Clinical Patterns

Acne is a polymorphic disease that occurs on the face (99%),back (60%) and chest (15%). 

Acne vulgaris is the most common type of acne. The individual lesions of acne vulgaris are divisible into three types non-inflamed lesions, inflamed lesions and scars (Table 11.2). 

Atrophic scars (icepick, rolling, boxcar) Hypertrophic scars (keloids) 

Non-inflamed lesions are called comedones. Comedones may be microscopic (microcomedones) or evident to the eye as blackheads or whiteheads (Figs. 11.1,11.2). The microcomedo 

Most patients have a mixture of non-in-flamed and inflamed lesions. Inflamed lesions can be superficial or deep, and arise from non-inflamed lesions. The superficial lesions are usually papules and pustules (5 mm or less in diameter), and the deep lesions are large pustules and nodules. Papules are small, raised, red spots, while pustules are predominantly yellow (Figs. 11.3,11.4). Pustules frequently start as solid lesions, like papules, which soon liquefy. Usually, the roof of the pustule bursts, allowing the pus to escape. The pustule represents a par- 

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Myoclonic epilepsy with ragged-red fibers (MERPF) is a rare syndrome which shows clear maternal inheritance and a variable clinical pattern including progressive myoclonus, cerebellar ataxia, dementia, and muscle weakness. It is associated with an A-to-G transition at position 8344 of the tRNA Lys gene in the mtDNA. The mutation is heteroplasmic and produces similar multicomplex deficiencies as are seen in KSS. 

Clinical features of melasma usually evolve rapidly, especially after UV exposure. Lesions are uniformly light to dark brown, often symmetric, and three clinical patterns can be distinguished ... 

In adult patients, the manifestations of PCP use can be grouped into nine clinical patterns of intoxication. Four of these are called major patterns because they may be associated with severe toxicity and often necessitate hospitalization. Patients with major patterns are usually unpredictable symptoms wax and wane, and the patient may abruptly change from one pattern of intoxication to another. Five other symptom complexes are designated as minor patterns since toxicity is usually mild and of short duration. Major Patterns consist of coma, catatonic syndrome, toxic psychosis, and acute brain syndrome. Minor Patterns are lethargy, bizarre behavior, violent behavior, agitation, and euphoria (McCarron et al. 1981b). 

McCarron, M.M. Schulze, B.W. and Thompson, G.A., Conder, M.C. and Goetz, W.A. Acute phencyclidine intoxication Clinical patterns, complications, and treatment. Ann Emerg Med 10 290-297, 1981b. 

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. 

Quod, J.P. and Turquet, J., Ciguatera in Reunion Island (SW Indian Ocean) epidemiology and clinical patterns, Toxicon, 34, 7, 779, 1996. 

Occupational exposure of 12 male workers, whose hands were in contact with MDA several hours per day, caused toxic hepatitis. The clinical pattern of the cases included right upper quadrant pain, high fever, and chills with subsequent jaundice. A skin rash was seen in five of the cases. Percutaneous absorption was considered to be the major route of exposure because workers in the same occupational setting who did not have direct skin contact with MDA were not affected. All patients recovered within 7 weeks, and follow-up more than 5 years later showed no biochemical or clinical evidence of chronic hepatic disease. 

Liver injury is clinically defined as an increase of serum alanine amino transferase (ALT) levels of more than three times the upper limit of normal and a total bilirubin level of more than twice the upper limit of normal [4]. The clinical patterns of liver injury can be characterized as hepatocellular (with a predominant initial elevation of ALT), cholestatic (with an initial elevation of alkaline phosphatase) or mixed. The mechanisms of drug-induced hepatotoxicity include excessive generation of reactive metabolites, mitochondrial dysfunction, oxidative stress and inhibition of bile salt efflux protein [5]. Better understandings of these mechanisms in the past decades led to the development of assays and models suitable for studying such toxic mechanisms and for selecting better leads in the drug discovery stage. 

According to Kuhn s observations, the effect of imipramine became apparent in some cases after a few days in other cases several weeks passed before any therapeutic effect could be seen. He estimated his failure rate at 20 25%, but regarded his sample as too small for any reliable estimate to be made. If the medicament was discontinued too soon, there was said to be a danger of relapse. It was also not possible to ascertain from his observations whether imipramine shortened the natural duration of the depressive phase. The best therapeutic successes were recorded in endogenous depression and in cases of depression which first appeared at the menopause, in cases where vital symptoms were clearly in the foreground". Kuhn also provided a comprehensive list of side effects of imipramine. which nevertheless in his view did not appreciably restrict use of the medicament. (None of the claims regarding the clinical pattern of action of imipramine made by Kuhn on the basis of open... 

