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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2007  |  Volume : 18  |  Issue : 2  |  Page : 151-158
Childhood Henoch Schonlein Purpura in Middle East Countries


University of Jordan, Amman, Jordan

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   Abstract 

HSP is the most common systemic vasculitis in children that is characterized by small vessel leukocytoclastic vasculitis. However, it is a self limiting disease, with few documented cases in Middle Eastern countries. Classic symptoms of the disease have been established in the literature, but new clinical features have recently been reported from Middle Eastern countries which include penile swelling, temperomandibular joint involvement, skin rash over the flexor surfaces of the extremities, and pleural hemorrhagic effusion. Familial Mediterranean fever (FMF) may present as HSP. The prevalence of the FMF gene in Middle Eastern countries raises interesting questions regarding the use of colchicine in HSP patients.

Keywords: Henoch, Shonlein, Purpura, Middle East countries

How to cite this article:
Akl K. Childhood Henoch Schonlein Purpura in Middle East Countries. Saudi J Kidney Dis Transpl 2007;18:151-8

How to cite this URL:
Akl K. Childhood Henoch Schonlein Purpura in Middle East Countries. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2020 May 26];18:151-8. Available from: http://www.sjkdt.org/text.asp?2007/18/2/151/32303

   Introduction Top


Henoch Schoenlein purpura (HSP) is the most common systemic vasculitis in children.[1] It is a leukocytoclastic vasculitis characterized by IgA deposition. It affects small blood vessels (arterioles, venules and capillaries) and causes damage and narrowing of the lumen. It usually involves skin, gastrointestinal tract, joints and kidneys. In children, the diagnosis is clinical. In rare cases one may confirm the diagnosis with a skin or renal biopsy. [1]

In this report, clinical manifestations of HSP in Middle East countries are reviewed. The data was obtained from a Medline search and local medical journals.


   Features of HSP Top


The incidence of HSP varies by country. Around 15 cases /100,000 children/year are reported in Norway [2], and it afflicts up to 20.4/100,000 children between 4-6 years in the United Kingdom.[3] It affects children more than adults, and males more than females. It is most common in children between the ages of 2 to 8.

The etiology of HSP is still unknown, though various triggering factors have been implicated in the precipitation of the disease, which include viruses, Group A beta hemo­lytic streptococci, drugs, vaccines, and insect bites.[4] Rare cases of acute poststreptococcal glomerulonephritis may present as HSP..[5],[6] Deposition of the IgA 1 subclass[7] is noted in the skin, kidneys, and other affected organs. There is evidence for genetic predisposition since the disease has been reported in mono­zygotic twins[8], and in members of the same family after exposure to a precipitating factor.[9]

There is an obscure relationship between HSP and IgA Nephropathy.[10] Both IgA nephro­pathy and HSP are poorly understood in their pathogenesis, which may involve synthesis of abnormal IgA molecules. Both Ig A nephro­pathy and HSP have abnormal IgA glycol­sylation (IgA1 rather than IgA2 ),[7] may occur in members of the same family,[9] and may represent variants of the same disease process

with different clinical manifestations.[11],[12],[13] However, HSP is a multisystem disease, where as only the kidney is involved in IgA nephro­pathy.[14],[15]

Familial  Mediterranean fever More Details (FMF) patients and carriers of the FMF gene muta­tion may present as HSP patients in 5-10% of the cases.[16],[17]

The classic skin rash is the presenting feature in 50% of patients, and can initially be urti­carial, macular, vesiculobullous, or hemo­rrhagic, which also may be petechial, purpuric, or ecchymotic.[7] The rash may recur once or more up to ten years after disease onset.

The gastrointestinal tract is involved in about 63% of HSP cases.[7] It may precede the rash in 36 % of reported cases. The involve­ment varies from mild abdominal pain to acute abdominal pain.[18] Severe involvement includes intussusception, [19] which is usually ileoileal rather than ileocolic in 65% of cases. Abdominal ultrasound [22],[21] or barium enema [22] aid in the diagnosis. Protein losing entero­pathy, hemorrhagic ascites, [23] and jejunal hemorrhage [24] may occur, and ileal strictures may ensue as a late complication of HSP.[25] Massive gastric hemorrhage may occur.[26]

Joint involvement may occur as arthralgia or arthritis. Larger joints are involved in 50­82% of cases,[7] with ankles and knees most commonly affected.[18] It is the presenting feature in 25% of patients.

