy.
Alopecia Areata* ; Alopecia* ; Dermatitis ; Dermatitis, Contact ; Eyelashes ; Female ; Humans ; Phenol ; Pruritus ; Scalp ; Urticaria ; Vitiligo ; Young Adult

Conventional dual chamber pacing (DDD) preserves atrioventricular synchrony but depend on appropriate sinus node function to achieve physiological heart rate with exercise by atrial tracking. Other indirect indicators of metabolic demand have been used to modulate pacing rate increases with exercise including sensing of pH, respiratory rate, ventricular repolarization and oxygen saturation. The activity sensing approach is unique in that noise generated by activity modulates the response and empirical programming of the unit allows for attaining the desired rate for a given level of activity. Physiologic rate increases can be obtained in patients with sinus node dysfunction or even atrial fibrillation. The lead can either be positoned in the atria for patients without atrial fibrillation or AV conduction disturbance or in the ventricle. We present two cases of rate responsive pacing using the Activitrax.
Atrial Fibrillation ; Heart Rate ; Humans ; Hydrogen-Ion Concentration ; Noise ; Oxygen ; Respiratory Rate ; Sick Sinus Syndrome ; Sinoatrial Node