Regarding these pathomechanisms, the clinical pattern of symptoms observed after ingestion of harmful food may be helpful in clinical classification to differentiate the onset of immediate (quick), semi-delayed, and delayed (late) reactions (Table 3.3.1) (Sicherer, 2002 Bock, 2003 Hpst et al., 2003 Nowak-Wegrzyn, 2003 Bindslev-Jensen et al., 2004 Chapman et al., 2006). 

Staden, U., C. Rolinck-Weminghaus, F. Brewe, U. Wahn, B. Niggemann, and K. Beyer. 2007. Specific oral tolerance induction in food allergy in children Efficacy and clinical patterns of reaction. Allergy 62 (11) 1261—1269. 

The classic clinical pattern of PICA territorial infarct is the Wallenberg s syndrome. However, symptoms... 

Della Sala S, Francescani A, Spinnler H (2002) Gait apraxia after bilateral supplementary motor area lesion. J Neurol Neurosurg Psychiatry 72 77-85 Devuyst G, Bogousslavsky J, Meuli R et al (2002) Stroke or transient ischemic attacks with basilar artery stenosis or occlusion clinical patterns and outcome. Arch Neurol 59 567-573... 

In the past several clinical patterns have been described. The most important recognized clinical patterns or types of Al toxicity include two types of encephalopathy. Firstly, the classical dialysis dementia sometimes referred to as dialysis encephalopathy syndrome (DES) or dementia dialytica [24, 28, 37, 42, 70-74] and secondly, the acute or subacute Al encephalopathy [41]. There are also two types of bone disease - either osteomalacia with bone fractures and proximal myopathy or aplastic bone disease [41, 75, 76]. There is quite some confusion in the definitions of Al toxicity in the literature. Because there seems to be an obligatory lag phase of at least several days to weeks for symptoms to occur, acute Al encephalopathy, defined as a direct result of a single overdose, probably does not exist. Because of the long lag phase of several months to years necessary to develop the chronic dialysis encephalopathy and also because acute Al encephalopathy has an abrupt, sudden onset of symptoms one can understand why the term acute is used instead of the more descriptive subacute . The descriptions dialysis dementia [37, 42, 46, 73, 74] and dialysis encephalopathy [33-36, 38, 40, 41, 78] are also unfortunate because true dementia is rare in Al encephalopathy [73] and non-dialyzed patients can also develop these symptoms [78]. There are also many dialysis-related encephalopathy syndromes unrelated to Al. As an example,... 

Tsai MJ, Huang YB, Wu PC. A novel clinical pattern of visual hallucination after zolpidem use. J Toxicol Clin Toxicol 2003 41 (6) 869-72. 

Four major and five minor clinical patterns of acute phencyclidine intoxication have been described in 1000 patients (7). Major patterns were acute brain syndrome (24.8%), toxic psychosis (16.6%), catatonic syndrome (11.7%), and coma (10.6%). Minor patterns included lethargy or stupor (3.8%) and combinations of bizarre behavior, violence, agitation, and euphoria in patients who were alert and oriented (32.5%). Patients with major patterns of toxicity usually required hospitalization and had most of the complications. Patients with minor patterns generally had mild intoxication and did not require hospitalization, except for treatment of injuries or autonomic effects of phencyclidine. There were various types of injuries in 16%, and aspiration pneumonia in 1.0%. There were 22 cases of rhabdomyolysis (2.2%), and three patients required dialysis for renal insufficiency. One patient who had been comatose died suddenly with a pulmonary embolism. 

Most channelopathies known to date do not lead to death, but rather they require an abnormal situation, a so-called trigger, to present with recognizable symptoms. Frequently, the attacks can be provoked by rest after physical activity or by exercise itself, hormones, stress, and certain types of food. Most channelopathies have a certain clinical pattern in common Typically, the symptoms occur as episodic attacks lasting from minutes to days that show spontaneous and complete remission, onset in the first or second decade of life, and—for unknown reason—show amelioration at the age of 40 or 50 years. Surprisingly, many patients with channelopathies respond to acetazolamide, a carbonic anhydrase inhibitor. Most channelopathies show no chronic progression however, a few exceptions exist. Chaimelopathies are caused by mutations or by autoantibodies. Although rare, they are important models for frequent disorders. 

J., Tygstrup, N., Wiiiiams, R. Clinical pattern and course of disease in primary biliary cirrhosis based on an analysis of 236 patients. Gastroenterology 1980 78 236-246... 

Jara, P, Rest , M., Hierro, L., Giacchino, R., Barbara, C., Zancan, L., Crivellaro, C., Sokal, E., Azzari, C., Guido, M., Bortolotti, F. Chronic hepatitis C virus infection in childhood clinical patterns and evolution in 224 white children. CUn. Infect. Dis. 2003 36 275 -280... 

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