Renal involvement usually manifests within three months of the rash. It occurs in 20% to 50% of older children and in 25% of children aged less than two years.[18] Children older than 5 years of age are more susceptible to severe renal manifestations.[26] Renal manifestations range from microscopic to gross hematuria, from mild proteinuria to the nephrotic syndrome, and from normal renal function to advanced renal dysfunction. Risk factors for renal manifestations include age > 4, severe abdominal pain with gastrointestinal bleeding and recurrent purpura.[27],[28] There is no apparent relationship between the severity of the nephritis and that of extrarenal manifestations.

Edema of penis, [29] priapism, [30] and renal colic secondary to blood clots may occur.[31],[32] Acute scrotal swelling, which may be the presenting feature, occurs in 2% to 38% of cases.[32],[33],[34],[35] Pulmonary involvement may occur in HSP [36],[37] but pulmonary hemorrhage is rare [38], and survival has been reported to occur in 75% of cases.[39] Chylothorax has been reported once.[40]

The most common central nervous system manifestation is headache. Seizures may occur as well as focal neurological deficit, and behavioural changes as a result of cerebral vasculitis.[41],[42] Symmetrical muscle involve­ment may occur in patients with HSP.[43],[44],[45]

Thrombocytosis occurs in 67% of cases. It is strongly associated with abdominal pain and gastrointestinal bleeding but does not correlate with nephritis or arthritis.[46] The qualitative function of platelets was found to be disturbed in one report.[47] At onset there may be neutrophilic leukocytosis. The bleeding, clotting, prothrombin, and partial thromboblastin times are normal. Factor 13, a fibrin stabilizing factor is significantly decreased in children with HSP.[48] The erythro­cyte sedimentation rate may be normal or elevated. Hemorrhagic diathesis may be associated with hemorrhaging into multiple organs such as the lungs, [38] ascites, [23] bullae, [49] muscles, Subcutaneous tissue, eyelids, conjun­ctivae, and scrotum.

Involvement of the eye is rare. Ocular manifestations include recurrent episcleritis, anterior uveitis, and keratitis.[50]

There are no specific laboratory markers to diagnose HSP. The white blood cell count may be normal or elevated.[51] Serum albumin may be decreased if there is an association with nephrotic syndrome or protein losing enteropathy.[52] Serum complement levels are usually normal. Factor XIII is decreased in around 50% of the cases, and factor VIII is also decreased in some cases. Stool guaiac may reveal occult blood.

The disease is usually self limited and therapy is symptomatic. Supportive care to control fluids and electrolytes along with antihypertensive agents may be required. Steroids do not prevent recurrences.[7],[53],[54] Although controversial, a short course of steroids may hasten the resolution of the abdominal pain as shown in a review of published studies by Haroon[55] and from other retrospective studies and case reports. Factor XIII may help in cases showing steroid resistance.[56] Arthralgias may be treated with analgesics, and will not benefit from steroids. There is some controversy as to whether the early use of steroids prevents renal complications. [57] A recent randomized placebo controlled trial of prednisone in early HSP could not reduce the risk of renal involvement at one year.[58] Steroid use is not beneficial in established mild nephri­tis,[7],[26] but a high dose of methylpredni-solone along with azathioprine or cyclophospha­mide may help in severe renal involve-ment, especially if glomerular crescents are greater than 50% on renal biopsy. [7],[60],[61],[62],[63],[64] Plasmapheresis may be also beneficial but the effect is transient.[65],[66]

The prognosis of HSP in children is excellent; however, it is largely affected by clinical presentation.[67],[68] The outcome is worse in adults.[69] Risk factors that may result in renal failure include hypertension, elevated serum creatinine, or nephrotic syndrome at the onset of disease. In patients with both nephritic and the nephrotic syndromes 50% will develop end-stage renal disease (ESRD) within 10 years; in patients with the nephritic syndrome, 15 % will develop ESRD. It is important to follow up the HSP patients for a long period of time as chronic kidney disease (CKD) may develop later, although the presentation may be mild at the onset of the disease.[67] CKD usually occurs in 1%, and ESRD in < 1%.[70] Moreover, HSP nephritis may recur after renal transplantation. If the FMF gene is present in certain cases of HSP, colchicine therapy should be considered.[16]


   HSP in Middle East countries Top


HSP has a seasonal incidence in Middle East countries, with a clustering of cases in the summer and winter,[70],[71],[72] which is similar to the literature from other parts of the world.[1],[2] The majority were males. Annual incidence ranged from 6.7- 8.5 / 100, 000 children less than 12 years of age.[73],[74] This is much lower than that reported in the literature.[2],[3] In Saudi Arabia, the age of onset is more than five years in 73 % of cases.[75] Antecedent upper respiratory tract infection, usually viral, has been reported in Jordan , Kuwait , Saudi Arabia, Qatar, and Bahrain.[70],[71],[72],[73],[74],[75],[76] Streptococcal infection has been emphasized from Northern Jordan[74] as an important triggering factor in that area. IgA nephropathy has been reported in two adults with FMF from Jordan.[77] Mesangial prolife­rative glomerulonephritis was reported in a child with FMF from Turkey.[78] In a report from Northern Jordan seven out of 192 children with FMF developed the rash from HSP.[79] In another report of 102 patients with FMF, HSP occurred in 3.9%. One FMF child presented as HSP.[80] Ozdogan et al from Turkey, mentioned the occurrence of HSP in fifteen out of 207 (7.2 %) patients with FMF.[81] It is known that vasculitis may coexist with FMF.[16],[81] Skin rash occurred in all patients with similar patterns as reported elsewhere in the world. [7],[72],[73] However, the distribution of the typical rash over the flexor surfaces of the lower extremities may be unique to a series in the Middle East.[73]

Gastrointestinal involvement ranges from 30% to 73%.[70],[71] It included abdominal pain, gastrointestinal bleeding in the form of hema­temesis or hematochezia that requires blood transfusions,[72] as well as intussusception,[70] ,[72],[76] which is similar in incidence to that mentioned in the literature.[7],[18],[19]

Affliction of the tempomandibular joint has not been reported before.[73]

Renal involvement in studies from the Middle East show similar patterns to that reported elsewhere but at lower percentages, which range from 17% to 24%. [28]

The urologic manifestations include penile swelling, first reported from Qatar,[72] then from Jordan, [71],[72],[77] and Bahrain.[29] One child from Qatar had stenosing ureteritis with resultant hydronephrosis and hypertension.[73]

Regarding pulmonary manifestations, one patient from Jordan had recurrent chest pain and gross hematuria that responded to a short course of steroids.[71] Pulmonary hemorrhage was reported from Saudi Arabia,[82] and Turkey.[83] Pleural hemorrhage , which has not been reported before, was reported from Qatar in a child with HSP.[84]

Neurological manifestations were not mentioned in reports from Middle East countries. Calf muscle pain has been reported from Qatar in 12.5% of cases, and was symmetrical as was mentioned in the literature.[43],[44],[45]

Ocular involvement, which is rare, occurred as subperiosteal orbital hematomas in a communication from Lebanon.[85]

The laboratory findings are similar to what was reported elsewhere.[7] Thrombocytosis occurred mainly in children with gastro­intestinal hemorrhage,[72] which was similar to other reports.[46],[51] Antistreptococcal titers were negative in most reports except for one from Northern Jordan.[75] Group A beta hemolytic streptococci was mentioned as one of many precipitating factors.[4],[5],[6]

In a retrospective report from Qatar, steroid therapy seemed to hasten the recovery from abdominal pain, but had no effect on renal manifestations.[73]

In summary, the reports from Middle Eastern countries regarding HSP are lacking, however, they include new clinical features that have not been reported previously. These include symptoms such as rash on the flexor surfaces of the lower extremities, penile swelling, tempoman­dibular joint involvement, and pleural hemorrhage. The prevalence of the FMF gene in the Middle East and the fact that FMF may present as HSP raises interesting questions regarding the treatment of such patients with colchicine[86].

 
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Correspondence Address:
Kamal Akl
Consultant Pediatric Nephrologist, University of Jordan, P.O. Box 831373, Amman 11183
Jordan
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PMID: 17496388

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